scholarly journals Influence of forearm muscle metaboreceptor activation on sweating and cutaneous vascular responses during dynamic exercise

2016 ◽  
Vol 310 (11) ◽  
pp. R1332-R1339 ◽  
Author(s):  
Tatsuro Amano ◽  
Masashi Ichinose ◽  
Yoshimitsu Inoue ◽  
Takeshi Nishiyasu ◽  
Shunsaku Koga ◽  
...  
Keyword(s):  
Sweat Rate ◽  
Voluntary Contraction ◽  
Esophageal Temperature ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Cycling Exercise ◽  
Isometric Handgrip Exercise ◽  
Ischemic Period ◽  
C 50 ◽  
Forearm Muscle

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.

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 ◽  
...  
Keyword(s):  
Sweat Rate ◽  
Pressure Control ◽  
Voluntary Contraction ◽  
Treadmill Running ◽  
Maximal Heart Rate ◽  
Isometric Handgrip ◽  
Young Males ◽  
Isometric Handgrip Exercise ◽  
Postexercise Recovery ◽  
Cutaneous Vascular Conductance

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.

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

2014 ◽  
Vol 306 (2) ◽  
pp. H251-H260 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Rei Tahara ◽  
Takeshi Nishiyasu
Keyword(s):  
Individual Differences ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Coefficients Of Variation ◽  
Isometric Handgrip Exercise ◽  
Induced Changes

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.

Cutaneous vascular responses to isometric handgrip exercise

1989 ◽  
Vol 66 (4) ◽  
pp. 1586-1592 ◽  
Author(s):  
W. F. Taylor ◽  
J. M. Johnson ◽  
W. A. Kosiba ◽  
C. M. Kwan
Keyword(s):  
Maximum Voluntary Contraction ◽  
Voluntary Contraction ◽  
Dynamic Exercise ◽  
Laser Doppler ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Local Skin ◽  
Vascular Responses ◽  
Arterial Blood ◽  
Isometric Handgrip Exercise

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)

Cutaneous vascular responses to isometric handgrip exercise during local heating and hyperthermia

2005 ◽  
Vol 98 (6) ◽  
pp. 2011-2018 ◽  
Author(s):  
Gregg R. McCord ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Local Heating ◽  
Whole Body ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Hyperthermic Condition ◽  
Isometric Handgrip Exercise

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.

scholarly journals Platelet ADP-Hypersensitivity by Aging and Isometric Exercise in Diabetics and its Prevention by EG-626

1977 ◽  
Author(s):  
T. Sano ◽  
T. Motomiya ◽  
Y. Itoh ◽  
N. Mashimo ◽  
H. Yamazaki ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Camp Phosphodiesterase ◽  
Minimum Effective Concentration ◽  
Isometric Handgrip Exercise ◽  
Thrombotic Tendency

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.

Autonomic mediation of the pressor responses to isometric exercise in humans

1988 ◽  
Vol 64 (5) ◽  
pp. 2190-2196 ◽  
Author(s):  
D. R. Seals ◽  
P. B. Chase ◽  
J. A. Taylor
Keyword(s):  
Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Pressor Responses ◽  
Isometric Handgrip Exercise ◽  
The Right ◽  
Exercise In Humans

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)

Effects of exercise intensity on the sweating response to a sustained static exercise

2000 ◽  
Vol 88 (5) ◽  
pp. 1590-1596 ◽  
Author(s):  
Narihiko Kondo ◽  
Hirotaka Tominaga ◽  
Manabu Shibasaki ◽  
Ken Aoki ◽  
Shuichi Okada ◽  
...  
Keyword(s):  
Exercise Intensity ◽  
Marked Change ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Time Courses ◽  
Response To Exercise ◽  
Male Subjects ◽  
Skin Temperatures

To investigate how the sweating response to a sustained handgrip exercise depends on changes in the exercise intensity, the sweating response to exercise was measured in eight healthy male subjects. Each subject lay in the supine position in a climatic chamber (35°C and 50% relative humidity) for ∼60 min. This exposure caused sudomotor activation by increasing skin temperature without a marked change in internal temperature. After this period, each subject performed isometric handgrip exercise [15, 30, 45, and 60% maximal voluntary contraction (MVC)] for 60 s. Although esophageal and mean skin temperatures did not change with a rise in exercise intensity and were similar at all exercise intensities, the sweating rate (SR) on the forearm increased significantly ( P < 0.05) from baseline (0.094 ± 0.021 mg ⋅ cm−2 ⋅ min−1at 30% MVC, 0.102 ± 0.022 mg ⋅ cm−2 ⋅ min−1at 45% MVC, 0.059 ± 0.009 mg ⋅ cm−2 ⋅ min−1at 60% MVC) in parallel with exercise intensity above exercise intensity at 30% MVC (0.121 ± 0.023 mg ⋅ cm−2 ⋅ min−1at 30% MVC, 0.242 ± 0.051 mg ⋅ cm−2 ⋅ min−1at 45% MVC, 0.290 ± 0.056 mg ⋅ cm−2 ⋅ min−1at 60% MVC). Above 45% MVC, SR on the palm increased significantly from baseline ( P < 0.05). Although SR on the forearm and palm tended to increase with a rise in exercise intensity, there was a difference in the time courses of SR between sites. SR on the palm showed a plateau after abrupt increase, whereas SR on the forearm increased progressively during exercise. These results suggest that the increase in SR with the increase in sustained handgrip exercise intensity is due to nonthermal factors and that the magnitude of these factors during the exercise may be responsible for the magnitude of SR.

