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5 Minerals INTRODUCTION horses, balance studies need to be conducted that compare the amount of mineral consumed by the animal to the While constituting only a minor part of the equine diet amount of mineral lost in the feces and urine and deter- by weight, minerals play a critical role in the health of mined via total collections of both feces and urine. Collect- horses. Minerals are involved in a number of functions in ing the total amount of urine voided in a 24-hour period can the body, including physiological roles such as in acid-base be labor intensive. The use of a urinary fractional electrolyte balance, formation of structural components, enzymatic co- excretion test (FE test) has been used, which requires col- factors, and energy transfer. Some minerals are integral lecting only a single urine sample. Unfortunately, fractional parts of vitamins, hormones, and amino acids. The horse excretion values of minerals do not always agree with re- obtains most of the necessary minerals from forages and sults obtained through total volumetric urinary collection, concentrates. The mineral content of feeds and the avail- suggesting less accuracy (McKeever et al., 2002; McKenzie ability of minerals vary with soil mineral concentrations, et al., 2003). Some minerals are present in such minute con- plant species, stage of maturity, and conditions of harvest- centrations that determining requirements through balance ing. The resulting variations in feed mineral content should studies is extremely difficult. Furthermore, mineral balance be considered in assessing an animalâs mineral status and studies have not been done in all ages and classes of horses. formulating appropriate diets, as minerals are elements that In such cases, requirements are estimated by examining cannot be created or destroyed under normal circumstances what amounts have been fed without negative effects being and must be provided in the ration. Minerals are typically observed and, as a result, might be more appropriately classified as macromineralsâthose typically found and termed ârecommendations.â Sulfur and many of the mi- needed in concentrations in the diet measured in g/kg or crominerals would fit this description. For minerals such as percentageâand micromineralsâthose measured in ppm these, the research has tended to examine concentrations in or mg/kg. While the amounts of individual minerals in the the diet. Besides still being provided as a concentration, the ration are important, the ratios of all minerals should be committee has made a transformation, based on expected taken into consideration, as minerals often influence the ab- daily intakes, in an attempt to determine what would be a sorption, metabolism, and/or excretion of other nutrients. reasonable recommendation for a daily allotment on a body Therefore, excesses or deficiencies of certain minerals can weight basis. The committee encourages researchers to re- alter the requirements of others. When appropriate, the port data from future studies on a body weight basis instead maximum tolerable concentration of a mineral is provided of simply as a dietary concentration to aid in determining from the publication Mineral Tolerance of Animals (NRC, actual requirements. The committee also encourages more 2005). This concentration is defined as the dietary amount studies aimed at determining mineral requirements for that, when fed for an extended period of time, will not im- growth, exercise, and pregnancy, as these are areas in which pair animal health and performance. This differs from a data seemed to be insufficient to adequately determine min- toxic amount. Also, this tolerable concentration is based eral requirements. For instance, in pregnancy, it is recog- upon all other nutrients in the diet being at or near the ani- nized that additional minerals are needed for embryonic and malâs requirement. When other minerals are provided at fetal growth, including those needed in the uterine fluid and higher or lower concentrations, absorption of the mineral in for growth of the uterus. Though the additional amount question can be altered, thus influencing the maximum tol- needed might be small, it is likely important, but not enough erable concentration. To determine mineral requirements of data are available to make strong conclusions. 69
70 NUTRIENT REQUIREMENTS OF HORSES When sufficient data are available, the apparent di- Serum ferritin status is believed to be a better indicator of gestibility of a given mineral can be calculated by subtract- iron status than is blood or plasma iron concentration. With ing the amount of a mineral in the feces from the amount fed most minerals, ration evaluation and case history are still to the horse, then dividing that difference by the total often needed to confirm problems. Additionally, proper amount ingested. While easier to determine than the true di- sampling techniques and analysis need to be performed to gestibility, the apparent digestibility often is lower as some ensure the greatest likelihood of meaningful results. of the nutrient found in the feces can come from endogenous In some studies on mineral requirements of horses, the losses instead of a mineral that was not absorbed. To deter- daily intake of the mineral of interest is reported on a body mine the true digestibility of a mineral, endogenous losses weight basis. However, in other studies, intake is reported as need to be determined and, to do so, various concentrations a concentration of the diet. Whenever possible, daily intake of a mineral are fed. The regression line obtained by plotting was converted to a body weight basis using feed intake and the amount of a mineral apparently absorbed (Y-axis) body weight information presented in individual studies. against the amount of a mineral fed (X-axis) can be used to When feed intake was not reported, assumptions were made estimate endogenous mineral losses, or the point where the as to the average intake of each class of horse so that it was mineral intake is at zero. In this procedure, various assump- possible to provide an estimate of the amount of a given tions have to be made. One assumption is that absorption of mineral needed per kg of body weight (BW). Obviously the mineral follows a linear function. Another assumption is these estimates of feed intakes are not constant among that endogenous secretions are constant. True digestibility is horses but are needed to provide estimates of daily nutrient then represented as the amount absorbed (which is the intakes. Horses at maintenance were assumed to eat 2 per- amount of mineral fed minus the amount of mineral in feces cent of their BW/d in dry matter feed, while growing horses and in the endogenous secretions) divided by the amount were assumed to eat 2.5 percent, pregnant mares were as- fed. Alternatively, true digestibility of the nutrient can be sumed to eat 2 percent of their nonpregnant body weight, represented by the slope of the regression of the amount of and lactating mares were assumed to eat 2.5 percent feed on mineral absorbed on dietary mineral intake (Pagan, 1994). a dry matter basis. With increasing intensities and durations By plotting retention (Y-axis) against intake (X-axis), a pre- of exercise, dry matter intake typically increases, though this diction can be made as to what dietary intake would result does not necessarily occurâparticularly if fat is substituted in no mineral being retained and the mineral balance would for carbohydrates in the diet. For light exercise, a dry matter be zero, thus representing minimal requirements (Hintz and intake of 2 percent was assumed, while 2.25 percent and 2.5 Schryver, 1972). Limitations to these methods include im- percent of BW/d were assumed to be the intake of moderate proper mineral recovery from the urine or feces due to im- and heavily working horses, respectively. As noted previ- proper laboratory procedures (OâConnor and Nielsen, 2006) ously, these assumptions were only used when there was in- or not accounting for minerals lost through avenues other sufficient information reported in an individual study to cal- than the urine or feces. Concentrations of minerals such as culate mineral intake on a body weight basis. These sodium and chloride need to be examined in other body se- estimates of intake are somewhat liberal and thus may over- cretions such as sweat, particularly in the exercising animal estimate the actual feed intake of study animals. However, (Coenen, 2005). Animals retaining more mineral than they by using a liberal estimate of intake, it seemed less likely are losing are considered to be in a positive mineral balance. that a requirement expressed on a body weight basis would This is expected when an animal is growing and accreting be underestimated. As there is an apparent lack of research minerals in various tissues. Once an animal is mature and in in determining mineral requirements of breeding stallions, a homeostatic state, it is more likely that an animal should they can be considered to be similar to maintenance values, be in a near zero balance, though a slight positive balance though it is possible some differences do exist. may exist due to unaccounted-for mineral losses in tissues, such as hair or hoof growth. While analyzing substances, MACROMINERALS such as the hair of horses, has been performed by some in- vestigators in an attempt to determine mineral status of Calcium horses (Asano et al., 2002), such techniques are of question- able use as they can be influenced by factors, such as coat Function color, that are independent of nutrition (Cape and Hintz, 1982; Asano et al., 2005). In contrast, mineral concentra- About 99 percent of the calcium (Ca) in the body is found tions in the blood can sometimes be useful in determining in the bones and teeth, with calcium constituting about 35 whether a dietary deficiency or excess is present. Blood percent of equine bone (El Shorafa et al., 1979). Calcium samples are more likely to provide information about phos- also plays an important role in various functions within the phorus, magnesium, potassium, sodium, chloride, copper, body such as muscle contraction, the function of cell mem- manganese, selenium, and zinc status of a horse than they branes, blood coagulation, and the regulation of many en- are the calcium, iodine, and cobalt status (Lewis, 1995). zymes. Calcium homeostasis within the blood is critical. The
MINERALS 71 skeleton, besides serving as structural support for the body, cium digestibility of 72 percent for alfalfa compared to only can serve as a readily available storage location for calcium. 40 percent for Bermudagrass. When mature ponies were fed 316 and 535 mg Ca/kg BW/d, van Doorn et al. (2004b) re- ported the apparent digestibility of calcium was around 28 Sources and Factors Influencing Absorption percent as compared to 42 percent when the ponies were fed Calcium carbonate, sulfate, and oxide are common inor- 148 mg Ca/kg of BW/d (dietary concentration equal to 0.78 ganic forms of calcium (Highfill et al., 2005). A calcium- percent calcium, which is still excessive for a maintenance amino acid proteinate did not differ from calcium carbonate diet). All ponies were in positive calcium balance, though in absorption rate though more calcium was absorbed in the calcium retention was greatest at the highest concentration two supplemented groups than in a nonsupplemented diet of calcium fed. As mature animals would be expected to (Highfill et al., 2005). Free-choice feeding of calcium supple- maintain a balance close to zero by adapting the digestibil- ments is not an effective means of ensuring adequate intake ity or urinary excretion, van Doorn et al. (2004b) suggested (Hintz, 1987a). Calcium supplements should be mixed with that when the amount of absorbed calcium exceeds the grain or other palatable materials to help ensure consumption. amount that can be excreted with urine, the additional cal- The portion of dietary calcium that is absorbed varies in cium is retained, resulting in a positive balance. In what tis- order to maintain normal calcium homeostasis (Jones and sue(s) the extra calcium is retained is unclear, though it is Rasmusson, 1980). In response to lowered ionized serum expected that the animals would need to eventually return to calcium concentrations, parathyroid hormone (PTH) secre- a homeostatic state if they were examined long enough, un- tion is stimulated in order to reestablish normal concentra- less calcium is lost from hair, hoof, or sweat and not ac- tions through stimulation of bone resorption and renal tubu- counted for. While Hintz and Schryver (1973) reported that lar calcium reabsorption (Bushinsky and Monk, 1998). increasing the dietary concentration of magnesium in- Vitamin D mediates intestinal absorption of calcium and creased calcium absorption, the absorption efficiency of cal- adaptation to dietary intake in most species, though Brei- cium decreases as phosphorus increases in the diet due to denbach et al. (1998) suggest that it does not play a key role the competitive nature of calcium and phosphorus absorp- in regulating calcium and inorganic phosphate homeostasis tion in the small intestine. This likely varies somewhat de- in the horse. Horses have a moderate or lacking increase of pending upon mineral source. Schryver et al. (1987b) re- plasma calcium and at the same time a pronounced increase ported true calcium digestibility increasing from 51 to 69 in plasma inorganic phosphate during vitamin D intoxifica- percent as the percentage of sodium chloride in the diet in- tion, potentially suggesting a different regulatory role of vi- creased. Dietary oxalate decreases absorption of calcium tamin D in horses than in other species (Harmeyer and quite dramatically and can play a role in a deficiency of ab- Schlumbohm, 2004). More research would need to be done sorbed calcium when not taken into consideration when bal- to confirm this theory. ancing diets. Swartzmann et al. (1978) reported a reduction An absorption efficiency of 50 percent is used for all ages of calcium absorption by about 66 percent by the inclusion of horses. The true absorption efficiency can be as high as of 1 percent oxalic acid in equine diets. McKenzie et al. 70 percent with young horses but appears to decline as a (1981) reported total dietary oxalate concentrations of 2.6 to horse matures. Throughout a horseâs life, calcium absorp- 4.3 percent decreased calcium absorption as evidenced by a tion can vary depending upon many factors, so determining negative calcium balance resulting from a doubling of fecal a specific absorption rate in an individual animal is difficult. calcium and decreased urinary calcium in comparison to Additionally, many mineral balance studies last 10 days or control horses. Similar negative balances for calcium were less, and horses likely are able to modulate the absorption observed by Blaney et al. (1981) in horses fed various trop- efficiency of calcium to account for lowered dietary intakes ical grass hays containing more than 0.5 percent total ox- (Hintz, 2000). Thus, a 50 percent absorption efficiency may alate. When the calcium:oxalate ratio on a weight-to-weight be low, especially when calcium concentrations in the diet basis was less than 0.5, it was concluded that horses could are low. However, Hintz (2000) contended making a liberal be at risk for nutritional secondary hyperparathyroidism. No estimate is better than making a conservative estimate, as it difference in calcium absorption was reported by Hintz et al. will decrease the likelihood of developing a calcium defi- (1984) from alfalfas containing 0.5 and 0.87 percent oxalic ciency. Pagan (1994) reported true calcium digestibility es- acid in which the calcium:oxalate ratios were 3 and 1.7, re- tablished over the course of many trials to be around 75 per- spectively. By contrast, there have been a few reports of cal- cent in mature horses. Other factors affecting calcium cinosis in horses due to the consumption of calcinogenic absorption include concentrations of calcium, phosphorus, plants (Mello, 2003). The plants that have been documented phytate, and oxalate in the diet. As calcium concentrations to affect horses are Cestrum diurnum (in Florida) and Trice- increase, the absorption efficiency typically decreases; how- tum flavescens (in Austria). These plants increase release of ever, apparent calcium absorption was higher in horses fed 1,25(OH)2D3, and can greatly increase calcium absorption, alfalfa than grass hays (Cuddeford et al., 1990; Crozier et thereby resulting in hypercalcemia. Fortunately, such situa- al., 1997). Sturgeon et al. (2000) reported an apparent cal- tions are rare.
72 NUTRIENT REQUIREMENTS OF HORSES Both intake and type of diet influence renal calcium ex- maintain blood calcium concentration within such a tight cretion (Meyer, 1990). Calcium is not absorbed from the range renders total serum calcium a poor indicator of cal- large intestine, emphasizing the need to have sufficient cium status (Krook and Lowe, 1964) so even when an un- amounts to ensure adequate absorption from the small intes- balanced diet is fed, calcium concentrations in the blood can tine (Stadermann et al., 1992). Dietary constituents can in- remain relatively constant (de Behr et al., 2003). When frac- fluence digestibility as prececal apparent digestibility of cal- tionated out using a micropartition system, Lopez et al. cium is higher with alfalfa hay than with concentrate (2006) reported total calcium in the serum of healthy horses (Stadermann et al., 1992). Hoffman et al. (2000) reported to be composed of ionized calcium (48.5 Â± 0.7 percent), lowered bone mineral content of the third metacarpus when protein-bound calcium (47.4 Â± 0.9 percent), and calcium feeding a fat- and fiber-based diet compared to a sugar- and complexed with weak acids (4.1 Â± 0.9 percent). The ionized starch-based diet, and thus expressed concerns over the po- fraction is thought to be the only physiologically active form tential binding of calcium by fat and fiber. A follow-up study and thus is the form that should be evaluated for clinical showed that supplementing more than 0.9 percent calcium work. A normal reference range for total serum calcium has in a sweet feed had no effect on mineral content of the third been given as 10.8 to 13.5 mg/dl serum and for ionized metacarpus in fat- and fiber-fed foals, thus leading the au- serum calcium as 6.44 to 6.74 mg/dl serum (Garcia-Lopez et thors to conclude that the transient lower bone mineral con- al., 2001). An ionized serum calcium concentration of less tent observed in the prior study may be better attributed to than 6 mg/dl serum has also been used to define horses as nutrient-endocrine interactions than to calcium insufficiency hypocalcemic by Toribio et al. (2001). Calcium deficiencies (Hoffman et al., 2001). Grace et al. (2003) reported no often have a dramatic impact on skeletal integrity. A defi- change in apparent absorption of calcium when weanlings ciency of calcium in the developing foal can lead to os- were fed diets ranging in concentration from 3.5 to 12 g teopenia. This condition is characterized by poor mineral- Ca/kg DM. Additionally, no changes in bone strength were ization of the osteoid tissue and the probability of enlarged related to dietary calcium concentration. Though hypothe- joints and crooked long bones. A survey of the severity of sized that diets high in protein increase urinary calcium ex- metabolic bone disease in yearlings and diet analysis on 19 cretion with potential detriment to bone, no influence on Ohio and Kentucky horse farms revealed a negative linear bone density was reported due to varying protein intakes relationship between dietary calcium intake and perceived (Schryver et al., 1987a; Spooner et al., 2005) or protein severity of metabolic bone disease in young horses (Knight quality (Smith et al., 2005). Besides diet, other factors can et al., 1985). Farms with yearlings having the lowest inci- influence absorption. Cymbaluk et al. (1989) reported true dence of metabolic bone disease were fed diets containing calcium digestibilities decreased substantially from 6 to 24 1.2 percent calcium, whereas yearlings with the most severe months of age (though this was confounded with a change metabolic bone disease were on farms that fed diets with 0.2 in calcium source), and the efficiency of calcium absorption percent calcium. It should be noted that this report did not was influenced by varying requirements during different have data on what the horses were consuming prior to the stages of training (Stephens et al., 2001). At times when survey and it did not report differences in exercise afforded mineral deposition is occurring in bone, requirements would to the young horsesâboth of which likely could have influ- be expected to increase. Bone serves as a reservoir for enced results. In the mature horse, inadequate dietary cal- calcium, and more calcium is needed from the diet when cium can result in weakening of the bones and an insidious calcium is being placed into bone as compared to when cal- shifting lameness (Krook and Lowe, 1964). cium is being removed from bone during periods of disuse Whitlock et al. (1970) fed diets with calcium:phosphorus (Bronner, 1993). During initial periods of disuse, the cal- ratios of 1.16:1 (0.43 percent calcium) and 4.12:1 (1.96 per- cium goes into the plasma, from which excess is secreted cent calcium) and observed a greater proportion of lamellar from the body. This appears to decrease calcium require- bone than osteonic bone in high-calcium horses; however, ments (Nielsen et al., 1998a). Likewise, when mineral is no clinically deleterious effects or gross morphological dif- being deposited into bone at times when exercise intensity is ferences were detected. Krook and Maylin (1988) proposed increasing, requirements are likely higher than when inten- that osteochondrosis may be associated with excess dietary sity of training is relatively constant. Exercise in mature calcium (e.g., from alfalfa hay) by producing hypercalci- horses did not alter apparent calcium digestibility (about 54 toninism. However, calcium has been fed at more than five percent: Pagan et al., 1998). times the required concentration without detrimental ef- fects, provided the phosphorus concentration is adequate (Jordan et al., 1975). When provided adequate, but not ex- Signs of Deficiency or Excess cessive, amounts of phosphorus, the maximum tolerable Removing calcium from the skeleton to meet metabolic concentration of calcium in horse feed has been given as 2 demands when dietary calcium intake is inadequate can re- percent of the diet (NRC, 2005). Recent work in other sult in a weakened skeleton if done in excess. The need to species has shown that calcium influences gastrin secretion
