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

Abstract

Increases in sweating during heat stress occur secondarily to increases in internal and skin temperatures. 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.Isometric handgrip (IHG) exercise increases heart rate, arterial blood pressure, and muscle and skin sympathetic nerve activity (Mark et al. 1985;Vissing et al. 1991;Joyner, 1992). In warm conditions IHG exercise increased sweat rate due to non-thermal factors since internal and skin temperatures did not increase during the bout of IHG exercise (Kondo et al. 1999). 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. 1. Isometric handgrip (IHG) exercise increases sweat rate and arterial blood pressure, and both remain elevated during post-exercise ischaemia. The purpose of this study was to identify whether the elevation in arterial blood pressure during post-exercise ischaemia contributes to the increase in sweating.2. In normothermia and during whole-body heating, 2 min IHG exercise at 40 % maximal voluntary contraction, followed by 2 min post-exercise ischaemia, was performed with and without bolus intravenous administration of sodium nitroprusside during the ischaemic period. Sodium nitroprusside was administered to reduce blood pressure during post-exercise ischaemia to pre-exercise levels. Sweat rate was monitored over two microdialysis membranes placed in the dermal space of forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine, while the other was perfused with the vehicle.3. In normothermia, IHG exercise increased sweat rate at the neostigmine-treated site but not at the control site. Sweat rate remained elevated during post-exercise ischaemia even after mean arterial blood pressure returned to the pre-IHG exercise baseline. Subsequent removal of the ischaemia stimulus returned sweat rate to pre-IHG exercise levels. Sweat rate during postexercise ischaemia without sodium nitroprusside administration followed a similar pattern.4. During whole-body heating, IHG exercise inc...

Sweating response to passive stretch of the calf muscle during activation of forearm muscle metaboreceptors in heated humans

“…However, it has been reported that skin sympathetic nerve activity and SR are not altered by phenylephrine-administered increases in arterial blood pressure during mild heating (46). Furthermore, the SR remained elevated during activation of the muscle metaboreceptors, even after MAP returned to baseline levels, with administration of sodium nitroprusside (38). These results suggest that the arterial baroreflex does not influence the sweating response.…”

“…It is well known that group III muscle afferents are stimulated predominantly by mechanically sensitive muscle mechanoreceptors, whereas group IV muscle afferents are stimulated mainly by chemically sensitive muscle metaboreceptors. Activation of muscle metaboreceptors by postexercise muscle ischemia (PEMI) under normothermic and mildly hot conditions induces sweating (2,4,22,38). Additionally, Kondo et al (23) reported that activating the muscle mechanoreceptors by passive limb movement for 2 min evoked slight sweating under hot conditions.…”

Hyperthermia modifies muscle metaboreceptor and baroreceptor modulation of heat loss in humans

“…heat stress; thermoregulation; isometric handgrip exercise; postexercise ischemia EXTENSIVE STUDIES HAVE SHOWN that mechano-and baroreceptors (cardiopulmonary and arterial) modulate the heat loss responses of cutaneous vasodilation and sweating during passive heating, exercise, and postexercise recovery, while central command can influence sweating and cutaneous vasodilation during exercise (12,13,23,24,31,34). In contrast, information regarding the influence of metaboreceptors on thermoeffector activity during and following exercise remains limited, largely because of the difficulties associated with isolating the muscle metaboreflex.Much of our understanding of the influence of metaboreceptor activity on heat loss responses has been limited to findings obtained using an isometric handgrip (IHG) exercise model (18,20,30). After an IHG exercise bout at a given percentage of maximal voluntary contraction (MVC), a 2-min period of ischemia is induced by occlusion of all limb blood flow to the exercising arm, which is thought to trigger group III and IV chemosensitive afferents (26).…”

“…Much of our understanding of the influence of metaboreceptor activity on heat loss responses has been limited to findings obtained using an isometric handgrip (IHG) exercise model (18,20,30). After an IHG exercise bout at a given percentage of maximal voluntary contraction (MVC), a 2-min period of ischemia is induced by occlusion of all limb blood flow to the exercising arm, which is thought to trigger group III and IV chemosensitive afferents (26).…”

Effects of exercise intensity, posture, pressure on the back and ambient temperature on palmar sweating responses due to handgrip exercises in humans

“…increases heart rate, mean arterial pressure, sweating rate, and sympathetic nerve activity to skin and muscle [Nishiyasu et al, 1994;Rowell & O'Leary, 1990;Saito et al, 1990;Shibasaki et al, 2001;Vissing et al, 1991]. These physiological responses associated with the IHG are related to mechanisms involving central command such as stimulation from the parallel activation of motor and autonomic pathways and the activation of mechanosensitive or metabosensitive receptors in exercising muscle [Crandall et al, , 1998Kondo et al, 1998Kondo et al, ,1999Rowell & O'Leary, 1990].…”