Cover Image

PAPERBACK
$99.00



View/Hide Left Panel

7
The Effect of Exercise and Heat on Mineral Metabolism and Requirements

Carl L. Keen1

INTRODUCTION

During the last decade there has been increasing interest in the idea that individuals engaged in strenuous exercise may have an increased need for several of the essential minerals. This idea has resulted in the widespread perception that mineral supplements may be advantageous for this subpopulation. The concept is based on two basic perceptions: (a) that individuals engaged in strenuous exercise have a higher requirement for some minerals compared to sedentary individuals due to increased rates of urinary and sweat losses of select minerals and (b) that the perceived inadequate intake of some minerals results in a lowering of endurance capacity and ultimately may lead to the development of some disease states. Although a significant number of athletes, coaches, and professionals in the sports medicine field believe in the salutary effects of mineral supplements, there are remarkably few data supporting a positive effect of dietary mineral supplementation on athletic performance. However, as discussed below, strenuous exercise does influence the metabolism of several minerals, and the amount of minerals lost via sweat (due to either intense heat or exercise) can be significant.

This chapter examines the current understanding of the effects of exercise on mineral metabolism and the potential consequences of these effects. The metabolism of at least eight minerals—copper, chromium, iodine, iron,

1  

Carl L. Keen, Departments of Nutrition and Internal Medicine, University of California, Davis, CA 95616–8669



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations 7 The Effect of Exercise and Heat on Mineral Metabolism and Requirements Carl L. Keen1 INTRODUCTION During the last decade there has been increasing interest in the idea that individuals engaged in strenuous exercise may have an increased need for several of the essential minerals. This idea has resulted in the widespread perception that mineral supplements may be advantageous for this subpopulation. The concept is based on two basic perceptions: (a) that individuals engaged in strenuous exercise have a higher requirement for some minerals compared to sedentary individuals due to increased rates of urinary and sweat losses of select minerals and (b) that the perceived inadequate intake of some minerals results in a lowering of endurance capacity and ultimately may lead to the development of some disease states. Although a significant number of athletes, coaches, and professionals in the sports medicine field believe in the salutary effects of mineral supplements, there are remarkably few data supporting a positive effect of dietary mineral supplementation on athletic performance. However, as discussed below, strenuous exercise does influence the metabolism of several minerals, and the amount of minerals lost via sweat (due to either intense heat or exercise) can be significant. This chapter examines the current understanding of the effects of exercise on mineral metabolism and the potential consequences of these effects. The metabolism of at least eight minerals—copper, chromium, iodine, iron, 1   Carl L. Keen, Departments of Nutrition and Internal Medicine, University of California, Davis, CA 95616–8669

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations magnesium, potassium, sodium, and zinc—has been suggested to be influenced by exercise. Due to space constraints, this chapter will focus on four elements—iron, magnesium, zinc, and copper—to exemplify concepts involved in exercise-and heat-induced alterations in mineral metabolism and nutrition. However, prior to this discussion a few comments will be made concerning iodine, selenium, and chromium. The reader is directed to Chapters 12 and 13 for information on exercise-and heat-induced changes in sodium and potassium metabolism. EFFECTS OF EXERCISE AND HEAT ON IODINE, CHROMIUM, AND SELENIUM METABOLISM Consolazio (1966) reported that a considerable amount of iodine can be lost via sweat. In that study, 12 adult males were maintained at a temperature of 38.5°C during the day and 33.1°C during the night. During the 24-hour period, the men exercised at a moderate rate on a bicycle ergometer for 1 hour. The average total sweat loss of the men over the 24-hour period was 5576 g, which resulted in an average loss of 146 µg of iodine. Given that the 1989 U.S. recommended dietary allowance (RDA) (NRC, 1989) for iodine for adult men and women is 150 µg per day, and the observation that typical iodine intakes exclusive of iodized salt range from 250 to 170 µg per day for men and women, respectively (Pennington et al., 1989), it is evident that sweat-associated iodine loss can be significant. The above findings suggest that it is critical that iodized salt (which provides >70 µg of iodine per g of salt) be consumed when an individual is in an exceptionally hot area and/or engaged in strenuous activity. Studies examining the influence of combined heat exposure and endurance exercise on iodine metabolism are needed. As with iodine, there is limited literature on the influence of exercise and heat on selenium metabolism, although it has been suggested that athletes may benefit from selenium supplements due to its role in glutathione peroxidase synthesis. Singh et al. (1991) reported that plasma selenium concentrations decreased in men exposed to a 5-day rigorous training program conducted by the U.S. Navy, despite an increase in dietary selenium intake during the program. Singh and colleagues suggested that the decrease in plasma selenium might have reflected a shift in selenium from the plasma pool to tissues requiring increased antioxidant protection. This hypothesis would be consistent with the observation that exercise can result in increased rates of tissue lipid peroxidation (Davies et al., 1982). Although the above observations suggest that selenium metabolism may be influenced by exercise, to date there is no compelling evidence that selenium supplementation is necessary for individuals engaged in endurance activities (Lane, 1989; Lang et al., 1987).

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Consolazio et al. (1964) reported an average loss of 340 µg of selenium in sweat over an 8-hour period in men maintained at a temperature of 37.8°C. However, given the observation that typical selenium intakes are only on the order of 100 µg per day (Pennington et al., 1984), the loss reported by Consolazio seems excessive, and may reflect the technical difficulties involved in measuring this element. With the exception of the data by Consolazio, there are no current reports suggesting that selenium requirements are higher in hot environments compared to temperate regions. Although the metabolic functions of chromium have not been clearly defined, chromium is known to be involved in the regulation of carbohydrate and lipid metabolism, presumably via a role in insulin action. Although not clearly defined in humans, signs associated with marginal chromium status in experimental animals include impaired glucose tolerance, elevated circulating insulin, elevated cholesterol and triglycerides, and increased incidence of aortic plaques (Campbell and Anderson, 1987). The dietary intake of chromium has been reported to be suboptimal for the general population based on dietary survey studies (Anderson and Kozlovsky, 1985). Recent research has indicated that chromium requirements may be influenced by strenuous exercise. Anderson et al. (1984) reported that serum chromium concentrations were increased in adult males immediately after a 6-mile run at near-maximal running capacity. This increase in serum chromium was still evident 2 hours after the completion of the run, and urinary chromium loss was elevated twofold on the run day compared to non-run days. Basal urinary chromium excretions have been shown to be lower in individuals routinely engaged in strenuous activity compared to sedentary controls (Anderson et al., 1988), which suggests either that chronic exercise results in a partial depletion of body chromium stores or that it induces metabolic changes that result in a reduction in urinary chromium excretion. Consistent with the latter idea, Vallerand et al. (1984) reported that, in rats, exercise training is associated with an increase in soft tissue chromium concentrations. In addition to exercise-induced increases in urinary chromium excretion, it would be expected that chromium losses would also be increased with excessive sweating. However, due to analytical difficulties in measuring this element, accurate data on sweat-associated losses of chromium are not currently available. Consolazio et al. (1964) reported that chromium loss in sweat over an 8-hour period averaged 60 µg in men maintained at 37.8°C, a value that would be double that of the typical dietary intake of the element. Studies aimed at better defining the amount of chromium lost in sweat at different amounts of sweat loss are clearly needed. Chromium deficiency per se has not been accepted as a health problem in endurance athletes. However, it seems prudent, given the above findings, to monitor chromium status of individuals engaged in strenuous activity for prolonged periods of time, particularly if the activity is performed in a hot