MINERALS 73 (Cheng et al., 1999; Dufner et al., 2005), indicating unnec- quirements likely go up, even if horses are just returned to essarily high dietary calcium may be implicated in gastric a pasture setting to compensate for bone loss associated ulcers and should be avoided. More details on the cal- with disuse. cium:phosphorus ratio are given in the phosphorus section Using the estimate of Schryver et al. (1974) that growing and in Chapter 12. foals deposit approximately 16 g Ca/kg of gain, a 215-kg Some work has been done in utilizing dietary cation- foal gaining 0.85 kg/d and having a calcium absorption effi- anion difference (DCAD) to influence calcium utilization. A ciency of 50 percent would require 27.2 g/d (16 g Ã 0.85 kg low DCAD (defined as mEq (sodium + potassium) â chloride/ of gain/0.5) of dietary calcium for skeletal growth plus 8.6 kg dry matter) has been shown to increase urinary calcium g/d (215 kg Ã 20 mg/0.5) to meet endogenous losses. How- loss in exercising horses (Wall et al., 1992) and perhaps ever, a study by Cymbaluk et al. (1989) estimated endoge- leads to a calcium deficiency in growing horses (Wall et al., nous fecal calcium to be 36 mg/kg BW in growing Quarter 1997). However, Cooper et al. (2000) reported that when fed horses. While Hintz (1996) suggested there is little evidence a lower DCAD (defined as mEq (sodium + potassium) â for the calcium requirements of growing horses to be greatly (chloride + sulfur)/kg of diet DM), horses increased intes- changed from the 1989 NRCâs recommendations, the appar- tinal calcium absorption to compensate for increased urinary ent greater endogenous losses in growing horses compared excretion of calcium. Using that same definition, Baker et al. to mature horses would increase the requirements of a 215- (1998) indicated a low DCAD diet formulated with ammo- kg foal by an additional 6.9 g/d over what the 1989 NRC nium chloride resulted in a decrease in apparent calcium suggestedâup to 42.7 g. While these horses were on a rela- balance. Cooper et al. (2000) suggested the horse is able to tively high-forage diet during the study (about 50 to 90 per- maintain metabolic equilibrium despite the ratio of cations cent), it is reasonable to believe growing horses have greater to anions in the diet and that horses can tolerate a wide vari- endogenous losses than a mature horse. In addition, Moffett ation in DCAD without experiencing adverse effects on et al. (2001) reported increased daily gains, as well as in- skeletal growth. Likewise, McKenzie et al. (2002) found creased calcium retention, when yearlings were fed 0.48 that varying DCAD did not alter daily balance of calcium percent calcium compared to 0.32 percent. Thus, the cal- and phosphorus. Data from Cooper et al. (1998) obtained cium requirement for growing horses not in training was in- after a 21-day diet adaptation period suggested horses are creased to meet endogenous losses of 36 mg Ca/kg BW with able to maintain normal acid-base status regardless of the di- a 50 percent absorption rate and to meet growth require- etary cation-anion balance of the diet. Whether this would ments of 16 g Ca/kg BW gain with a 50 percent absorption be true in a longer duration study is not known. rate. The resultant requirement for calcium is (0.072 g Ã kg BW) + (32 g Ã ADG in kg). In late gestation, calcium requirements for the mare are Recommendations increased to meet the needs of fetal growth and tissue de- Endogenous losses of calcium have been estimated to be velopment. Approximately 11.1, 25.3, and 11.4 mg of Ca/kg 20 mg Ca/kg BW/d (Schryver et al., 1970, 1971a). Using of mare body weight are deposited daily in the fetus and that estimate and the absorption efficiency of 50 percent, membranes of mares in months 9, 10, and 11, respectively the 1989 NRC proposed a 500-kg horse would require 20 g (Meyer and Ahlswede, 1978; Drepper et al., 1982). Though (500 kg Ã 20 mg/0.5) of dietary calcium (0.04 g of Ca/kg the substantial increase at 10 months of gestation is suspect, BW) or 1.22 g Ca/Mcal DE (digestible energy)/d for main- their findings may be supported by a study by House and tenance. Using data compiled from many studies, Pagan Bell (1993) that examined fetal calves from slaughtered (1994) estimated endogenous calcium loss to be 17.4 g/d cows. At the end of gestation, calcium accretion in the fetus (R2 = 0.94) for a 550-kg horse (about 31.6 mg/kg BW), was 10.3 g/d at 280 days of gestation. Using the average cow which is higher than the 1989 NRC values. The true di- weight of 714 kg, 14.4 mg of calcium were being deposited gestibility of calcium was estimated at 74.7 percent, which per kg of BW, which is comparable to the 11.4 mg Ca/kg of is also higher than 1989 NRC values. However, the result- BW reported in horses at the end of gestation. Given that ing requirement for a 500-kg horse (21.2 g Ca/d) is similar fetal calf growth increased from 329 g/d at 200 days post- to the 1989 NRC requirement (20 g/d). Regression analyses mating to 456 g/d at 242 days post-mating and then declined on the calcium data of Buchholz-Bryant et al. (2001) using to 296 g/d at 280 days of gestation, it seems plausible that 12 sedentary geldings of three different age groups at four the increased deposition of calcium in the 10th month of time periods gives a calculated requirement of 0.043 g gestation in horses also represents the greatest period of Ca/kg of BW. This would represent 21 g Ca/d for a 500-kg fetal foal growth and the greatest need for calcium. Using an horse, which is similar to the recommendation of the 1989 absorption efficiency of 50 percent, the calcium requirement NRC. Thus, the subcommittee saw no reason to change the during months 9, 10, and 11 of gestation for a 500-kg mare maintenance calcium requirements. As noted in the section would be 11, 25, and 11 g/d, respectively, for fetal develop- on exercise, after extended periods of stall rest, calcium re- ment. As data on the deposition rate of minerals in the fetus
74 NUTRIENT REQUIREMENTS OF HORSES are very limited, a mean deposition rate (15.9 mg Ca/kg partum week to 0.8 g/kg of fluid milk during weeks 15 to 17 BW) was used for the last 3 months (NRC, 1989). Using the postpartum. This is consistent with the data of Baucus et al. 50-percent absorption rate, 0.032 g Ca/kg BW is needed in (1987). For a 500-kg mare producing 16 kg milk/d in early addition to maintenance requirements during the last 3 lactation and with a calcium absorption efficiency of 50 per- months of gestation. Martin et al. (1996) evaluated prepar- cent, the daily dietary calcium requirement would be 38.4 g tum mares fed either 0.55 percent calcium (0.076 g Ca/kg (16 kg Ã 1.2 g/0.5) for milk production, in addition to 20 g BW; above the 1989 NRC suggested minimum of 0.45 per- for maintenance. This estimate of calcium requirement for cent) or 0.35 percent calcium (0.045 g Ca/kg BW; below the milk production is consistent with that of Jarrige and suggested minimum) and concluded that the optimal dietary Martin-Rosset (1981). When fed at the 1989 NRC recom- calcium concentration for prepartum mares was closer to mended concentration, mares still lost bone density from the 0.55 percent than 0.35 percent. The dietary concentration of third metacarpal bone during the first 12 weeks of lactation 0.45 percent calcium recommended by the 1989 NRC for but density was restored by 24 weeks postpartum (Glade, pregnant mares was not evaluated in this study, which ap- 1993). Mares fed 20 percent less calcium had not fully re- peared to confirm that 0.35 percent dietary calcium was not covered third metacarpal bone density by 20 weeks after adequate for prepartum mares. However, in the study by milk production had ceased (40 weeks after parturition). Martin et al. (1996), the two treatment groups were main- This suggests that rebred mares not fed sufficient calcium tained on separate farms and the treatment groups were not during lactation would have a greater demand for calcium balanced for breed. In addition, the dietary calcium concen- throughout gestation as they attempt to restore the mineral tration was determined from estimated pasture intake lost from the skeleton during lactation. This work reaffirms (which was very different for the two groups), so the results that the dietary calcium recommendation of the 1989 NRC may have been influenced by factors other than dietary cal- for lactation should not be reduced, though it is uncertain if cium concentration. However, Glade (1993) confirmed that the recommendation should be increased. Thus, the recom- the dietary amount of calcium recommended for brood- mendations remain unchanged, although new estimates of mares is a minimum and should not be reduced. Foals of milk production are used. Milk production is estimated at mares fed calcium lower than the 1989 NRC requirements 0.032 kg milk per kg BW from foaling to 3 months, 0.026 had mechanically weaker bones at birth compared to foals kg milk per kg BW from 4 to 5 months, and 0.020 kg milk of mares fed the 1989 NRC recommended amounts. While per kg BW after 5 months. The resultant equations for cal- the 1989 NRC based its recommendation on DE, the current cium requirements during lactation are: method of determination results in a similar requirement and, at this time, there is no strong evidence to suggest a re- Foaling to 3 months = (0.04 g Ã kg BW) + vision of that requirement. However, considering there is (0.032 Ã kg BW Ã 2.4 g) substantial fetal growth during months 7 and 8 of gestation, the requirement for those months is suggested as being an 4â5 months = (0.04 g Ã kg BW) + (0.026 Ã kg BW Ã 1.6 g) average of maintenance and late gestation. In summary, to meet endogenous losses of 20 mg Ca/kg BW with an ab- > 5 months = (0.04 g Ã kg BW) + (0.020 Ã kg BW Ã 1.6 g) sorption rate of 50 percent and to meet fetal deposition rate of 15.9 mg Ca/kg BW with a 50 percent absorption rate, the Previously, it had been assumed that any additional cal- calcium requirement during months 9, 10, and 11 of preg- cium required for exercise would be met through the addi- nancy is calculated as (0.04 g Ca Ã kg BW) + (0.032 g Ca Ã tional feed consumed to meet energy demands (NRC, 1989). kg BW) or simply (0.072 g Ca Ã kg BW). To meet endoge- The need for calcium is greatly influenced by bone develop- nous losses of 20 mg Ca/kg BW with an absorption rate of ment. Bone formation is impacted by exercise, or the lack 50 percent and to meet fetal deposition rate of 8 mg Ca/kg thereof. When net bone deposition is increased, so is the BW with a 50 percent absorption rate, the requirement for need for calcium. When bone loss is occurring, requirements pregnancy during months 7 and 8 of gestation is calculated for calcium are lower as calcium is removed from the skele- as (0.04 g Ã kg BW) + (0.016 g Ã kg BW) or simply (0.056 g ton, goes into the plasma, and is lost through the urine and Ã kg BW). feces with an accompanying decreased need for calcium ab- Though commonly recognized, additional demand for sorption (Nielsen et al., 1998a). Unfortunately, plasma cal- calcium during lactation was reconfirmed by Martin et al. cium concentrations are of little use in assessing net calcium (1996), who reported an increase in serum parathyroid hor- balance as horses in a negative calcium balance commonly mone concentrations with a lactation-induced decrease in have normal plasma or serum values (Rose, 1990) despite serum total and ionized calcium beginning 3 days prepartum measurable changes in bone mineral content. Estimates of and continuing until 2 days postpartum. Schryver et al. mineral content of the lower leg are reduced in young horses (1986b) reported that the daily calcium requirements for lac- that are stalled without sufficient access to exercise as com- tation range from 1.2 g/kg of fluid milk during the first post- pared to horses kept on pasture (Hoekstra et al., 1999; Bell
MINERALS 75 et al., 2001; Brama et al., 2002). Porr et al. (1998) reported 1989 NRC recommended calcium amount were fed com- stall rest for 12 weeks in mature Arabians similarly de- pared to 97 percent and 136 percent. Likewise, Michael et creased third metacarpal bone mineral content estimates, al. (2001) reported increased markers of bone formation and which was not prevented by dietary calcium intake at twice decreased markers of bone resorption in horses fed the two the 1989 NRC recommended concentration (an excess of higher percentages of calcium compared to the two lower about 20 g of calcium). To compensate for mineral loss from percentages. Unfortunately, neither Nolan et al. (2001) nor the skeleton, Meyer (1987) suggested feeding 20 percent Michael et al. (2001) reported weight of the horses or feed above the recommended amounts of calcium and phospho- intake, so calculating absolute intake on a body weight basis rus if horses have a prolonged period without activity once is not possible. If the feed intake of the horses was relatively normal activity has returned. Short sprints are sufficient to low, the absolute amount taken in may have been closer to stimulate bone formation, while exercising for longer dis- the amount recommended by the 1989 NRC than the con- tances, but at slower speeds, is less efficient. Vervuert et al. centrations would make it appear. Stephens et al. (2004) re- (2005a) reported draught load exercise with low velocities ported calcium retention to be maximal when calcium intake had no effect on calcium metabolism. was 123 mg Ca/kg BW/d, which represents a 36 percent in- In contrast, despite receiving the exact same diet, a single crease over the 1989 NRC recommendations for exercise. 82-m sprint five days per week increased indirect measures However, variation was great (R2 = 0.23) for calcium reten- of third metacarpal bone mineral content and improved third tion vs. intake. Total concentrate and hay intake averaged metacarpus architecture in stalled weanlings compared to 18 g/kg BW. Calcium intake was 135 Â± 6 mg/kg BW/d at the stalled weanlings afforded no exercise (Hiney et al., 2004). start of the study and was 123 Â± 4 mg/kg BW/d at the com- These studies demonstrate the importance of exercise in pletion of the study at day 128. In these studies, the effects stimulating calcium deposition in the skeleton. Interestingly, of additional calcium are often confounded with varying a 10-year study in humans showed that calcium intake over amounts of phosphorus and magnesium but demonstrate po- that period was not associated with bone gain or bone tential improvements in bone mineral content, and poten- strength (Lloyd et al., 2004). Instead, only exercise during tially strength, by feeding additional calcium over what was adolescence, as determined by a sports exercise question- recommended by the 1989 NRC. When only the calcium naire, was significantly associated with increased bone min- concentration was altered, Schryver et al. (1978) suggested eral density and bone bending strength (P < 0.01). Similarly, that 0.6 percent dietary calcium was not needed, compared Nielsen (2005) reported a much greater role in influencing to 0.4 percent calcium, when fed to yearling Standardbreds markers of bone turnover in studies related to differences in entering training. For horses consuming 2 percent of their exercise as compared to nutrition. Hence, the importance of body weight per day, as was the case in many of these stud- exercise in young horses to maximize bone strength is un- ies, this would equate to 0.08 g Ca/kg BW. This is also sup- derscored. If sufficient exercise is provided, extra dietary ported by the data of Buchholz-Bryant et al. (2001). When calcium can likely be utilized to improve bone strength. Ex- their data for calcium intake for young horses in training are ercise, particularly in the young horse, appears to increase plotted against the amount retained, the linear regression re- calcium requirements above maintenance requirements. sponse shows a requirement of 0.079 g Ca/kg BW. For Gray et al. (1988) found horses in training had lower urinary horses that are rapidly growing (typically under 24 months calcium excretion, despite receiving more calcium, than of age), these requirements would usually be met by the re- horses not working, suggesting exercise increases the need quirements for growth ((0.072 g Ca Ã kg BW) + (32 g Ca Ã for calcium. Exercised horses had a higher calcium balance ADG in kg)) that have been increased from the 1989 NRC. than horses that were sedentary for 2 months and then exer- As a result, the requirement for growing horses that are ex- cised for 2 months (Elmore-Smith et al., 1999). In response ercising is the same as the requirement for growth. Typi- to previously measured declines in mineral content of the cally, this is equal or greater than the apparent recommen- third metacarpal bone (Nielsen et al., 1997, 1998a), calcium dation for heavy exercise (0.08 g Ca Ã kg BW) only when balance and retention were determined in 2-year-old race- average daily gain drops to 0.1 kg. It is likely the calcium re- horses placed into training receiving a total diet containing quirement associated with exercise is less for mature horses. either 0.31 percent calcium (0.063 g Ã kg BW) or 0.38 per- Mansell et al. (1999) found little difference in the response cent calcium (0.074 g Ã kg BW) on an as-fed basis and con- of bone to varying concentrations of dietary calcium but suming about 2 percent of their body weight daily (Nielsen found bigger differences depending upon the age of horses. et al., 1998b). Calcium retention was greater, as was mineral When calcium intake data of Buchholz-Bryant et al. (2001) content of the third metacarpal bone, in horses fed 0.38 per- for mature horses are plotted against retention, linear re- cent calcium (0.074 g Ã kg BW). Other studies also support gression reveals a requirement of 0.04 g Ca/kg BW/dâthe the need for additional calcium for horses in training. Nolan same as is required for maintenance. While it is likely the et al. (2001) reported increased mineralization of the third calcium requirement for mature horses is less than that of metacarpal bone when 151 percent and 169 percent of the the younger horse, an insufficient number of studies have
76 NUTRIENT REQUIREMENTS OF HORSES been performed to warrant lowering the requirement for in dietary sodium chloride from 1 percent to 5 percent in- heavy exercise in mature horses at this time. Because forces creased phosphorus absorption from 28 to 40 percent applied to the skeleton primarily regulate bone mineral dep- (Schryver et al., 1987b). Despite concern with aluminum osition, which is one of the major needs for additional cal- interference in phosphorus absorption, phosphorus absorp- cium, establishing calcium requirements for exercise is dif- tion was not affected by feeding an aluminum (Al) supple- ficult and will vary depending upon the intensity of training ment (931 ppm Al/kg feed or 12 mg of Al/kg BW/d) for 1 and the influence upon the skeleton. The requirement will month (Roose et al., 2001). likely be closer to maintenance for horses not experiencing Diets containing high concentrations of oxalates depress any high-speed work and for horses that are not increasing phosphorus retention (Blaney et al., 1981; McKenzie et al., their intensity of training. Thus, the calcium recommenda- 1981). Phytate phosphorus, the salt of phytic acid and a pre- tions for light and moderate exercise can be expected to dominant form of phosphorus in plants, is poorly absorbed be lower than that of heavy exercise and have been set at by horses, though some phytase exists in the hindgut (Hintz 0.06 g Ca Ã kg BW for light exercise and 0.07 g Ca Ã kg BW et al., 1973). To meet phosphorus requirements, inorganic for moderate exercise. While a heavily exercising horse may phosphates are often added to the equine diet and this could have only a small increased need for extra calcium com- be at least partially avoided if the absorbability of phytate pared to a lightly exercising horse if the exercise intensity phosphorus could be increased by an appropriate use of phy- has been constant, these recommendations are established to tates (Eeckhout and De Paepe, 1994). Despite an abundance minimize or eliminate problems as the intensity of exercise of research on the use of phytase to increase phosphorus increases. availability in other species, Morris-Stoker et al. (2001) re- ported no benefit to horses of feeding phytase (200 units/g) at the rate of 1 g/kg of feed. Patterson et al. (2002) also Phosphorus found no improvement in phosphorus apparent digestibility with the addition of phytase up to 900 Phytase unit Function (FTU)/kg of diet. When horses were fed four different diets Like calcium, phosphorus (P) is a major constituent of (Coasta Bermudagrass with whole oats, alfalfa cubes, a tex- bone, making up 14 to 17 percent of the skeleton (El Shorafa tured sweet feed, or a pelleted concentrate), Hainze et al. et al., 1979). In addition, it is required for many energy (2004) found phytase decreased fecal phosphorus only for transfer reactions associated with adenosine diphosphate the sweet feed-based diet, due largely to decreased fecal out- (ADP) and adenosine triphosphate (ATP), and for the syn- put of the insoluble fraction of phosphorus. Because horse thesis of phospholipids, nucleic acids, and phosphoproteins. manure contains a lower proportion of total phosphorus as the water-soluble phosphorus fraction compared with that from other farm animals, phosphorus in horse feces may be Sources and Factors Influencing Absorption less prone to runoff in typical pasture-based management True phosphorus absorption is quite variable and typi- systems. Hainze et al. (2004) concluded that under normal cally ranges from 30â55 percent. It varies depending upon feeding conditions, phytase probably has limited potential other dietary constituents, how much and what type of for decreasing concerns over environmental phosphorus phosphorus is fed, and the age of the horse. High calcium contamination as the proportion of fecal phosphorus repre- concentrations in the diet depress phosphorus absorption. sented by the soluble fraction is increased. However, Warren In diets averaging 0.89 percent calcium, Pagan (1994) re- (2003) cautioned that, though equine research has not shown ported true phosphorus absorption to be around 25 percent. phytase to be useful in reducing phosphorus excretion, eval- Similarly, phosphorus absorption of a high-phosphorus diet uated diets have had sufficient phosphorus. A better test is to (0.125 g P/kg BW) decreased from 25 percent in horses determine if phytase can increase phosphorus utilization by receiving a diet containing 0.148 g Ca/kg BW/d to 11 per- the horse when dietary phosphorus concentrations are below cent and 13 percent when fed diets containing 0.316 required amounts (Warren, 2003). and 0.535 g Ca/kg BW/d, respectively (van Doorn et al., Phosphorus absorption is assumed to be higher by foals 2004b). All horses were in positive phosphorus balance. consuming milk than it is in mature horses, though Grace et High dietary phosphorus concentrations (1.19 percent al. (1999a) suggested creep feed be fed to nursing foals as phosphorus) have been shown to increase phosphorus re- milk may be insufficient in phosphorus (as well as calcium) tention and plasma phosphorus concentrations (Schryver et for optimal growth of foals. A phosphorus absorption effi- al., 1971b). Buchholz-Bryant et al. (2001) reported similar ciency of 35 percent is used for mature horses (except for findings when examining the effect of calcium and phos- lactating mares) as they primarily consume plant sources of phorus supplementation in young, mature, and aged horses phosphorus. For lactating mares and growing horses, a 45- with different training regimens. All groups retained phos- percent efficiency is used because their diets are often sup- phorus regardless of whether they were fed normal (0.24 plemented with inorganic phosphorus. Horses at 8 months percent) or high (0.57 percent) phosphorus diets. Increases were more efficient at utilizing phosphorus than horses at 12
