Serial estimations of exchangeable (42)K showed that six volunteer subjects undergoing intensive physical conditioning in a hot climate sustained a mean deficit of 517 mEq. This deficit occurred despite a daily potassium intake of 100 mEq. Simultaneous values for lean body mass rose suggesting that potassium deficiency was not the result of catabolism. Although sweating was the major avenue by which the deficit occurred, daily excretion of potassium into the urine when each subject was maximally deficient ranged from 46 to 75 mEq and thus was inappropriately high for potassium-depleted subjects. Despite high intakes of sodium and excretion of corresponding quantities into the urine, Na/K ratios in sweat were low thus indicating unsuppressed activity of aldosterone on sweat glands. Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake. These findings suggest that intense physical work in the heat stimulates higher production of aldosterone than would occur in nonexercising subjects on similar sodium intakes. Similar to the phenomenon of mineralocorticoid escape, such overproduction of aldosterone in the presence of conditions permitting excretion of sodium into the urine could facilitate continued excretion of potassium by the kidney despite serious potassium depletion. As a consequence, the kidney played a role in the genesis of potassium depletion in these subjects. In contrast to subjects undergoing conditioning in the summer months, potassium depletion did not occur in 16 subjects during identical training under cooler environmental conditions.