scholarly journals Muscle metaboreceptors modulate postexercise sweating, but not cutaneous blood flow, independent of baroreceptor loading status

2015 ◽  
Vol 309 (11) ◽  
pp. R1415-R1424 ◽  
Author(s):  
Gabrielle Paull ◽  
Sheila Dervis ◽  
Ryan McGinn ◽  
Baies Haqani ◽  
Andreas D. Flouris ◽  
...  

We examined whether sustained changes in baroreceptor loading status during prolonged postexercise recovery can alter the metaboreceptors' influence on heat loss. Thirteen young males performed a 1-min isometric handgrip exercise (IHG) at 60% maximal voluntary contraction followed by 2 min of forearm ischemia (to activate metaboreceptors) before and 15, 30, 45, and 60 min after a 15-min intense treadmill running exercise (>90% maximal heart rate) in the heat (35°C). This was repeated on three separate days with continuous lower body positive (LBPP, +40 mmHg), negative (LBNP, −20 mmHg), or no pressure (Control) from 13- to 65-min postexercise. Sweat rate (ventilated capsule; forearm, chest, upper back) and cutaneous vascular conductance (CVC; forearm, upper back) were measured. Relative to pre-IHG levels, sweating at all sites increased during IHG and remained elevated during ischemia at baseline and similarly at 30, 45, and 60 min postexercise (site average sweat rate increase during ischemia: Control, 0.13 ± 0.02; LBPP, 0.12 ± 0.02; LBNP, 0.15 ± 0.02 mg·min−1·cm−2; all P < 0.01), but not at 15 min (all P > 0.10). LBPP and LBNP did not modulate the pattern of sweating to IHG and ischemia (all P > 0.05). At 15-min postexercise, forearm CVC was reduced from pre-IHG levels during both IHG and ischemia under LBNP only (ischemia: 3.9 ± 0.8% CVCmax; P < 0.02). Therefore, we show metaboreceptors increase postexercise sweating in the middle to late stages of recovery (30–60 min), independent of baroreceptor loading status and similarly between skin sites. In contrast, metaboreflex modulation of forearm but not upper back CVC occurs only in the early stages of recovery (15 min) and is dependent upon baroreceptor unloading.

2014 ◽  
Vol 306 (1) ◽  
pp. R82-R89 ◽  
Author(s):  
Ryan McGinn ◽  
Brendan Swift ◽  
Konrad Binder ◽  
Daniel Gagnon ◽  
Glen P. Kenny

Metaboreceptor activation during passive heating is known to influence cutaneous vascular conductance (CVC) and sweat rate (SR). However, whether metaboreceptors modulate the suppression of heat loss following dynamic exercise remains unclear. On separate days, before and after 15 min of high-intensity treadmill running in the heat (35°C), eight males underwent either 1) no isometric handgrip exercise (IHG) or ischemia (CON), 2) 1 min IHG (60% of maximum, IHG), 3) 1 min IHG followed by 2 min of ischemia (IHG+OCC), 4) 2 min of ischemia (OCC), or 5) 1 min IHG followed by 2 min of ischemia with application of lower body negative pressure (IHG+LBNP). SR (ventilated capsule), cutaneous blood flow (Laser-Doppler), and mean arterial pressure (Finometer) were measured continuously before and after dynamic exercise. Following dynamic exercise, CVC was reduced with IHG exercise ( P < 0.05) and remained attenuated with post-IHG ischemia during IHG+OCC relative to CON (39 ± 2 vs. 47 ± 6%, P < 0.05). Furthermore, the reduction in CVC was exacerbated by application of LBNP during post-IHG ischemia (35 ± 3%, P < 0.05) relative to IHG+OCC. SR increased during IHG exercise ( P < 0.05) and remained elevated during post-IHG ischemia relative to CON following dynamic exercise (0.94 ± 0.15 vs. 0.53 ± 0.09 mg·min−1·cm−2, P < 0.05). In contrast, application of LBNP during post-IHG ischemia had no effect on SR (0.93 ± 0.09 mg·min−1·cm−2, P > 0.05) relative to post-IHG ischemia during IHG+OCC. We show that CVC is reduced and that SR is increased by metaboreceptor activation following dynamic exercise. In addition, we show that the metaboreflex-induced loading of the baroreceptors can influence the CVC response, but not the sweating response.


2016 ◽  
Vol 310 (11) ◽  
pp. R1332-R1339 ◽  
Author(s):  
Tatsuro Amano ◽  
Masashi Ichinose ◽  
Yoshimitsu Inoue ◽  
Takeshi Nishiyasu ◽  
Shunsaku Koga ◽  
...  