The effect of extracellular hyperosmolality on sweat rate during metaboreflex activation in passively heated young men

2021 ◽  
Author(s):  
Maura M. Rutherford ◽  
Ashley P. Akerman ◽  
Robert D. Meade ◽  
Sean R. Notley ◽  
Madison D. Schmidt ◽  
...  
Keyword(s):  
Sweat Rate ◽  
Nervous Activity ◽  
Maximum Voluntary Contraction ◽  
Young Men ◽  
Weighted Average ◽  
Whole Body ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Body Regions ◽  
Isometric Handgrip Exercise

Metaboreflex activation augments sweating during mild-to-moderate hyperthermia in euhydrated (isosmotic isovolemic) individuals. Recent work indicates that extracellular hyperosmolality may augment metaboreflex-mediated elevations in sympathetic nervous activity. Our primary objective was therefore to test the hypothesis that extracellular hyperosmolality would exacerbate metaboreflex-mediated increases in sweat rate. On two separate occasions, 12 young men (mean (SD): 25 (5) years) received a 90-min intravenous infusion of either 0.9% saline (isosmotic condition, ISO) or 3.0% saline (hyperosmotic condition, HYP), resulting in a post-infusion serum osmolality of 290 (3) and 301 (7) mOsm/kg, respectively. A whole-body water perfusion suit was then used to increase esophageal temperature by 0.8°C above resting. Participants then performed a metaboreflex activation protocol consisting of 90 s isometric handgrip exercise (40% of their pre-determined maximum voluntary contraction), followed by 150 s of brachial occlusion (trapping produced metabolites within the limb). Metaboreflex-induced sweating was quantified as the change in global sweat rate (from pre-isometric handgrip exercise to brachial occlusion), estimated as the surface area-weighted average of local sweat rate on the abdomen, axilla, chest, bicep, quadriceps, and calf, measured using ventilated capsules (3.8 cm2). We also explored whether this response differed between body regions. The change in global sweat rate due to metaboreflex activation was significantly greater in HYP compared to ISO (0.03 mg/min/cm2 [95% confidence interval: 0.00, 0.06]; p=0.047), but was not modulated by body region (site*condition interaction: p=0.679). These findings indicate that extracellular hyperosmolality augments metaboreflex-induced increases in global sweat rate, with no evidence for region-specific differences.

scholarly journals Platelet Aggregation and Plasma Catecholamines in Hypertension

1977 ◽  
Author(s):  
N. D. Vlachakis ◽  
L. Aledort
Keyword(s):  
Platelet Aggregation ◽  
Light Transmission ◽  
Platelet Rich Plasma ◽  
Plasma Catecholamines ◽  
Voluntary Contraction ◽  
Upright Position ◽  
Plasma Norepinephrine ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise

In 19 patients, with essential hypertension (EH) while on placebo therapy and 8 age matched normals (NC), platelet aggregation studies and plasma norepinephrine (NE) and epinephrine (E) were obtained at rest and at the end of 3 min isometric handgrip exercise (IHE) (2/3 of maximal voluntary contraction) in the upright position. The percent of light transmission at 1 μM ADP concentration (LT) and the biphasic aggregation threshold (BAT) in response to ADP were measured in fresch platelet rich plasma at 300,000 platelets. In NC the LT was 26±4.8, the BAT was 2.8±0.9, NE was 242±30, pg/ml and E was 36±3.3, while in EH the corresponding values were 27.6±2.6 for LT, 3.4±1 for BAT, 222±22 for NE and 36±2.8 for E. The IHE increased LT significantly in both groups and decreased BAT significantly only in EH, while NE and E increased significantly in both groups. In 7 patients the administration of propranolol (PR) for 6 weeks or longer decreased LT and increased BAT as well as increased both NE and E, but neither change was significant. The sudden discontinuation of PR did not produce significant changes in NE, E, LT and BAT from the placebo period, when measurements were obtained one to ten days thereafter. To 7 subjects the intravenously administration of NE for 15 min produced an increase of plasma NE from 338±43 to 1774±159 associated with a significant increase in LT and significant decrease in BAT. Thus uncomplicated EH does not appear to be associated with abnormal platelet aggregation or increased NE or E. However, plasma catecholamines affect platelet function.

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