Sweat samples were collected from the forearms of eight male volunteers using light gauze pads applied for 20-min periods. Preliminary trials indicated that this technique yielded realistic figures for both sweat volume and sweat composition. Tests were conducted under three conditions: a) outdoor exercise, cool environment; b) indoor exercise, normal room temperatures; and c) sauna exposure. In all environments, proximal forearm samples indicated a larger sweat secretion than distal forearm or hand samples. [Mg2+] decreased as sweat flow increased, but after allowance for interindividual differences of sweat volume, [Na+], [K+], [Ca2+], and [Cl-] were independent of sweat flow rates. The differential effect of sweat flow suggests active regulation rather than contamination. Interindividual differences of sweat composition could not be explained in terms of differences in personal fitness. Sauna bathing yielded sweat with a higher [Mg2+] and [Ca2+] content than did exercise; however, [Na+], [K+], and [Cl-] were similar for the three experimental conditions. Again, the data are best explained in terms of an active regulation of sweat composition. Total ionic losses do not seem sufficient to deplete body mineral reserves unless many days of training are undertaken in a hot climate.
Ten elite male runners (age, 29.8 +/- 1.7 yr; maximum oxygen consumption, 65.3 +/- 4.9 ml.kg-1.min-1; 10-km times, 31 min 43 s +/- 1 min 46 s) deliberately increased training schedules by an average of 38% for 3 wk. Resting heart rate and maximal oxygen intake were unchanged, but the heart rate response to acute exercise was decreased. Following heavy training, blood samples taken at rest showed trends to a decreased helper/suppressor cell ratio, an increased phytohemagglutinin (PHA)- and concanavalin (ConA)-stimulated lymphocyte proliferation, and a decreased production of immunoglobulins IgG and IgM. Whereas PHA-stimulated lymphocyte proliferation was initially unchanged by acute exercise, after 3 wk of heavy training the same acute exercise caused an 18% suppression of proliferation. Acute exercise following heavy training did not alter pokeweed-stimulated IgG or IgM synthesis. There was no correlation between changes in lymphocyte subpopulations, helper/suppressor ratios, and mitogen-induced cellular proliferation. The immune system of endurance-trained athletes at rest seemed to tolerate the stress of heavy training, but superimposition of a bout of acute exercise on the chronic stress of heavy training resulted in immunosuppression, which was transient and most likely not of clinical significance.
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