MINERALS 77 months (Cymbaluk, 1990). Environment appears to influ- often in the United States, but Hintz (1997) cautioned that ence phosphorus absorption as horses housed in a warm horse owners still need to be made aware of this potential barn had greater true phosphorus digestibility than those problem, particularly if horses are fed large amounts of housed in a cold barn (Cymbaluk, 1990). Similar to the find- grain-based feedstuffs such as wheat bran or oats. While this ings for calcium, Stephens et al. (2001) reported the effi- condition is rare, it can still occur in situations when horses ciency of absorption can vary with requirements. Absorp- are fed grains not supplemented with calcium and are re- tion, at least to a degree, apparently increases when demand ceiving forage relatively low in calcium or that contains sub- for phosphorus increases and may change with stage of stantial amounts of oxalates (Mason et al., 1988; Ronen et training though more studies are needed. al., 1992; Luthersson et al., 2005). Though typically not a concern with forages, certain types, such as orchardgrass, can have inverted calcium:phosphorus ratios. With grains Signs of Deficiency or Excess being naturally higher in phosphorus than calcium, it is quite Inadequate dietary phosphorus will, like calcium and vi- easy to feed too much phosphorus in relation to calcium tamin D, produce rachitic-like changes in growing horses when raw grains or grain byproducts are fed in large quanti- and osteomalacic changes in mature horses. Excess phos- ties. Clinical signs vary depending on the degree of the phorus reduces the rate of calcium absorption and leads to imbalance of calcium to phosphorus, oxalate content of chronic calcium deficiency and nutritional secondary hyper- the diet, age of the horse, performance level, and environ- parathyroidism (NSH). Clinically, NSH is characterized by mental conditions (Ramirez and Seahorn, 1997). While a shifting lameness and, in advanced cases, by enlargement of low calcium:phosphorus ratio can be quite detrimental, ra- the upper and lower jaws and facial crest (Krook and Lowe, tios as high as 6:1 in the growing horse may be acceptable if 1964). Savage et al. (1993a) reported that foals fed 388 per- phosphorus intake is adequate (Jordan et al., 1975). The cent of the 1989 NRC recommendation for phosphorus calcium:phosphorus ratio in milk has been reported to range showed numerous, severe lesions of osteochondrosis but no between 1.8 and 2.5:1 between weeks 16 and 24 of lactation clinical signs of NSH, though Savage et al. (1993b), in a his- (Sonntag et al., 1996). tomorphometric assessment of bone biopsies from the foals, reported that the changes were consistent with NSH. Recommendations Both organic and inorganic phosphorus exist in serum, though serum inorganic phosphorus is derived entirely from Endogenous losses of phosphorus by the mature horse inorganic compounds and is the value utilized in clinical have been estimated at 10 mg/kg BW/d (Schryver et al., practice (Lau, 1986). Serum inorganic phosphorus concen- 1971b). Combined with a 35 percent absorption efficiency, trations are high at birth and decline over several months to the 1989 NRC estimated the maintenance phosphorus re- normal adult values. Serum inorganic phosphorus values quirements for a 500-kg horse to be 14.3 g (0.028 g P/kg may be more indicative of dietary phosphorus status than BW). Using data from a number of studies, Pagan (1994) serum calcium is of calcium status because homeostatic estimated endogenous phosphorus loss to be 4.7 g/d (R2 = mechanisms for phosphorus are less sensitive than for cal- 0.33) for a 550-kg horse (about 8.5 mg/kg BW), which is cium (Schryver et al., 1970, 1971b). Caple et al. (1982) slightly lower than the 1989 NRC estimates. The true di- determined that horses excreting more than 15 Âµmol of gestibility of phosphorus was estimated to be 25.2 percent, P/mOsm of urine solute and having a phosphorus: creatinine which is also lower than the 35 percent used by the 1989 clearance ratio greater than 4 had excessive phosphorus in- NRC. However, the resulting requirement for a 500-kg take and were subject to NSH. It has been suggested that a horse was estimated at 17 g P/d which, although slightly maximum tolerable concentration of dietary phosphorus in higher, is similar to 1989 NRC values. This emphasizes the horses fed adequate dietary calcium is 1 percent assuming importance of knowing the availability of a phosphorus an appropriate calcium:phosphorus ratio (NRC, 2005). source when formulating rations as the absorption effi- ciency can greatly influence the amount of phosphorus needed in the diet. Due to concerns with extra phosphorus Calcium:Phosphorus Ratio being introduced into the environment, the subcommittee The absolute intakes of calcium and phosphorus by has chosen to remain with the lower estimate for phospho- horses must be adequate, but secondarily, it is important to rus requirements. evaluate the calcium:phosphorus ratio of equine rations. If As foals deposit about 8 g P/kg BW gain (Schryver et al., calcium intake is less than phosphorus intake (ratio less than 1974), the 1989 NRC suggested growing horses require 17.8 1:1), calcium absorption may be impaired. Even if the diet g (8 g/0.45 percent efficiency) for each kg of gain in addi- contains adequate calcium, excessive phosphorus intake tion to the maintenance requirements. Thus, a 215-kg foal may cause skeletal abnormalities (Schryver et al., 1971b). gaining 0.85 kg/d would require about 15.1 g of phosphorus Nutritional secondary hyperparathyroidism is covered more (8 g/0.45 Ã 0.85 kg gain) in addition to its maintenance re- completely in Chapter 12. This condition does not occur quirement of 4.8 g (215 kg Ã 10 mg/0.45). While Furtado et
78 NUTRIENT REQUIREMENTS OF HORSES al. (2000) estimated endogenous fecal losses in growing absorption) for lactation would be 26.7 g for a mare produc- horses to be 10.3 mg P/kg of BW/d, Pagan (1989) argued ing 16 kg milk/d in early lactation and 11.1 g for a mare pro- that endogenous phosphorus losses in young horses are ducing 10 kg milk/d during late lactation. At these rates of double those used by the NRC (1989) in estimating dietary milk production, a 500-kg mare would require 37.8 and phosphorus requirement. This agrees with Cymbaluk et al. 22.2 g P/d in early and late lactation, respectively. No data (1989), who estimated endogenous fecal phosphorus to be have been found suggesting the 1989 NRC recommendation 18 mg/kg BW/d in growing Quarter horses. Using the higher for lactation should be changed other than to account for a estimate for endogenous loss (215 kg Ã 18 mg/0.45), the revision of milk production estimates. To meet endogenous total phosphorus requirements would be increased to 23.7 g losses of 10 mg P/kg BW with an absorption rate of 45 per- P/d. Grace et al. (1999b) suggested 21 g of P/d is the re- cent and to meet milk production needs estimated at 0.032 quired amount compared to the 16 to 20 g recommended by kg milk/kg BW containing 0.75 g P/kg milk that is absorbed the 1989 NRC for growing horses expected to reach 500 kg. at a 45 percent rate, the phosphorus requirement for lacta- Their calculations were based upon a 200-kg horse gaining tion from foaling to 3 months is (0.022 g Ã kg BW) + (0.032 1 kg/d and using an absorption efficiency of 0.5. With a Ã kg BW Ã 1.67 g). To meet endogenous losses of 10 mg lower absorption efficiency, requirements would be even P/kg BW with an absorption rate of 45 percent and to meet greater. The results of these studies suggest that the endoge- milk production needs estimated at 0.026 kg milk/kg BW nous losses, and hence, maintenance phosphorus require- containing 0.5 g P/kg milk that is absorbed at a 45 percent ments, for young horses are greater than previously assumed rate, the phosphorus requirement for lactation from 4 to 5 and an endogenous loss of 18 mg/kg BW/d was used in de- months is (0.022 g Ã kg BW) + (0.026 Ã kg BW Ã 1.11 g). termining the requirements. The requirement for growth To meet endogenous losses of 10 mg P/kg BW with an ab- recommended in this publication thus contains both a main- sorption rate of 45 percent and to meet milk production tenance component (0.018 g/0.45 absorption efficiency Ã kg needs estimated at 0.020 kg milk/kg BW containing 0.5 g BW) and a growth component (8 g/0.45 percent absorption P/kg milk that is absorbed at a 45 percent rate, phosphorus efficiency Ã kg gain). Phosphorus requirements increase requirement for lactation after 5 months is (0.022 g Ã kg during late gestation and lactation. Phosphorus requirements BW) + (0.020 Ã kg BW Ã 1.11 g). for the products of conception for mares in months 9, 10, The influence of exercise on phosphorus requirements and 11 of pregnancy have been estimated to be 7, 12, and 6.7 has been studied in combination with calcium. During the mg/kg BW/d, respectively (Drepper et al., 1982). At 35 per- first 4 months of race training in 2-year-old Quarter horses, cent absorption efficiency, the daily phosphorus require- Nielsen et al. (1998b) reported phosphorus retention re- ments for a 500-kg mare for products of conception during mained relatively constant over a range of phosphorus con- gestation months 9, 10, and 11 would be 10, 17.1, and 9.6 g, centrations in the diet (0.21 to 0.30 percent on an as-fed respectively (mean 12.2 g/d). The mean daily phosphorus basis). Likewise, 0.24 percent of the total diet (average deposition for the last 3 months of gestation ((8.6 mg/kg amount fed to control group) appeared to be adequate and BW)/0.35 absorption efficiency) was added to maintenance no apparent benefit was seen by feeding 0.29 percent, needs to determine the requirements. An average of mainte- though both the minimum and maximum amounts are above nance and late gestation was used for the phosphorus re- the 1989 NRC recommended amount based upon a percent- quirements during months 7 and 8 to allow for fetal growth age of the diet. In similarly trained horses, Stephens et al. occurring during that period. Thus, to meet endogenous (2004) reported phosphorus requirements to be at least 66 losses of 10 mg P/kg BW with an absorption rate of 35 mg/kg BW/d, which was 32 percent over the 1989 NRC rec- percent and to meet fetal deposition rate of 4.3 mg P/kg ommendation. While feeding various amounts of calcium, BW with a 35 percent absorption rate, the requirement for phosphorus, and magnesium to horses in race training, pregnancy during months 7 and 8 is (0.028 g Ã kg BW) + Nolan et al. (2001) reported diminished mineralization of (0.012 g Ã kg BW), or simply 0.04 g Ã kg BW. To meet the third metacarpus when feeding phosphorus at the 1989 endogenous losses of 10 mg P/kg BW with an absorp- NRC suggested amount, even when additional calcium and tion rate of 35 percent and to meet a fetal deposition rate of magnesium was provided. Only when phosphorus was at 8.6 mg P/kg BW with a 35 percent absorption rate dur- 130 percent of the NRC recommendation (calcium and mag- ing months 9, 10, and 11 of pregnancy, the requirement nesium both above 150 percent) was mineralization in- is (0.028 g Ã kg BW) + (0.0245 g Ã kg BW), or simply creased. Furthermore, exercised horses had a higher phos- 0.0525 g Ã kg BW. phorus balance than did horses that were sedentary for 2 The phosphorus concentration of maresâ milk ranges months and then exercised for 2 months (Elmore-Smith et from 0.75 g/kg of fluid milk in early lactation to 0.50 g/kg al., 1999). Young et al. (1989) also found an increase in daily of fluid milk in late lactation. If the absorption efficiency of phosphorus retention when miniature horses were exercised. lactating mares is 45 percent, the daily phosphorus require- In contrast, Lawrence et al. (2003) reported no differences in ments above maintenance (adjusted for the higher percent phosphorus retention between exercising horses and seden-
MINERALS 79 tary horses in a review of studies reporting phosphorus in- sorption (Kapusniak et al., 1988), though the apparent di- take and excretion. Likely, the majority of the horses from gestibility of magnesium was still between 41 and 45 per- the studies that were reviewed were mature horses and un- cent when mature ponies were fed excess phosphorus of ap- dergoing a relatively constant training protocol in contrast to proximately 125 mg P/kg BW/d (van Doorn et al., 2004b). many of the studies reporting requirements higher than the In a small study, Weidenhaupt (1977) reported high potas- 1989 NRC that were conducted in young horses just enter- sium concentrations slightly decreased magnesium apparent ing training. Like with calcium, any potentially higher re- digestibility. In contrast, high concentrations of aluminum quirements associated with exercise in the rapidly growing did not alter magnesium absorption (Schryver et al., 1986a) horse (typically under 24 months) should be met by the and neither did varying the consumption of salt (Schryver et phosphorus requirements for growth that have been in- al., 1987b). Wall et al. (1992) reported that varying DCAD creased from the 1989 NRC. With no strong evidence to did not alter mean daily urinary excretion of magnesium. suggest mature exercising horses have a higher requirement Schryver et al. (1987b) found that the calculated true ab- than was suggested by the 1989 NRC, the requirements re- sorption of magnesium was between 62 and 67 percent. Ols- main unchanged and are 0.058 g P Ã kg BW for heavy exer- man et al. (2004) reported a diet rich in sugar beet pulp did cise, 0.042 g P Ã kg BW for moderate exercise, and 0.036 g not alter magnesium absorption even though pH of intestinal P Ã kg BW for light exercise. contents should have theoretically been lowered, resulting in increased mineral solubility. Pagan et al. (1998) reported that the apparent digestibility of magnesium in mature Magnesium horses did not differ between exercised (28.5 percent) and nonexercised (35 percent) groups. Magnesium is absorbed Function from both the small and large intestine, though the majority Magnesium (Mg) constitutes approximately 0.05 percent appears to be absorbed from the small intestine (Kapusniak of the body mass. Sixty percent of magnesium in the body is et al., 1988). found in the skeleton and about 30 percent can be found in muscle (Grace et al., 1999b). Magnesium is an important ion Signs of Deficiency or Excess in the blood, plays a role as an activator of many enzymes, and participates in muscle contractions. Meyer (1990) suggested that renal creatinine/magnesium quotients greater than 7.5 indicate an insufficient dietary supply. Stewart et al. (2004) reported that determination of Sources and Factors Influencing Absorption urinary magnesium excretion during a 24-hour period was a Many commonly used feedstuffs contain 0.1â0.3 percent better method to indicate decreased magnesium intake as magnesium, and magnesium absorption from these feed- compared to serum total and ionized magnesium, as well as stuffs appears to be 40â60 percent (Hintz and Schryver, muscle magnesium concentrations, but a spot sample of the 1972, 1973; Meyer, 1979). According to Harrington and fractional clearance of magnesium can be conveniently used Walsh (1980), inorganic supplemental sources such as mag- to identify horses consuming a magnesium-deficient diet. nesium oxide, magnesium sulfate, and magnesium carbon- Hypomagnesemia was reported in foals with magnesium in- ate appear to be essentially equivalent as supplemental di- take at 7â8 mg/kg diet/d (Harrington, 1974). Assuming a etary sources of magnesium for growing foals and have a feed intake equivalent to 3 percent BW, magnesium intake higher absorption rate (70 percent) than the magnesium would have been only 0.2 mg/kg BW in comparison to the found in natural sources. Data from human studies indicate control animals receiving 390 mg/kg diet or 11.7 mg/kg the absorption rate of magnesium oxide to be lower than BW. Clinical signs of magnesium deficiency include nerv- magnesium citrate (Lindberg et al., 1990; Walker et al., ousness, muscle tremors, and ataxia, with the potential for 2003) and magnesium chloride, magnesium lactate, and collapse, hyperpnea, and death. Meyer and Ahlswede (1977) magnesium aspartate (Firoz and Graber, 2001). Stadermann indicated that a magnesium intake of 5â6 mg/kg BW/d re- et al. (1992) reported apparent digestibility of magnesium sulted in hypomagnesemia (less than 1.6 mg/dl serum) and was higher with alfalfa hay (51 percent) than with concen- a marked reduction in renal excretion of magnesium, trate (31 percent). McKenzie et al. (1981) reported magne- whereas 20 mg of Mg/kg BW/d resulted in normal serum sium to be 42â45 percent digestible and not affected by ox- magnesium values of 1.6â2.0 mg/dl. Hypomagnesemia in- alate. Supplemental phytase also did not affect magnesium duces mineralization (focal calcium and phosphorus de- absorption (van Doorn et al., 2004a). Further, van Doorn et posits) in the aorta. Histologic changes occur within 30 days al. (2004b) reported no differences in the apparent di- of initiation of a low-magnesium diet (Harrington, 1974). gestibility of magnesium (approximately 41â45 percent) The 1989 NRC indicated pastures that are conducive to when horses were fed rations ranging from 0.148â0.535 g magnesium deficiency, tetany, and death in ruminants do not Ca/kg BW/d. Excess phosphorus decreased magnesium ab- affect horses similarly, though no evidence was found in the
80 NUTRIENT REQUIREMENTS OF HORSES literature to provide support for this claim. However, while nous fecal loss, for a total of 4.25 g/d. By comparison, using uncommon, tetany in transported horses has been attributed the factorial method, Grace et al. (1999b) calculated the di- to hypocalcemia and potentially hypomagnesemia (Green et etary magnesium requirement of a 200-kg horse gaining 1 al., 1935; Merck Veterinary Manual, 2005). kg/d at 0.7 g Mg/kg DM intake. Assuming an intake of 3 Controlled studies evaluating the toxicity of magnesium percent BW, this would result in a similar intake of 4.2 g of in horses have not been done, though the maximum tolera- magnesium. The magnesium requirement for growth con- ble concentration has been estimated at 0.8 percent (NRC, sists of 0.015 g Ã kg BW to account for endogenous losses 2005), up from 0.3 percent in the 1980 NRC. Some alfalfa and 1.25 g magnesium for every kg of daily gain. hays with magnesium concentrations of 0.5 percent have The magnesium requirement of the mare associated with been fed to horses without apparent ill effects (Lloyd et al., products of conception has been estimated at 0.23, 0.31, and 1987). The source of magnesium may be important for 0.36 mg/kg BW of the mare for months 9, 10, and 11, re- horses, since mature ponies fed diets containing 0.86 per- spectively (Drepper et al., 1982). To meet the magnesium re- cent magnesium for 1 month had no noted adverse effects quirement for these periods, and assuming an absorption when the magnesium source was magnesium oxide (Hintz rate of 40 percent, a 500-kg mare would need 287, 387, and and Schryver, 1973). Historically, magnesium sulfate was 450 mg of dietary magnesium daily for fetal growth. Given used intravenously as an anesthetic agent in horses prior to that data on deposition rate of minerals in the fetus are very the advent of barbiturates and inhalation anesthetics (Kato et limited, a mean deposition rate of 0.30 mg/kg gain was used al., 1968). At normal dietary concentrations, there is no in- as the magnesium requirement for development of the prod- dication that magnesium sulfate has an anesthetic effect. ucts of conception for the last 3 months. Mean dietary mag- However, magnesium sulfate is used as a saline laxative for nesium required for fetal growth was added to maintenance treatment of intestinal impactions, but can cause magnesium needs for the same period to determine the requirement. toxicosis when overdosed, resulting in renal insufficiency, This relatively minor increase in magnesium requirements hypocalcemia, or a compromise of intestinal integrity (Hen- for a mare during late gestation is supported by a similar ninger and Horst, 1997). Magnesium supplementation is a finding in cattle (House and Bell, 1993). Little research is practice done to calm horses that could greatly influence available to determine magnesium requirements during magnesium intake if done often. months 7 and 8 of gestation, but an additional amount be- Normal serum magnesium concentrations in the horse tween that of maintenance and late gestation was added to range from 18â35 Âµg/dl (Puls, 1994). However, Edwards accommodate the growth of the products of conception. (2004) reported that serum magnesium concentrations in Thus, to meet endogenous losses of 6 mg Mg/kg BW with both Grantâs and common zebras are reported to be 14 to 15 an absorption rate of 40 percent and to meet a fetal deposi- ppm. tion rate of 0.08 mg Mg/kg BW with a 40 percent absorption rate, the magnesium requirement for months 7 and 8 of ges- tation is (0.015 g Ã kg BW) + (0.0002 g Ã kg BW), or sim- Recommendations ply 0.0152 g Ã kg BW. To meet endogenous losses of 6 mg Endogenous magnesium excretion was estimated at 6 Mg/kg BW with an absorption rate of 40 percent and to meet mg/kg BW/d (NRC, 1989), though Pagan (1994), summa- fetal deposition rate of 0.12 mg Mg/kg BW with a 40 per- rizing results from numerous studies, reported endogenous cent absorption rate, the magnesium requirement for months magnesium excretion of 2.2 mg/kg BW (R2 = 0.76). A study 9, 10, and 11 of gestation is (0.015 g Ã kg BW) + (0.0003 g by van Doorn et al. (2004b) reported magnesium retention Ã kg BW), or simply 0.0153 g Ã kg BW. to be around 4.4 mg/kg BW/d despite varying magnesium Grace et al. (1999a) reported magnesium concentrations concentrations in the diet (from 31.4 to 38.4 mg/kg BW/d) to be greater in colostrum (302 mg/L) than the average in as well as varying calcium concentrations (from 148 to 535 milk from day 55 to day 150 (47 mg/L). Concentrations of mg/kg BW/d). Using the initial value and a 40 percent ab- magnesium in milk declined during the course of lactation sorption rate, a 500-kg horse at maintenance requires 7.5 g (Schryver et al., 1986b) and concentrations during early lac- of dietary Mg/d or 15 mg/kg BW, which is lower than the 20 tation were double that of late lactation (NRC, 1989). As- mg/kg BW proposed by Drepper et al. (1982). While mag- suming a 40 percent absorption efficiency, a mare producing nesium requirements need to be better defined, Hintz (2000) 16 kg of milk/day with a magnesium concentration of 90 suggested there are no strong reasons that the 1989 NRC Âµg/g of milk during early lactation would require an addi- magnesium requirements for maintenance are not satisfac- tional 3.6 g of dietary Mg/d for milk production in addition tory and that the Pagan (1994) data suggest they could po- to her maintenance requirement of 7.5 g. Magnesium re- tentially be lower. Requirements for gain range from 0.85 to quirements for milk would be (0.015 g Ã kg BW) + (0.032 1.25 g Mg/kg BW gained per day (Schryver et al., 1974). Ã kg BW Ã 0.23) from foaling to 3 months to meet endoge- Using the higher value, a 200-kg foal gaining 1 kg/d would nous losses of 6 mg Mg/kg BW with an absorption rate of need 1.25 g of magnesium for growth plus 3 g for endoge- 40 percent and to meet milk production needs estimated at