We examined whether the sustained activation of metaboreceptor in forearm during cycling exercise can modulate sweating and cutaneous vasodilation. On separate days, 12 young participants performed a 1.5-min isometric handgrip exercise at 40% maximal voluntary contraction followed by 1) 9-min forearm ischemia (Occlusion, to activate metaboreceptor) or 2) no ischemia (Control) in thermoneutral conditions (27°C, 50%) with mean skin temperature clamped at 34°C. Thirty seconds after the handgrip exercise, participants cycled for 13.5 min at 40% V̇o2 max. For Occlusion, forearm ischemia was maintained for 9 min followed by no ischemia thereafter. Local sweat rate (SR, ventilated capsule) and cutaneous vascular conductance (CVC, laser-Doppler perfusion units/mean arterial pressure) on the contralateral nonischemic arm as well as esophageal and skin temperatures were measured continuously. The period of ischemia in the early stages of exercise increased SR (+0.03 mg·cm−2·min−1, P < 0.05) but not CVC ( P > 0.05) above Control levels. No differences were measured in the esophageal temperature at which onset of sweating (Control 37.19 ± 0.09 vs. Occlusion 37.07 ± 0.09°C) or CVC (Control 37.21 ± 0.08 vs. Occlusion 37.08 ± 0.10°C) as well as slopes for these responses (all P > 0.05). However, a greater elevation in SR occurred thereafter such that SR was significantly elevated at the end of the ischemic period relative to Control (0.37 ± 0.05 vs. 0.23 ± 0.05 mg·cm−2·min−1, respectively, P < 0.05) despite no differences in esophageal temperature. We conclude that the activation of forearm muscle metaboreceptor can modulate sweating, but not CVC, during cycling exercise without affecting the core temperature-SR relationship.


2003 ◽  
Vol 94 (5) ◽  
pp. 1829-1835 ◽  
Author(s):  
Narihiko Kondo ◽  
Shuji Yanagimoto ◽  
Takeshi Nishiyasu ◽  
Craig G. Crandall

Given differences in sympathetic innervation to glabrous and nonglabrous skin, we tested the hypothesis that muscle metaboreceptor regulation of cutaneous vascular conductance (CVC) differs between these skin regions. Subjects ( n = 21) performed isometric handgrip exercise (IHG; 50% maximal voluntary contraction for 60 s), followed by 2 min of postexercise ischemia. Throughout IHG and postexercise ischemia, CVC was measured from glabrous (palm) and nonglabrous (forearm and chest) regions contralateral to the exercising arm. These procedures were conducted after the subjects had been exposed to an ambient temperature of 35°C and a relative humidity of 50% for 60 min. These thermal conditions were intended to cause slight increases in cutaneous blood flow via sympathetic withdrawal. Esophageal, sublingual, and mean skin temperatures did not change markedly during IHG or postexercise ischemia. During IHG, forearm CVC did not change, chest CVC increased slightly, and palm CVC decreased substantially (from 100 to 34.8 ± 3.5%; P = 0.001). During muscle metaboreceptor stimulation due to postexercise ischemia, CVC from nonglabrous regions returned to preexercise baselines, whereas CVC at the palm remained below preexercise baseline (68.2 ± 4.2%; P = 0.001 relative to preexercise baseline). These results indicate that in mildly heated humans muscle metaboreflex stimulation is capable of modulating CVC in glabrous, but not in nonglabrous, skin.


2014 ◽  
Vol 306 (2) ◽  
pp. H251-H260 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Rei Tahara ◽  
Takeshi Nishiyasu

We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise ( r = −0.751, P < 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI ( r = 0.568 and 0.512, respectively, P < 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses.


1989 ◽  
Vol 66 (4) ◽  
pp. 1586-1592 ◽  
Author(s):  
W. F. Taylor ◽  
J. M. Johnson ◽  
W. A. Kosiba ◽  
C. M. Kwan