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations environment where chromium losses in sweat would be predicted to be high. Studies on the functional consequences of activity-induced changes in chromium metabolism are needed. EFFECTS OF EXERCISE AND HEAT ON IRON METABOLISM It is well recognized that iron-deficiency anemia can be associated with a diminished performance in maximal and submaximal physical exercise (Andersen and Barkve, 1970; Edgerton et al., 1981; Gardner et al., 1977; McDonald and Keen, 1988 and references cited therein). However, there is considerable controversy about the extent to which exercise contributes to the development of iron deficiency. Although there is a common perception that athletes as a group tend to have a high incidence of anemia compared to sedentary populations, hematological surveys of elite athletes have typically not supported this idea (Brotherhood et al., 1975; de Wijn et al., 1971; Stewart et al., 1972). Thus, overt iron-deficiency anemia does not appear to be a common complication of chronic intense exercise. High levels of physical activity have been suggested to cause ''sports anemia'' (typically defined as a drop in hemoglobin concentration, hematocrit, and red blood cell count; Balaban et al., 1989; Yoshimura, 1970). The phenomenon of sports anemia has been associated with increased erythrocyte destruction, depressed iron absorption, increased sweat loss of iron, and gastrointestinal blood loss (Dressendorfer et al., 1991; Ehn et al., 1980; Frederickson et al., 1983; Paulev et al., 1983; Puhl et al., 1981; Stewart et al., 1984). Although most investigators agree that sports anemia is common in athletes who initiate rigorous training programs, this "anemia" is typically transitory in nature with hematological values often returning to pretraining values within 3 weeks despite continued training (Frederickson et al., 1983). Based on these findings, it has been suggested by some that sports anemia may be in part a consequence of plasma volume expansion and a functional dilution of the red blood cell count because blood volume can increase by as much as 20 percent during training (Brotherhood et al., 1975; Hegenauer et al., 1983). In recent years there has been interest in the idea that exercise training can result in reduced tissue iron stores. Ehn at al. (1980) reported low bone marrow iron stores and evidence of increased iron absorption in elite distance runners who were characterized by normal hemoglobin and serum iron levels. Low serum ferritin concentrations have been reported by numerous investigators to be a consequence of prolonged, strenuous exercise (primarily when the subject is involved in weight-bearing sports) (Magazanik et al., 1988; Nickerson et al., 1985; Parr et al., 1984; Roberts and Smith, 1990; Snyder et al., 1989). Although there is considerable debate about the extent to which iron supplements may prevent exercise-induced reductions in tis-

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations sue iron stores, Snyder et al. (1989) and Nickerson et al. (1985) have reported that providing highly bioavailable iron (heme iron in meat) or iron supplements (105 mg per day) can retard the development of low serum ferritin concentrations. Given the observation that endurance athletes are typically not characterized by a higher than normal frequency of iron-deficiency anemia (see above), many investigators have questioned the significance of the finding of low serum ferritin concentrations in these individuals. However, it is important to note that the occurrence of low tissue iron stores in these individuals could present a problem with regard to recovery from injuries that result in extensive tissue damage or blood loss. It should be noted that marginal iron deficiency resulting in impaired thermoregulation has recently been observed (Beard et al., 1990); thus exercise-induced alterations in iron status may pose particular risks for individuals exposed to extreme temperatures. As discussed above, an increased rate of sweat loss of iron is thought to contribute to the depletion of iron stores with chronic endurance exercise. Although the loss of iron via sweat is not normally considered to be a major explanation for the iron depletion, sweat iron concentrations can range from 0.1 to 0.3 mg per liter for men and up to 0.4 mg per liter for women (Aruoma et al., 1988; Brune et al., 1986; Lamanca et al., 1988; Paulev et al., 1983). Given these concentrations, sweat can be an appreciable route of iron loss particularly when sweat rates exceed 5 liters per day. The potential interaction between prolonged exposure to high temperatures and vigorous activity with regard to iron status, and an individual's ability to thermoregulate and recover from injury is an area that needs further clarification. In sum, dietary iron supplementation may in some instances be justified to ensure good health of the individual. However, caution must be used in advocating excessive iron supplementation, given the potential negative side effects that can be associated with its use, including possible gastrointestinal discomfort, and interactions with other metals that have similar physiochemical properties. For example, it has been suggested that high levels of supplemental iron can inhibit the absorption of zinc (Keen and Hackman, 1986; Solomons, 1986). Given that prolonged exposure to a regimen of strenuous exercise and/or exposure to conditions resulting in high rates of sweat loss is associated with marked changes in zinc metabolism (see below), the potential negative effects of excess iron supplementation are clear. EFFECTS OF EXERCISE AND HEAT ON ZINC METABOLISM Lichti et al. (1970) first demonstrated that strenuous exercise can result in marked changes in zinc metabolism. They reported a marked increase in plasma zinc concentrations in dogs following short bouts of intense exercise. This observation was extended by Hetland et al. (1975) who found that

