Heat stress and baroreflex regulation of blood pressure

Abstract

In healthy, noninjured, individuals, passive (i.e., nonexercising) whole-body heating has the potential to cause significant cardiovascular stress that may be second only to the cardiovascular stress associated with exercise. For example, such a heat stress can increase heart rate to well over 100 beats min(-1) with cardiac output increasing upward to 13 L min(-1). This increase in cardiac output is necessary to maintain blood pressure due to profound reductions in total vascular conductance associated with cutaneous vasodilation. These responses are accompanied with elevations in sympathetic activity and reductions in vascular conductance (i.e., increased vascular resistance) from noncutaneous beds. While heat-stressed, blood pressure control is compromised resulting in orthostatic intolerance. A plausible explanation for such an event is that heat stress impairs baroreflex responsiveness perhaps due to the reduced range by which baroreflexes can increase heart rate, cardiac output, sympathetic activity, and vascular resistance during a hypotensive challenge. Given that dynamic exercise has the potential to cause large increases in internal temperature, possibly a component of the response to exercise, with respect to baroreflex control of blood pressure, may be affected by the thermal load during the exercise bout. Within this context, the purpose of this review was to summarize findings investigating the effects of heat stress on baroreflex regulation of blood pressure.

FIGURE 1

Carotid–cardiac (left panels) and carotid–vascular (right panels) baroreflex responses during normothermia (solid lines) and whole-body heat stress (dashed lines). Whole-body heat stress did not alter the maximum gain of the carotid–cardiac baroreflex (lower left panel), whereas this heat stress significantly (P < 0.01) reduced the maximum gain of the carotid–vascular baroreflex by approximately 35% (lower right panel). Notice how the heat stress shifted the carotid–cardiac baroreflex curve to the prevailing elevated heart rate (upper left panel) that occurs during this thermal exposure. The operating point, defined as the heart rate or blood pressure before perturbing the carotid sinus are depicted as open symbols. bpm indicates beats per minute; mm Hg, millimeters of mercury; ECSP, estimated carotid sinus pressure; MAP, mean arterial blood pressure. Figure used with permission Crandall (2).

FIGURE 2

Linear regression between muscle sympathetic nerve activity (MSNA) and an index of central blood flow (thoracic impedance) during progressive lower-body negative pressure (LBNP) for a representative subject. Squares depict baseline MSNA and thoracic impedance before LBNP. The average slope of this relationship across all subjects was significantly elevated by heat stress (normothermia = 235 ± 103 units·min⁻¹·Ω⁻¹, heat stress = 523 ± 230 units·min⁻¹·Ω⁻¹, P < 0.01). r indicates the correlation coefficients for this subject’s data. Figure used with permission from Cui et al. (7).

FIGURE 3

Effects of whole-body heat stress (solid line) on transfer function gain and coherence values during fixed breathing (A and B) and spontaneous breathing (C and D) protocols. Regardless of whether breathing was fixed or spontaneous, heat stress significantly reduced the transfer function gain between spontaneous changes in systolic arterial blood pressure and corresponding changes in heart rate within the high-frequency range (0.2–0.3 Hz) relative to when the subjects were normothermic (dashed lines). Heat stress did not significantly affect transfer function gain between systolic blood pressure and heart rate in the low-frequency range (0.03–0.15 Hz). Regardless of breathing protocol or frequency range, heat stress did not significantly affect coherence. Reduced cardiac vagal neural activity due to heat stress is the likely cause for reduced transfer function gain between systolic blood pressure and heart rate within the high-frequency range. Figure used with permission from Crandall et al. (4).

FIGURE 4

Mean arterial blood pressure (MAP; dashed line) and cutaneous vascular conductance (CVC; solid line) responses when a representative subject was normothermic (leftmost data set) and during 30-mm Hg lower-body negative pressure (LBNP) while the subject was heat-stressed. Numerical values above the CVC data indicate an index of skin blood flow (SkBF) derived from laser Doppler flowmetry. Notice that, at the onset of syncopal symptoms (i.e., presyncope) and corresponding large reductions in MAP, SkBF and CVC remained three- to fourfold higher relative to when the subject was normothermic. These data depict what could be construed as an inadequate reduction in CVC leading up to and at the onset of syncopal symptoms, given that, during heat stress, a large fraction of cardiac output is directed to the skin.

FIGURE 5

Change in mean arterial blood pressure (upper panel), systemic vascular resistance (middle panel), and systemic vascular conductance (lower panel) to systemic infusions of three graded doses of the α₁ agonist phenylephrine. Before drug administration, heat stress (closed circles) significantly reduced systemic vascular resistance, significantly increased systemic vascular conductance, without significantly affecting mean arterial blood pressure. Notice the pronounced differences in the elevation in mean arterial blood pressure and systemic vascular resistance during graded infusions of the same concentrations of phenylephrine. *Significant differences (P < 0.05) between thermal conditions for that dose of phenylephrine. Figure used with permission from Cui et al. (6).