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Review
. 2010 Aug;199(4):407-23.
doi: 10.1111/j.1748-1716.2010.02119.x. Epub 2010 Mar 24.

Cardiovascular function in the heat-stressed human

C G Crandall  1 , J González-Alonso
Affiliations
Review

Cardiovascular function in the heat-stressed human

C G Crandall et al. Acta Physiol (Oxf). 2010 Aug.

Abstract

Heat stress, whether passive (i.e. exposure to elevated environmental temperatures) or via exercise, results in pronounced cardiovascular adjustments that are necessary for adequate temperature regulation as well as perfusion of the exercising muscle, heart and brain. The available data suggest that generally during passive heat stress baroreflex control of heart rate and sympathetic nerve activity are unchanged, while baroreflex control of systemic vascular resistance may be impaired perhaps due to attenuated vasoconstrictor responsiveness of the cutaneous circulation. Heat stress improves left ventricular systolic function, evidenced by increased cardiac contractility, thereby maintaining stroke volume despite large reductions in ventricular filling pressures. Heat stress-induced reductions in cerebral perfusion likely contribute to the recognized effect of this thermal condition in reducing orthostatic tolerance, although the mechanism(s) by which this occurs is not completely understood. The combination of intense whole-body exercise and environmental heat stress or dehydration-induced hyperthermia results in significant cardiovascular strain prior to exhaustion, which is characterized by reductions in cardiac output, stroke volume, arterial pressure and blood flow to the brain, skin and exercising muscle. These alterations in cardiovascular function and regulation late in heat stress/dehydration exercise might involve the interplay of both local and central reflexes, the contribution of which is presently unresolved.

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Conflict of interest statement

Conflict of interest

There is no conflict of interest.

Figures

Figure 1
Figure 1
Classic cardiovascular responses to increases in skin temperature (Ts) resulting in a large increases in body temperature (Tb) reported as a per cent change in the indicated value relative to pre-heat stress baseline. CO, cardiac output; HR, heart rate; SV, stroke volume; CBV, central blood volume; AoMP, aortic mean arterial blood pressure; RAMP, right atrial mean blood pressure; TPR, total peripheral resistance. Note that the effects of heat stress on central blood volume have recently been shown to decrease as opposed to slight increases observed by these investigators (see Fig. 2). Figure from Rowell et al. (1969a); republished with permission from The American Physiological Society.
Figure 2
Figure 2
Percent change in blood volume from the indicated regions between experimental (i.e. heat stressed) and time control subjects. In each of the indicated regions heat stress significantly reduced blood volume relative to the time control trials. Figure from Crandall et al. (2008); republished with permission from Wiley-Blackwell.
Figure 3
Figure 3
Peak septal and lateral mitral annular systolic velocities (S′; panel a) and isovolumic acceleration of the septal and lateral mitral annulus (panel b). Individual (left-hand side of each panel) and group averaged (right-hand side of each panel) echocardiographic measurements of the indicated data during normothermic (NT) and whole-body heat-stress (WBH) conditions. Increases in the indicated parameters by heat stress are indicative of an increase in cardiac systolic function. Figure from Brothers et al. (2009a); used with permission from The American Physiological Society.
Figure 4
Figure 4
Effect of thermal stress on the Frank–Starling relation via plotting the relation between pulmonary capillary wedge pressure and stroke volume. Data points were generated via lower body negative pressures (LBNP) of 0, 15 and 30 mmHg. The arrows indicate the operating point for the respective thermal conditions. The operating point is defined as the prevailing pulmonary capillary wedge pressure and stroke volume prior to the onset of LBNP. Figure from Wilson, Brothers, Tollund, Dawson, Nissen, Yoshiga, Jons, Secher and Crandall. J Physiol 587, 3383–3392, 2009; republished with permission from Wiley-Blackwell.
Figure 5
Figure 5
End-tidal carbon dioxide tension and middle cerebral artery blood velocity (MCA Vmean) during normothermia, heat stress, and heat stress after end-tidal carbon dioxide (PETCO2) concentration was returned to pre-heat stress levels. The reduction in PETCO2 concentration during heat stress was completely abolished by the PETCO2 clamping procedure (panel a). Heat stress reduced MCA Vmean relative to normothermia. Restoration of PETCO2 to the normothermic level while subjects were heat stressed (heat stress + clamp) attenuated the decrease in MCA Vmean relative to control heat stress without the clamp; however MCA Vmean remained reduced when compared with normothermia (panel b). These data indicate that mechanisms other than reduced PETCO2 contribute to the reduced cerebral perfusion that occurs in heat-stressed individuals. *Significantly different relative to normothermia; §significantly different relative to control heat stress. Figure from Brothers et al. (2009b); republished with permission from Wiley-Blackwell.
Figure 6
Figure 6
Haemodynamics during maximal whole-body exercise in heat-stressed humans. Systemic and exercising limb blood flow and vascular conductance during constant maximal exercise with heat stress and control conditions. Note the significant reductions in cardiac output and leg blood flow and arterial blood pressure leading to unchanged vascular conductance. *Significantly lower than corresponding peak exercise values, P < 0.05. †Significantly lower than control (normal) trials, P < 0.05. Figure from González-Alonso & Calbet (2003); republished with permission from the American Heart Association.
Figure 7
Figure 7
Cerebral circulation and oxygenation during maximal whole-body exercise in heat-stressed humans. Left and right middle cerebral artery blood velocity and near-infrared spectroscopy-determined cerebral tissue oxygenation at rest, during submaximal and maximal cycling and during 10 min of recovery in heat stress and control conditions. Note the marked reductions in blood velocity accompanying the declines in tissue oxygenation. *Higher than value at start of exercise, P < 0.05. †Lower than peak value during maximal exercise, P < 0.05. From González-Alonso et al. (2004); republished with permission from Wiley-Blackwell.
Figure 8
Figure 8
Haemodynamics with dehydration during prolonged exercise in the heat. Systemic and peripheral blood flow during prolonged cycling in the heat with and without dehydration and hyperthermia. Note that the declines in cardiac output are accompanied by reductions in blood flow to the exercising legs, the skin and possible visceral blood flow. *Significantly lower than 20 min value, P < 0.05. †Significantly lower than control, P < 0.05. From González-Alonso et al. (1998); republished with permission from Wiley-Blackwell.
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