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations plasma zinc concentrations in men participating in a 5-hour, 70-km cross-country ski race were 19 percent higher immediately postrace compared to prerace values. However, by day 1 postrace, zinc concentrations were back to control levels. The observation that plasma zinc concentrations can increase significantly during strenuous exercise has since been verified by numerous investigators (Dressendorfer et al., 1982; Lukaski et al., 1984; Ohno et al., 1985; Van Rij et al., 1986). The magnitude of the increase in plasma zinc concentration with exercise is such that it cannot be due to hemoconcentration (Hetland et al., 1975; Lukaski et al., 1984); rather it is thought to reflect the result of muscle leakage of zinc into the extracellular fluid following muscle breakdown (Karlson et al., 1968). Following the cessation of exercise, there is normally a rapid drop in plasma zinc levels back to preexercise concentrations within a short period. It is thought that this rapid postexercise drop in plasma zinc is due to a high urinary excretion of the element coupled with a shift in the distribution of the element from the plasma fraction into the liver (Anderson et al., 1984; Campbell and Anderson, 1987; McDonald and Keen, 1988). The shift of zinc from the plasma into the liver is thought to be in part a consequence of the so-called acute-phase response, which occurs as a consequence of stressors such as infection, inflammation, and trauma. These stressors can result in the elaboration of cytokines, which result in the stimulation of the synthesis of several liver proteins (Cannon and Kluger, 1983; Cousins, 1985; Dinarello, 1989; Keen and Hackman, 1986; Singh et al., 1991). With regard to zinc, one component of the acute-phase response is an increase in liver metallothionein concentration, which can result in a sequestering of zinc in the liver (Cousins, 1985; Whanger and Oh, 1978). (Serum ferritin concentrations can increase as a result of the acute-phase response, a fact that must be considered when collecting samples for assessment of iron status; Singh et al., 1991; Taylor et al., 1987.) Reductions in plasma zinc concentrations were also observed in men who participated in a 5-day intensive training course conducted by the U.S. Navy (Singh et al., 1991). This reduction in plasma zinc occurred despite an increase in dietary zinc intake during the training period. The authors attributed the reduction in plasma zinc primarily to a redistribution of plasma zinc into liver as a consequence of metallothionein synthesis stimulated by interleukin-6 (IL-6). (The observed increase in plasma IL-6 concentrations was associated with tissue trauma.) Consistent with the above finding, Lichton et al. (1988) observed a reduction in plasma zinc concentrations in male soldiers engaged in a 34-day field exercise at an elevation of 1800 m. The field exercise was simulated combat in which the men performed combat-support activities during both day and night and during which time they lost sleep. Activities included digging foxholes, building lava-stone walls, and walking. During the study, subjects were given a military operational

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations ration, the meal, ready-to-eat (MRE), as their only food. Although the average zinc intake during the field exercise was lower than zinc intakes in a sedentary control group of soldiers who were fed the same food, intakes by both groups were considered adequate. Urinary zinc concentrations in the active soldiers increased from an average basal level of 400 µg per day to about 700 µg per day during the study. Sweat mineral losses were not assessed. This finding shows that there are short-term effects of exercise on zinc metabolism; however, the immediate physiological consequences of these effects are not known. Dressendorfer and Sockolov (1980) have suggested that a high level of constant exercise can have long-lasting effects on zinc metabolism. This suggestion was based on the observation that a significant number of endurance runners were characterized by low serum zinc concentrations even when tested prior to an exercise bout. This hypozincemia in endurance runners has since been reported by other laboratories (Couzy et al., 1990; Deuster et al., 1986; Dressendorfer et al., 1982; Hackman and Keen, 1986; Haralambie, 1981). The mechanisms underlying the development of exercise-induced hypozincemia are presumably multifactorial and may include impaired absorption of zinc, excessive sweat and urinary loss of the element, and an altered metabolism of zinc (Anderson et al., 1984; Deuster et al., 1989; Miyamura et al., 1987). Although there is considerable debate about the value of plasma zinc in diagnosing zinc deficiency, most investigators agree that prolonged low plasma zinc concentrations are indicative of suboptimal zinc status. Given that the consequences of a suboptimal zinc status can include behavioral abnormalities, impaired immunocompetence, and reduced rate of recovery from injury (Hambidge, 1989; Keen and Gershwin 1990), it is evident that the functional significance of exercise-induced hypozincemia needs to be defined in future studies. In addition, the interactive effect of prolonged exposure to high temperatures and intense exercise needs to be defined. Exposure to extremes in temperature by itself can result in a stimulation of the acute-phase response with subsequent changes in zinc metabolism (Sugawara et al., 1983; Uhari et al., 1983); sweat losses of zinc can range from 0.5 to 1 mg per liter (Aruoma et al., 1988; Van Rij et al., 1986). Thus a strong synergistic effect of prolonged exposure to exercise and heat would be predicted. To illustrate the above scenario, the following calculations can be made. First, assume a dietary zinc intake of 15 mg, with a typical absorption of 20 percent (King and Turnlund, 1989), resulting in an uptake of 3 mg of zinc. By assuming a sweat zinc concentration of 0.5 mg per liter, it is evident that sweat losses in excess of 8 liters can present a significant problem. In addition, typical urinary zinc losses under conditions of stress will average 0.5 to 0.8 mg per day. Zinc absorption may also be reduced under conditions of stress. Given the above calculations, sus-

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations tained exercise in a hot environment would be predicted to have a negative impact on an individual's zinc balance. Note that an intermediate value for zinc absorption was used for these calculations. Zinc absorption from typical foods ranges from 10 to 40 percent (King and Turnlund, 1989); thus the type of meal fed will have a significant effect on the zinc balance of individuals exposed to the above conditions. Given the frequent observation of exercise-induced hypozincemia and the potentially high amounts of the element that can be lost via sweat, there may be a need for zinc supplementation in situations where prolonged exposure to exercise and heat is anticipated. However, as discussed for iron, caution must be used when advocating zinc supplements because this element at high levels can interfere with copper absorption due to the similar physiochemical properties of zinc and copper (Keen and Hackman, 1986). Chronic (more than 6 weeks) consumption of zinc supplements in excess of 50 mg per day has been linked to the induction of copper deficiency in humans (Fischer et al., 1984; Fosmire, 1990; Prasad et al., 1978; Samman and Roberts, 1988). Lower levels of zinc supplementation have not been reported to result in copper deficiency. INFLUENCE OF EXERCISE AND HEAT ON MAGNESIUM METABOLISM There are considerable data demonstrating an effect of exercise on magnesium metabolism. Rose et al. (1970) reported that serum magnesium concentrations in marathon runners immediately following a race were significantly lower than prerace values, a phenomenon that was attributed to sweat losses of the element during the run. The idea that excessive sweating could result in a high loss of magnesium from the body is consistent with the work of Consolazio et al. (1963) who found that, under normal conditions, sweat loss accounted for over 12 percent of the total daily excretion of magnesium in men working in temperatures of 49° to 50°C. (Typical magnesium losses via sweat are on the order of 3 to 4 mg per liter [Beller et al., 1975; Consolazio et al., 1963].) The observed lowering of plasma magnesium with intense exercise has since been verified by numerous investigators (Beller et al., 1975; Deuster et al., 1987; Franz et al., 1985; Haralambie et al., 1981; Laires et al., 1988; Lijnen et al., 1988; Refsum et al., 1973; Stendig-Lindberg et al., 1987, 1989). The typical reduction in plasma magnesium following intense exercise is on the order of 10 percent. Stendig-Lindberg et al. (1989) reported that low plasma magnesium concentrations can be demonstrated in young men for up to 18 days after strenuous exertion (a 70-km march). In addition to an increased loss of magnesium via sweat, urinary magnesium loss can increase by up to 30 percent following a bout of intense exercise (Deuster et al., 1987; Lijnen et al., 1988). Although

