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.
1Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX; and 2Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX
Address for correspondence: Craig G. Crandall, Ph.D., Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Ave, Dallas, TX 75231; E-mail: CraigCrandall@texashealth.org.
Submitted for publication December 2007.
Accepted for publication February 2008.