from 53.3 to 56.4 mEq/kg. This represented a significant change and suggested that there was an increase in the potassium concentration in skeletal muscle as a result of training. As is pointed out below, subsequent studies in dogs confirmed this notion. The fact that the men who trained in hot weather did not show an increase in potassium per kilogram of lean body mass indeed suggested that muscle injury might have prevented such a change. Although none of the subjects became frankly hypokalemic, most values were in the low normal range, that is, between 3.4 and 3.7 mEq/liter at the time of peak potassium deficiency. The absence of frank hypokalemia possibly indicates coincident muscle injury. Other studies showed that aldosterone was produced excessively in terms of sodium intake. However, when expressed as a function of sodium excretion, both secretory rates and excretory rates of aldosterone were perfectly appropriate. Renin activity measured before the men arose each day was often markedly elevated and became more elevated following maintenance of an upright posture during the morning hours, as would be expected. There also occurred a substantial rise in total body water, an expansion of extracellular fluid volume, and an increase of inulin clearance from an average value of 101 ml/min per 1.72 m2 of body surface area to a value of 123 ml/min (Knochel et al., 1974).
Serum creatine kinase activity was within normal limits at the time of initial measurement. However, this value and the value for creatine excretion rose markedly by week 2 of training (Knochel et al., 1974), suggestive of muscle injury. Subsequently, both values fell to the normal range. Other indices suggestive of skeletal muscle injury that peaked on week 2 of training included a drop in the total serum calcium concentration that was not associated with changes in the serum protein concentration and an elevation of serum phosphorus. Frank hyperuricemia occurred in all of these individuals. In addition, uric acid excretion into the urine became abnormally high and was compatible with major muscle injury or rhabdomyolysis (Knochel and Carter; 1976; Knochel et al., 1974). These values also peaked during week 2 of training. At the time of peak potassium deficiency, average values for potassium excretion into the urine were 72 mEq/day. This is considered to be greatly in excess of that anticipated in potassium depletion and suggests either an obligatory loss as a result of muscle injury or that losses were the result of renal tubular sodium-potassium exchange mediated by aldosterone.
The foregoing studies were interpreted to indicate that modestly severe potassium deficiency occurs as a result of intense training in hot weather. This did not occur under identical training conditions during cool weather. Although sweat cannot be collected accurately under such conditions, canteen counts confirmed water intakes of between 10 and 15 liters/day during hot weather. Since body weight did not change appreciably or fell,