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations the reduction in plasma magnesium may be due in part to an increased rate of magnesium loss from the body, redistribution of magnesium from the plasma pool into other sites may also contribute to exercise-induced decreases in plasma magnesium. For example, Costill et al. (1976) reported an increased magnesium content in exercising muscle during prolonged work that paralleled the decline in plasma magnesium. Redistribution of serum magnesium into red blood cells (Abbasciano et al., 1988; Deuster et al., 1987; Lukaski et al., 1983) and into adipocytes (Franz et al., 1985) with exercise has also been reported. Researchers generally agree that prolonged exercise can result in lower than normal plasma magnesium concentrations; however, they have not agreed on the functional consequences of this reduction. Jooste et al. (1979) reported that in some cases the reduction can be severe enough to trigger epileptic-type convulsions in runners. Similarly, Liu et al. (1983) reported a case in which an exercise-induced reduction in plasma magnesium was associated with the induction of carpopedal spasms in a 24-year-old woman. Marginal magnesium deficiency has been associated with the etiology of some cardiac diseases (Rayssiguier, 1984), hypertension (Altura and Altura, 1984), and reduced work capacity (Conn et al., 1986; Keen et al., 1987; Lowney et al., 1990; Lukaski et al., 1983). Marginal magnesium status has also been implicated in a number of human psychiatric disturbances and in chronic fatigue syndrome (Cox et al., 1991). Given the above reports, it is clear that prolonged strenuous exertion can result in reductions in plasma magnesium concentrations. These reductions can be attributed in part to an increased rate of magnesium loss via sweat, which could be significantly amplified in hot environments. Given the recognition that marginal magnesium deficiency can present a significant health risk to an individual, studies are needed that define the functional consequences of exercise-and heat-induced reductions in plasma magnesium concentrations. EFFECTS OF EXERCISE AND HEAT ON COPPER METABOLISM Acute, strenuous exercise has been reported by several investigators to result in a marked increase in plasma copper concentrations, which has been attributed to an increase in plasma ceruloplasmin concentrations (Haralambie, 1975; Ohno et al., 1984; Olha et al., 1982). An increase in ceruloplasmin concentrations is consistent with the induction of an acute-phase response as discussed above. The effects of intense exercise on increasing plasma copper levels can continue for prolonged time periods. Dressendorfer et al. (1982) reported that men engaged in a 20-day, 500-km road race were characterized by plasma copper levels that increased constantly during the first week, after which they remained fairly constant. This increased copper out-

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations put into the plasma as a result of exercise may have long-lasting effects, as suggested by the observation that plasma copper levels at rest tend to be higher in athletes than in untrained individuals (Haralambie, 1975; Lukaski et al., 1983; Olha et al., 1982). Given the putative antioxidant properties of ceruloplasmin (Goldstein et al., 1979; Gutteridge, 1986), one explanation for the exercise-induced increase in the concentration of this plasma protein is as a response to tissue injury associated with oxidative damage or to the presence of an increased concentration of free radicals (Alessio et al., 1988; Davies et al., 1982; Jenkins, 1988; Kanter et al., 1986). An additional possibility is that the increased ceruloplasmin output from the liver, and hence increased levels in the plasma, is an adaptive response by the body to an increased requirement for extrahepatic copper. It is known that the higher values of maximal oxygen uptake in trained individuals are correlated to an increase in oxidative enzymes within the cell. One of the enzymes increased is the copper-containing protein, cytochrome oxidase (Terjung et al., 1973). It has been shown that ceruloplasmin copper can be incorporated into cytochrome oxidase, and cell receptor sites for ceruloplasmin have been identified (Stevens et al., 1984). Ceruloplasmin copper has also been demonstrated to be transferred to apo-copper, zinc superoxide dismutase (Percival and Harris, 1991). An increase in cellular copper, zinc superoxide dismutase activity could represent an adaptive response to exercise-induced intracellular oxidative stress (Jenkins, 1988; Lukaski et al., 1990). In contrast to reports of increased plasma copper concentrations, Anderson et al. (1984) reported that plasma copper concentrations were similar in men prior to and after completing a 6-mile run; Lukaski et al. (1990) reported no influence of training on plasma copper concentrations in elite swimmers, and Singh et al. (1991) observed no change in plasma copper concentrations in men engaged in intense physical activity over a 5-day period. Resina et al. (1990) reported that plasma copper concentrations were lower in long-distance runners than in sedentary controls, and Dowdy and Burt (1980) reported that plasma copper concentrations and ceruloplasmin activity decreased in competitive swimmers over a 6-month period. Uhari et al. (1983) reported that plasma copper concentrations decreased in male and female subjects following exposure to hot temperatures in a sauna bath. Reasons for the above differences in reported effects of exercise on plasma copper concentrations are various, including differences in copper status of the subjects; type, intensity, and duration of the exercise; physical condition of the individual; and extent of exercise-induced tissue trauma. Presumably, increases in plasma copper occur primarily when there is tissue damage that triggers an acute-phase response. However, note that in the study by Singh et al. (1991), despite evidence of significant tissue damage (see zinc section above), plasma copper concentrations were not elevated.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Additional studies are needed that define the mechanisms underlying exercise-induced increases in plasma copper concentrations. It is important to point out that the occurrence of high plasma copper concentrations does not necessarily translate into high tissue copper concentrations; indeed, high plasma copper concentrations in some disease states have been correlated to low soft tissue copper concentrations (Clegg et al., 1987; Dubick et al., 1987). Although the interpretation of normal to high plasma copper concentrations with regard to assessing an individual's copper status can be difficult, there is general agreement that low plasma copper concentrations typically reflect a compromised copper status. Thus the report of low plasma copper concentrations in some endurance athletes (see above) is of concern. Although loss of basal copper via sweat is typically considered negligible (Gutteridge et al., 1985; Jacob et al., 1981), Consolazio et al. (1964) reported that the amount of copper lost via sweat can be considerable; men who were maintained at 37.8°C and 50 percent relative humidity lost as much as 1 mg per day in sweat. This value should be contrasted to typical dietary copper intakes, which are on the order of 1 to 2 mg (Pennington et al., 1989). Thus prolonged, excessive loss of copper via sweat during strenuous exercise could result in a marginal copper status. The simultaneous exposure to hot temperatures would be expected to accelerate the development of a marginal copper condition. CONCLUSIONS Prolonged strenuous exercise can result in marked changes in chromium, copper, iron, magnesium, and zinc metabolism. Evidence of these changes can persist for several days after the exercise is discontinued. Some of the observed changes in plasma mineral concentrations may be attributed in part to an acute-phase response, which occurs as a result of tissue trauma or stress. Reductions in plasma mineral concentrations may also in part reflect an increased loss of these minerals from the body via urine and sweat. The increased rate of mineral loss that occurs in sweat with exercise is amplified by the simultaneous exposure to hot temperatures. Given the above observations, the following questions emerge: Do endurance-associated changes in mineral metabolism result in some or all of the following: a compromised endurance capacity? a compromised immune defense system? a compromised antioxidant defense system? a slower rate of recovery from injury? Additional work on the influence of prolonged exposure to strenuous exercise and heat is urgently needed. The influence of diet on the above

