Skin blood flow and sweating changes following exercise training and heat acclimation

1977 ◽  
Vol 43 (1) ◽  
pp. 133-137 ◽  
Author(s):  
M. F. Roberts ◽  
C. B. Wenger ◽  
J. A. Stolwijk ◽  
E. R. Nadel
Keyword(s):  
Blood Flow ◽  
Exercise Training ◽  
Forearm Blood Flow ◽  
Sweat Rate ◽  
Heat Acclimation ◽  
Lower Body ◽  
Body Temperatures ◽  
Internal Temperature ◽  
Exercise Training Program ◽  
Lower Blood

Eight subjects underwent an exercise training program (10 days at 75% VO2max for 1 h/day at 25 degrees C db/13 degrees C wb) and a heat-acclimation program (10 days at 50% VO2max for 1 h/day at 35 degrees C db/32 degrees C wb). The relations of chest sweat rate and of forearm blood flow to internal temperature were determined for each subject at a 25 degrees C ambient temperature before training, between training and acclimation, and following acclimation. Training shifted the vasodilation and sweating thresholds toward lower internal temperatures, and acclimation further lowered these thresholds. All threshold shifts were statistically significant (P less than 0.05). Training and acclimation both appeared to increase the slope of the sweating relation, but these effects were not statistically significant. Changes in the slope of the blood flow relation were small and inconsistent. Since arm blood flow is higher at any given internal temperature after acclimation, the lower blood flow which is reported to accompany heat acclimation must result from the lower body temperatures.

scholarly journals Heat acclimation improves cutaneous vascular function and sweating in trained cyclists

2010 ◽  
Vol 109 (6) ◽  
pp. 1736-1743 ◽  
Author(s):  
Santiago Lorenzo ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Vascular Function ◽  
Structural Changes ◽  
Forearm Blood Flow ◽  
Sweat Rate ◽  
Local Heating ◽  
Heat Acclimation ◽  
Control Group ◽  
Doppler Flowmetry

The aim of this study was to explore heat acclimation effects on cutaneous vascular responses and sweating to local ACh infusions and local heating. We also sought to examine whether heat acclimation altered maximal skin blood flow. ACh (1, 10, and 100 mM) was infused in 20 highly trained cyclists via microdialysis before and after a 10-day heat acclimation program [two 45-min exercise bouts at 50% maximal O2 uptake (V̇o2max) in 40°C ( n = 12)] or control conditions [two 45-min exercise bouts at 50% V̇o2max in 13°C ( n = 8)]. Skin blood flow was monitored via laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC) was calculated as LDF ÷ mean arterial pressure. Sweat rate was measured by resistance hygrometry. Maximal brachial artery blood flow (forearm blood flow) was obtained by heating the contralateral forearm in a water spray device and measured by Doppler ultrasound. Heat acclimation increased %CVCmax responses to 1, 10, and 100 mM ACh (43.5 ± 3.4 vs. 52.6 ± 2.6% CVCmax, 67.7 ± 3.4 vs. 78.0 ± 3.0% CVCmax, and 81.0 ± 3.8 vs. 88.5 ± 1.1% CVCmax, respectively, all P < 0.05). Maximal forearm blood flow remained unchanged after heat acclimation (290.9 ± 12.7 vs. 269.9 ± 23.6 ml/min). The experimental group showed significant increases in sweating responses to 10 and 100 mM ACh (0.21 ± 0.03 vs. 0.31 ± 0.03 mg·cm−2·min−1 and 0.45 ± 0.05 vs. 0.67 ± 0.06 mg·cm−2·min−1, respectively, all P < 0.05), but not to 1 mM ACh (0.13 ± 0.02 vs. 0.18 ± 0.02 mg·cm−2·min−1, P = 0.147). No differences in any of the variables were found in the control group. Heat acclimation in highly trained subjects induced local adaptations within the skin microcirculation and sweat gland apparatus. Furthermore, maximal skin blood flow was not altered by heat acclimation, demonstrating that the observed changes were attributable to improvement in cutaneous vascular function and not to structural changes that limit maximal vasodilator capacity.

Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise

1992 ◽  
Vol 73 (4) ◽  
pp. 1340-1350 ◽  
Author(s):  
S. J. Montain ◽  
E. F. Coyle
Keyword(s):  
Blood Flow ◽  
Prolonged Exercise ◽  
Forearm Blood Flow ◽  
Sweat Rate ◽  
Sodium Concentration ◽  
O2 Consumption ◽  
Esophageal Temperature ◽  
Warm Environment ◽  
Cardiovascular Drift ◽  
Highly Correlated

This investigation determined the effect of different rates of dehydration, induced by ingesting different volumes of fluid during prolonged exercise, on hyperthermia, heart rate (HR), and stroke volume (SV). On four different occasions, eight endurance-trained cyclists [age 23 +/- 3 (SD) yr, body wt 71.9 +/- 11.6 kg, maximal O2 consumption 4.72 +/- 0.33 l/min] cycled at a power output equal to 62-67% maximal O2 consumption for 2 h in a warm environment (33 degrees C dry bulb, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or ingested a small (SF), moderate (MF), or large (LF) volume of fluid that replaced 20 +/- 1, 48 +/- 1, and 81 +/- 2%, respectively, of the fluid lost in sweat during exercise. The protocol resulted in graded magnitudes of dehydration as body weight declined 4.2 +/- 0.1, 3.4 +/- 0.1, 2.3 +/- 0.1, and 1.1 +/- 0.1%, respectively, during NF, SF, MF, and LF. After 2 h of exercise, esophageal temperature (Tes), HR, and SV were significantly different among the four trials (P < 0.05), with the exception of NF and SF. The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20–22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials. In each subject, the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality (r = 0.81-0.98, P < 0.02-0.19) and the increase in serum sodium concentration (r = 0.87-0.99, P < 0.01-0.13) from 5 to 120 min of exercise. In summary, the magnitude of increase in core temperature and HR and the decline in SV are graded in proportion to the amount of dehydration accrued during exercise.

Circadian rhythm in sweating and cutaneous blood flow

1984 ◽  
Vol 246 (3) ◽  
pp. R321-R324 ◽  
Author(s):  
L. A. Stephenson ◽  
C. B. Wenger ◽  
B. H. O'Donovan ◽  
E. R. Nadel
Keyword(s):  
Blood Flow ◽  
Circadian Rhythm ◽  
Body Temperature ◽  
Forearm Blood Flow ◽  
Sweat Rate ◽  
Circadian Variation ◽  
Esophageal Temperature ◽  
Cutaneous Blood Flow ◽  
Cutaneous Vasodilation ◽  
Cutaneous Blood

To characterize the changes in the control of the heat loss responses associated with the circadian variation in body temperature, we studied five men during 20 min of exercise in 25 degrees C on 6 separate days. Experiments were conducted at six times, equally spaced over the 24-h day. Esophageal temperature (Tes) and chest sweat rate (msw) were measured continuously, and forearm blood flow (FBF) was measured one to two times per minute. The thresholds for sweating and forearm vasodilation were significantly higher at 1600 and 2000 than at 2400 and 0400, averaging 0.57 and 0.65 degrees C higher, respectively, at 1600 than at 0400. Resting Tes and the Tes thresholds for cutaneous vasodilation and sweating during exercise all showed a similar circadian rhythm. The level at which core temperature is regulated therefore varies over the 24-h day with the zenith occurring around 1600 and the nadir at 0400. However, whereas the slope of the msw-to-Tes relation did not change over the 24-h day, the slope of the FBF-to-Tes relation tended to increase between 0400 and 2400, implying that the circadian rhythm may be more complex than just a shift in the central reference temperature.

