Muscle mechanoreceptor modulation of sweat rate during recovery from moderate exercise

2004 ◽  
Vol 96 (6) ◽  
pp. 2115-2119 ◽  
Author(s):  
Manabu Shibasaki ◽  
Mieko Sakai ◽  
Mayumi Oda ◽  
Craig G. Crandall

The objective of this study was to identify whether muscle mechanoreceptor stimulation is capable of modulating sweat rate. Seven healthy subjects performed two 20-min bouts of supine exercise on a tandem cycle ergometer (60 rpm at 65% of maximal heart rate). After one bout, the subject stopped exercising (i.e., no pedaling), whereas, after the other bout, the subject's legs were passively cycled (at 60 rpm) via a second person cycling the tandem ergometer. This allows for mechanical stimulation of muscle with minimal activation of central command. Esophageal temperature (Tes), mean skin temperature (T̄sk), heart rate, mean arterial blood pressure, oxygen consumption, cutaneous vascular conductance (CVC), and sweat rate were not different during the two exercise bouts. Regardless of the mode of exercise recovery, there were no differences in Tes, T̄sk, or CVC. In contrast, early in the recovery period, chest and forearm sweat rate were significantly greater in the passive cycling recovery mode relative to the no-pedaling condition (chest: 0.57 ± 0.13 vs. 0.39 ± 0.14, forearm: 0.30 ± 0.05 vs. 0.12 ± 0.02 mg·cm-2·min-1; both P < 0.05). These results suggested that muscle mechanoreceptor stimulation to the previously activated muscle is capable of modulating sweat rate.

2004 ◽  
Vol 96 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Thad E. Wilson ◽  
Robert Carter ◽  
Michael J. Cutler ◽  
Jian Cui ◽  
Michael L. Smith ◽  
...  

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (Tcore), mean skin temperature (Tsk), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure ( n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, Tcore, and Tsk. Baroreceptor loading and thermal status were similar during trials because MAP (90 ± 4, 88 ± 4 mmHg), thoracic impedance (29 ± 1, 28 ± 2 Ω), central venous pressure (5 ± 1, 4 ± 1 mmHg), Tcore (37.5 ± 0.1, 37.5 ± 0.1°C), and Tsk (34.1 ± 0.3, 34.2 ± 0.2°C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 ± 6% of maximum) and inactive (28 ± 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 ± 0.16 mg·cm-2·min-1) compared with inactive (0.34 ± 0.19 mg·cm-2·min-1; P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.


2002 ◽  
Vol 93 (6) ◽  
pp. 1918-1924 ◽  
Author(s):  
Robert Carter ◽  
Thad E. Wilson ◽  
Donald E. Watenpaugh ◽  
Michael L. Smith ◽  
Craig G. Crandall

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 ± 3, forearm: 48 ± 3%max) compared with during inactive recovery (chest: 21 ± 2, forearm: 25 ± 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 ± 0.10, forearm: 0.46 ± 0.10 mg · cm−2 · min−1) compared with during inactive recovery (chest: 0.28 ± 0.10, forearm: 0.14 ± 0.20 mg · cm−2 · min−1); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.


1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.


1988 ◽  
Vol 64 (2) ◽  
pp. 753-758 ◽  
Author(s):  
J. K. Kalis ◽  
B. J. Freund ◽  
M. J. Joyner ◽  
S. M. Jilka ◽  
J. Nittolo ◽  
...  

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)


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 24 (5) ◽  
pp. 489-496 ◽  
Author(s):  
Tiago Peçanha ◽  
Marcelle Paula-Ribeiro ◽  
Edson Campana-Rezende ◽  
Rhenan Bartels ◽  
João Carlos Bouzas Marins ◽  
...  