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations changes in mineral metabolism, or whether dietary manipulations may attenuate some of the negative consequences of these changes, is an area of research that needs to be expanded. REFERENCES Abbasciano, V., F. Levato, M.G. Reali, I. Casoni, M. Patracchini, D. Mazzotta, F. Fagioli, and C. Guglielmini 1988 Reduction of erythrocyte magnesium concentration in heterozygote β-thalassaemic subjects and in normal subjects submitted to physical stress. Magnesium Res. 1:213–217. Alessio, H.A., A.H. Goldfarb, and R.G. Cutler 1988 MDA content increases in fast and slow twitch skeletal muscle with intensity of exercise in a rat. Am. J. Physiol. 255:C874–C877. Altura, B.M., and B.T. Altura 1984 Interactions of magnesium and potassium on blood aspects in view of hypertension: Review of present status and new findings. Magnesium 3:175–194. Andersen, H.T., and H. Barkve 1970 Iron deficiency and muscular work performance: An evaluation of cardio-respiratory function of iron deficient subjects with and without anemia. Scand. J. Lab. Invest. 25(suppl. 144): 1–39. Anderson, R.A., and A.S. Kozlovsky 1985 Chromium intake, absorption, and excretion of subjects consuming self-selected diets . Am. J. Clin. Nutr. 41:1177–1183. Anderson, R.A., M.M. Polansky, and N.A. Bryden 1984 Strenuous running: Acute effects on chromium, copper, zinc and selected variables in urine and serum of male runners. Biol. Trace Elem. Res. 6:327–336. Anderson, R.A., N.A. Bryden, M.M. Polansky, and P.A. Deuster 1988 Exercise effects on chromium excretion of trained and untrained men consuming a constant diet. J. Appl. Physiol. 64:249–252. Aruoma, O.I., T. Reilly, D. MacLaren, and B. Halliwell 1988 Iron, copper and zinc concentrations in human sweat and plasma; the effect of exercise. Clin. Chim. Acta 177:81–88. Balaban, E.P., J.V. Cox, P. Snell, R.H. Vaugh, and E.P. Frenkel 1989 The frequency of anemia and iron deficiency in the runner. Med. Sci. Sports Exerc. 21:643–648. Beard, J.L., M.J. Borel, and J. Derr 1990 Impaired thermoregulation and thyroid function in iron-deficiency anemia. Am. J. Clin. Nutr. 52:813–819. Beller, G.A., J.T. Maher, L.H. Hartley, D.E. Bass, and W.E.C. Wacker 1975 Changes in serum and sweat magnesium levels during work in the heat. Aviat. Space Environ. Med. 46:709–712. Brotherhood, J., B. Brozovic, and L.G.C. Pugh 1975 Haematological status of middle-and long-distance runners. Clin. Sci. Mol. Med. 48:139–145. Brune, M., B. Magnusson, H. Petsson, and L. Hallberg 1986 Iron losses in sweat. Am. J. Clin. Nutr. 43:438–443. Campbell, W.W., and R.A. Anderson 1987 Effects of aerobic exercise and training on the trace minerals chromium, zinc and copper. Sports Med. 4:9–18.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Cannon, J.G., and M.J. Kluger 1983 Endogenous pyrogen activity in human plasma after exercise. Science 220:617–619. Clegg, M.S., F. Ferrell, and C.L. Keen 1987 Hypertension-induced alterations in copper and zinc metabolism in Dahl rats. Hypertension 9:624–628. Conn, C.A., E. Ryder, R.A. Schemmel, P. Ku, V. Seefeldt, and W.W. Heusner 1986 Relationship of maximal oxygen consumption to plasma and erythrocyte magnesium and to plasma copper levels in elite young runners and controls. Fed. Proc. 45:972. Consolazio, C.F. 1966 Comparisons of nitrogen, calcium and iodine excretion in arm and total body sweat. Am. J. Clin. Nutr. 18:443–448. Consolazio, C.F., L.O. Matoush, R.A. Nelson, R.S. Harding, and J.E. Canham 1963 Excretion of sodium, potassium, magnesium and iron in human sweat and the relation of each to balance and requirements. J. Nutr. 79:407–415. Consolazio, C.F., R.A. Nelson, L.O. Matoush, R.C. Hughes, and P. Urone 1964 Trace mineral losses in sweat. Pp. 1–12 in report no. 284 of U.S. Army no. 3A12501A283 (Military Internal Medicine), Subtask no. 03 (Biochemistry), U.S. Army Medical Research and Nutrition Laboratory, Fitzsimmons General Hospital, Denver, Colo. Costill, D.L., R. Cote, and W. Fink 1976 Muscle water and electrolytes following varied levels of dehydration in man. J. Appl. Physiol. 40:6–11. Cousins, R.J. 1985 Absorption, transport, and hepatic metabolism of copper and zinc: Special reference to metallothionein and ceruloplasmin. Physiol. Rev. 65:238–309. Couzy, F., P. Lafargue, and C.Y. Guezennec 1990 Zinc metabolism in the athletes: Influence of training, nutrition and other factors. Int. J. Sports Med. 11:263–266. Cox, I.M., M.J. Campbell, and D. Dowson 1991 Red blood cell magnesium and chronic fatigue syndrome. Lancet 337:757–760. Davies, K.J.A., A.T. Quintanilha, G.A. Brooks, and L. Packer 1982 Free radicals and tissue damage produced by exercise. Biochem. Biophys. Res. Commun. 107:118–125. de Wijn, J.F., J.L. de Jongste, W. Mosterd, and D. Willebrand 1971 Haemoglobin, packed cell volume, serum iron and iron binding capacity of selected athletes during training. J. Sports Med. Phys. Fitness 11:42–51. Deuster, P.A., S.B. Kyle, P.B. Moser, R.A. Vigersky, A. Singh, and E.B. Schoomaker 1986 Nutritional survey of highly trained women runners. Am. J. Clin. Nutr. 45:954–962. Deuster, P.A., E. Dolev, S.B. Kyle, R.A. Anderson, and E.B. Schoomaker 1987 Magnesium homeostasis during high-intensity anaerobic exercise in men. J. Appl. Physiol. 