Effects of posture on peripheral vascular responses to lower body positive pressure

2007 ◽  
Vol 293 (1) ◽  
pp. H670-H676 ◽  
Author(s):  
Takeshi Nishiyasu ◽  
Shigeko Hayashida ◽  
Asami Kitano ◽  
Kei Nagashima ◽  
Masashi Ichinose
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Positive Pressure ◽  
Upper Limbs ◽  
Lower Body ◽  
Peripheral Vascular ◽  
Vascular Responses ◽  
Lower Body Positive Pressure ◽  
Body Positive

We tested the hypothesis that peripheral vascular responses (in the lower and upper limbs) to application of lower body positive pressure (LBPP) are dependent on the posture of the subjects. We measured heart rate, stroke volume, mean arterial pressure, leg and forearm blood flow (using the Doppler ultrasound technique), and leg (LVC) and forearm (FVC) vascular conductance in 11 subjects (9 men, 2 women) without and with LBPP (25 and 50 mmHg) in supine and upright postures. Mean arterial pressure increased in proportion to increases in LBPP and was greater in supine than in upright subjects. Heart rate was unchanged when LBPP was applied to supine subjects but was reduced in upright ones. Leg blood flow and LVC were both reduced by LBPP in supine subjects [LVC: 4.8 (SD 4.0), 3.6 (SD 3.5), and 1.4 (SD 1.8) ml·min−1·mmHg−1 before LBPP and during 25 and 50 mmHg LBPP, respectively; P < 0.05] but were increased in upright ones [LVC: 2.0 (SD 1.2), 3.4 (SD 3.4), and 3.0 (SD 2.0) ml·min−1·mmHg−1, respectively; P < 0.05]. Forearm blood flow and FVC both declined when LBPP was applied to supine subjects [FVC: 1.3 (SD 0.6), 1.0 (SD 0.4), and 0.9 (SD 0.6) ml· min−1·mmHg−1, respectively; P < 0.05] but remained unchanged in upright ones [FVC: 0.7 (SD 0.4), 0.7 (SD 0.4), and 0.6 (SD 0.5) ml·min−1·mmHg−1, respectively]. Together, these findings indicate that the leg vascular response to application of LBPP is posture dependent and that the response differs in the lower and upper limbs when subjects assume an upright posture.

Comparison of two indices for forearm noradrenaline release in humans

2000 ◽  
Vol 99 (5) ◽  
pp. 363-369 ◽  
Author(s):  
Gerard A. RONGEN ◽  
Jacques W. M. LENDERS ◽  
Paul SMITS ◽  
John S. FLORAS
Keyword(s):  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Noradrenaline Release ◽  
Negative Pressure ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Release Of Noradrenaline ◽  
Appearance Rate

Although there is as yet no method which measures directly the neuronal release of noradrenaline in humans in vivo, the isotope dilution technique with [3H]noradrenaline has been applied to estimate forearm neuronal noradrenaline release into plasma. Two different equations have been developed for this purpose: one to estimate the spillover of noradrenaline into the venous effluent, and a modified formula (often referred to as the appearance rate) which may reflect more closely changes in the neuronal release of noradrenaline into the synaptic cleft, particularly during interventions that alter forearm blood flow. The present study was performed to compare the effects of two interventions known to exert contrasting actions on neuronal forearm noradrenaline release and forearm blood flow. Intra-arterial infusion of sodium nitroprusside at doses without systemic effect increases forearm blood flow, but not neuronal noradrenaline release. In contrast, lower-body negative pressure at -25 mmHg causes forearm vasoconstriction by stimulating neuronal noradrenaline release. During sodium nitroprusside infusion, forearm noradrenaline spillover increased from 1.1±0.3 to 2.2±1.0 pmol·min-1·100 ml-1 (P < 0.05), whereas the forearm noradrenaline appearance rate was unchanged. Lower-body negative pressure did not affect the forearm noradrenaline spillover rate, but increased the forearm noradrenaline appearance rate from 3.4±0.4 pmol·min-1·100 ml-1 at baseline to 5.0±0.9 pmol·min-1·100 ml-1 (P < 0.05). These results indicate that the noradrenaline appearance rate provides the better approximation of changes in forearm neuronal noradrenaline release in response to stimuli which alter local blood flow.

