Baroreceptor modulation of cutaneous vasodilator and sudomotor responses to thermal stress in humans.

Abstract

1. The influence of baroreceptor unloading on cutaneous vasodilatation was investigated in ten human subjects during dynamic supine cycle ergometer exercise at 28 degrees C. Increases in forearm skin blood flow (venous occlusion plethysmography) and arterial blood pressure (non-invasive) were measured and used to calculate forearm vascular conductance while local chest sweating rate was measured by dew-point hygrometry. Subjects performed two similar exercise protocols with and without baroreceptor unloading induced by application of -40 mmHg lower body negative pressure (LBNP). The LBNP condition was reversed (i.e. either removed or applied) after 15 min while exercise continued for an additional 20 min. 2. During exercise without LBNP, the body core temperature threshold for vasodilatation (measured as oesophageal temperature, Tc) averaged 37.06 +/- 0.12 degrees C (+/- S.E.M.) and increased to 37.30 +/- 0.09 degrees C (P < 0.05) during exercise with LBNP. The rate of rise of forearm vascular conductance (FVC) per unit increase in Tc (an expression of thermal sensitivity) and peak FVC at 15 min was significantly attenuated during baroreceptor unloading. These effects were rapidly reversed when LBNP was turned off. 3. Baroreceptor unloading during the first 15 min of exercise attenuated the local chest sweating rate, which was also reversed when LBNP was removed. 4. The time course and quickness in which baroreceptor unloading modulated thermoregulatory control of skin blood flow and local chest sweat rate suggests that the interaction between these two homeostatic mechanisms is primarily neurally mediated. The ability of baroreceptor activity to modulate both control of skin blood flow and sweating suggests a common site of interaction, more proximal than the effector organs, and involving the active vasodilator system.

Evidence for metaboreceptor stimulation of sweating in normothermic and heat‐stressed humans

“…Given previous findings that demonstrate a relationship between muscle metaboreceptor stimulation and the elevation in blood pressure and muscle sympathetic nerve activity during post-exercise ischaemia (Victor et al 1988;Nishiyasu et al 1994), it is clear that muscle metaboreceptors during post-exercise ischaemia were activated in the present procedure. Since baroreceptors have been shown to modulate sweat rate (Mack et al 1995), it was possible Role of metaboreflex and/or baroreflex on sweating J. Physiol. 534.2 Figure 2.…”

“…Moreover, this increase in sweating was attributed to muscle metaboreceptor simulation since sweat rate remained elevated during post-IHG exercise ischaemia under moderately warmed and hyperthermic conditions (Crandall et al 1998;Kondo et al 1999). However, given prior findings that baroreceptors modulate sweating (Mack et al 1995), coupled with elevations in mean arterial blood pressure during exercise and post-exercise ischaemia, it may be that baroreceptor loading contributes to increases in sweat rate during IHG exercise and post-exercise ischaemia. To our knowledge, the contribution of elevated arterial blood pressure during exercise on the control of sweat rate remains unknown.…”

“…In addition to these thermal factors, non-thermal factors, such as central command, muscle mechano/metaboreceptor activation and baroreflexes, have been shown to modulate sweating during whole-body heating and during exercise (Van Beaumont & Bullard, 1963;Solack et al 1985;Mack, 1995;Yamazaki et al 1996;Kondo et al 1999;Kondo, 2001). However, independent roles of these non-thermal factors in the control of sweating, particularly during exercise, remain unclear.…”

Heat Illness during Working and Preventive Considerations from Body Fluid Homeostasis

“…Fortney et al 16) examined the effect of isotonic hypovolemia by 9% on local SR during exercise at 65-70% of VO 2max in a hot environment (T a =30°C, relative humidity [r.h.]=40%) and suggested that the T es threshold for sweating remained unchanged while SR on the chest and arm in response to increased T es was significantly reduced. Moreover, Mack et al 10) suggested that the reduction in cardiac filling pressure by LBNP reduced SR during exercise. Dodt et al 17) suggested that skin sympathetic nervous activity was reduced by LBNP.…”

“…They suggested that hypovolemia significantly increased esophageal temperature (T es ) threshold for cutaneous vasodilation by 0.42°C and decreased the maximal SkBF by 50%. Moreover, Mack et al 10) reported that -40 mmHg of lower body negative pressure (LBNP), a maneuver that reduced the venous return to the heart, suppressed cutaneous vasodilation in response to increased T es during exercise while the cessation of LBNP released the suppression. Similarly, other maneuvers to increase the venous return to the heart; acute blood volume expansion 11) , a supine position 12,13) , headout-of-water immersion 14) , or continuous negative pressure breathing 15) all enhanced cutaneous vasodilation during exercise.…”