62(2):545–550. Deuster, P.A., B.A. Day, A. Singh, L. Douglass, and P.B. Moser-Veillon 1989 Zinc status of highly trained women runners and untrained women. Am. J. Clin. Nutr. 49:1295–1301. Dinarello, C.A. 1989 The endogenous pyrogens in host-defense interactions. Hosp. Pract. 24:111–128. Dowdy, R.P., and J. Burt 1980 Effect of intensive, long term training on copper and iron nutriture in man. Fed. Proc. 39:786.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Dressendorfer, R.H., and R. Sockolov 1980 Hypoxincemia in runners. Physician Sports Med. 8:97–100. Dressendorfer, R.H., C.E. Wade, C.L. Keen, and J.H. Scaff 1982 Plasma mineral levels in marathon runners during a 20-day road race. Physician Sports Med. 10:113–118. Dressendorfer, R.H., C.L. Keen, C.E. Wade, J.R. Claybaugh, and G.C. Timmis 1991 Development of runners' anemia during a 20-day road race: Effect of iron supplements. Int. J. Sports Med. 12:332–336. Dubick, M.A., G.C. Hunter, S.M. Casey, and C.L. Keen 1987 Aortic ascorbic acid, trace elements, and superoxide dismutase activity in human aneurysmal and occlusive disease. Proc. Soc. Exp. Biol. Med. 184:138–143. Edgerton, V.R., Y. Ohira, J. Hettiarachchi, B. Senewiratne, G.W. Gardner, and R.J. Barnard 1981 Elevation of hemoglobin and work tolerance in iron-deficient subjects. J. Nutr. Sci. Vitaminol. 27:77–86. Ehn, L., B. Carlmark, and S. Hoglund 1980 Iron status in athletes involved in intense physical activity. Med. Sci. Sports Exerc. 12:61–64. Fischer, P.W.F., A. Giroux, and M.R. L'Abbe 1984 Effect of zinc supplementation on copper status in adult man. Am. J. Clin. Nutr. 40:743–746. Fosmire, G.J. 1990 Zinc toxicity. Am. J. Clin. Nutr. 51:225–227. Franz, R.B., H. Ruddel, G.L. Todd, T.A. Dorheim, J.C. Buell, et al. 1985 Physiologic changes during a marathon with special references to magnesium. J. Am. Coil. Nutr. 4:187–194. Frederickson, L.A., J.L. Pulh, and W.S. Runyan 1983 Effects of training on indices of iron status of young female cross-country runners. Med. Sci. Sports Exerc. 15:271–276. Gardner, G.W., V.R. Edgerton, B. Senewiratne, R.J. Barnard, and Y. Ohira 1977 Physical work capacity and metabolic stress in subjects with iron deficiency anemia. Am. J. Clin. Nutr. 30:910–917. Goldstein, I.M., H.B. Kaplan, H.S. Edelson, and G. Weissmann 1979 Ceruloplasmin. A scavenger of superoxide anion radicals. J. Biol. Chem. 254:4040–4045. Gutteridge, J.M.C. 1986 Antioxidant properties of the proteins caeruloplasmin, albumin, and transferrin. A study of their activity in serum and synovial fluid from patients with rheumatoid arthritis. Biochem. Biophys. Acta 869:119–127. Gutteridge, J.M.C., D.A. Rowley, B. Halliwell, D.F. Cooper, and D.M. Heeley 1985 Copper and iron complexes catalytic for oxygen radical reaction in sweat from human athletes. Clin. Chim. Acta 145:267–273. Hackman, R.M., and C.L. Keen 1986 Changes in serum zinc and copper levels after zinc supplementation in running and non-running men. Pp. 89–99 in Sport, Health and Nutrition: 1984 Olympic Scientific Congress Proceedings, Vol. 2, F. Katch ed. Champaign, Ill: Human Kinetics. Hambidge, K.M. 1989 Mild zinc deficiency in human subjects. Pp. 281–296 in Zinc in Human Biology, C.F. Mills, ed. Great Britain: Springer-Verlag.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Haralambie, G. 1975 Changes in electrolytes and trace elements during long-lasting exercise. Pp. 340–351 in Metabolic Adaptation to Prolonged Physical Exercise, H. Howard and J.R. Poortmans, eds. Basel, Switzerland: Birkhäuser Verlag. 1981 Serum zinc in athletes in training. Int. J. Sports Med. 2:135–138. Haralambie, G., L. Senser, and R. Sierra-Chavez 1981 Physiological and metabolic effects of a 25 km race in female athletes. Eur. J. Appl. Physiol. 47:123–131. Hegenauer, J., L. Strause, P. Saltman, D. Dann, J. White, and R. Green 1983 Transitory effects of moderate exercise are not influenced by iron supplementation. Eur. J. Appl. Physiol. 52:57–61. Hetland, O., E.A. Brubak, H.E. Refsum, and S.B. Stromme 1975 Serum and erythrocyte zinc concentrations after prolonged heavy exercise. Pp. 367–370 in Metabolic Adaptation to Prolonged Physical Exercise, H. Howard and J.R. Poortmans, eds. Basel, Switzerland: Birkhäuser Verlag. Jacob, P.A., H.H. Sandstead, J.M. Munoz, L.M. Klevay, and D.B. Milne 1981 Whole body surface loss of trace metals in normal males. Am. J. Clin. Nutr. 34:1379–1383. Jenkins, R.R. 1988 Free radical chemistry. Relationship to exercise. Sports Med. 5:156–170. Jooste, P.L., J.M. Wolfswinkel, J.J. Schoeman, and N.B. Strydom 1979 Epileptic-type convulsions and magnesium deficiency. Aviat. Space Environ. Med. 50:734–735. Kanter, M.M., G.R. Lesmes, N.D. Neguin, K.A. Kaminsky, and J.M. Saeger 1986 Serum lipid levels and lipid peroxidation in ultramarathon runners. Ann. Sports Med. 3:39–41. Karlson, J., R. Diamant, and B. Saltin 1968 Lactic dehydrogenase activity in muscle after prolonged exercise in man. J. Appl. Physiol. 