PubMed1981
The effect of low potassium (K+) intake on its excretion, concentration in sweat and on physiological responses during heat stress was evaluated on eight Indian male soldiers in winter months at Delhi. After a stabilization period of 3 days on each diet, i.e., 85 mEq of K+/d (diet I, normal), 55 mEq of K+/d (diet II), and 45 mEq of K+/d (diet III), the physiological responses and the sodium and potassium concentrations in sweat, plasma, RBC, and urine were measured when the subjects were exposed to heat for 3 h daily in a climatic chamber maintained at 40 degrees C DB and 32 degrees C WB. The subjects worked in the chamber at the rate of 465 W/h for 20 min periods with 40 min rest between each period of exercise. The whole body sweat was collected after the spell of work and was analysed for sodium and potassium levels. Throughout the study the subjects remained on positive sodium balance except on day 4 in diet III. Fluid balance also remained positive while potassium balance was negative in subjects on diet II and diet III. There was no significant change in heart rate, sweat volume, oral temperature, sodium, and potassium concentrations in plasma and RBC during the entire period of the study. Even in the subjects with negative potassium balance there was no change in the sodium and potassium concentrations in sweat during exercise in heat. The only evidence of potassium conservation was a reduced excretion in urine. Out of the eight subjects, in one subject there was a flattening of the 'T' wave in the ECG and reduction in amplitude of the 'T' wave in two more subjects. As there is no reduction in sweat potassium concentration and the urine volume is low, the marginal level of reduced excretion of potassium in urine with a high rate of sweating (7-81) in subjects doing work in the tropics, there is every likelihood of potassium deficiency if a liberal intake is not ensured. In our earlier studies (Malhotra et al. 1976) we found that the concentration of potassium (K+) in sweat is much higher than in plasma even in acclimatised subjects. A large amount of K+ is therefore likely to be lost in sweat during exposure to heat. In that study there was no evidence of a reduction in K+ concentration in the sweat or urine upon repeated exposure of the subjects to heat, indicative of a compensatory mechanism for conservation of K+ losses. However, these earlier studies were done on subjects who were on a normal diet which contained 75-80 mEq of K+ per day. Since a compensatory mechanism may be triggered only when the body K+ becomes dificient and not earlier, as is the case with sodium (Malhotra et al. 1959), we have now investigated the effects of a sequential reduction of reduced dietary K+ on the dermal and urinary losses of K+. The effects of K+ deficiency on the physiological responses to heat have also been studied. The results of these studies are reported here.