MINERALS 81 0.032 kg milk/kg BW containing 0.09 g Mg/kg of milk that support increasing magnesium requirements for mature is absorbed at a 40 percent rate; (0.015 g Ã kg BW) + (0.026 horses above what was recommended in the 1989 NRC, the Ã kg BW Ã 0.23) from 4 to 5 months to meet endogenous amount previously recommended for heavy exercise (0.030 losses of 6 mg Mg/kg BW with an absorption rate of 40 per- g Mg Ã kg BW) and moderate exercise (0.023 g Mg Ã kg cent and to meet milk production needs estimated at 0.026 BW) were greater than what was recommended for both the kg milk/kg BW containing 0.09 g Mg/kg milk that is ab- long yearling and 2-year-old in training (0.022 g Mg Ã kg sorbed at a 40 percent rate; and (0.015 g Ã kg BW) + (0.020 BW). Therefore, the recommendation for young horses Ã kg BW Ã 0.11) after 5 months to meet endogenous losses (under 24 months) in training of any intensity is the same as of 6 mg Mg/kg BW with an absorption rate of 40 percent the requirement for heavy exercise to accommodate in- and to meet milk production needs estimated at 0.020 kg creased needs associated with the onset of training. milk/kg BW containing 0.045 g Mg/kg that is absorbed at a To meet endogenous losses of 6 mg Mg/kg BW with an 40 percent rate. absorption rate of 40 percent and to meet additional require- Much of the work done with magnesium nutrition in ex- ment for light work of 1.6 mg Mg/kg BW with a 40 percent ercising horses is confounded with varying concentrations absorption rate, the magnesium requirement for light exer- of calcium and phosphorus. For instance, in a study com- cise is estimated at (0.015 g Ã kg BW) + (0.004 g Ã kg BW), paring various concentrations of calcium, phosphorus, and or simply 0.019 g Ã kg BW. To meet endogenous losses of magnesium in young horses, Nielsen et al. (1998b) found an 6 mg Mg/kg BW with an absorption rate of 40 percent and to increase in mineral content of the third metacarpus after 3 meet an additional requirement for moderate work of 3.2 mg months of training in horses supplemented with extra cal- Mg/kg BW with a 40 percent absorption rate, the magnesium cium. Likewise, magnesium retention increased at that point requirement for moderate exercise is estimated at (0.015 g Ã in training. As substantial amounts of magnesium are found kg BW) + (0.008 g Ã kg BW), or simply 0.023 g Ã kg BW. in bone mineral (Jee, 1988), it was hypothesized that the in- To meet endogenous losses of 6 mg Mg/kg BW with an ab- creased magnesium retention was caused by increased bone sorption rate of 40 percent and to meet an additional require- formation that was permitted by the additional calcium in ment for heavy work of 6 mg Mg/kg BW with a 40 percent the diet. The authors suggested that the 1989 NRC recom- absorption rate, the magnesium requirement for heavy exer- mendations for magnesium in the young horse in training cise is estimated at (0.015 g Ã kg BW) + (0.015 g Ã kg BW), were too low and appear to be between 0.15 and 0.20 per- or simply 0.030 g Ã kg BW. cent on an as-fed basis. Nolan et al. (2001) reported in- creased mineralization of the third metacarpus when the Potassium magnesium in the diet was above 150 percent of the NRC recommended amount, though their findings were also con- Function founded with varying calcium and phosphorus concentra- tions. Stephens et al. (2004) reported an intake of 36 mg/kg As the major intracellular cation, potassium (K) is in- BW/d resulted in maximal retention of magnesium at day 64 volved in maintenance of acid-base balance and osmotic of race training in young horses fed varying amounts of cal- pressure and is the most quantitatively important ion in- cium, phosphorus, and magnesium. These studies suggest volved in neuromuscular excitability (Kronfeld, 2001). The the magnesium requirements during training are too low, total amount of body potassium in a 500-kg horse has been though Pagan (1994) suggested that the requirement for estimated to be about 28,000 mEq (Rose, 1990). Most of the magnesium may be about half of the NRC requirement. bodyâs potassium is found in skeletal muscle (Johnson, Most likely, exercise and stage of training influence magne- 1995), while less than 1.5 percent of the total body potas- sium requirements (Stephens et al., 2001), and this may ex- sium is found in the extracellular fluid (Rose, 1990). Meyer plain the difference between conclusions of Pagan (1994) (1987) estimated 75 percent of potassium is found in the and those drawn from the other studies. Matsui et al. (2002) skeletal muscle, 5 percent is in the skeleton, 5 percent is in reported that in a cool ambient temperature, magnesium loss the blood and skin, 4.5 percent is in the ingesta, and 10.5 due to exercise-related sweating was small (less than 2 per- percent is found in other tissues. After chronic potassium de- cent of the 1989 NRC requirement). Drepper et al. (1982) pletion, the greatest total amount of potassium lost was from suggested that light to medium work increased magnesium muscle (7.5 percent of the bodyâs total), while 3 percent of requirements by 1 to 2 g/d for a 600-kg horse. Wolter et al. the bodyâs total was lost from the skeleton (representing 60 (1986) suggested supplementing 0.18 percent dietary mag- percent of the skeletonâs reserves). nesium for horses in training, especially if supplemental fat has been incorporated in the diet. In contrast to calcium and Sources and Factors Influencing Absorption phosphorus, additional magnesium requirements associated with growth appear to be less than the extra requirements Forages and oilseed meals generally contain 1â2 percent needed for exercise. While there is not sufficient evidence to potassium on a dry matter basis, whereas cereal grains
82 NUTRIENT REQUIREMENTS OF HORSES (corn, oats, wheat) contain 0.3â0.4 percent potassium. Nor- effective method of restoring fluids and electrolytes (Ecke et mally, potassium intake greatly exceeds requirements due to al., 1998a,b; Schott, 1998). While most intravenous and oral the high potassium concentrations in most types of forage fluid replacement products are higher in sodium than potas- (Coenen, 2005). When potassium supplementation is re- sium, combined fecal and urinary losses resulted in greater quired, potassium chloride and potassium carbonate are ef- potassium losses than sodium. As a result, potassium deple- fective sources of supplemental potassium. Pagan and Jack- tion can occur if horses are not eating. Metabolic acidosis son (1991b) reported the apparent digestibility of potassium can also occur due to an increase in plasma chloride con- to be between 61 and 65 percent, though it has been shown centrations resulting in a greater decrease in strong ion dif- to be as high as 99.8 percent (Reynolds et al., 1998). Pagan ference after oral rehydration therapy. Attention should be (1994) estimated true potassium digestibility to be around paid to these concerns when preparing such solutions. 75 percent. Jansson et al. (1999) reported that in response to Despite the NRC (2005) maximum tolerable concentra- an increase in dietary potassium, urinary excretion is in- tion of potassium being listed as 1 percent of intake, many creased first, followed by an increase in fecal excretion. forages commonly fed to horses without any apparent prob- Hence, the equine kidney is particularly efficient at excret- lems have a much greater concentration of potassium. Thus, ing extra potassium, but the horse may not be efficient at the true maximum concentration is likely much greater as conserving potassium when intake is inadequate (Johnson, excess dietary potassium is excreted readily, primarily via 1995). The body attempts to maintain a balance between di- the urine, when water intake is unrestricted. Lewis (1995) etary intake of electrolytes and excretion of them through concluded that if adequate water is not available, horses will the feces, urine, and sweat, though the amount of elec- refuse to eat if potassium concentrations are too great, in ef- trolytes excreted through the kidneys is the primary variable fect negating the likelihood of potassium toxicity. Addition- that can be controlled in an attempt to respond to varying in- ally, the required potassium concentration in a purified-type take (Coenen, 2005). The redistribution of electrolytes is diet for growing foals was estimated at 1 percent by Stowe needed during exercise and the gastrointestinal tract can (1971), further suggesting the maximum tolerable amount is serve as a temporary reservoir, but its capacity depends on greater than suggested by the 2005 NRC. However, Hintz diet and the time between feeding and exercise. If a diet con- and Schryver (1976) suggested the recommendation by taining lower concentrations of potassium is desired, feed- Stowe to be excessive based upon studies of body composi- ing hay harvested from fields not heavily fertilized with tion and balance trials they conducted. The effects of excess potash may be advised (Hintz, 1995). Exercise in mature potassium have not been studied in the horse; however, hy- horses decreased apparent potassium digestibility from 74.3 perkalemia, induced by parenteral administration of excess percent to 66.3 percent (Pagan et al., 1998). McKenzie et al. potassium, would be expected to cause cardiac arrest (2002) reported that varying DCAD did not alter the daily (Tasker, 1980), though hyperkalemia during exercise does balance of potassium. not cause any cardiac issues. Horses with hyperkalemic pe- riodic paralysis (HYPP) syndrome are sensitive to high potassium concentrations in their diet, but being afflicted Signs of Deficiency or Excess with the problem does not seem to alter potassium balance Foals fed potassium-deficient, pelleted, purified diets (Reynolds et al., 1998). More information on HYPP can be gradually refused to eat and, therefore, lost weight, became found in Chapter 12. unthrifty in appearance, and had moderately lowered serum The normal range for serum potassium concentrations potassium concentration (hypokalemia). On addition of has been given as 2.4 to 5.6 mEq/L by Puls (1994). The potassium carbonate to the purified diet, an immediate re- potassium concentration of the middle gluteal muscle in sumption of normal feed intake occurred (Stowe, 1971). healthy adult horses was reported as 91.1 Â± 3.0 ÂµM potas- Given that fluid losses during exercise can reach 10 to 15 L sium/g muscle (wet weight) but decreased (P < 0.05) to 73.6 per hour in the horse and that horseâs sweat is hypertonic Â± 1.9 ÂµM potassium/g muscle after 7 days of food depriva- with respect to plasma, large amounts of sodium, chloride, tion (Johnson et al., 1991). and potassium can be lost during prolonged exercise (Flaminio and Rush, 1998). Hence, a deficiency in the exer- Recommendations cising horse, particularly in the endurance horse, can de- velop. As sweat fluid losses are almost double when horses Drepper et al. (1982) estimated the daily potassium re- compete in a hot, humid climate as compared to a cool, dry quirements for a 600-kg horse to be 22 g for maintenance climate (McCutcheon and Geor, 1996), dietary intake of (0.037 g/kg BW). Hintz and Schryver (1976), however, using potassium, sodium, and chloride may not be sufficient in a series of balance trials, calculated that mature ponies re- hard working horses in warm, humid climates when supple- quired 0.048 g of K/kg BW/d, though their data was derived mentation is not provided. In cases of diarrhea in horses, it only from fecal and urine losses and did not include sweat has been suggested that using an oral rehydration solu- and dermal losses of potassium. As a result of not including tion as an alternative to intravenous fluids may be a cost- sweat losses, Hintz and Schryver (1976) suggested that the
MINERALS 83 maintenance requirement would actually be greater than (0.05 g Ã kg BW) + (0.032 Ã kg BW Ã 1.4) to meet endoge- 0.048 g K/kg of BW. Not being able to quantify loss of min- nous losses of 40 mg K/kg BW with an absorption rate of 80 erals (such as potassium, sodium, and chloride) through the percent and to meet milk production needs estimated at sweat during digestibility trials tends to underestimate the re- 0.032 kg milk/kg BW containing 0.7 g K/kg milk that is ab- quirements for those minerals by inadequately predicting the sorbed at a 50 percent rate. The requirement from 4 to 5 amount of mineral retained and the resulting calculated en- months is (0.05 g Ã kg BW) + (0.026 Ã kg BW Ã 0.8) to dogenous losses. An endogenous loss of 40 mg/kg BW/d meet endogenous losses of 40 mg K/kg BW with an absorp- with an absorption rate of 80 percent has been proposed by tion rate of 80 percent and to meet milk production needs es- GEH (1994) and results in a maintenance requirement of timated at 0.026 kg milk/kg BW containing 0.4 g K/kg milk 0.05 g K/kg BW. A 500-kg horse would thus require 25 g that is absorbed at a 50 percent rate. The requirement for (500 kg Ã 0.05 g) of dietary potassium daily for maintenance. lactation after 5 months is estimated to be (0.05 g Ã kg BW) Since forages are usually high in potassium concentration + (0.020 Ã kg BW Ã 0.8) to meet endogenous losses of 40 and since forages usually constitute a major proportion of the mg K/kg BW with an absorption rate of 80 percent and to horseâs diet, requirements are typically easily satisfied. meet milk production needs estimated at 0.020 kg milk per For growth of foals with an anticipated mature body kg BW containing 0.4 g K/kg milk that is absorbed at a 50 weight of 600 kg, Drepper et al. (1982) estimated the daily percent rate. potassium requirements to be 11 g (about 0.05 g/kg BW) for Renal excretion of potassium increases in reaction to ex- months 3 to 6, 14 g for months 7 to 12 (about 0.04 g/kg ercise and, combined with heavy sweating losses, can lead to BW), and 18 g for months 12 to 24 (about 0.03 g/kg BW). a potential potassium deficit (Meyer, 1987; Schott et al., Jarrige and Martin-Rosset (1981) suggested 0.6 percent 1991; Johnson, 1998). Jarrige and Martin-Rosset (1981) in- potassium in the diet of 6- to 12-month-old foals, and 0.8 dicated that the optimal potassium concentrations of equine percent for horses 18 to 24 months of age. Growing horses diets were 0.4 to 0.5 percent for light to medium work. Drep- have been shown to deposit 1.5 g of K/kg gain (Schryver et per et al. (1982) estimated the daily potassium requirements al., 1974). Thus, a 215-kg foal gaining 0.85 kg BW/d and for a 600-kg horse to be 32 g for light work (0.053 g/kg having a true potassium retention efficiency of 50 percent BW), 43 g for medium work (0.072 g/kg BW), and 53 g requires 2.6 g (1.5 g K Ã 0.85 kg BW/0.5) of dietary K/d for (0.088 g/kg BW) for heavy work. When maintenance re- skeletal growth in addition to 10.8 g (0.05 g K Ã 215 kg BW) quirements are applied to the work of Drepper et al. (1982), for maintenance. The 50 percent absorption rate, used by the the requirement for light, medium, and heavy work become 1989 NRC, may be low but helps to ensure that potassium 1.1, 1.4, and 1.8 times maintenance, respectively. This rela- will not be limited for the growing horse. tionship has also been approximated by a potassium-to-DE Pregnant mares require little additional potassium relationship. Hoyt et al. (1995a) proposed diets for exercis- (Meyer and Ahlswede, 1978). Jarrige and Martin-Rosset ing horses should contain 4.5 g K/Mcal DE. (1981) indicated that the optimal dietary potassium concen- The main increase in requirements for the electrolytes tration was 0.4 percent for late gestation. Drepper et al. potassium, sodium, and chloride associated with exercise is (1982) indicated that the products of conception require 1.2, to replace the amounts lost in sweat. Typical equine diets 1.7, and 2.2 mg of K/kg of mare weight during gestation contain excess potassium, so inclusion of potassium in elec- months 9, 10, and 11, respectively. To determine require- trolytes for horses may not be needed. Supplementation ments for late gestation, potassium for maintenance was of an electrolyte mixture without potassium resulted in a added to an average of the amount needed for the product of similar completion rate to horses supplemented with a conception. Hence, to meet endogenous losses of 40 mg potassium-containing electrolyte mixture in an 80-km en- K/kg BW with an 80 percent absorption rate and to meet a durance ride (Hess et al., 2005). Exercise conditions greatly fetal deposition rate of 1.36 mg K/kg BW with an 80 percent influence sweat production but quantifying sweat produc- absorption rate, the potassium requirement for months 9, 10 tion in the field is not simple (Coenen, 2005). However, and 11 of gestation was estimated to be (0.05 g Ã kg BW) + sweat losses account for about 90 percent of the changes in (0.0017 g Ã kg BW), or simply 0.0517 g Ã kg BW. body weight during exercise (Meyer et al., 1990). Thus, Co- Drepper et al. (1982) estimated the potassium require- enen (2005) proposed that, for practical purposes, the ment for a 600-kg mare to be 34 g during lactation, which is change in body weight during exercise can be used as an es- lower than recommended by the 1989 NRC. No research has timate of sweat losses. Using data from Meyer et al. (1990) demonstrated the requirement for lactation is different than and McCutcheon and Geor (1998), Coenen (2005) esti- that established by the 1989 NRC, so it was not changed. mated equine sweat to contain 1.4 g K/L, so the potassium However, the percent absorption (50 percent) used to calcu- recommendation for exercise can be expressed as mainte- late the additional potassium needed for milk may be low. nance plus 2.8 g (1.4 g/0.50 percent absorption) for every Additionally, new estimates of milk production are used to kilogram of weight lost during exercise. Some weight loss determine requirements. The recommended potassium re- obviously can occur through defecation and urination, but quirement for lactating mares from foaling to 3 months is this amount is relatively small compared to sweat losses
84 NUTRIENT REQUIREMENTS OF HORSES (Butudom et al., 2002). An exception to this is when tracellular fluid is 138 to 140 mmol/L, which is about furosemide is administered, as furosemide greatly increases 14,000 mmol for a 500-kg horse with an extracellular fluid urine production (Hinchcliff et al., 1995) and likely in- volume of 100 L (Rose, 1990). This is referred to as the ex- creases urinary loss of electrolytes. This could result in an changeable sodium. The skeleton contains 51.1 percent of increased transient requirement associated with the esti- the sodium in the body, the ingesta contains 12.4 percent, mated 700,000 doses given to Thoroughbred and Standard- both blood and muscle contain 10.8 percent, the skin con- bred racehorses a year in the United States (Hinchcliff, tains 8.5 percent, and the organs contain 2.1 percent, ac- 2005). While requiring weighing a horse before and after ex- cording to Meyer (1987). During chronic sodium comple- ercise, and though not applicable after furosemide adminis- tion, the greatest loss is from the ingesta (9.9 percent of the tration, using weight loss as an estimate of sweat loss likely bodyâs total sodium), with the next greatest loss coming provides an accurate estimate of the additional potassium re- from the skeleton (5.2 percent of the bodyâs total). quirements associated with exercise. Because it is not always practical to weigh horses before and after exercise, estimates Sources and Factors Influencing Absorption of sweat loss for horses performing different levels of exer- cise have been made in order to estimate the electrolyte re- The sodium concentration of natural feedstuffs for quirements of exercising horses. It is important to note that horses is often lower than 0.1 percent. Sodium chloride sweat loss will be greatly influenced by environmental tem- ((NaCl) common salt) is often added to concentrates at perature and whether the animal is acclimated to the im- rates of 0.5 percent to 1 percent or fed free-choice as plain, posed exercise and the environmental conditions. A discus- iodized, cobalt-iodized, or trace-mineralized salt. In exer- sion of factors affecting sweat losses can be found in Chapter cising horses, Jansson and Dahlborn (1999) reported 7. McConaghy (1994) has suggested that 1 liter of sweat is sodium intake solely from a salt block was equal to or less necessary to dissipate 580 kcal of heat in the horse. There- (range from 0 to 62 mg/kg BW/d) than the maintenance re- fore, sweat loss may be approximated from heat production quirement in four out of six horses, suggesting supplemen- during exercise. The factors affecting heat production during tation in feed may be required for some exercising horses to exercise are discussed in Chapter 1. For the purposes of this meet losses associated with sweating. Ingesta in the large document, daily sweat loss associated with work for horses intestine has been shown to be a reservoir for water, as well in the light, moderate, heavy, and very heavy exercise cate- as for sodium, chloride, and potassium, when exercising gories are estimated at 0.25, 0.5, 1, and 2 percent of body (Meyer, 1996a,b), and may be why exercising horses rarely weight, respectively. These estimates are based on weekly develop severe hyponatraemia despite losing substantial workloads expected for the horses in different categories and amounts of sodium through their sweat. Sosa Leon et al. do not necessary account for losses associated with a stren- (1998) concluded administration of electrolyte paste is ad- uous competition, such as a race or a 3-day event. After a vantageous over water alone in restoring fluid, electrolyte, strenuous event, particularly in a hot environment, additional and acid-base balance after fluid and electrolyte loss attrib- supplementation may be necessary to replace electrolyte utable to furosemide administration. Butudom et al. (2002) losses. A sweat loss of 2.4 percent of body weight has been reported 0.45 and 0.9 percent saline solutions, offered dur- reported in horses becoming acclimated to and exercising in ing the first 5 minutes after completing exercise, were more hot, humid conditions (McCutcheon et al., 1999). This per- effective in maintaining elevated plasma sodium concentra- centage, greater than the estimate used for very heavy exer- tions and restoring body weight loss during exercise than cise, demonstrates the impact environmental conditions have was water alone. It was cautioned that this should be pur- on sweating rate and serves as a reminder that the estimates sued after horses have been trained to drink salt water dur- for sweat loss for varying intensities of work are only a guide ing and after exercise to prevent greater dehydration. Addi- and can be much greater. tionally, repeated oral administration of an electrolyte solution has been associated with an exacerbation of gastric ulcers (Holbrook et al., 2005). Urinary sodium loss is min- Sodium imized when sodium is relatively deficient in the diet and temperatures are cool (Tasker, 1967), as well as after exer- Function cise (Jansson et al., 1995). Lindinger et al. (2000) also re- Sodium (Na) is critical for normal function of the central ported an improved conservation of sodium after heat ac- nervous system, generation of action potentials in excitable climation and training. However, sodium excretion in the tissues, and transport of many substances such as glucose feces may exceed that in urine under some conditions across cell membranes (Johnson, 1995). Sodium is the (Alexander, 1977). When dietary sodium is increased, an major extracellular cation and the major electrolyte involved increase in urinary excretion will maintain the total ex- in maintenance of acid-base balance and osmotic regulation changeable sodium pool (Rose, 1990). Sodium concentra- of body fluids. The average sodium concentration in the ex- tions have been reported to increase in equine sweat in re-