Cutaneous vascular responses to dynamic exercise have been well characterized, but it is not known whether that response pattern applies to isometric handgrip exercise. We examined cutaneous vascular responses to isometric handgrip and dynamic leg exercise in five supine men. Skin blood flow was measured by laser-Doppler velocimetry and expressed as laser-Doppler flow (LDF). Arterial blood pressure was measured noninvasively once each minute. Cutaneous vascular conductance (CVC) was calculated as LDF/mean arterial pressure. LDF and CVC responses were measured at the forearm and chest during two 3-min periods of isometric handgrip at 30% of maximum voluntary contraction and expressed as percent changes from the preexercise levels. The skin was normothermic (32 degrees C) for the first period of handgrip and was locally warmed to 39 degrees C for the second handgrip. Finally, responses were observed during 5 min of dynamic two-leg bicycle exercise (150–175 W) at a local skin temperature of 39 degrees C. Arm LDF increased 24.5 +/- 18.9% during isometric handgrip in normothermia and 64.8 +/- 14.1% during isometric handgrip at 39 degrees C (P less than 0.05). Arm CVC did not significantly change at 32 degrees C but significantly increased 18.1 +/- 6.5% during isometric handgrip at 39 degrees C (P less than 0.05). Arm LDF decreased 12.2 +/- 7.9% during dynamic exercise at 39 degrees C, whereas arm CVC fell by 35.3 +/- 4.6% (in each case P less than 0.05). Chest LDF and CVC showed similar responses.(ABSTRACT TRUNCATED AT 250 WORDS)


2005 ◽  
Vol 98 (6) ◽  
pp. 2011-2018 ◽  
Author(s):  
Gregg R. McCord ◽  
Christopher T. Minson

The dramatic increase in skin blood flow and sweating observed during heat stress is mediated by poorly understood sympathetic cholinergic mechanisms. One theory suggests that a single sympathetic cholinergic nerve mediates cutaneous active vasodilation (AVD) and sweating via cotransmission of separate neurotransmitters, because AVD and sweating track temporally and directionally when activated during passive whole body heat stress. It has also been suggested that these responses are regulated independently, because cutaneous vascular conductance (CVC) has been shown to decrease, whereas sweat rate increases, during combined hyperthermia and isometric handgrip exercise. We tested the hypothesis that CVC decreases during isometric handgrip exercise if skin blood flow is elevated using local heating to levels similar to that induced by pronounced hyperthermia but that this does not occur at lower levels of skin blood flow. Subjects performed isometric handgrip exercise as CVC was elevated at selected sites to varying levels by local heating (which is independent of AVD) in thermoneutral and hyperthermic conditions. During thermoneutral isometric handgrip exercise, CVC decreased at sites in which blood flow was significantly elevated before exercise (−6.5 ± 1.8% of maximal CVC at 41°C and −10.5 ± 2.0% of maximal CVC at 43°C; P < 0.05 vs. preexercise). During isometric handgrip exercise in the hyperthermic condition, an observed decrease in CVC was associated with the level of CVC before exercise. Taken together, these findings argue against withdrawal of AVD to explain the decrease in CVC observed during isometric handgrip exercise in hyperthermic conditions.


1977 ◽  
Author(s):  
T. Sano ◽  
T. Motomiya ◽  
Y. Itoh ◽  
N. Mashimo ◽  
H. Yamazaki ◽  
...  

The important role of platelet aggregation in the pathophysiology of diabetic vascular disease has been emphasized. The authors devised a new method to assess platelet sensitivity to aggregation performed without centrifugation (Sano et al. Thrombos. Haemostasis April '77 issue, in press). Using this technique, platelet aggregability in diabetics was assessed concerning to age and to. the effect of isometric exercise. The effect of EG-626, a potent cAMP phosphodiesterase inhibiting and thromboxane A2-antagonistic substance, administered prior to exercise was also observed.In 52 diabetics without macroangiopathy, platelet sensitivity to ADP-aggregation was assessed. The sensitivity was expressed by ‘n’ of the minimum effective concentration of serially two-fold diluted ADP, 2-n mg/ml, to give aggregation. In males, both diabetics and healthy, the sensitivity correlated significantly with age. The regression lines obtained were Y=2.15+0,13X (Y: sensitivity, X:age in years) in the diabetics and Y=6.58+0.04X in the healthy subjects respectively. The value of the slope was significantly higher in the diabetics comparing to the healthy subjects. An enhancement of the platelet sensitivity was disclosed significantly in the diabetics but not in the healthy subjects, after isometric handgrip exercise at 50% maximal voluntary contraction for 2 minutes.. This enhancement was prevented when the patients were treated orally with 300 mg of EG-626, 1.5 hours before exercise. These findings would suggest the thrombotic tendency in diabetics and anti-thrombotic effect of this compound.


