Mechanisms of heat acclimation with endurance training in humans: A role of active cutaneous vasodilator

Abstract

Hypovolemia and hyperosmolality due to thermal dehydration suppress thermoregulatory responses of sweating and cutaneous vasodilation in humans, resulting in increasing a risk of heat illness. Recently, we found in young and older subjects that an ingestion of carbohydrate-protein supplement immediately after a bout of exercise during training accelerated an increase in plasma volume and an improvement of thermoregulatory responses. These results suggest that change in plasma volume alters cutaneous vasodilation and sweat rate through baroreflexes; however, no electrical signals in the efferent path of the reflex loop have not been identified. We have recently successfully recorded skin sympathetic nerve signal components synchronized and non-synchronized with cardiac cycles, separately, in passively heated young subjects, and found that although both components increased with cutaneous vasodilation and sweat rate in hyperthermia, an increase in synchronized component was suppressed by hypovolemia with suppressed cutaneous vasidilation, while an increase in non-synchronized component was not suppressed as sweat rate. On the other hand, we found that hyperosmolality suppressed the increases of both components with suppressed cutaneous vasodilation and sweat rate. These results suggest that a synchronized component controls cutaneous vasodilation while a non-synchronized component controls sweat rate, and also that beat-by-beat changes in atrial pressure due to a fluctuation of venous return to the heart varies cutaneous vasodilation through baroreflexes but not sweat rate.