25:88–91. Keen, C.L., and M.E. Gershwin 1990 Zinc deficiency and immune function. Annu. Rev. Nutr. 10:415–431. Keen, C.L., and R.M. Hackman 1986 Trace elements in athletic performance. Pp. 51–65 in Sport, Health and Nutrition: 1984 Olympic Scientific Congress Proceedings, vol. 2, F.I. Katch, ed. Champaign, Ill.: Human Kinetics. Keen, C.L., M.E. Gershwin, P. Lowney, L.S. Hurley, and J.S. Stern 1987 The influence of dietary magnesium intake on exercise capacity and hematological parameters in rats. Metabolism 36:788–793. King, J.C., and J.R. Turnlund 1989 Human zinc requirements. Pp. 335–350 in Zinc in Human Biology, C.F. Mills, ed. Great Britain: Springer-Verlag. Laires, M.J., F. Alves, and M.J. Halpern 1988 Changes in serum and erythrocyte magnesium and blood lipids after distance swimming. Magnesium Res. 1:219–222. Lamanca, J.J., E.M. Haymes, J.A. Daly, R.J. Moffatt, and M.F. Waller 1988 Sweat iron loss of male and female runners during exercise. Int. J. Sports Med. 9:52–55. Lane, H.W. 1989 Some trace elements related to physical activity: Zinc, copper, selenium, chromium, and iodine. Pp. 301–307 in Nutrition in Exercise and Sports, J.E. Hickson and I. Wolinsky, eds. Boca Raton, Fla.: CRC Press.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Lang, J.K., K. Gohil, L. Packer, and R.F. Burk 1987 Selenium deficiency, endurance exercise capacity, and antioxidant status in rats. J. Appl. Physiol. 63:2532–2535. Lichti, E.L., M. Turner, M.S. Deweese, and J.H. Henzel 1970 Zinc concentration in venous plasma before and after exercise in dogs. Missouri Med. 67:303–309. Lichton, I.J., J.B. Miyamura, and S.W. McNutt 1988 Nutritional evaluation of soldiers subsisting on meal, ready-to-eat operational rations for an extended period: Body measurements, hydration, and blood nutrients. Am. J. Clin. Nutr. 48:30–37. Lijnen, P., P. Hespel, R. Fagard, R. Lysens, E. Vanden Eynde, and A. Amery 1988 Erythrocyte, plasma and urinary magnesium in men before and after a marathon. Eur. J. Appl. Physiol. 58:252–256. Liu, L., G. Borowski, and L.I. Rose 1983 Hypomagnesemia in a tennis player. Physician Sports Med. 11:79–80. Lowney, P., J.S. Stern, M.E. Gershwin, and C.L. Keen 1990 Magnesium deficiency and blood 2,3 diphosphoglycerate concentrations in sedentary and exercised male Osborne-Mendel rats. Metabolism 39:837–841. Lukaski, H.C., W.W. Bolonchuk, L.M. Klevay, D.B. Milne, and H.H. Sandstead 1983 Maximal oxygen consumption as related to magnesium, copper and zinc nutriture. Am. J. Clin. Nutr. 37:407–415. 1984 Changes in plasma zinc content after exercise in men fed a low-zinc diet. Am. J. Physiol. 247:E88–E93. Lukaski, H.C., B.S. Hoverson, S.K. Gallagher, and W.W. Bolonchuk 1990 Physical training and copper, iron, and zinc status of swimmers. Am. J. Clin. Nutr. 51:1093–1099. Magazanik, A., Y. Weinstein, R.A. Dlin, M. Derin, S. Schwartzman, and D. Allalouf 1988 Iron deficiency caused by 7 weeks of intensive physical exercise. Eur. J. Appl. Physiol. 57:198–202. McDonald, R., and C.L. Keen 1988 Iron, zinc and magnesium nutrition and athletic performance. Sports Med. 5:171–184. Miyamura, J.B., S.W. McNutt, I.J. Lichton, and N.S. Wenkam 1987 Altered zinc status of soldiers under field conditions. J. Am. Diet. Assoc. 87:595–597. NRC (National Research Council) 1989 Recommended Dietary Allowances, 10th ed. Washington, D.C.: National Academy Press. Nickerson, H.J., M. Holubets, A.D. Tripp, and W.E. Pierce 1985 Decreased iron stores in high school female runners. Am. J. Dis. Child. 139:1115–1119. Ohno, H., T. Yahata, F. Hirata, K. Yamamura, R. Doi, M. Harada, and N. Taniguchi 1984 Changes in dopamine-b-hydroxylase, and copper, and catecholamine concentrations in human plasma with physical exercise. J. Sports Med. Phys. Fitness 24:315–320. Ohno, H., K. Yamashita, R. Doi, K. Yamamura, T. Kondo, and N. Taniguchi 1985 Exercise-induced changes in blood zinc and related proteins in humans. J. Appl. Physiol. 58:1453–1458. Olha, A.E., V. Klissouras, J.D. Sullivan, and S.C. Skoryna 1982 Effect of exercise on concentration of elements in the serum. J. Sports Med. Phys. Fitness 22:414–425.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Parr, R.B., L.A. Bachman, and R.A. Moss 1984 Iron deficiency in female athletes. Physician Sports Med. 12:81–86. Paulev, P-E., R. Jordal, and N.S. Pedersen 1983 Dermal excretion of iron in intensely training athletes. Clin. Chim. Acta 127:19–27. Pennington, J.A.T., D.B. Wilson, R.F. Newell, B.F. Harland, R.D. Johnson, and J.E. Vanderveen 1984 Selected minerals in foods surveys, 1974 to 1981/82. J. Am. Diet. Assoc. 84:771–780. Pennington, J.A.T., B.E. Young, and D.B. Wilson 1989 Nutritional elements in U.S. diets: Results from the Total Diet Study, 1982 to 1986. J. Am. Diet. Assoc. 89:659–664. Percival, S.S., and E.D. Harris 1991 Regulation of Cu, Zn superoxide dismutase with copper. Caeruloplasmin maintains levels of functional enzyme activity during differentiation of K562 cells. Biochem, J. 274:153–158. Prasad, A.S., G.J. Brewer, E.B. Shoomaker, and P. Rabbani 1978 Hypocupremia induced by zinc therapy in adults. J. Am. Med. Assoc. 240:2166–2168. Puhl, S.H., W.B. Runyan, and S.J. Kruse 1981 Erythrocyte changes during training in high school women cross-country runners. Res. Q. Exerc. Sport 52:484–494. Rayssiguier, Y. 1984 Role of magnesium and potassium in the pathogenesis of atherosclerosis. Magnesium 3:226–238. Refsum, H.E., H.D. Meen, and S.B. Stromme 1973 Whole blood, serum and erythrocyte magnesium concentrations after repeated heavy exercise of long duration. Scand. J. Clin. Lab. Invest. 