scholarly journals Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans

2010 ◽  
Vol 109 (5) ◽  
pp. 1301-1306 ◽  
Author(s):  
Jonathan E. Wingo ◽  
David A. Low ◽  
David M. Keller ◽  
R. Matthew Brothers ◽  
Manabu Shibasaki ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Temperature ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Local Temperature ◽  
Whole Body ◽  
Local Cooling ◽  
Mean Body Temperature ◽  
Local Skin ◽  
Doppler Flowmetry

Sweat rate (SR) is reduced in locally cooled skin, which may result from decreased temperature and/or parallel reductions in skin blood flow. The purpose of this study was to test the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating. In protocols I and II, eight subjects rested supine while wearing a water-perfused suit for the control of whole body skin and internal temperatures. While 34°C water perfused the suit, four microdialysis membranes were placed in posterior forearm skin not covered by the suit to manipulate skin blood flow using vasoactive agents. Each site was instrumented for control of local temperature and measurement of local SR (capacitance hygrometry) and skin blood flow (laser-Doppler flowmetry). In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ∼1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm−2·min−1·°C−1 for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm−2·min−1·°C−1 for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.

Control of skin blood flow by whole body and local skin cooling in exercising humans

1996 ◽  
Vol 270 (1) ◽  
pp. H208-H215 ◽  
Author(s):  
P. E. Pergola ◽  
J. M. Johnson ◽  
D. L. Kellogg ◽  
W. A. Kosiba
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Threshold Level ◽  
Tissue Temperature ◽  
Whole Body ◽  
Internal Temperature ◽  
Local Cooling ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Rate Of Increase

We examined the independent roles of whole body skin temperature (Tsk) and tissue temperature (local temperature, Tloc) in the control of skin blood flow (SBF) during cooling and the roles of the vasoconstrictor (VC) and active vasodilator (AVD) systems in mediating these effects. SBF was monitored by laser-Doppler flowmetry (LDF) at untreated sites and sites with local VC blockade by pretreatment with bretylium (BT). Seven subjects underwent four sessions of moderate bicycle exercise (20-30 min duration) at neutral Tsk and Tloc (34 degrees C), neutral Tsk and cool Tloc (27 degrees C), low Tsk (28 degrees C) and neutral Tloc, and low Tsk and Tloc. Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed relative to the maximum. Cool Tsk increased the threshold level of internal temperature at which CVC began to rise equally at BT-treated and untreated sites (P < 0.05). The rate of increase in CVC relative to internal temperature was reduced by local cooling. BT pretreatment partially reversed this effect (P < 0.05). Thus a cool environment results in reflex inhibition of the onset of AVD activity by cool Tsk and a reduced rate of increase in CVC due, in part, to norepinephrine release stimulated by cool Tloc.

The role of baseline in the cutaneous vasoconstrictor responses during combined local and whole body cooling in humans

2007 ◽  
Vol 293 (5) ◽  
pp. H3187-H3192 ◽  
Author(s):  
Gary J. Hodges ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
Guy E. Alvarez ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Laser Doppler ◽  
Whole Body ◽  
Local Cooling ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Body Cooling ◽  
Whole Body Cooling

Previous work showed that local cooling (LC) attenuates the vasoconstrictor response to whole body cooling (WBC). We tested the extent to which this attenuation was due to the decreased baseline skin blood flow following LC. In eight subjects, skin blood flow was assessed using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was expressed as LDF divided by blood pressure. Subjects were dressed in water-perfused suits to control WBC. Four forearm sites were prepared with microdialysis fibers, local heating/cooling probe holders, and laser-Doppler probes. Three sites were locally cooled from 34 to 28°C, reducing CVC to 45.9 ± 3.9, 42 ± 3.9, and 44.5 ± 4.8% of baseline ( P < 0.05 vs. baseline; P > 0.05 among sites). At two sites, CVC was restored to precooling baseline levels with sodium nitroprusside (SNP) or isoproterenol (Iso), increasing CVC to 106.4 ± 12.4 and 98.9 ± 10.1% of baseline, respectively ( P > 0.05 vs. precooling). Whole body skin temperature, apart from the area of blood flow measurement, was reduced from 34 to 31°C. Relative to the original baseline, CVC decreased ( P < 0.05) by 44.9 ± 2.8 (control), 11.3 ± 2.4 (LC only), 29 ± 3.7 (SNP), and 45.8 ± 8.7% (Iso). The reductions at LC only and SNP sites were less than at control or Iso sites ( P < 0.05); the responses at those latter sites were not different ( P > 0.05), suggesting that the baseline change in CVC with LC is important in the attenuation of reflex vasoconstrictor responses to WBC.

scholarly journals Sustained increases in skin blood flow are not a prerequisite to initiate sweating during passive heat exposure

2017 ◽  
Vol 313 (2) ◽  
pp. R140-R148 ◽  
Author(s):  
Nicholas Ravanelli ◽  
Ollie Jay ◽  
Daniel Gagnon
Keyword(s):  
Blood Flow ◽  
Vapor Pressure ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Heat Exposure ◽  
Mean Body Temperature ◽  
Local Skin ◽  
Sweat Production ◽  
Sweating Efficiency ◽  
Change In Mean

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiSeff) or low (LoSeff) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiSeff at 36°C (HiSeff: 99 ± 11 vs. LoSeff: 77 ± 11 min, P < 0.01) and 42°C (HiSeff: 72 ± 16 vs. LoSeff: 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions ( P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating.