2012 ◽  
Vol 302 (4) ◽  
pp. R417-R423 ◽  
Author(s):  
Konrad Binder ◽  
Aaron G. Lynn ◽  
Daniel Gagnon ◽  
Narihiko Kondo ◽  
Glen P. Kenny

The relative influence of muscle metabo- and baroreflex activity on heat loss responses during post-isometric handgrip (IHG) exercise ischemia remains unknown, particularly under heat stress. Therefore, we examined the separate and integrated influences of metabo- and baroreceptor-mediated reflex activity on sweat rate and cutaneous vascular conductance (CVC) under increasing levels of hyperthermia. Twelve men performed 1 min of IHG exercise at 60% of maximal voluntary contraction followed by 2 min of ischemia with simultaneous application of lower body positive pressure (LBPP, +40 mmHg), lower body negative pressure (LBNP, −20 mmHg), or no pressure (control) under no heat stress. On separate days, trials were repeated under heat stress conditions of 0.6°C (moderate heat stress) and 1.4°C (high heat stress) increase in esophageal temperature. For all conditions, mean arterial pressure was greater with LBPP and lower with LBNP than control during ischemia (all P ≤ 0.05). No differences in sweat rate were observed between pressure conditions, regardless of the level of hyperthermia ( P > 0.05). Under moderate heat stress, no differences in CVC were observed between pressure conditions. However, under high heat stress, LBNP significantly reduced CVC by 21 ± 4% ( P ≤ 0.05) and LBPP significantly elevated CVC by 14 ± 5% ( P ≤ 0.05) relative to control. These results show that sweating during post-IHG exercise ischemia is activated by metaboreflex stimulation, and not by baroreflexes. In contrast, our results suggest that baroreflexes can influence the metaboreflex modulation of CVC, but only at greater levels of hyperthermia.


2015 ◽  
Vol 309 (8) ◽  
pp. R912-R919 ◽  
Author(s):  
Naoto Fujii ◽  
Lyra Halili ◽  
Maya Sarah Singh ◽  
Robert D. Meade ◽  
Glen P. Kenny

Acetylcholine released from cholinergic nerves is a key neurotransmitter contributing to heat stress-induced cutaneous vasodilation and sweating. Given that sympathetic cholinergic nerves also release ATP, ATP may play an important role in modulating cholinergic cutaneous vasodilation and sweating. However, the pattern of response may differ between males and females given reports of sex-related differences in the peripheral mechanisms governing these heat loss responses. Cutaneous vascular conductance (CVC, laser-Doppler perfusion units/mean arterial pressure) and sweat rate (ventilated capsule) were evaluated in 17 young adults (8 males, 9 females) at four intradermal microdialysis skin sites continuously perfused with: 1) lactated Ringer (Control), 2) 0.3 mM ATP, 3) 3 mM ATP, or 4) 30 mM ATP. At all skin sites, methacholine was coadministered in a concentration-dependent manner (0.0125, 0.25, 5, 100, 2,000 mM, each for 25 min). In both males and females, CVC was elevated with the lone infusion of 30 mM ATP (both P < 0.05), but not with 0.3 and 3 mM ATP compared with control (all P >0.27). However, 0.3 mM ATP induced a greater increase in CVC compared with control in response to 100 mM methacholine infusion in males ( P < 0.05). In females, 0.3 mM ATP infusion resulted in a lower concentration of methacholine required to elicit a half-maximal response (EC50) ( P < 0.05). In both males and females, methacholine-induced sweating was unaffected by any concentration of ATP (all P > 0.44). We demonstrate that ATP enhances cholinergic cutaneous vasodilation albeit the pattern of response differs between males and females. Furthermore, we show that ATP does not modulate cholinergic sweating.


1988 ◽  
Vol 64 (5) ◽  
pp. 2190-2196 ◽  
Author(s):  
D. R. Seals ◽  
P. B. Chase ◽  
J. A. Taylor

The purpose of this study was to determine the respective contributions of tachycardia and increases in sympathetic nerve activity (SNA) in mediating the pressor responses to fatiguing vs. nonfatiguing levels of isometric handgrip exercise (IHE) in humans. We performed direct (microneurographic) measurements of muscle SNA from the right peroneal nerve in the leg and recorded arterial pressure (AP) and heart rate (HR) in eight healthy subjects before (control), during, and after 2.5 min of IHE at 15, 25, or 35% of maximal voluntary contraction (MVC). At 15% MVC, AP increased during the initial 1.5 min of IHE (7 mmHg, P less than 0.05) and remained at this level; at 25 and 35% MVC, AP increased throughout IHE (22 and 34 mmHg vs. control, respectively, P less than 0.05). HR increased during the initial 1.5 min of IHE at all three levels (5, 12, and 19 beats/min, respectively, P less than 0.05) but did not increase further over the last minute. At 15% MVC, muscle SNA did not increase above control; during 25 and 35% MVC, muscle SNA did not increase during the 1st min of IHE but increased progressively thereafter (109 and 205% vs. control, respectively, P less than 0.05). The magnitudes of the average increases in AP and muscle SNA over the last minute of IHE were directly related (r = 0.99, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)


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