It has been shown that water intake (WI) improves postexercise parasympathetic recovery after moderateintensity exercise session. However, the potential cardiovascular benefit promoted by WI has not been investigated after high-intensity exercise.Purpose:To assess the effects of WI on post high-intensity parasympathetic recovery.Methods:Twelve recreationally active young men participated in the study (22 ± 1.4 years, 24.1 ± 1.6 kg.m−2). The experimental protocol consisted of two visits to the laboratory. Each visit consisted in the completion of a 30-min high-intensity [~80% of maximal heart rate (HR)] cycle ergometer aerobic session performing randomly the WI or control (CON, no water consumption) intervention at the end of the exercise. HR and RR intervals (RRi) were continuously recorded by a heart rate monitor before, during and after the exercise. Differences in HR recovery [e.g., absolute heart rate decrement after 1 min of recovery (HRR60s) and time-constant of the first order exponential fitting curve of the HRR (HRRτ)] and in postexercise vagalrelated heart rate variability (HRV) indexes (rMSSD30s, rMSSD, pNN50, SD1 and HF) were calculated and compared for WI and CON.Results:A similar HR recovery and an increased postexercise HRV [SD1 = 9.4 ± 5.9 vs. 6.0 ± 3.9 millisecond, HF(ln) = 3.6 ± 1.4 vs. 2.4 ± 1.3 millisecond2, for WI and CON, respectively; p < .05] was observed in WI compared with CON.Conclusion:The results suggest that WI accelerates the postexercise parasympathetic reactivation after high-intensity exercise. Such outcome reveals an important cardioprotective effect of WI.


1995 ◽  
Vol 79 (3) ◽  
pp. 781-785 ◽  
Author(s):  
F. Leweke ◽  
K. Bruck ◽  
H. Olschewski

According to the most customary exercise protocols, core temperature (Tc) rises in parallel with workload (WL) and experimental time. Physiological variables, however, may be related to each of these factors. To investigate effects of WL independent of experimental time and body temperature, we employed four moderate WLs in 4-min steps between 35 and 65% peak O2 uptake (VO2 peak) in randomized order. To investigate independent effects of body temperature, the same work protocol was performed both after resting in comfortable ambient temperature [control test (Cont)] and after a double cold exposure [precooling test (Pret)], where Tc and the temperature set point are decreased by approximately 0.6 and 0.3 degrees C, respectively. Eight male subjects (24 +/- 1.9 yr, VO2 peak 4.9 +/- 0.5 l/min) worked on a cycle ergometer in a climatic chamber. Heart rate (HR) and breathing frequency (BF), but not preferred pedal rate (PR), were positively correlated to Tc, the slopes amounting to 17 and 3.75 min-1/degree C for HR and BF, respectively. The regression appeared linear over the whole temperature range, and the regression lines were not shifted by precooling. PR was increased by time, but Pret-Cont differences of PR and Tc were inversely correlated (r = -0.50, P < 0.01). The effects of WL were highly significant on HR, O2 uptake, and rate of perceived exertion but not on BF, PR, and sweat rate. The relation of rate of perceived exertion to HR was shifted by precooling.


2017 ◽  
Vol 23 (6) ◽  
pp. 578-582
Author(s):  
Emrah Aytac ◽  
Murat Gonen ◽  
Orhan Dogdu ◽  
Mehmet Balin

Objective Although carotid artery stenting (CAS) is an effective treatment for severe carotid stenosis, it has been associated with alterations in autonomic functions long term after the procedure. Patients with CAS have been reported to have autonomic nervous system (ANS) dysfunction. This study aimed to evaluate heart rate recovery (HRR) indices and exercise test parameters after CAS. Methods Patients (10 male, 11 female) suitable for CAS, without a history of hypertension, diabetes mellitus, severe coronary artery or valvular heart disease, were enrolled in our study. Basal electrocardiography, echocardiography, and treadmill exercise testing were performed in all patients pre- and post-procedure. The HRR index was defined as the reduction in the heart rate from the rate at peak exercise to the rate first minute (HRR1), second minute (HRR2), third minute (HRR3) and fifth minute (HRR5) after the cessation of exercise stress testing. Results The exercise time, maximal heart rate, maximal blood pressure and maximal metabolic equivalents values were significantly decreased after the procedure. The first- and second-minute HRR indices of patients before procedure were significantly lower than after procedure (23.5 ± 6.6 vs 25.8 ± 8.3; p < 0.001 and 41.8 ± 12.3 vs 50.2 ± 16.3; p < 0.001, respectively). Similarly, HRR indices after the third and fifth minutes of the recovery period were significantly lower in patients before procedure, when compared with those indices after procedure (52.9 ± 13.1 vs 60.7 ± 14.4; p < 0.001 and 62.4 ± 12.8 vs 71.9 ± 14.1; p < 0.001). Conclusion We have demonstrated that HRR indices increased in the first, second, third and fifth minutes of the recovery period after maximal exercise testing in patients after the CAS procedure, which may be a reflection of parasympathetic dominance after CAS.