Influence of female reproductive hormones on local thermal control of skin blood flow

1999 ◽  
Vol 87 (5) ◽  
pp. 1719-1723 ◽  
Author(s):  
Nisha Charkoudian ◽  
Dan P. Stephens ◽  
Kenna C. Pirkle ◽  
Wojciech A. Kosiba ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Thermal Control ◽  
Reproductive Hormones ◽  
Whole Body ◽  
Vascular Control ◽  
Local Cooling ◽  
Doppler Flowmetry ◽  
Vasodilator Response ◽  
Local Warming

Progesterone and estrogen modify thermoregulatory control such that, when both steroids are elevated, body temperature increases and the reflex thermoregulatory control of cutaneous vasodilation is shifted to higher internal temperatures. We hypothesized that the influence of these hormones would also include effects on local thermal control of skin blood flow. Experiments were conducted in women in high-hormone (HH) and low-hormone (LH) phases of oral contraceptive use. Skin blood flow was measured by laser-Doppler flowmetry, and local temperature (Tloc) was controlled over 12 cm2 around the sites of blood flow measurement. Tloc was held at 32°C for 10–15 min and was then decreased at one site from 32 to 20°C in a ramp over 20 min. Next, Tloc was increased from 32 to 42°C in a ramp over 15 min at a separate site. Finally, Tloc at both sites was held at 42°C for 30 min to elicit maximum vasodilation; data for cutaneous vascular conductance (CVC) are expressed relative to that maximum. Whole body skin temperature (Tsk) was held at 34°C throughout each study to minimize reflex effects from differences in Tsk between experiments. Baseline CVC did not differ between phases [8.18 ± 1.38 (LH) vs. 8.41 ± 1.31% of maximum (HH); P > 0.05]. The vasodilator response to local warming was augmented in HH ( P < 0.05, ANOVA). For example, at Tloc of 40–42°C, CVC averaged 76.41 ± 3.08% of maximum in HH and 67.71 ± 4.43% of maximum in LH ( P < 0.01 LH vs. HH). The vasoconstrictor response to local cooling was unaffected by phase ( P > 0.05). These findings indicate that modifications in cutaneous vascular control by female steroid hormones include enhancement of the vasodilator response to local warming and are consistent with reports of the influence of estrogen to enhance nitric oxide-dependent vasodilator responses.

Forearm cutaneous vascular and sudomotor responses to whole body passive heat stress in young smokers

2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  
Keyword(s):  
Heat Stress ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Whole Body ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Local Sweat Rate ◽  
Vasomotor Activity ◽  
Young Smokers

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.

Active cutaneous vasodilation in resting humans during mild heat stress

2005 ◽  
Vol 98 (3) ◽  
pp. 829-837 ◽  
Author(s):  
Yoshi-Ichiro Kamijo ◽  
Kichang Lee ◽  
Gary W. Mack
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Mean Skin Temperature ◽  
Local Skin ◽  
Mild Heat ◽  
Normal Core ◽  
Local Sweat Rate

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40°C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3°C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVCBT) and sweat expulsion number increased at 38 and 40°C compared with 34°C ( P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40°C ( P < 0.05, different from 34°C). However, SSNA burst amplitude increased ( P < 0.05), whereas SSNA burst duration decreased ( P < 0.05), at the same time as we observed the increase in CVCBT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.

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)

scholarly journals Temperature of water ingested before exercise alters the onset of physiological heat loss responses

2019 ◽  
Vol 316 (1) ◽  
pp. R13-R20 ◽  
Author(s):  
Nathan B. Morris ◽  
Georgia K. Chaseling ◽  
Anthony R. Bain ◽  
Ollie Jay
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Body Temperature ◽  
Relative Humidity ◽  
Body Mass ◽  
Sweat Rate ◽  
Vascular Conductance ◽  
Mean Body Temperature ◽  
Local Sweat Rate ◽  
Cutaneous Vascular Conductance