MINERALS 85 sponse to exercise (McCutcheon and Geor, 1998; Jansson et mately 1.9 mg/kg BW/d during the 10th month of gestation. al., 1999). The requirement for months 9, 10, and 11 of pregnancy has Schryver et al. (1987b) found 75â94 percent of ingested been estimated as (0.02 g Ã kg BW) + (0.002 g Ã kg BW), sodium was absorbed. Pagan et al. (1998) reported the ap- or simply 0.022 g Ã kg BW, to meet endogenous losses of 18 parent digestibility of sodium to be increased in four mature mg Na/kg BW with a 90 percent absorption rate and to meet horses from 48.9â83.6 percentâpresumably to meet the in- a fetal deposition rate of 1.9 mg Na/kg BW based upon the creased sodium needs that accompany additional sweat work of Drepper et al. (1982). losses. Apparent absorption of sodium was 99.6 percent in Schryver et al. (1986b) reported sodium concentrations mature broodmares (Reynolds et al., 1998). during the first 3 months after foaling to average 180 mg/kg fluid milk, but had dropped to 115 mg/kg milk from 12 to 17 weeks. Grace et al. (1999a) reported sodium concentrations Signs of Deficiency or Excess to average 130 mg/L milk in pasture-fed mares during the Chronic sodium depletion results in decreased skin tur- first 5 months after foaling, which would equate to about gor, a tendency for horses to lick objects such as sweat- 126 mg/kg milk. Using an average of the two estimates and contaminated tool handles, a slowed rate of eating, de- an absorption rate of 90 percent, each kg of milk would re- creased water intake, and eventually a cessation of eating quire 0.17 g sodium during the first 3 months of lactation (Meyer et al., 1984). In acute sodium deficiency, muscle and 0.14 g sodium after that. Thus, from foaling to 3 contractions and chewing were uncoordinated and horses months, the sodium requirement for lactating mares is (0.02 had an unsteady gait; serum sodium and chloride concentra- g Ã kg BW) + (0.032 Ã kg BW Ã 0.17) to meet endogenous tions decreased markedly, whereas serum potassium in- losses of 18 mg Na/kg BW with an absorption rate of 90 per- creased (Meyer et al., 1984). As ambient temperatures and cent and to meet milk production needs estimated at 0.032 exercise intensity increased, sodium concentrations in sweat kg milk/kg BW containing 0.153 g Na/kg milk that is ab- increased and sodium losses could result in relatively large sorbed at a 90 percent rate. From 4 to 5 months, the esti- ion deficits (McCutcheon and Geor, 1998). This can lead to mated requirement is (0.02 g Ã kg BW) + (0.026 Ã kg BW alterations in skeletal muscle ion content and potentially Ã 0.14) to meet endogenous losses of 18 mg Na/kg BW with muscular dysfunction. As long as sufficient water is avail- an absorption rate of 90 percent and to meet milk production able, excess sodium will typically be excreted in the urine. needs estimated at 0.026 kg milk/kg BW containing 0.126 g The maximum tolerable concentration of sodium chloride in Na/kg milk that is absorbed at a 90 percent rate. After 5 the diet has been set at 6 percent of intake (NRC, 2005). months, the sodium requirement for lactating mares is esti- mated as (0.02 g Ã kg BW) + (0.020 Ã kg BW Ã 0.14) to meet endogenous losses of 18 mg Na/kg BW with an ab- Recommendations sorption rate of 90 percent and to meet milk production Optimal sodium concentrations for equine diets have needs estimated at 0.020 kg milk/kg BW containing 0.126 g been reported to be between 1.6 and 1.8 g/kg dry matter for Na/kg milk that is absorbed at a 90 percent rate. growth, maintenance, and late gestation and 3.6 g/kg dry Even though sodium excretion has been shown to be re- matter for moderate to heavy work (Jarrige and Martin- duced by as much as 73 percent during the early stages of Rosset, 1981). Endogenous sodium loss in the idle adult training (McKeever et al., 2002), prolonged exercise and el- horse has been estimated at 15 to 20 mg/kg BW/d (Meyer et evated temperatures increase the sodium requirement be- al., 1984; Schryver et al., 1987b). If sodium is 90 percent ab- cause sweat contains a notable amount of sodium. Sodium sorbed, and using an endogenous loss of 18 mg/kg BW/d, losses in sweat are estimated to range from 8.25 to 82.5 g the maintenance requirement is 0.02 g Na/kg BW daily. A (Meyer, 1987). Butudom et al. (2002) calculated sodium 500-kg horse would meet that requirement by consuming losses due to sweat losses during endurance exercise to be 25 g NaCl/day. between 1,500 to 2,000 mmol (34.5 to 46 g), with an addi- Based upon whole body analyses of euthanized foals, tional loss of 1,500 mmol (34.5 g) due to administration of Grace et al. (1999b) determined 0.85 g Na/d were deposited furosemide, a diuretic. Meyer et al. (1984) reported that a at an absorption rate of 80 percent, resulting in a calculated negative sodium balance could be demonstrated transiently daily sodium requirement of 1 g sodium for a 200-kg horse in nonexercised horses and ponies after initial restriction of gaining 1 kg/d. The requirement for growing horses has been sodium intake to 5 mg/kg BW/d. However, over time, these set at (0.02 g Ã kg BW) + (1.0 g Ã average daily gain in kg) horses adapted to sodium restriction and, ultimately, could to meet endogenous losses of 18 mg Na/kg BW with a 90 be in positive sodium balance while consuming only 1.6 mg percent absorption rate and to meet growth requirements of Na/kg BW/day. Hoyt et al. (1995a) proposed diets for horses 0.85 g Na/kg BW gain with an 80 percent absorption rate. exercising in hot, humid conditions should contain 1.3 g Drepper et al. (1982) reported that the sodium require- Na/Mcal DE. Because of limited data on specific require- ment of pregnant mares, above maintenance, is approxi- ments for sodium and the influence of activity, adaptation,
86 NUTRIENT REQUIREMENTS OF HORSES and environment on animal needs, precise recommendations to those reported in ruminants, which include decreased cannot be made. However, the 1989 NRC suggested sodium food intake, weight loss, muscle weakness, decreased milk concentration in the maintenance diet should be at least 0.1 production, dehydration, constipation, and depraved ap- percent. For intensely exercising horses in a hot climate, petite (Fettman et al., 1984). Hoyt et al. (1995b) indicated that 0.41 percent sodium in the Horses are considered tolerant of high concentrations of diet of horses drinking tap water would be necessary to meet salt in their diets if they have free access to fresh drinking sodium demands and that adding 0.9 percent salt to the diet water. High salt concentrations in feeds are sometimes used would meet those demands. This represents a large salt in- to limit feed intake, especially of supplements. Parker take that would not normally be required under less stringent (1984) reported that ponies consumed a 3-day grain ration conditions. A more precise estimate of sodium requirements over 3 days when the grain contained 16 percent salt but can be determined with exercising horses by measuring consumed the same ration in 1â2 days when the grain con- weight losses during exercise, and using weight loss as an tained only 4â8 percent salt. The elevated dietary salt con- estimate of sweat loss. Sweat contains 2.8 g Na/L (Coenen, centrations were associated with marked increases in water 2005), so adding 3.1 g Na/kg weight loss during exercise to intake. Regulating the concentrate intake by salt addition is maintenance requirements provides a reasonable estimate of generally not as effective in horses as in ruminants. The sodium requirements during exercise. Thus, the requirement maximum percentages of the daily salt requirements toler- for sodium in exercising horses has been estimated as (0.02 ated in drinking water for 450-kg working and lactating g Ã kg BW) + (3.1 g Ã BW loss in kg during exercise) to horses were estimated at 840 and 1,050 percent, respectively meet endogenous losses of 18 mg Na/kg BW with an ab- (NRC, 1974). Central nervous system manifestations of salt sorption rate of 90 percent and to meet additional require- toxicity occur in some species. Horses can be expected to re- ment for work associated with sweat loss of 2.8 g of Na/kg spond similarly, though it has not been documented. of BW loss as an estimate of sweat loss during exercise with Chloride concentrations in serum or plasma provide a a 90 percent absorption rate. good guide to chlorine balance (Rose, 1990). Normal range for plasma chloride concentrations in mature performance horses has been given as 94â104 mmol/L (Hodgson and Chlorine Rose, 1994). Function Recommendations Chlorine (Cl) normally accompanies sodium in the diet as the anion chloride. Chloride is an important extracellular While the chlorine requirements of horses have not been anion involved in acid-base balance and osmotic regulation. strongly established, chlorine requirements are presumed to It is an essential component of bile and is important in the be adequate when the sodium requirements are met with formation of hydrochloric acid, a component of gastric se- sodium chloride. However, a review of studies by Coenen cretions necessary for digestion. (1999) revealed fecal chlorine excretion to be 2.3 Â± 1.2 mg/kg BW/d without any major influence of chlorine intake. Given that chloride absorption can be 100 percent (Schryver Sources and Factors Influencing Absorption et al., 1987b), this likely represents the fecal endogenous Common salt is 61 percent chloride and is often used to losses. Coenen (1999) proposed using 3 mg Cl/kg BW to meet chlorine needs. Some chloride concentrations of com- account for fecal endogenous losses, 2 mg/kg BW for renal mon equine feedstuffs range from 0.05 percent for corn and endogenous losses, and 1 mg/kg BW for cutaneous endoge- soybean meal to 3 percent for molasses (NRC, 1982). nous losses for a total of 6 mg Cl/kg BW/d for total en- Schryver et al. (1987b) reported chloride absorption to be dogenous losses. Another 14 mg Cl/kg BW/d was suggested 100 percent and did not vary as dietary sodium chloride con- to replace that loss through perspiration for a total minimum centrations increased. maintenance requirement of 20 mg Cl/kg BW/d. However, 80 mg/kg BW/d were required to prevent changes in acid- base balance and hypochloremia and this likely represents Signs of Deficiency or Excess the recommended minimum daily chlorine intake and has A chlorine deficiency is unlikely to occur without a been set as the maintenance requirement. sodium deficiency, although it could occur if horses were Coenen (1999) suggested the requirements for growth being administered sodium bicarbonate (Lewis, 1995). up to 6 months of age equals maintenance plus 13 mg Cl/kg Chlorine deficiency was clearly correlated to metabolic al- BW/d, and maintenance plus 5 mg Cl/kg BW/d for 6â12 kalosis as observed in horses with minimized chlorine in- months. Though specific requirements for growth from take (Coenen, 1988, 1991) because of a compensatory in- 12â24 months have not been specifically determined, an in- crease in bicarbonate during the chlorine deficit (Tasker, termediate value between the long weanling and maintenance 1980). Clinical signs of chlorine deficiency may be similar is used. Thus, the requirement for growing horses is esti-
MINERALS 87 mated as (0.08 g Ã kg BW) + (0.013 g Ã kg BW), or simply sulfur in plants is organic sulfur present in the amino acids 0.093 g Cl Ã kg BW, to meet maintenance requirements and in the plant proteins (Georgievskii et al., 1982). Some di- to meet growth requirements. The requirement for growing etary inorganic sulfur is incorporated into sulfur-containing horses 6 to 12 months of age is estimated to be (0.08 g Ã kg microbial protein in the equine hindgut, but amino acid BW) + (0.005 g Ã kg BW), or simply 0.085 g Cl Ã kg BW, absorption from this region is limited. Inorganic forms of to meet maintenance requirements and to meet growth re- dietary sulfur are used in the synthesis of some sulfur- quirements. For growing horses 12 to 24 months, the re- containing substances such as chondroitin sulfate, heparin, quirement has been set at (0.08 g Ã kg BW) + (0.0025 g Ã and insulin. Adequate, high-quality dietary protein (e.g., kg BW), or simply 0.0825 g Cl Ã kg BW, to meet mainte- from soybean meal) usually provides at least 0.15 percent nance requirements and to meet growth requirements. organic sulfur. No studies were found that specifically ex- During the last 3 months of pregnancy, requirements amined sulfur absorption rates, though Wall et al. (1992) re- equal maintenance plus 2 mg Cl/kg BW/d or simply 0.082 g ported that anaerobically exercised horses that had a sulfur Cl Ã kg BW. Lactation requirements are maintenance plus intake of 16 g/d had urinary excretion of 22 g/d regardless 11 mg Cl/kg BW/d (0.091 g Cl Ã kg BW) based upon data of dietary cation-anion balance. While this suggests a tre- from literature related to milk composition (Coenen, 1999). mendous loss of sulfur from the body is possible, the work Hoyt et al. (1995a) proposed rations for exercising horses also suggests sulfur absorption may be high. should contain 3.1 g Cl/Mcal DE. For a 500-kg horse con- suming 24.6 Mcal DE, this would equate to 76.3 g Cl or 150 Signs of Deficiency or Excess mg Cl/kg BW. Alternatively, Hoyt et al. (1995b) proposed intensely exercising horses in a hot climate consuming tap Sulfur deficiency in horses has not been described. The water would need 0.88 percent chlorine in the ration, which maximum tolerable dietary sulfur concentration has been es- could be met by adding 1.14 percent salt to the ration. Al- timated at 0.5 percent from data in other species (NRC, ternatively, Coenen (1999) suggested chlorine requirements 2005). Corke (1981), however, reported the effects of excess for exercising horses equal maintenance requirements plus sulfur on 5- to 12-year-old horses that were accidentally fed 5.5 mg Cl/g sweat/kg BW. An average of 5.3 g Cl/L sweat between 200 and 400 g of flowers of sulfur (> 99 percent was given later by Coenen (2005), and that average was used sulfur). The horses became lethargic within 12 hours, and in establishing the requirement for horses based upon sweat colic often supervened. Other signs included a yellow, loss. Thus, the requirement for exercise is (0.08 g Ã kg BW) frothy discharge from the external nares, jaundiced mucous + (5.3 g Ã BW loss in kg during exercise) to meet mainte- membranes, and labored breathing. Two of the 12 horses de- nance requirements and to meet the additional requirement veloped an expiratory snort and cyanosis; despite treatment, for work associated with sweat loss assuming a concentra- they died following convulsions. Chronic consumption of tion of 5.3 g Cl/kg sweat and using BW loss as an estimate excess sulfur in ruminants depresses copper absorption and of sweat loss during exercise with a 100 percent Cl absorp- can induce secondary copper deficiencies. No evidence has tion rate. been found that the equine species is subject to this effect of sulfur (Strickland et al., 1987). Sulfur Recommendations Function The sulfur requirements of the horse have not been es- Sulfur, in the form of sulfur-containing amino acids, B tablished, though the sulfur in high-quality dietary protein vitamins (thiamin and biotin), heparin, insulin, and chon- appears adequate to meet the sulfur requirements of the droitin sulfate, makes up about 0.15 percent of the body horse (NRC, 1978; Jarrige and Martin-Rosset, 1981). Until weight. The sulfur-containing amino acids cysteine and further studies verify the need for adjustment, the recom- methionine play a major role in the structural component of mendations of the 1989 NRC (0.15 percent sulfur on a DM almost all proteins and enzymes in the body. Thiamin is in- basis) remain unchanged. volved in carbohydrate metabolism, biotin is a co-enzyme involved with intermediary metabolism, heparin serves as an MICROMINERALS anticoagulant, insulin helps regulate carbohydrate metabo- lism, and chondroitin sulfate is important to joint health. Cobalt Sources and Factors Influencing Absorption Function Horses must meet their sulfur requirements from organic Cecal and colonic microflora of horses use dietary cobalt forms such as cystine and methionine. Although about (Co) in the synthesis of vitamin B12 (Davies, 1971; Salmi- 10â15 percent of total plant sulfur is inorganic, most of the nen, 1975), and cobalt, in the form of vitamin B12, is inter-
88 NUTRIENT REQUIREMENTS OF HORSES related with iron and copper in hematopoiesis or blood cell for cane molasses. Although few controlled studies on com- formation (Ammerman, 1970). parative copper availability have been reported for the horse, salts such as cupric chloride, cupric sulfate, and cupric car- bonate are effective supplemental copper sources in other Sources and Factors Influencing Absorption nonruminants (Cromwell et al., 1978, 1984). Though Cym- Common horse feeds typically contain between 0.05 to baluk et al. (1981a) suggested the efficiency of copper ab- 0.6 mg Co/kg dietary dry matter (DM). Cobalt-iodized salt sorption is inversely related to the dietary copper concentra- often contains around 100 mg cobalt/kg DM. The lower At- tion, Lawrence (2004) did not find such a relationship when lantic Coastal Plain and parts of New England have soils doing a retrospective analysis of nine studies reported be- that are deficient in cobalt, as do other areas of the world in- tween 1981 and 2003. It should be noted that the reviewed cluding Australia, New Zealand, East Africa, and Norway studies used a variety of copper sources, which may have (Ammerman, 1970). Information regarding the availability confounded the results. Schryver et al. (1987b) reported of various compounds is limited, but the carbonate, chloride, copper absorption to range between 24 and 48 percent. and sulfate forms of cobalt have been proposed as adequate Pagan (1994) estimated true copper digestibility to be sources for beef cattle (Cunha et al., 1964). around 40 percent in the mature horse (calculated endoge- nous loss estimated at 38 mg/d), while Pagan and Jackson (1991b) reported apparent digestibilities of copper ranging Signs of Deficiency or Excess from 27.2â32.5 percent. Hudson et al. (2001) did not detect A cobalt deficiency would result in a vitamin B12 defi- differences in true copper digestibility between sedentary ciency. However, no known cases of either a cobalt or vita- horses (41.8 percent) and exercised horses (54.4 percent). min B12 deficiency have been reported or experimentally in- Pagan and Jackson (1991a) reported apparent copper di- duced in horses. A maximum tolerable concentration of 25 gestibility to be higher in a pelleted blend of alfalfa and mg/kg DM intake has been set for cobalt from data in other Bermuda straw (36.2 percent) as compared to alfalfa hay (10 species (NRC, 2005). percent) or alfalfa pellets (9.2 percent). Wagner et al. (2005) reported the absorption of copper oxide, sulfate, and an organic-chelate to be 5.3, 6.6, and 2.8 percent, respectively, Recommendations and these did not differ between sources. However, it was The cobalt requirements of horses have not been studied noted that these values were lower than previous studies. No specifically. Filmer (1933) reported that horses remained in differences on bone metabolism (Baker et al., 2003) or liver good health while grazing pastures that were inadequate in copper concentrations (Siciliano et al., 2001) were found be- cobalt for ruminants. The 1989 NRC set the minimum rec- tween an inorganic copper source and a mix of organic and ommended amount for horses at 0.1 mg cobalt/kg DM. Con- inorganic copper sources. However, Miller et al. (2003) re- sidering that the occurrence of deficiency symptoms in cat- ported an increase in copper retention and apparent di- tle and sheep were observed at concentrations of less than gestibility of yearling horses supplemented with an organic 0.04 to 0.07 mg/kg dietary DM, and considering that horses copper source (proteinate) as compared to copper sulfate. In are tolerant of lower concentrations than cattle, the mini- contrast, Baker et al. (2005) showed that apparent copper di- mum recommended amount has been set at 0.05 mg/kg di- gestibility and retention were greater in mature horses sup- etary DM. This should typically be met through the con- plemented with copper sulfate as compared to the same or- sumption of normal feedstuffs. ganic copper proteinate. Several factors can influence copper metabolism. Copper interacts with many other minerals, including molybdenum, Copper sulfur, zinc, selenium, silver, cadmium, iron, and lead (Un- derwood, 1981). There are limited quantitative studies in the Function horse that explore these relationships; however, some dis- Copper (Cu) is essential for several copper-dependent en- tinct species differences are known. Molybdenum intakes at zymes involved in the synthesis and maintenance of elastic 1 to 3 mg/kg of the ration interfered with copper utilization connective tissue, mobilization of iron stores, preservation in ruminants (Underwood, 1981), but much higher concen- of the integrity of mitochondria, melanin synthesis, and trations of molybdenum were tolerated by the horse (Under- detoxification of superoxide. wood, 1977; Cymbaluk et al., 1981b). Molybdenum at 20 mg/kg of the ration did not interfere with copper absorption (Rieker et al., 1999). Therefore, the likelihood of a molyb- Sources and Factors Affecting Absorption denum problem in the horse is minimal (Strickland et al., The copper concentration of common feedstuffs ranges 1987). In contrast, a secondary copper deficiency was in- widely from approximately 1 mg/kg for corn to 80 mg/kg duced after 5 to 6 weeks in weanling foals fed a basic ration