1983 ◽  
Vol 54 (5) ◽  
pp. 1368-1373 ◽  
Author(s):  
R. J. Butland ◽  
J. A. Pang ◽  
D. M. Geddes

Ventilation, heart rate, and arterial blood gas tensions were measured at rest and during incremental exercise in 10 patients with emphysema after intravenous placebo or 7 mg metoprolol. Metoprolol reduced heart rate by 14% (P less than 0.001) and ventilation by 11% (P less than 0.01), but there was no significant difference in arterial O2 or CO2 tension (Pao2 and PaCO2, respectively). Metoprolol increased the time to exhaustion on a cycle ergometer (P less than 0.05) but did not improve the 12-min walking distance. A double-blind randomized crossover comparison of 4 wk treatment with atenolol (100 mg/day), metoprolol (100 mg/day), or matched placebo was performed in 12 patients with emphysema. Both beta-adrenoceptor antagonists reduced resting heart rate by 33% (P less than 0.001) and resting minute ventilation by 11% (P less than 0.025). There was no change in resting or exercise Pao2 or Paco2. During steady-state exercise on a cycle ergometer, atenolol and metoprolol reduced ventilation by 14 and 4%, respectively. This was accompanied by 11 and 5% reductions in O2 consumption (P less than 0.05) and 13 and 6% falls in CO2 production (P less than 0.05). There were no significant changes in tests of exercise tolerance, but forced expiratory volume in 1 s and forced vital capacity were reduced during beta 1-adrenergic blockade. beta 1-Blocking drugs reduce hyperventilation in emphysema by reducing pulmonary gas exchange without a change in arterial blood gas tensions. Increased airflow obstruction prevents this reduction being of therapeutic value.


2010 ◽  
Vol 5 (4) ◽  
pp. 535-545 ◽  
Author(s):  
Carl J. Petersen ◽  
Marc R. Portus ◽  
David B. Pyne ◽  
Brian T. Dawson ◽  
Matthew N. Cramer ◽  
...  

Cricketers are often required to play in hot/humid environments with little time for heat adaptation.Purpose:We examined the effect of a short 4-d hot/humid acclimation program on classical physiological indicators of heat acclimation.Methods:Male club cricketers were randomly assigned into heat acclimation (ACC, n = 6) or control (CON, n = 6) groups, and 30 min treadmill trials (10 km/h, approx. 30 ± 1.0°C, approx. 65 ± 6% RH) were conducted at baseline and postacclimation. The ACC group completed four high intensity (30–45 min) acclimation sessions on consecutive days at approx. 30°C and approx. 60% RH using a cycle ergometer. The CON group completed matched cycle training in moderate conditions (approx. 20°C, approx. 60% RH). Physiological measures during each treadmill trial included heart rate; core and skin temperatures; sweat Na+, K+ and Cl– electrolyte concentrations; and sweat rate.Results:After the 4-d intervention, the ACC group had a moderate decrease of -11 (3 to -24 beats/min; mean and 90% CI) in the 30 min heart rate, and moderate to large reductions in electrolyte concentrations: Na+ -18% (–4 to -31%), K+ -15% (0 to -27%), Cl– -22% (-9 to -33%). Both ACC and CON groups had only trivial changes in core and skin temperatures and sweat rate. After the intervention, both groups perceived they were more comfortable exercising in the heat. The 4-d heat intervention had no detrimental effect on performance.Conclusions:Four 30–45 min high intensity cycle sessions in hot/humid conditions elicited partial heat acclimation. For full heat acclimation a more intensive and extensive (and modality-specific) acclimation intervention is needed for cricket players.


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