This study sought to determine whether the temperature of water ingested before exercise alters the onset threshold and subsequent thermosensitivity of local vasomotor and sudomotor responses after exercise begins. Twenty men [24 (SD 4) yr of age, 75.8 (SD 8.1) kg body mass, 52.3 (SD 7.7) ml·min−1·kg−1peak O2consumption (V̇o2peak)] ingested 1.5°C, 37°C, or 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50% V̇o2peakfor 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (Tb), local sweat rate (LSR), and skin blood flow (SBF) were measured. In a subset of eight men [25 (SD 5) yr of age, 78.6 (SD 8.3) kg body mass, 48.9 (SD 11.1) ml·min−1·kg−1V̇o2peak], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in Tbwas greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔTb= 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔTb= 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔTb= 0.18 (SD 0.15) °C, 0.11 (SD 0.13) °C, and 0.09 (SD 0.09) °C with 1.5°C, 37°C, and 50°C water, respectively, P = 0.07]. Conversely, the thermosensitivity of LSR and SBF was not different [LSR = 1.11 (SD 0.75), 1.11 (SD 0.75), and 1.34 (SD 1.11) mg·min−1·cm−2·°C−1with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.46); SBF = 717 (SD 882), 517 (SD 606), and 857 (SD 904) %baseline arbitrary units (AU)/°C with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.95)]. After 15 min of exercise, LSR and SBF were greater with ingestion of 50°C than 1.5°C water [LSR = 0.40 (SD 0.17) vs. 0.31 (SD 0.19) mg·min−1·cm−2( P = 0.02); SBF = 407 (SD 149) vs. 279 (SD 117) %baseline AU ( P < 0.001)], but not 37°C water [LSR = 0.50 (SD 0.22) mg·min−1·cm−2; SBF = 324 (SD 169) %baseline AU]. CVC was statistically unaffected [275 (SD 81), 340 (SD 114), and 384 (SD 160) %baseline CVC with 1.5°C, 37°C, and 50°C ingested water, respectively, P = 0.30]. Collectively, these results support the concept that visceral thermoreceptors modify the central drive for thermoeffector responses.

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.

Differences in the postexercise threshold for cutaneous active vasodilation between men and women

2006 ◽  
Vol 290 (1) ◽  
pp. R172-R179 ◽  
Author(s):  
Glen P. Kenny ◽  
Jane E. Murrin ◽  
W. Shane Journeay ◽  
Francis D. Reardon
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Mean Skin Temperature ◽  
Local Skin ◽  
Men And Women ◽  
Cutaneous Vasodilation ◽  
Vasodilatory Response

The purpose of this study was to evaluate the possible differences in the postexercise cutaneous vasodilatory response between men and women. Fourteen subjects (7 men and 7 women) of similar age, body composition, and fitness status remained seated resting for 15 min or cycled for 15 min at 70% of peak oxygen consumption followed by 15 min of seated recovery. Subjects then donned a liquid-conditioned suit. Mean skin temperature was clamped at ∼34°C for 15 min. Mean skin temperature was then increased at a rate of 4.3 ± 0.8°C/h while local skin temperature was clamped at 34°C. Skin blood flow was measured continuously at two forearm skin sites, one with (UT) and without (BT) (treated with bretylium tosylate) intact α-adrenergic vasoconstrictor activity. The exercise threshold for cutaneous vasodilation in women (37.51 ± 0.08°C and 37.58 ± 0.04°C for UT and BT, respectively) was greater than that measured in men (37.33 ± 0.06°C and 37.35 ± 0.06°C for UT and BT, respectively) ( P < 0.05). Core temperatures were similar to baseline before the start of whole body warming for all conditions. Postexercise heart rate (HR) for the men (77 ± 4 beats/min) and women (87 ± 6 beats/min) were elevated above baseline (61 ± 3 and 68 ± 4 beats/min for men and women, respectively), whereas mean arterial pressure (MAP) for the men (84 ± 3 mmHg) and women (79 ± 3 mmHg) was reduced from baseline (93 ± 3 and 93 ± 4 mmHg for men and women, respectively) ( P < 0.05). A greater increase in HR and a greater decrease in the MAP postexercise were noted in women ( P < 0.05). No differences in core temperature, HR, and MAP were measured in the no-exercise trial. The postexercise threshold for cutaneous vasodilation measured at the UT and BT sites for men (37.15 ± 0.03°C and 37.16 ± 0.04°C, respectively) and women (37.36 ± 0.05°C and 37.42 ± 0.03°C, respectively) were elevated above no exercise (36.94 ± 0.07°C and 36.97 ± 0.05°C for men and 36.99 ± 0.09°C and 37.03 ± 0.11°C for women for the UT and BT sites, respectively) ( P < 0.05). A difference in the magnitude of the thresholds was measured between women and men ( P < 0.05). We conclude that women have a greater postexercise onset threshold for cutaneous vasodilation than do men and that the primary mechanism influencing the difference between men and women in postexercise skin blood flow is likely the result of an altered active vasodilatory response and not an increase in adrenergic vasoconstrictor tone.

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