32:123–127. Resina, A., S. Fedi, L. Gatteschi, M.G. Rubenni, M.A. Giamberardino, E. Trabassi, and F. Imreh 1990 Comparison of some serum copper parameters in trained runners and control subjects. Int. J. Sports Med. 11:58–60. Roberts, D., and D. Smith 1990 Serum ferritin values in elite speed and synchronized swimmers and speed skaters. J. Lab. Clin. Med. 116:661–665. Rose, L.I., D.R. Carroll, S.L. Lowe, E.W. Peterson, and K.H. Cooper 1970 Serum electrolyte changes after marathon running. J. Appl. Physiol. 29:449–451. Samman, S., and D.C.K. Roberts 1988 The effect of zinc supplements on lipoproteins and copper status. Atherosclerosis 70:247–252. Singh, A., B.L. Smoak, K.Y. Patterson, L.G. LeMay, C. Veillon, and P.A. Deuster 1991 Biochemical indices of selected trace minerals in men: Effect of stress. Am. J. Clin. Nutr. 53:126–131. Snyder, A.C., L.L. Dvorak, and J.B. Roepke 1989 Influence of dietary iron source on measures of iron status among female runners. Med. Sci. Sports Exerc. 21:7–10. Solomons, N. 1986 Competitive interaction of iron and zinc in the diet: Consequences for human nutrition. J. Nutr. 116:927–935. Stendig-Lindberg, G., Y. Shapiro, Y. Epstein, E. Galun, E. Schonberger, E. Graff, and W.E.C. Wacker 1987 Changes in serum magnesium concentration after strenuous exercise. J. Am. Coil. Nutr. 6:35–40.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations Stendig-Lindberg, G., Y. Shapira, E. Graff, E. Schonberger, and W.E.C. Wacker 1989 Delayed metabolic changes after strenuous exertion in trained young men. Magnesium Res. 2:211–218. Stevens, M.D., R.A. Disilvestro, and E.P. Harris 1984 Specific receptor for ceruloplasmin in membrane fragments for aortic and heart tissue. Biochemistry 23:261–266. Stewart, G.A., J.E. Steel, A.H. Toyme, and M.J. Stewart 1972 Observations on the haematology and the iron and protein intake of Australian Olympic athletes. Med. J. Austr. 2:1339–1343. Stewart, J.G., D.A. Ahlquist, D.B. McGill, D.M. Ilstrup, S. Schwartz, and R.A. Owen 1984 Gastrointestinal blood loss and anemia in runners. Ann. Intern. Med. 100:843–845. Sugawara, N., C. Sugawara, N. Maehara, T. Sadamato, I. Harabuchi, and K. Yamamura 1983 Effect of acute stresses on Zn-thionein production in rat liver. Eur. J. Appl. Physiol. 51:365–370. Taylor, C., G. Rogers, C. Goodman, R.D. Baynes, T.H. Bothwell, W.R. Bezwoda, F. Kramer, and J. Hattingh 1987 Hematologic, iron-related, and acute-phase protein responses to sustained strenuous exercise. J. Appl. Physiol 62:464–469. Terjung, R.L., W.W. Winder, K.M. Baldwin, and J.O. Holloszy 1973 Effect of exercise on the turnover of cytochrome C in skeletal muscle. J. Biol. Chem. 248:7404–7406. Uhari, M., A. Pakarinen, J. Hietala, T. Nurmi, and K. Kouvalainen 1983 Serum iron, copper, zinc, ferritin, and ceruloplasmin after intense heat exposure. Eur. J. Appl. Physiol. 51:331–335. Vallerand, A.L., J.-P. Cuerrier, D. Shapcott, R.J. Vallerand, and P.F. Gardiner 1984 Influence of exercise training on tissue chromium concentrations in the rat. Am. J. Clin. Nutr. 39:402–409. Van Rij, A.M., M.T. Hall, G.L. Dohm, J. Bray, and W.J. Pories 1986 Changes in zinc metabolism following exercise in human subjects. Biol. Trace Element Res. 10:99–106. Whanger, P.D., and S.H. Oh 1978 Nutritional and environmental factors affecting metallothionein levels. Experientia (Suppl.) 34:281–291. Yoshimura, H. 1970 Anemia during physical training (sports anemia). Nutr. Rev. 28:251–253. DISCUSSION DR. NESHEIM: Thank you. We will have a few questions before we break for lunch. PARTICIPANT: Could you elaborate some more on the magnesium uptake by lymphocytes? You mentioned in passing that there could be an increase in uptake by lymphocytes? DR. KEEN: Yes, this has been suggested by Franz (Franz et al., 1985). And the argument is, although there is no hard data to support it, that for lipolysis, you will have an increase in a lymphocyte magnesium uptake. While the current data for this idea are not very strong, it is in the literature that it should be considered a possibility.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations An exercise-induced erythrocyte uptake of magnesium, has also been argued based on the idea that it is needed for 2, 3-diphosphoglycerate synthesis (Lukaski et al., 1983). However, we have done a study (Lowney et al., 1990) where we looked at the influence of magnesium deficiency on erythrocyte 2, 3-diphosphoglycerate production, and it had no influence on 2, 3-diphosphoglycerate levels. PARTICIPANT: How about the endurance study with magnesium deficiency in the animal. Why didn't that continue to go on down as you have a more severe deficiency. Here is a plateau in fact. DR. KEEN: Yes, it is a plateau. Unfortunately, you can't get animals much more deficient and get meaningful data. We were curious if we could get a dose response using animals fed diets containing less than 50 µg of magnesium per gram, however once pronounced signs of magnesium deficiency occurred, it was difficult to get the males to run. DR. NESHEIM: Thank you, Carl. That was very interesting and challenging and indeed reports some of the work that needs to be done.

OCR for page 117
Nutritional Needs in Hot Environments: Applications for Military Personnel in Field Operations This page in the original is blank.