MINERALS 89 containing 7.7 mg Cu/kg of ration and containing either per concentrations than obtained for using plasma (Paynter, 1,000 or 2,000 mg zinc/kg of the ration, but not when the ra- 1982). Meyer and Tiegs (1995) proposed that liver copper tion contained either 29.1 or 250 mg zinc/kg (Bridges and concentrations in the 10- and 11-month-old fetus of greater Moffitt, 1990). than 300 Âµg Cu/g DM and in newly born foals of greater than 400 Âµg of Cu/g DM reflect an adequate copper supply of their dams. Signs of Deficiency or Excess Osteochondrosis and osteodysgenesis reportedly are as- Recommendations sociated with hypocupremia (Carbery, 1978; Bridges et al., 1984). When foals were fed a liquid milk-replacer diet con- Jarrige and Martin-Rosset (1981) and Drepper et al. taining 1.7 mg Cu/kg DM for 13â16 weeks, lameness was (1982) recommended 10 mg Cu/kg ration for all ages of observed 2â6 weeks after serum copper concentrations had horses, regardless of degree of work or stage of production, decreased to less than 0.1 Âµg/ml (Bridges and Harris, 1988). though Jeffcott and Davies (1998) suggested that there are A decline in serum copper with increasing age of mares ap- differences in copper requirements for horses of different peared to be related to the incidence of usually fatal rupture breed, age, sex, and pregnancy status. Hudson et al. (2001) of the uterine artery in aged, parturient mares (Stowe, 1968). showed endogenous copper losses to be 15.7 mg/d (0.029 Feeding 8 ppm copper, as compared to 25 ppm, resulted in mg Cu/kg BW with a true copper digestibility of 41.8 per- declining liver copper values, osteochondritis, epiphysitis, cent) for sedentary horses and 20.3 mg/d (0.038 mg Cu/kg and limb deformities over a 6-month period (Hurtig et al., BW with a true copper digestibility of 54.5 percent) for ex- 1993). However, van Weeren et al. (2003) found no rela- ercising horses averaging 534 kg, with a resultant require- tionship between liver copper concentrations and osteo- ment ranging from 35 to 44 mg Cu/d (0.066 to 0.083 mg chondrosis (see Chapter 12 for further discussion on the role Cu/kg BW/d). By comparison, in evaluating the results of of Cu in developmental orthopedic disease). many prior studies, Pagan (1994) estimated endogenous Horses are relatively tolerant of high dietary copper con- copper loss to be about 0.069 mg/kg BW and the true di- centrations. Pony mares fed 791 mg of Cu/kg ration for 183 gestibility of copper to be 40 percent. The resulting require- days had elevated liver copper, but no adverse clinical signs ment for a 500-kg horse would be 86 mg Cu/d or 0.172 mg were observed in the mares or their foals (Smith et al., Cu/kg BW. Assuming an intake of 2 percent of BW, this 1975). Single oral doses of 20 and 40 mg of Cu/kg BW (as would result in a dietary copper concentration of 8.6 mg/kg copper sulfate) were administered to mature ponies without DM feed, suggesting the 10 mg/kg DM requirement given in apparent adverse effects (Stowe, 1980). The maximum tol- the 1989 NRC is adequate for maintenance. Noting the erable concentration of copper for horses has been estimated lower copper absorption rate in various feedstuffs, a 35 per- to be approximately 250 mg/kg ration (NRC, 2005), though cent absorption rate was used with the endogenous copper the report by Smith et al. (1975) provided evidence that it losses estimated by Pagan (1994) to ensure adequate dietary may be substantially higher. Other dietary factors such as copper with the resultant copper requirement for mainte- zinc or iron concentrations, as well as the source of copper, nance being 0.2 mg/kg BW/d. can influence this also. Only one study could be found that made an attempt at Bathe and Cash (1995) suggested serum copper concen- factoring out the true copper requirement for growth based trations may be of limited clinical usefulness in assessing on whole body analysis. Grace et al. (1999b) determined copper status. Mee and McLaughlin (1995) reported a wide 1 mg Cu/d was deposited at an estimated absorption rate of range in what is considered to be ânormalâ serum copper 30 percent for gain of 1 kg/d in 200-kg foals. The result concentrations, depending upon what procedures are used would increase requirements over maintenance by only and whether the population of horses being routinely sam- 0.017 mg Cu/kg BW/d. That would result in a requirement pled is supplemented or not. Auer et al. (1989) reported an of 0.217 mg Cu/kg BW for growing horses. If that were increase in plasma copper concentrations in response to an converted to a concentration basis assuming a 2.5 percent acute reaction after localized injury, suggesting another lim- feed intake, it would result in a recommendation of 8.68 mg itation of sampling blood to assess dietary copper status. Cu/kg DM intake. Satisfactory growth was attained by foals Suttle et al. (1996) proposed a threshold value for serum fed 9 mg Cu/kg ration (Cupps and Howell, 1949), whereas copper of 16 Âµmol/L to distinguish normal from subnormal normal copper homeostasis was maintained in mature copper status and 11.5 Âµmol/L as an interim threshold to ponies fed 3.5 mg of Cu/kg ration (Cymbaluk et al., 1981a). distinguish a deficient from a marginal copper status. New- Knight et al. (1985) reported a negative correlation between born foals have low serum copper concentrations as com- the copper concentrations of weanling rations and a per- pared to mature horses (Cymbaluk et al., 1986). Addition- ceived degree of affliction with metabolic bone disease. The ally, an apparent sedimentation of ceruloplasmin copper 1989 NRC subcommittee reviewed the data by Knight et al. occurs during clot retraction resulting in lower serum cop- (1985) and a follow-up study by Knight et al. (1988) that re-
90 NUTRIENT REQUIREMENTS OF HORSES ported histologic lesions without statistical inference. The Interestingly, Voges et al. (1990) found copper concen- subcommittee considered the data to be inconclusive and trations in equine bone increase up to age 8 and then begin left the copper requirements for growth, pregnancy, and lac- to decrease. It was proposed that the lower amount in older tation unchanged from the previous NRC (1978). In support horses may be the result of differences in feeding horses in of this, Kronfeld et al. (1990) pointed out that the correlation more recent years, when supplementation is more frequent, reported by Knight et al. (1985) becomes nonsignificant providing some support for the greater incorporation of (P > 0.05) if two outlier values (32 and 40 ppm of copper) copper into the skeleton if it is available. This finding raises were eliminated from the 19 points. the question as to whether increased copper concentrations Subsequently, Knight et al. (1990) published greater de- in the ration are efficacious in reducing the incidence of os- tails of the 1988 study. Mares were fed either 13 ppm or 32 teochondrosis. Despite most commercially prepared feeds ppm during the last 3 to 6 months of gestation and the first for growing horses typically containing substantially higher 3 months of lactation. Their respective foals were fed a pel- amounts of copper than the amount recommended by the leted concentrate containing 15 ppm or 55 ppm and were 1989 NRC, the incidence of osteochondrosis remains high then euthanized at 3 or 6 months and necropsied. Foals re- in certain populations of horses. Interestingly, Gabel (2005) ceiving the ration containing the lower copper concentra- reported that the optimum concentration of copper from a tion had more lesions than did the ones receiving supple- follow-up study of the farms used in the Knight et al. (1985) mentation at the higher rate though one foal in the low study appeared to be 25 ppm. However, Gabel (2005) re- copper group accounted for a disproportional percentage of ported that in the follow-up study, yearlings were consum- the lesions. Similarly, Hurtig et al. (1993) reported defec- ing 160 percent of the protein requirements and 120 percent tive cartilage and bone growth in foals fed 8 ppm as com- of the energy requirements recommended by the NRC. Sav- pared to those receiving 25 ppm. Though the information age (1992) reported that when 48 foals were fed 11.1 to 11.7 may be useful, the animals in that study were housed by ppm Cu, there was no increase in osteochondrosis provided treatment in two pens so the experimental number is ar- the DE and phosphorus content were similar to what was guably only one (n = 1), thus, the statistical inference lacks suggested by the 1989 NRC. These studies emphasized the validity. Supplementation with copper at the rate of 0.5 mg apparent need to feed a balanced ration rather than simply Cu/kg BW to foals on pasture containing 4.4 to 8.6 ppm increase the concentration of a single nutrient. Furthermore, copper had no effect on bone or cartilage parameters, but in a study using 629 Hanoverian foals from 83 farms, similar supplementation of mares decreased radiographic Winkelsett et al. (2005) reported no relationship between indices of physitis in the distal third metatarsal bone of their copper intake of the pregnant mare and osteochondrosis in foals at 150 days and the prevalence of articular cartilage the foals. Though the requirement, based upon the replace- lesions (Pearce et al., 1998a). These results led the investi- ment of endogenous losses and an allotment for growth, gators to conclude that mare supplementation probably had may be slightly lower, a recommendation has been set at an effect on foal skeletal development in utero rather than 0.25 mg/kg BW for growing horses as studies have indicated through the provision of greater copper stores in the liver of potential problems when the concentration of copper is neonates. (It should be noted that the zinc:copper ratio ap- under 10 ppm. Assuming an intake of 2.5 percent of BW, pears to be over three times greater in the unsupplemented this recommendation will meet that minimum. As there is group than in the supplemented group [Pearce et al., some evidence that additional copper may be useful in the 1998c], and the horses in the study also had low calcium pregnant mare in increasing fetal copper stores, which may and phosphorus intakes, as well as calcium:phosphorus ra- be of use after birth, the requirement for the pregnant mare tios below 1 for 6 of the 11 months of the trial [Pearce et during months 9, 10, and 11 of gestation has been set at 0.25 al., 1998a], and these factors certainly could have influ- mg/kg BW, which would work out to a concentration of 12.5 enced the results). Gee et al. (2000) reported parenteral mg/kg DM for a mare consuming 2 percent of her body copper supplementation of broodmares in late gestation had weight. Further studies in a tightly controlled setting will no effect on liver copper concentration of foals at birth, need to be conducted to determine the adequacy of this though copper liver concentrations can be increased recommendation. through supplementation beginning after birth (Pearce et Anderson (1992) reported milk copper concentration as al., 1998b). Though all the broodmares were consuming the 0.155 mg/kg milk. Grace et al. (1999a) determined milk same pasture, Van Weeren et al. (2003) reported that foals copper concentrations to be 0.23 mg/L milk during the first born with low liver copper concentrations had worsening 3 months after gestation and 0.18 mg/kg during months 4 osteochondrosis scores from 5 to 11 months, while foals and 5, which would equate to about 0.22 and 0.17 mg/L born with higher liver copper concentrations showed im- milk, respectively. Milk copper concentrations ranged from provement. This finding led them to propose that copper a high of 0.6 mg/kg milk at birth to about 0.17 mg/kg milk may be involved in the repair process of existing lesions for weeks 3 to 8 postpartum and was not influenced by di- during growth. etary copper concentration (Breedveld et al., 1987). Like-
MINERALS 91 wise, foal blood mineral concentrations also were not influ- px) activity during thyroid stimulation, whereas a moder- enced by the copper concentration of the mareâs ration. Sim- ately low selenium intake normalized circulating T4 concen- ilar results were reported by Baucus et al. (1987). Using an tration in the presence of iodine deficiency. average of the three milk concentrations (0.185 mg Cu/kg milk) and an absorption rate of only 35 percent, the esti- Sources and Factors Influencing Absorption mated milk production of 3.2 percent of body weight used during the first 3 months of lactation results in an increased Laboratory analyses of feedstuffs usually do not report io- requirement of only 0.017 mg Cu/kg BW more than mainte- dine concentrations, though iodine concentrations in most nance. The resulting 0.217 mg Cu/kg BW would result in a common feedstuffs vary from 0 to 2 mg/kg DM (NRC, 1989). need for 108.5 mg copper for a 500-kg lactating mare. If that This depends on the concentrations of iodine in the soil on mare were consuming 2.5 percent of her body weight, the which the feedstuffs were grown. Kelp and other seaweed are resulting concentration would be 8.68 mg/kg DM. As feed- sometimes fed to horses and can have concentrations as high ing rations containing about 9 ppm copper to broodmares re- as 1,850 mg of I/kg DM (Baker and Lindsey, 1968). Ethyl- sult in milk with normal copper concentrations (Hintz, enediaminedihydroiodide (EDDI) is used as an equine anti- 1987b), and since no increases in either milk concentrations fungus supplement and can contribute to excess dietary io- or foal serum concentrations are reported with additional dine. Typically, iodine supplementation is accomplished by supplementation, the amount recommended by the 1989 feeding iodized or trace mineralized salts that often contain 70 NRC appears to be adequate. Assuming a 2.5 percent intake mg of I/kg DM. Cobalt-iodized salt is not required, nor is it for the lactating mare, the recommended daily copper allot- detrimental. Potassium iodate is more stable and, hence, is ment is 0.25 mg/kg BW. preferred to potassium iodide. Digestibility of iodine appears The lack of data for copper requirements in mature, exer- to be quite high as renal excretion goes up linearly with in- cising horses precludes any changes to recommendations creasing iodine intake while fecal excretion remained rela- and remains at 10 mg/kg of dietary DM. Assuming a 2 per- tively low, but constant, with only a small increase in response cent of BW intake for light exercise, this would result in a to increased iodine intake (Wehr et al., 2002). copper intake of 0.2 mg/kg BW; assuming a 2.25 percent of BW intake for moderate exercise, an intake of 0.225 mg/kg Signs of Deficiency or Excess BW; for heavy exercise with an assumed intake of 2.5 per- cent of BW, an intake of 0.25 mg/kg BW. The classic symptom of either a severe deficiency or ex- cess of iodine in the ration is hypothyroidism resulting in thyroid gland hypertrophy or goiter. As concentrations of io- Iodine dine in the newborn foal are determined by the maternal in- take (Meyer, 1996c), reproduction of the mare and health of Function foals can be affected when iodine concentrations in the ra- Most of the bodyâs iodine (I) is found in the thyroid gland tion are inappropriate, even when goiter is not present in (Schryver, 1990). Iodine is necessary for the synthesis of thy- broodmares. Meyer and Klug (2001) indicated that both a roxine (T4) and triiodothyronine (T3), which are thyroid hor- deficiency and excess of iodine depressed the viability of mones that regulate basal metabolism. In the thyroid glands foals and probably influenced embryonic and fetal develop- and in peripheral tissues, T4 is deiodinated to T3. An increase ment. In 1935, Rodenwold and Simms reported losing about in either results in decreased thyroid stimulating hormone 50 percent of foals born to mares receiving iodine-deficient (TSH) secretion and an increase in metabolic rate. Both defi- feedstuffs with the foals showing signs of goiter. Supple- ciencies and toxicities of iodine may result in hypothy- mentation of 15 grains per week of potassium iodide (equiv- roidism. When an iodine deficiency is present, sufficient thy- alent to about 100 mg I/day) during the second half of ges- roid hormones are unable to be produced. If excess iodine is tation ended the problem, while supplementation with 5 present, it can directly inhibit the synthesis and release of grains per week was not effective. Iodine content below 0.2 thyroid hormones. In both situations, TSH production is in- mg/kg DM in the majority of feedstuffs fed to horses on a creased in an attempt to elevate the reduced concentrations of Japanese farm without supplementation resulted in seven thyroid hormones and alleviate the hypothyroidism. The re- foals showing bilateral thyroid enlargement, and four of the sultant increase in TSH causes an increase in the size of the seven had extensive flexion of the lower forelegs (Osame thyroid gland in a condition known as goiter. and Ichijo, 1994). Stillborn foals, or foals born weak with Dietary iodine and selenium have also been shown to in- difficulty in standing to suckle, can result if broodmares are teract to affect thyroid hormone metabolism (Hotz et al., fed an iodine-deficient ration even when the symptom of 1997). A high iodine intake, when selenium is deficient, thyroid gland enlargement is not present in the mare. Like- may permit thyroid tissue damage as a result of low thy- wise, iodine-deficient mares have been reported to have ab- roidal selenium-dependent glutathione peroxidase (GSH- normal estrous cycles (Kruzhova, 1968). Feedstuffs such as
92 NUTRIENT REQUIREMENTS OF HORSES uncooked soybeans, cabbage, kale, and mustard are known (McLaughlin and Doige, 1981; McLaughlin et al., 1986). to have an anti-thyroid activity (goitrogens) that can also This does not suggest that the recommended range is too cause goiter (Jackson and Pagan, 1996). Supplemental io- low, but does reflect the limitations of depending upon the dine is not particularly effective at inhibiting the goitrogenic intake of one nutrient to guarantee the intake of another. For response, but heating these feedstuffs can inactivate the en- calculating iodine requirements of horses, endogenous io- zyme responsible for this action. dine losses were assumed to be 7 Âµg/kg BW/d (Wehr et al., The maximum tolerable concentration of iodine has been 2002). Given that Osame and Ichijo (1994) reported foals set at 5 mg/kg of dietary intake (NRC, 2005), though the developed goiter when fed feedstuffs that were generally Merck Veterinary Manual (2005) indicated iodine toxicities below 0.2 mg I/kg DM, with only alfalfa hay at 0.6 mg I/kg in mares have been reported at an intake as low as 40 mg/d. DM, and that the foals were returned to normal by oral ad- Toxicities seem to be more common than deficiencies in re- ministration of 2 mg I/d (approximately 0.33 mg I/kg DM) cent years (Hintz, 1989). An iodine toxicity usually results for 2â4 weeks, it is questionable whether the concentration only when iodine is oversupplemented or when animals are of 0.1 mg I/kg DM is sufficient. Thus, the average (0.35 mg receiving feeds containing unusually high amounts of iodine I/kg DM) of the range (0.1 to 0.6 mg I/kg DM) given in the such as some types of seaweed. Silvia et al. (1987) reported second printing of the 1989 NRC is likely a safe minimum that excess iodine supplementation of 700 mg inorganic recommendation. Assuming a near 100 percent absorption, iodine in foals and of more than 350 mg in pregnant and the maintenance requirement would be 0.007 mg/kg BW lactating mares caused a high incidence of goiters in the (which would account for the endogenous losses suggested newborn, as well as causing abortions and foal mortality. by Wehr et al. in 2002) or 0.35 mg/kg DM assuming 2 per- Eroksuz et al. (2004) reported goiter in newborn foals whose cent of BW intake. Due to limited data from equine studies, mares had been supplemented with 299 mg I/d during the this dietary concentration is used with all classes except for last 24 weeks of pregnancy. Iatrogenic iodism and an asso- the broodmare in late gestation. The increased amount allot- ciated alopecia were reported in a horse being treated with ted for humans during the final trimester of pregnancy 90 g/d for 18 days of EDDI for dermatophilosis (Fadok and (Donoghue et al., 1990) appears to be prudent and the di- Wild, 1983). An increase is susceptibility to infectious dis- etary concentration has been set at 0.4 mg I/kg DM. ease may also occur with excessive dietary iodine (Baker and Lindsey, 1968). Wehr et al. (2002) reported the renal excretion of iodine Iron was nearly equivalent to iodine intake when iodine supple- mentation ranged from 0 to 80 Âµg/kg BW/d. No changes Function were seen in concentrations of thyroid hormones. Hence, Iron (Fe) is contained in hemoglobin, myoglobin, cy- urinary iodine can be used to estimate the amount of iodine tochromes, and many enzyme systems. Iron plays a critical being fed. As the clinical signs of an iodine deficiency or role in oxygen transport and cellular respiration (Schryver, toxicity appear similar, a simple evaluation of the ration 1990). The body of a 500-kg horse contains about 33 g of should reveal whether iodine concentrations are excessive or iron. The approximate distributions are hemoglobin (60 per- deficient and the appropriate corrections can then be made. cent), myoglobin (20 percent), storage and transport forms (20 percent), and cytochromic and other enzymes (0.2 per- cent) (Moore, 1951). Recommendations Using data from other species, a range of 0.1 to 0.6 mg/kg Sources and Factors Influencing Absorption ration was used in the second printing of the 1989 NRC for all classes of horses. It has been proposed that a 500-kg Forage and by-product ingredients commonly contain horse at light work requires 1.75 mg of iodine, 2.5 mg for 100â250 mg Fe/kg DM. Grains usually contain less than moderate work, and 2.7 to 3 mg/d for intense work (Jackson, 100 mg/kg DM, some milled concentrates can have greater 1997), but research to support the higher requirements for than 500 to 1,400 mg/kg DM, and calcium and phosphorus work have not been substantiated. Likewise, Donoghue et al. supplements often contain 2â3 percent iron. Dietary iron ab- (1990) suggested that, like in humans, requirements during sorption in nonruminants fed adequate iron is likely to be 15 the third trimester of pregnancy may be slightly increased. percent or less. Iron is absorbed more efficiently in newborn As feed intake increases to meet the increased caloric de- animals. A small amount of orally administered iron may mand of work, daily intake of iodine would be increased if exceed the iron-binding capacity of the serum, resulting in concentrations in the ration remained constant. However, in- free iron reaching the liver and causing liver necrosis and sufficient iodine may be consumed when iodine intake de- failure (Schryver, 1990). Iron utilization increases in iron- pends on free-choice iodized salt intake. This was reported deficient rations and diminishes with higher than normal in- as the possible cause of iodine deficiency in some pregnant takes of cadmium, cobalt, copper, manganese, and zinc (Un- mares whose foals were born with leg abnormalities derwood, 1977).