Mechanisms of control of skin blood flow during prolonged exercise in humans

1993 ◽  
Vol 265 (2) ◽  
pp. H562-H568 ◽  
Author(s):  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. L. Kenney ◽  
P. E. Pergola ◽  
W. A. Kosiba
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Bicycle Ergometer ◽  
Dew Point ◽  
Whole Body ◽  
Internal Temperature ◽  
Vasodilator Activity ◽  
Forearm Skin ◽  
Reduced Rate

Exercise in a warm environment raises internal temperature and leads to a rapid increase in skin blood flow (SkBF). As exercise continues, and internal temperature approaches 38 degrees C, the rate of rise of SkBF is markedly attenuated despite further significant increases in internal temperature. To find whether this attenuation is mediated by increased cutaneous active vasoconstrictor activity or by a reduced rate of rise of active vasodilator activity, each of 12 male subjects had 0.64 cm2 forearm skin sites iontophoretically treated with bretylium tosylate for selective local blockade of noradrenergic vasoconstrictor nerves. SkBF was monitored there and at adjacent untreated control sites by laser-Doppler blood flowmetry (LDF). Whole body skin temperature (Tsk) was controlled by water-perfused suits, and esophageal temperature (Tes) was monitored as an index of internal temperature. Mean arterial pressure (MAP) was monitored and cutaneous vascular conductance was calculated as LDF/MAP. Sweat rate was also monitored by dew point hygrometry in 11 subjects. Tsk was raised to 38 degrees C, after which subjects began 20-30 min of exercise on a bicycle ergometer. The rate of the initial rapid increase in SkBF with increasing Tes was not altered by bretylium treatment (P > 0.05 between sites). The attenuation of the rate of rise during the latter phase of exercise was not abolished by bretylium treatment (P > 0.05 between sites); instead, there was a trend for the attenuation to be enhanced at those sites. We conclude that the attenuated rate of rise of SkBF is due to limitation of active vasodilator activity and not due to increased vasoconstrictor tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Forearm blood flow during body temperature transients produced by leg exercise

1975 ◽  
Vol 38 (1) ◽  
pp. 58-63 ◽  
Author(s):  
C. B. Wenger ◽  
M. F. Roberts ◽  
J. A. Stolwijk ◽  
E. R. Nadel
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Forearm Blood Flow ◽  
Bicycle Ergometer ◽  
Vapor Pressures ◽  
Internal Temperature ◽  
Ambient Temperatures ◽  
Forearm Skin ◽  
Leg Exercise ◽  
Skin Temperatures

Subjects exercised for 30 min on a bicycle ergometer at 30, 50, and 70% of maximal aerobic power in ambient temperatures of 15, 25, and 35 degrees C and vapor pressures of less than 18 Torr. Exercise was used to vary internal temperature during an experiment, and different ambient temperatures were used to vary skin temperatures independently of internal temperature. Forearm skin temperature was fixed at about 36.5 degrees C. Esophageal temperature (Tes) was measured with a thermocouple at the level of the left atrium, and mean skin temperature (Tsk) was calculated from a weighted mean of thermocouple temperatures at eight skin sites. Forearm blood flow (BF) was measured by electrocapacitance plethysmography. Our data are well accounted for by an equation of the form BF = a1Tes + q2Tsk + b, independent of exercise intensity, although some subjects showed an equivocal vasodilator effect of exercise. The ratios a1/a2 (7.5, 9.6, 11.7) are quite similar to the ratios (8.6, 10.4) of the corresponding coefficients in two recent models of thermoregulatory sweating.

scholarly journals Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human

2010 ◽  
Vol 299 (4) ◽  
pp. H1168-H1173 ◽  
Author(s):  
C. G. Crandall ◽  
M. Shibasaki ◽  
T. E. Wilson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Internal Temperature ◽  
Orthostatic Challenge ◽  
Head Up Tilt ◽  
Cutaneous Vasoconstriction

As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure ( N = 41) and head-up tilt ( N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure × 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 ± 0.3°C; P < 0.001) and CVC (29 ± 20 to 160 ± 58 CVC units; P < 0.001) without altering mean arterial pressure (83 ± 7 to 82 ± 6 mmHg). Mean arterial pressure was reduced to 57 ± 9 mmHg ( P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 ± 61 CVC units ( P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.).

