Haemodynamic responses to heat stress and hypohydration in resting and exercising humans: Implications for the regulation of skeletal muscle blood flow

Abstract

Heat stress-induced hyperthermia and exercise-induced hypohydration are associated with marked alterations in limb and systemic haemodynamics in humans. However, the mechanisms underlying these alterations their effects on muscle blood flow are not well understood. The present thesis examined whether whole body and local heat stresses increased limb skin and muscle blood flow (Study 1) and whether hypohydration and hyperthermia compromised leg muscle, skin and systemic haemodynamics (Study 2). The effects of heat stress and combined hypohydration and hyperthermia were examined at rest and during mild small muscle mass exercise in humans. The results from Study 1 suggested that heat stress was accompanied by vasodilation in both skeletal muscle and skin vasculatures. Therefore in line with concomitant elevations in blood flow, skeletal muscle and skin vasodilation contribute to increases in leg blood flow and vascular conductance with whole body heat stress. Furthermore, increases in leg muscle and skin blood flow with isolated elevations in leg tissue temperature accounted for at least one half of the total increase in leg blood flow with whole body heat stress. Enhanced leg blood flow owed to a net vasodilation as explained by an elevation in vasodilator activity that exceeded increases in vasoconstrictor activity. This phenomenon was closely related to increases in muscle temperature and intravascular adenosine triphosphate (ATP). The results from Study 2 demonstrated that mild and moderate hypohydration and hyperthermia do not compromise leg muscle and skin blood flow or cardiac output at rest or during mild exercise in humans. Furthermore, acute rehydration did not alter leg muscle and skin blood flow or cardiac output compared to hypohydration and hyperthermia despite large alterations in blood volume and haematological variables and the restoration of core temperature. Taken together, the findings of this thesis indicate that: 1) heat stress induces vasodilation in both skeletal muscle and cutaneous vasculature, 2) elevations in muscle temperature and intravascular ATP play a role in heat stress- and exercise-induced hyperaemia, and 3) moderate hypohydrationinduced hypovolemia and haemoconcentration and rehydration-induced hypervolaemia and haemodilution do not alter leg blood flow or cardiac output at rest and during low intensity exercise in humans when a large cardiovascular reserve is available.