MINERALS 93 Signs of Deficiency or Excess amount to be toxic. In comparison, ponies given 50 mg Fe/kg of BW/d from ferrous sulfate did not show signs of The primary sign of iron deficiency is a microcytic, poisoning, and it was concluded that administration of that hypochromic anemia. Although young, milk-fed foals are concentration for a period of less than 8 weeks would not most susceptible to this anemia, iron deficiency is not a cause iron toxicosis (Pearson and Andreasen, 2001). High practical problem in foals or mature horses at any perfor- concentrations of supplemental dietary iron (500 and 1,000 mance level if they have access to soil. This is true, in part, mg/kg feed) fed to ponies had no effect on feed intake, daily because the body efficiently salvages and retains iron de- gain, red blood cell count, hemoglobin concentration, rived from the catabolism of body constituents. However, packed cell volume, or serum iron, calcium, copper, and Brommer and Sloet van Oldruitenborgh-Oosterbaan (2001) manganese (Lawrence, 1986; Lawrence et al., 1987). The reported lowered hemoglobin concentrations and packed higher dietary iron concentration, however, depressed both cell volumes in exercised and unexercised, box-stalled serum and liver zinc. Johnson and Murphy (1988) also re- weanlings compared to foals raised on pasture. Blood iron ported that high iron concentrations decreased copper ab- concentrations were also lower (P < 0.05) in the two box- sorption in copper-deficient rats. Mills and Marlin (1996) stalled groups (101 Â± 61 Âµg/dL and 123 Â± 67 Âµg/dL) as com- concluded that possible adverse effects of excessive iron pared to the pastured group (212 Â± 67 Âµg/dL) though serum might outweigh any supposed advantages. It should be ferritin, a better indicator of dietary iron status, was not re- noted that supplemental iron can be toxic to newborn foals ported. This occurred even though box-stalled foals received and iron injections are dangerous to horses, often resulting fresh-cut grass harvested from the same pastures that the in severe reactions or death. pastured foals were grazing. Additionally, box-stalled foals Excess iron is especially toxic to young animals, and appeared to be listless compared to pastured foals. Oral sup- deaths among foals have been attributed to oral administra- plementation of iron increased hemoglobin concentrations tion of digestive inocula containing supplemental iron (Mul- and packed cell volumes and the stabled foals became as ac- laney and Brown, 1988). Foals dosed according to manufac- tive as the pastured foals. It was concluded that the pastured turerâs recommendations received 350 mg of elemental iron foals likely had increased iron consumption due to the con- as ferrous fumarate at birth and at 3 days of age. Prior to sumption of soil that contained high concentrations of iron, death, these foals exhibited diarrhea, icterus, dehydration, while stalled horses had no such opportunity due to the con- and coma. Morphologic changes included erosion of jejunal crete flooring of their stalls. Of interest, the iron concentra- villi, pulmonary hemorrhage, massive iron deposition in the tion of the grass being fed was sampled twice and the iron liver, and liver degeneration. Since the removal in the 1980s concentration was found to be 186 and 310 mg/kg DMâ of products containing ferrous fumurate for administration well above the minimum amount required. Thus, it is un- to neonates, iron poisoning has become less common (Cas- clear whether an iron deficiency truly existed or if the tim- teel, 2001). Ferrous fumurate toxicity in a mature horse has ing of the oral supplementation and resultant change in been reported by Arnbjerg (1981). Serum iron concentra- behavior was confounded with other factors. Kohn et al. tions exceeding 400 Âµg/dL suggest acute toxicosis (Puls, (1990) reported four doses (248 mg each) of supplemental 1994). Because serum iron content can be affected second- oral iron during the second and third weeks after birth in arily by several disorders, Smith et al. (1986) reported that foals had no beneficial effects on hematologic variables. serum ferritin content seems to be the best indicator of iron They concluded that most foals apparently have sufficient status in horses. Smith et al. (1984) reported serum ferritin body iron stores at birth and sufficient intake to support de- ranging from 70 to 250 ng/ml with a mean of 152 Â± 55 for mands for iron during early foalhood. normal horses. From data in other species, the maximum tolerable con- centration of iron has been set at 500 mg/kg ration (NRC, 2005). Some feedstuffs, particularly forages such as Recommendations sorghum hay, contain more than this concentration of iron, but there are no reports of iron toxicity from feeding these Daily endogenous losses of iron have not been reported feeds to horses. Although various iron supplements have for horses, and the dietary iron requirement is estimated to be been ineffective in improving the hemoglobin or oxygen- 50 mg/kg DM for growing foals or pregnant and lactating carrying capacity of red blood cells under natural feeding mares and 40 mg/kg DM for mature horses. Common feed- programs (Kirkham et al., 1971), some iron supplements stuffs should meet the iron requirements. According to have been implicated in chronic iron toxicity when fed at 0.6 Meyer (1986), approximately 37, 38, and 92 mg of iron are mg Fe/kg BW/d in the form of ferrous sulphate (Edens et al., deposited each day in the fetus and placental membranes dur- 1993). Clinical signs disappeared after discontinuation of ing months 9, 10, and 11 of gestation, respectively. For a the iron supplement. However, Edens et al. (1993) suggested 500-kg mare, this equates to 74, 76, and 184 Âµg Fe/kg mare that other factors such as iron amount in the primary feed weight. The iron content of mareâs milk ranges from 1.3 Âµg/g source, inaccurate reporting of dosage amount, or some at parturition to 0.49 Âµg/g at 4 months postpartum (Ullrey et other underlying problem may be the reason for such a small al., 1974), though an average of 0.22 Âµg/g has also been re-
94 NUTRIENT REQUIREMENTS OF HORSES ported (Anderson, 1992). A mare producing 15 kg milk/d genital contractures in newborn foals. However, no direct would require approximately 130 mg of iron daily for milk evidence exists to support this theory. Manganese is among production in early lactation and 32.6 mg of iron for 10 kg the least toxic of the trace elements (Underwood, 1977), and milk/d in late lactation, in addition to the iron requirement for there are no known instances of manganese intoxication in maintenance. Iron loss through sweat is small having been horses (Schryver, 1990). However, large amounts of man- reported to be only 0.6 percent of intake, so it would not con- ganese in the ration can interfere with phosphorus absorp- tribute appreciably to iron requirements for exercise (Inoue et tion. The 2005 NRC has suggested 400 ppm of dietary man- al., 2003). Without an accurate estimate of endogenous ganese may be the maximum tolerable amount based upon losses, and hence maintenance requirements, the 1989 NRC interspecies extrapolation. requirements are unchanged. Recommendations Manganese The manganese requirements of horses have not been firmly established; however, based upon data from other Function species, 40 mg Mn/kg DM (Rojas et al., 1965) was consid- Manganese (Mn) is essential for carbohydrate and lipid ered adequate by the 1989 NRC. Hudson et al. (2001) cal- metabolism and for synthesis of the chondroitin sulfate nec- culated endogenous losses in horses averaging 534 kg to be essary in cartilage formation. between 164 Â± 68 and 305 Â± 95 mg/d (0.31 and 0.57 mg/kg BW) with a resultant requirement ranging from 408 Â± 107 to 529 Â± 167 mg/d (0.76â0.99 mg Mn/kg BW or 380â495 mg Sources and Factors Influencing Absorption of Mn/d for a 500-kg horse). Pagan (1994) estimated en- Forages contain 40 to 140 mg of Mn/kg DM, and most dogenous manganese loss to be 110 mg/d (about 0.2 mg/kg concentrates (except corn) contain 15 to 45 mg/kg DM. BW) though the R2 for the calculation was only 0.40. The Wagner et al. (2005) reported the absorption of manganese true digestibility of manganese was estimated to be 28.5 oxide, sulfate, and an organic-chelate to be 13.6, 8.6, and percent. The resulting requirement for a 500-kg horse (350 15.5 percent, respectively, and these did not differ between mg of Mn/d) is lower than the 1989 NRC recommendation sources. Siciliano et al. (2001) found no difference in liver (400 mg Mn/d) assuming a 2 percent of BW intake; how- manganese concentrations between horses supplemented ever, the Pagan (1994) horses consumed less total feed. The with manganese-oxide or a combination of half manganese- results of the Pagan (1994) report do provide at least some oxide and half manganese-methionine. Pagan and Jackson evidence that the requirements established by the 1989 NRC (1991b) reported the apparent digestibility of manganese subcommittee should adequately meet the requirements of to range from 4.7â10.6 percent, while Pagan (1994) re- the horse. Sobota et al. (2001) reported decreased growth ported true manganese digestibility to be around 28.5 per- rates in yearlings receiving only 35.8 mg Mn/kg ration com- cent in mature horses. Exercise has been shown to decrease pared to yearlings receiving 101 mg Mn/kg ration. Though true digestibility of manganese from 58 percent to 40 per- not substantially lower than the 1989 NRC recommenda- cent (Hudson et al., 2001). The variation in reported di- tion, Sobota et al. (2001) concluded that the decreased gestibilities results in difficulties in precisely determining growth rates seen when feeding 35.8 mg Mn/kg ration pro- requirements. vide support for the minimum requirement of 40 mg Mn/kg ration. Milk manganese concentrations in mares have re- ported to be 0.255 Âµmol/L or 0.014 ppm (Anderson, 1992). Signs of Deficiency or Excess Until further studies are conducted that suggest a need to in- Manganese deficiency in other species results in abnor- crease the previous recommendations, or that they can be mal cartilage development. This is due to failure of chon- decreased without causing problems, the recommendation droitin sulfate synthesis, which results in bone malforma- remains at 40 mg Mn/kg DM. tion. The crooked limbs of newborn calves have been associated with manganese deficiency (Howes and Dyer, Selenium 1971). Similar afflictions (congenitally enlarged joints, twisted legs, and shortened forelimb bones) have been asso- Function ciated with âsmelter smoke syndromeâ in Oklahoma (Cowgill et al., 1980); the extensive liming required to off- Selenium (Se) is an essential component of selenium- set the acidic effects of smelter effluent on the soil was dependent glutathione peroxidase (Rotruck et al., 1973), thought to markedly reduce manganese availability. It has which aids in detoxification of lipo- and hydrogen peroxides been suggested since, but not proven, that manganese defi- that are toxic to cell membranes. Selenium also plays a role ciency may be associated with limb abnormalities and con- in the control of thyroid hormone metabolism (Hotz et al.,
MINERALS 95 1997). The deiodinating enzyme, which produces most of supplemental selenium (Hintz, 1999). These contain up to the circulating T3, type I iodothyronine 5-deiodinase, is a se- 120 ppm selenium. Shellow et al. (1985) reported blood se- lenoenzyme with most of the activity occurring in liver, kid- lenium concentrations increased linearly for 5â6 weeks and ney, and thyroid. then were unchanged for the remainder of a 12-week study when supplemental selenium was fed to horses receiving a basal ration of 0.06 ppm selenium. Hayes et al. (1987) re- Sources and Factors Influencing Absorption ported that dietary selenium concentrations often did not The concentration of selenium in feedstuffs commonly correlate with blood selenium concentrations. In a small sur- ranges from 0.01 to 0.3 mg/kg and is influenced by varia- vey of farms, the farm having the highest concentration of tions in soil selenium and pH. Alkaline soils are more con- dietary selenium had inadequate blood concentrations in the ducive to plants accumulating selenium. Drought conditions animals tested, leading the authors to conclude that interac- also encourage deeper root growth where selenium concen- tions with other minerals may have been influencing ab- trations in the soil may be greater. Drought conditions can sorption of selenium or that breed differences may have also encourage animals to eat accumulator plants that might played a role in the ability to absorb selenium. Besides other otherwise be ignored. Accumulator plants may store high dietary minerals, knowledge of the vitamin E status of the concentrations of selenium and can result in toxicities when animals is also important. consumed (Finley, 2005). Selenium in forages and seed grains is normally present as organic selenium in the form Signs of Deficiency or Excess of selenocystine, selenocysteine, and selenomethionine. Sodium selenite and sodium selenate are common inorganic Through veterinary and laboratory surveys of every state, sources of supplemental selenium, and no differences in Edmonson et al. (1993) reported selenium-deficiency dis- bioavailability between the two sources were observed by eases in 46 states. Deficiencies were an important livestock Podoll et al. (1992). Pagan et al. (1999) reported a trend problem in regions of 37 states, but deficiencies in wildlife (P < 0.1) for the apparent absorption of selenium from sele- were reported in only 10 states. By comparison, natural oc- nium-enriched yeast to be greater than from sodium selenite curring toxicosis is rare and was only reported in 7 states (57.3 vs. 51.1 Â± 1.4 percent). Janicki et al. (2001) reported even though oversupplementation was reported in 15 states. greater serum selenium concentrations in mares receiving Acute, subacute, and chronic forms of selenium deficiency supplementation of 3 mg/d of selenium as selenium-yeast in horses have been reported in China (Jiong et al., 1987). compared to mares receiving either 1 or 3 mg Se/d as The myopathy results in weakness, impaired locomotion, sodium selenite. Selenium in the colostrum and milk was difficulty in suckling and swallowing, respiratory distress, also greater in the mares receiving the supplemental organic and impaired cardiac function (Dill and Rebhun, 1985). selenium. By comparison, Richardson et al. (2006) reported Serum changes include elevations in creatine kinase, aspar- no clear difference in various markers of selenium status tate aminotransferase, potassium, and blood urea nitrogen (e.g., selenium concentration of plasma and middle gluteal (Dill and Rebhun, 1985). Elevated aspartic-pyruvic trans- muscle; GSH-px activity of plasma, red blood cells, and aminase and gamma-glutamyltransferase have also been as- middle gluteal muscle) was identified in 18-month-old sociated with the vitamin E/selenium-response disease. Oc- nonexercised horses fed diets containing either zinc-L- currence of the tying-up syndrome did not correlate with selenomethionine or sodium selenite (0.45 mg Se/kg DM) vitamin E or selenium status (Lindholm and Asheim, 1973; over a 56-d experimental period. Selenium is absorbed more Gallagher and Stowe, 1980; Blackmore et al., 1982). The efficiently in nonruminants than in ruminants (77 compared clinical and morphologic manifestations of selenium defi- to 29 percent: Wright and Bell, 1966). Selenium concentra- ciency are affected by the concomitant vitamin E status. tion of milk was shown to be one-fourth of that in colostrum Perkins et al. (1998) reported on four cases of neonatal foals 1 day postpartum and was considered a minor source of se- with rhabdomyolysis due to selenium deficiency both with lenium regardless of the selenium status of their mares dur- and without vitamin E deficiency. Nutritional myopathy ing gestation (Lee et al., 1995). Although the Food and Drug (white muscle disease or vitamin E/selenium-responsive Administration (FDA) has approved maximal selenium sup- disease) involves skeletal and cardiac muscles and is associ- plementation at 0.3 mg/kg DM in complete feeds for cattle, ated with glutathione peroxidase (GSH-px) values lower sheep, and swine (FDA, 1987), selenium supplementation of than 25 enzyme units (EU)/dl (Caple et al., 1978) and with equine feeds in the United States is not covered and is re- serum selenium values lower than 60 ng/ml (Blackmore et stricted only by nutritional recommendations and industry al., 1982). Though low selenium serum concentrations are practices (Ullrey, 1992). By comparison, the Feed Additive often used as evidence of a selenium deficiency, if no other Directive 70/524/EC allows maximal selenium supplemen- clinical problems are evident, it is questionable whether a tation of 0.5 mg/kg in complete feeds (assuming 88 percent deficiency is truly present. For example, Vervuert et al. dry matter). Selenized salt blocks are available to provide (2001) reported Icelandic horses had low plasma selenium