scholarly journals Sympathetic activation increases NO release from eNOS but neither eNOS nor nNOS play an essential role in exercise hyperemia in the human forearm

2013 ◽  
Vol 304 (9) ◽  
pp. H1225-H1230 ◽  
Author(s):  
Husain Shabeeh ◽  
Michael Seddon ◽  
Sally Brett ◽  
Narbeh Melikian ◽  
Barbara Casadei ◽  
...  
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Essential Role ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
No Synthase ◽  
Lower Body ◽  
Sympathetic Activation ◽  
Handgrip Exercise ◽  
No Release

Nitric oxide (NO) release from endothelial NO synthase (eNOS) and/or neuronal NO synthase (nNOS) could be modulated by sympathetic nerve activity and contribute to increased blood flow after exercise. We examined the effects of brachial-arterial infusion of the nNOS selective inhibitor S-methyl-l-thiocitrulline (SMTC) and the nonselective NOS inhibitor NG-monomethyl-l-arginine (l-NMMA) on forearm arm blood flow at rest, during sympathetic activation by lower body negative pressure, and during lower body negative pressure immediately after handgrip exercise. Reduction in forearm blood flow by lower body negative pressure during infusion of SMTC was not significantly different from that during vehicle (−28.5 ± 4.02 vs. −34.1 ± 2.96%, respectively; P = 0.32; n = 8). However, l-NMMA augmented the reduction in forearm blood flow by lower body negative pressure (−44.2 ± 3.53 vs. −23.4 ± 5.71%; n = 8; P < 0.01). When lower body negative pressure was continued after handgrip exercise, there was no significant effect of either l-NMMA or SMTC on forearm blood flow immediately after low-intensity exercise ( P = 0.91 and P = 0.44 for l-NMMA vs. saline and SMTC vs. saline, respectively; each n = 10) or high-intensity exercise ( P = 0.46 and P = 0.68 for l-NMMA vs. saline and SMTC vs. saline, respectively; each n = 10). These results suggest that sympathetic activation increases NO release from eNOS, attenuating vasoconstriction. Dysfunction of eNOS could augment vasoconstrictor and blood pressure responses to sympathetic activation. However, neither eNOS nor nNOS plays an essential role in postexercise hyperaemia, even in the presence of increased sympathetic activation.

Sweat rate vs. forearm blood flow during lower body negative pressure

1985 ◽  
Vol 58 (5) ◽  
pp. 1546-1552 ◽  
Author(s):  
S. D. Solack ◽  
G. L. Brengelmann ◽  
P. R. Freund
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Sweat Rate ◽  
Minor Component ◽  
Lower Body ◽  
Indirect Measure ◽  
System A ◽  
Forearm Vascular Conductance ◽  
A Minor

Skin blood flow is inhibited when hyperthermia and added hypovolemic stresses are superimposed. We tested the hypothesis that part of this inhibition is a reduced drive for cutaneous active vasodilatation (AVD) with sweat rate (SR) taken as an indirect measure of the efferent drive for cutaneous AVD. We also inquired whether SR itself changes with redistribution of blood volume. Six healthy supine men were subjected to lower body negative pressure (LBNP) after heating in water-perfused suits increased esophageal temperatures (Tes) to a mean of 37.2 degrees C and at least doubled SR and forearm vascular conductance (FVC). Heating continued throughout LBNP and recovery. Sweat rate did not decrease with LBNP onset, although SR-Tes slopes during LBNP were reduced 28% from control. In four subjects the SR-Tes slope did not recover when LBNP was discontinued. These observations suggest that SR is not an effector of the low-pressure baroreflex. In contrast to SR, FVC abruptly fell 22% at the onset of LBNP. Thereafter, FVC-Tes slopes near zero or less occurred. The major effector for FVC inhibition with LBNP appears to be the neural vasoconstrictor system. A minor component due to reduced drive for cutaneous AVD probably occurs as well.

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