Hemodynamic responses to heat stress in the resting and exercising human leg: insight into the effect of temperature on skeletal muscle blood flow

Abstract

Heat stress increases limb blood flow and cardiac output (Q) in humans, presumably in sole response to an augmented thermoregulatory demand of the skin circulation. Here we tested the hypothesis that local hyperthermia also increases skeletal muscle blood flow at rest and during exercise. Hemodynamics, blood and tissue oxygenation, and muscle, skin, and core temperatures were measured at rest and during exercise in 11 males across four conditions of progressive whole body heat stress and at rest during isolated leg heat stress. During whole body heat stress, leg blood flow (LBF), Q, and leg (LVC) and systemic vascular conductance increased gradually with elevations in muscle temperature both at rest and during exercise (r(2) = 0.86-0.99; P < 0.05). Enhanced LBF and LVC were accompanied by reductions in leg arteriovenous oxygen (a-vO(2)) difference and increases in deep femoral venous O(2) content and quadriceps tissue oxygenation, reflecting elevations in muscle and skin perfusion. The increase in LVC occurred despite an augmented plasma norepinephrine (P < 0.05) and was associated with elevations in muscle temperature (r(2) = 0.85; P = 0.001) and arterial plasma ATP (r(2) = 0.87; P < 0.001). Isolated leg heat stress accounted for one-half of the increase in LBF with severe whole body heat stress. Our findings suggest that local hyperthermia also induces vasodilatation of the skeletal muscle microvasculature, thereby contributing to heat stress and exercise hyperemia. The increased limb muscle vasodilatation in these conditions of elevated muscle sympathetic vasoconstrictor activity is closely related to the rise in arterial plasma ATP and local tissue temperature.

Mechanisms for the control of local tissue blood flow during thermal interventions: influence of temperature‐dependent ATP release from human blood and endothelial cells

“…1972; Pearson et al . 2011). It is therefore likely that blood and deep tissue temperature in the forearm varied by as much as 9–10°C after 1 h of heating and cooling.…”

“…Forearm oxygen consumption (${\dot{V}}_{{\mathrm{normalO}}_2}$) was estimated in the experimental and control arms using the Fick equation (${\dot{V}}_{{\mathrm{normalO}}_2}$ = BABF × arteriovenous O 2 difference), where arterial O 2 content was calculated assuming that the arterial [Hb] was the same as the measured venous [Hb] and that arterial O 2 saturation and partial pressure of oxygen ($P_{{\mathrm{normalO}}_2}$) remained unchanged at 98% and 100 mmHg, respectively, thoughout the 1 h heating and cooling protocols (Pearson et al . 2011; Chiesa et al . 2015).…”

“…2011; Pearson et al . 2011). In support of the responsiveness of skeletal muscle macro‐ and microcirculations to thermal stimuli, local cooling and heating have been shown to change perfusion in the human thenar eminence muscle group in proportion to variations in intramuscular temperature (Binzoni et al .…”

“…2011). This supports a coupling between the increase in intravascular ATP and the concomitant elevation in local perfusion (Ellsworth et al .…”

“…2010), because metabolic changes in response to local heating and cooling are relatively small (Barcroft & Edholm, 1943; Pearson et al . 2011). It remains unknown, however, whether reductions in temperature depress ATP release from isolated human erythrocytes.…”