96 NUTRIENT REQUIREMENTS OF HORSES concentrations (66.7 Â± 47.2 ng Se/ml) with no health prob- found in chronic selenosis and 2,000â2,500 Âµg/dl in acute lems and suggested those horses had an efficient metabolism intoxication (Traub-Dargatz et al., 1986). Whole blood ap- that allowed them to compensate for a low selenium supply. pears to be a more preferable indicator of serum status than Likewise, GSH-px activity was not correlated with selenium serum (McLaughlin and Cullen, 1986). The serum selenium intake or selenium plasma concentrations in a field study of of foals from selenium-adequate mares is typically much 106 horses (Wichert et al., 2002a). Without other symptoms lower than their dams and ranges from 70 to 80 ng of of a selenium deficiency, low concentrations of selenium in selenium per ml of serum (Stowe, 1967). If, according to the blood and low GSH-px activity should not be taken as a Blackmore et al. (1982), serum selenium values below 65 clear sign that a selenium deficiency is present. ng/ml are indicative of deficiency, young foals may be prone Based upon studies with other species, the maximum tol- to nutritional muscular dystrophy, especially if their vita- erable concentration of selenium in horses has been esti- min E status is low. Carmel et al. (1990) reported that of 202 mated at 5 mg/kg DM (NRC, 2005). However, the 1989 randomly sampled horses in Maryland, blood selenium con- NRC recognized that maximum tolerable concentration of centrations ranged from 50â266 ng/ml. Stowe and Herdt selenium to be 2 mg/kg DM and this seems to be a more ad- (1992) expected serum selenium values to increase gradu- visable upper limit. The LD50 for orally administered sele- ally with age from starting ranges for newborn foals of nium is considered to be approximately 3.3 mg of Se (as 70â90 ng/ml with expected or ânormalâ values for the adult sodium selenite)/kg BW (Miller and Williams, 1940). The horses to range from 130â160 ng/ml. Normal liver selenium chemical form of selenium can influence its toxicity, with concentrations are considered to range between 1.2 and 2.0 organic selenium compounds found in plants (selenocystine, Âµg/g on a dry weight basis, regardless of age (Stowe and selenocysteine, and selenomethionine) being the most toxic Herdt, 1992). (Schryver, 1990). Horses appear to be more susceptible to selenium toxicity than are cattle (Rogers et al., 1990). Cop- Recommendations per pretreatment can increase the LD50 markedly (Stowe, 1980). Acute selenium toxicityâblind staggersâis charac- The selenium requirement of the horse was estimated at terized by apparent blindness, head pressing, perspiration, 0.1 mg/kg ration (Stowe, 1967). This is consistent with the abdominal pain, colic, diarrhea, increased heart and respira- report of Shellow et al. (1985), who found that plasma sele- tion rates, and lethargy (Rosenfeld and Beath, 1964). Hair nium concentrations of mature horses reached a plateau at loss and changes in hooves could also be expected after an about 140 ng/ml in horses fed either 0.14 or 0.23 mg of acutely high dose of selenium (Fan and Kizer, 1990). Se/kg ration. They concluded that there was no advantage in Chronic selenium toxicityâalkali diseaseâis characterized supplementing the mature idle horse with more than 0.1 mg by alopecia, especially about the mane and tail, as well as Se/kg ration and that 140 ng of Se/ml plasma (or serum) was cracking of the hooves around the coronary band (Rosenfeld adequate to prevent problems associated with selenium de- and Beath, 1964; Traub-Dargatz et al., 1986). Orally admin- ficiency. A similar selenium supplementation rate, 1 mg/d istering mixtures of sulphates that antagonize selenium are a for horses 1 to 6 years of age, was reported by Maylin et al. suggested cure for chronic toxicity (Rogers et al., 1990). (1980) to increase blood selenium from 45 to 123 ng/ml There are anecdotal accounts of immediate death after ad- over an 11-week period. The higher blood selenium value ministration of injectable vitamin E/selenium preparations. was considered well above the concentration associated with These deaths appear due to an anaphylactoid sensitivity of myodegeneration. Glutathione peroxidase values for racing the horse to a carrier ingredient in the injectable prepara- Standardbred horses were reported to be 17 EU/mg hemo- tions and not to the toxicity of selenium or vitamin E. As a globin (Gallagher and Stowe, 1980). Maylin et al. (1980) result of chronically elevated selenium intake, it is believed and Roneus and Lindholm (1983) confirmed a strong rela- that sulfur is replaced by selenium in such sulfur-containing tionship between selenium intake and GSH-px activity and tissues as keratin, potentially resulting in weakened hooves noted that the GSH-px response to oral selenium was much and hair (Merck Veterinary Manual, 2005). Therefore, even lower than to parenteral selenium. Wichert et al. (2002b) re- though below toxic amounts, there appears to be no justifi- ported selenium intake in over half of 106 horses sampled cation for feeding selenium at a concentration greater than was below 1.25 Âµg/kg BW without signs of selenium defi- 0.5 mg Se/kg DM. ciency. This amount was almost half of what was recom- The selenium status of horses can be evaluated by mea- mended by the 1989 NRC, so there is a possibility that the suring serum, plasma, or whole blood selenium by the sen- minimum requirement may be somewhat overestimated. It sitive fluorometric selenium assay (Whetter and Ullrey, can be concluded the true requirement for selenium is un- 1978). Selenium-dependent GSH-px of serum and erythro- known, though a recommendation (0.1 mg/kg DM) can be cytes can also be measured (Paglia and Valentine, 1967); given that is known to prevent a classical deficiency. How- however, sample storage time and temperature are critical. ever, Janicki et al. (2001) found greater influenza antibodies Serum selenium concentrations of 100â500 Âµg/dl have been in foals from mares receiving 3 mg Se/d as compared to
MINERALS 97 1 mg Se/d suggesting that selenium intake necessary for op- rate, parakeratosis (especially on the lower limbs), alopecia, timum immune function could be greater than that needed to reduced serum and tissue zinc concentrations, and decreased prevent classical deficiency symptoms. alkaline phosphatase (Harrington et al., 1973). Horses ap- pear quite tolerant of excess dietary zinc and a maximum tolerable concentration has been set at 500 mg/kg ration Zinc based upon interspecies extrapolation (NRC, 2005). Except when homeostatic mechanisms that act on absorption are Function overwhelmed, zinc generally does not accumulate with con- Zinc (Zn) is present in the body as a component of more tinued exposure (Casteel, 2001). No detrimental effects than 100 enzymes including many metalloenzymes such as were observed in mares or foals fed rations containing up to carbonic anhydrase, alkaline phosphatase, and carboxypep- 700 mg Zn/kg feed (Graham et al., 1940). However, Messer tidase. The highest concentrations of zinc occur in the (1981) reported tibiotarsal effusion in three Arabian fillies choroid and iris of the eye and in the prostate gland. Inter- that had marked elevations in serum zinc. Foals fed 90 g mediate concentrations of zinc are present in skin, liver, Zn/d (equal to about 2 percent of the ration) developed en- bone, and muscle, whereas low concentrations are found in larged epiphyses, stiffness of gait, lameness, and increased blood, milk, lungs, and brain. tissue zinc (Graham et al., 1940). Similar signs were ob- served by Eamens et al. (1984) in four young horses grazed near industrial plants where the pasture contained high zinc Sources and Factors Influencing Absorption concentrations and by Gunson et al. (1982) in two young Many feedstuffs contain 15â40 mg Zn/kg DM. Sources foals raised near a zinc smelter. The cause appeared to be a of supplemental zinc include zinc sulfate, zinc oxide, zinc secondary copper deficiency induced by zinc toxicosis. Sim- chloride, zinc carbonate, and various organic sources of zinc ilarly, Bridges and Moffitt (1990) reported foals fed rations chelates. Zinc absorption is regulated by the zinc status of containing zinc (supplemented in the form of zinc oxide) at the animal and is typically in the 5â15 percent range. Pagan 1,000 and 2,000 mg/kg BW became hypocupremic within and Jackson (1991b) reported the apparent digestibility to be 5â6 weeks and were lame within 6 weeks because of carti- between 7.8 and 11.5 percent. Pagan (1994) reported an ap- lage defects. The ratio of copper to zinc should be consid- parent digestibility of 9.4 percent and a true digestibility of ered, as zinc is believed to compete for the same transport nearly 21 percent. A study by Hudson et al. (2001) showed mechanisms as copper and is a potent inducer of metalloth- true zinc digestibility to decrease to 14 percent when horses ionein synthesis, which binds copper. Thus, the amount of were exercised compared to 25 percent in sedentary horses. zinc necessary to cause a deficiency in copper is dependent Wagner et al. (2005) found the absorption of zinc oxide, sul- on the reserve amount of copper present in the liver and fate, and an organic-chelate to be 13.9, 12.8, and 10.6 per- other tissues (Bridges et al., 1984; Cymbaluk and Smart, cent, respectively, in mature horses. Baker et al. (2005) also 1993; Campbell-Beggs et al., 1994). As a result, dietary zinc reported mature horses retained more zinc when supple- excess or high dietary zinc:copper ratios may create a cop- mented with zinc oxide as compared to organically chelated per deficiency. By altering zinc:copper ratios from 6.3 to 3, zinc. No difference was found between an inorganic source Caure et al. (1998) was able to reduce osteochondrosis and a combination of organic and inorganic sources of zinc scores on one of two French farms, though they were not fed at higher than required concentrations on bone metabo- able to alter the prevalence of the lesions. It should be noted lism (Baker et al., 2003) or liver zinc concentrations (Sicil- that this study was not controlled and alterations in other nu- iano et al., 2001), though Miller et al. (2003) reported an in- trients were also made. Young et al. (1987) and Coger et al. creased zinc retention in yearlings fed the organic zinc as (1987) were unable to alter the copper absorption in grow- compared to the inorganic zinc. Wichert et al. (2002c) re- ing and mature ponies fed rations containing 580 or 1,200 ported higher bioavailability of inorganic zinc sulfate and mg Zn/kg feed. Therefore, the purported effect of elevated zinc sulfate chelate than zinc oxide after a high single dose. zinc intake on copper metabolism may involve postabsorp- These conflicting data make it hard to claim that organic or tive events rather than the actual site of absorption. inorganic zinc forms are better absorbed. When comparing Time between blood collection and separation, in addi- organic vs. inorganic minerals, cost is often an important tion to the contamination of blood samples from rubber consideration besides digestibility. stoppers, makes evaluation of zinc status from blood diffi- cult (English and Hambidge, 1988; Casteel, 2001). Concen- trations of zinc in the serum or plasma, while often used for Signs of Deficiency or Excess evaluating zinc intake, can vary from low to high within the Zinc deficiency has been produced in foals fed 5 mg of same herd and are not a good indicator of zinc status. Like- Zn/kg purified diet (Harrington et al., 1973). Zinc deficiency wise, serum zinc concentrations have been found to be quite in foals is accompanied by inappetence, reduced growth variable with respect to age (Bell et al., 1987).
98 NUTRIENT REQUIREMENTS OF HORSES Recommendations forms have been reported to range from 0.4â3 percent (An- derson, 1987), while chromium from sources such as Harrington et al. (1973) demonstrated that 40 mg Zn/kg brewerâs yeast has been reported to be absorbed at rates as purified-type diet was sufficient to prevent zinc deficiency high as 10â25 percent by rats (Underwood, 1977). in foals. Schryver et al. (1974) reported that foals fed 41 mg While no evidence has been found of a chromium defi- Zn/kg natural diet grew at acceptable rates and maintained ciency in horses, a chromium deficiency leads to symptoms normal body stores of zinc. Drepper et al. (1982) and Jar- associated with adult-onset diabetes and cardiovascular dis- rige and Martin-Rosset (1981) indicated that 50 mg Zn/kg ease in humans (Vincent, 1999). From data in other species, dry matter was adequate for all classes of horses. Accord- the maximum tolerable concentration of chromium in the ra- ing to Knight et al. (1985), based on farm surveys, the op- tion of horses is set at 3,000 mg/kg DM for the oxide form timal dietary zinc concentration in equine rations to mini- and 100 mg/kg DM for the chloride form of the trivalent mize the incidence of metabolic bone disease approaches forms of chromium (NRC, 2005). The hexavalent forms of 90 mg/kg feed. Although these workers suggested that the chromium appear to be much more toxic (NRC, 1997). 1978 NRC recommendations on zinc requirements be Chromosome damage in hamsters has been noted after treat- reevaluated, no controlled studies support a dietary zinc re- ment with chromium picolinate but not with chromium quirement greater than 50 mg/kg ration DM and the 1989 nicotinate, nicotinic acid, and trivalent chromium chloride NRC did not change the recommendations from 40 mg/kg hexahydrate at the same doses (Stearns et al., 1995). dietary DM. Likewise, Wichert et al. (2002b) reported that At this time, insufficient information is available to de- only 42 percent of 106 sampled horses had zinc intake of 1 termine if there is a chromium requirement for horses, mg/kg BW and 25 percent of the horses were fed < 0.5 mg though the recommended safe and adequate daily intake for Zn/kg BW with none of the horses showing signs of zinc humans is 50â200 Âµg/d (Anderson and Kozlovsky, 1985). deficiency. Mareâs milk contains 1.8â3.2 mg Zn/kg fluid Jackson (1997) suggested chromium requirements may be milk (NRC, 1989; Anderson, 1992). Thus, foals drinking 15 higher for exercising horses than for sedentary horses. While kg of milk/d would consume 27â48 mg of Zn/d. On a dry not strongly supported by research in horses, this is sup- matter basis, this is equivalent to 17â30 mg Zn/kg DM in- ported by Lukaski (2000) for humans in endurance training. take. The zinc in milk is assumed to be highly available. Pagan et al. (1995) reported that exercising horses supple- Kavazis et al. (2002) concluded that supplementing late mented with 5 mg of chromium from a chromium yeast gestating and lactating mares with zinc at higher concentra- product had lower plasma glucose concentrations during tions than recommended by the 1989 NRC did not have any several stages of a standardized exercise test. Likewise, sup- influence on foal growth and development or the zinc con- plemented horses had lower blood insulin 1 hour after grain centrations of mare milk or foal serum. feeding than did control horses. In contrast, Pagan et al. Pagan (1994) estimated endogenous zinc loss to be 54 (1995) indicated no response to supplementation in un- mg/d for a 550-kg horse (about 0.1 mg/kg BW), which is trained, sedentary horses. Ott and Kivipelto (1999) reported similar to Hudson et al. (2001). They estimated endogenous chromium tripicolinate supplementation resulted in peak zinc losses to be between 65 and 70 mg Zn/d for horses av- plasma glucose concentrations decreasing more rapidly fol- eraging 534 kg (about 0.12â0.13 mg Zn/kg BW). Pagan lowing an intravenous insulin sensitivity test. Likewise, (1994) calculated the true digestibility of zinc to be 20.8 per- mean glucose fractional turnover rate values increased in re- cent. The resulting requirement for a 500-kg horse (236 mg sponse to the chromium tripicolinate supplementation. Gen- Zn/d) is much lower than the 1989 NRC recommendation as- try et al. (1997) reported chromium tripicolinate supplemen- suming a 2 percent of BW intake (400 mg/d). However, until tation had only a marginal effect on metabolic, hormonal, studies are performed demonstrating lower amounts can be and immune responses. Vervuert et al. (2005b) reported that fed without problems for longer periods, the decision was horses supplemented with a chromium yeast product did not made to keep the requirements the same at 40 mg/kg of DM. have improved glucose âhandlingâ capabilities. Chromium- supplemented horses also had higher heart rates and blood lactate at the end of a standardized exercise test suggest- OTHER MINERALS OF INTEREST ing that the exercise capacity of chromium-supplemented horses was compromised. Supplementation of chromium-L- Chromium methionine to geriatric mares for a period of 4 weeks did not Chromium plays a role in carbohydrate and lipid metab- alter most immune parameters (Dimock et al., 1999). In ad- olism. It acts as a potentiator of insulin to facilitate glucose dition, 4 mg/d of chromium propionate supplementation did clearance and is considered an essential nutrient in humans not alleviate elevations in plasma leptin and insulin or alter (Mertz, 1992). glucose dynamics and insulin sensitivity in horses with a Trivalent and hexavalent are the two most common forms high body condition (Cartmill et al., 2005). While it has of chromium. Organic chromium appears to be more been suggested that dietary supplementation with chromium bioavailable than inorganic forms. Absorption of inorganic can calm horses and may be beneficial in horses with recur-
MINERALS 99 rent exertional rhabdomyolysis, because horses with trol animals, and had fewer injuries compared to controls. polysaccharide storage myopathy display abnormal sensitiv- Feeding a natural zeolite, as compared to the synthetic SZA, ity to insulin, chromium supplementation may be counter- did not increase plasma silicon (Mazzella et al., 2005). productive in those animals (Valberg, 2005). Porter et al. Greater rates of bone formation (Lang et al., 2001b) and (1999) suggested that, at least in humans, routine use of lower rates of bone resorption (Lang et al., 2001a) as chromium supplements is not warranted based upon current compared to the control horses were reported in SZA- data. supplemented horses, suggesting an overall increase in bone production. Turner et al. (2005) reported an increase in bone turnover in calves fed SZA and hypothesized that the reduc- Fluorine tion in injuries reported previously was due to rapid repair Fluorine (F) is known to be involved in bone and teeth of subclinical injuries. These studies suggested benefits as- development, but its dietary necessity for horses has not sociated with supplemental available silicon. Silicon ap- been established. pears to reduce aluminum absorption and toxicity (Jug- Forages often contain between 2 and 16 mg F/kg DM and daohsingh et al., 2000), though it is not certain to what cereal grains usually contain between 1 and 3 mg fluo- degree each element inhibits the absorption of each other. ride/kg DM (NRC, 1980). Phosphorus supplements that The relative abundance of silicon makes the deficiency of have not been adequately defluorinated are a common this element difficult to achieve. Likewise, silicon naturally source of excess dietary fluorine. found in the environment is not very absorbable and thus is A fluorine deficiency is not known to have been reported not likely to cause toxic effects through dietary intake. The in horses. Horses appear to be more tolerant than cattle of NRC (2005) did not set a maximum tolerable concentration excess fluorine (Buck et al., 1976). Fluorine intoxication for silicon in horses, but set one at 0.2 percent for cattle and may result from long-term ingestion of feed or water con- sheep. taminated by certain industrial operations or from consump- As a result of research demonstrating silicon can interact tion of water or mineral supplements that contain high con- with other nutrients for apparent beneficial effects (Nielsen, centrations of fluorine (Schryver, 1990). Excess intake 1991), the American Institute of Nutrition reformulated its results in discolored teeth (fluorosis), bone lesions, lame- published formulas of purified diets for experimental ro- ness, and unthriftiness. Shupe and Olson (1971) indicated dents and added silicon to the required nutrient profile at the horses can tolerate 50 mg F/kg ration for extended periods rate of 5 mg/kg ration (Reeves, 1997). Difficulty in produc- without detrimental effects, but the maximum tolerable con- ing a silicon-deficient purified diet for horses will make de- centration of fluorine has been set at 40 mg/kg DM intake termining a minimum requirement difficult, though a need based upon data with other species (NRC, 2005). for silicon in the ration likely exists for the equine. An equine requirement for fluorine has not been estab- lished, but given the concentrations of fluorine in normal Other Elements feedstuffs, any potential requirement is likely met and addi- tional supplementation is not suggested. Further elements are, in principle, accepted as essential constituents in a mammalian diet (e.g., boron, nickel, and vanadium). Based on the current status of knowledge, their Silicon natural occurrence is sufficient to ensure the required very Despite silicon being the second most common element small amounts of these elements. The supplementation of of Earthâs crust (Carlisle, 1972), surprisingly little is known these elements, including the rare earth elements, is not about the nutritional importance of it in the diet of mam- based on scientifically elaborated, valid data and has the po- malian species. 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