15° Head-down tilt attenuates the postexercise reduction in cutaneous vascular conductance and sweating and decreases esophageal temperature recovery time

2006 ◽  
Vol 101 (3) ◽  
pp. 840-847 ◽  
Author(s):  
Natalie H. McInnis ◽  
W. Shane Journeay ◽  
Ollie Jay ◽  
Emily Leclair ◽  
Glen P. Kenny
Keyword(s):  
Heat Loss ◽  
Sweat Rate ◽  
Peripheral Resistance ◽  
Cycle Ergometry ◽  
Dynamic Exercise ◽  
Esophageal Temperature ◽  
Vascular Conductance ◽  
Experimental Protocols ◽  
Cutaneous Vascular Conductance ◽  
Male Subjects

The following study examined the effect of 15° head-down tilt (HDT) on postexercise heat loss and hemodynamic responses. We tested the hypothesis that recovery from dynamic exercise in the HDT position would attenuate the reduction in the heat loss responses of cutaneous vascular conductance (CVC) and sweating relative to upright seated (URS) recovery in association with an augmented hemodynamic response and an increased rate of core temperature decay. Seven male subjects performed the following three experimental protocols: 1) 60 min in the URS posture followed by 60 min in the 15° HDT position; 2) 15 min of cycle ergometry at 75% of their predetermined V̇o2 peak followed by 60 min of recovery in the URS posture; or 3) 15 min of cycle ergometry at 75% of their predetermined V̇o2 peak followed by 60 min of recovery in the 15° HDT position. Mean skin temperature, esophageal temperature (Tes), skin blood flow, sweat rate, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance, and mean arterial pressure (MAP) were recorded at baseline, end exercise, 2, 5, 8, 12, 15, and 20 min, and every 5 min until end of recovery (60 min). Without preceding exercise, HDT decreased HR and increased SV ( P ≤ 0.05). During recovery after exercise, a significantly greater MAP, SV, CVC, and sweat rate and a significantly lower HR were found with HDT compared with URS posture ( P ≤ 0.05). Subsequently, a significantly lower Tes was observed with HDT after 15 min of recovery onward ( P ≤ 0.05). At the end of 60 min of recovery, Tes remained significantly elevated above baseline with URS ( P ≤ 0.05); however, Tes returned to baseline with HDT. In conclusion, extended recovery from dynamic exercise in the 15° HDT position attenuates the reduction in CVC and sweating, thereby significantly increasing the rate of Tes decay compared with recovery in the URS posture.

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women

2005 ◽  
Vol 99 (5) ◽  
pp. 1816-1821 ◽  
Author(s):  
W. shane Journeay ◽  
Francis D. Reardon ◽  
Natalie H. McInnis ◽  
Glen P. Kenny
Keyword(s):  
Blood Flow ◽  
Sweat Rate ◽  
Peripheral Resistance ◽  
Dynamic Exercise ◽  
Central Command ◽  
Active Recovery ◽  
Vascular Conductance ◽  
Ergometer Exercise ◽  
Cardiopulmonary Baroreceptors ◽  
Cutaneous Vascular Conductance

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (T̄sk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values ( P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery ( P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode ( P < 0.05). No differences in either Tes or T̄sk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.

Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans

2004 ◽  
Vol 96 (6) ◽  
pp. 2207-2212 ◽  
Author(s):  
W. Shane Journeay ◽  
Francis D. Reardon ◽  
C. Ryan Martin ◽  
Glen P. Kenny
Keyword(s):  
Blood Flow ◽  
Sweat Rate ◽  
Peripheral Resistance ◽  
Dynamic Exercise ◽  
Peak Oxygen Consumption ◽  
Central Command ◽  
Active Recovery ◽  
Vascular Conductance ◽  
Ergometer Exercise ◽  
Cutaneous Vascular Conductance

The purpose of the study was to examine the effect of 1) passive (assisted pedaling), 2) active (loadless pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), skin blood flow (SkBF), and sweating during recovery after 15 min of dynamic exercise. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, SkBF, and sweating during exercise recovery. Six male subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 15 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (T̄sk), esophageal temperature (Tes), SkBF, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, and 15 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active and passive recovery modes, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values ( P < 0.05). The passive mode was equally as effective as the active mode in maintaining CO, SV, MAP, CVC, and sweat rate above inactive recovery. Sweat rate was different among all modes after 8 min of recovery ( P < 0.05). TPR during active recovery remained significantly lower than during recovery in the passive and inactive modes ( P < 0.05). No differences in either Tes or T̄sk were observed among conditions. Given that MAP was higher during passive and active recovery modes than during inactive recovery suggests differences in CVC may be due to differences in baroreceptor unloading and not factors attributed to central command. However, differences in sweat rate may be influenced by factors such as central command and mechanoreceptor stimulation.

Can supine recovery mitigate the exercise intensity dependent attenuation of post-exercise heat loss responses?

2008 ◽  
Vol 33 (4) ◽  
pp. 682-689 ◽  
Author(s):  
Glen P. Kenny ◽  
Daniel Gagnon ◽  
Ollie Jay ◽  
Natalie H. McInnis ◽  
W. Shane Journeay ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Stroke Volume ◽  
Exercise Intensity ◽  
Sweat Rate ◽  
Maximal Oxygen Consumption ◽  
Peripheral Resistance ◽  
Esophageal Temperature ◽  
Post Exercise ◽  
Supine Posture ◽  
Cutaneous Vascular Conductance

Cutaneous vascular conductance (CVC) and sweat rate are subject to non-thermal baroreflex-mediated attenuation post-exercise. Various recovery modalities have been effective in attenuating these decreases in CVC and sweat rate post-exercise. However, the interaction of recovery posture and preceding exercise intensity on post-exercise thermoregulation remains unresolved. We evaluated the combined effect of supine recovery and exercise intensity on post-exercise cardiovascular and thermal responses relative to an upright seated posture. Seven females performed 15 min of cycling ergometry at low- (LIE, 55% maximal oxygen consumption) or high-(HIE, 85% maximal oxygen consumption) intensity followed by 60 min of recovery in either an upright seated or supine posture. Esophageal temperature, CVC, sweat rate, cardiac output, stroke volume, heart rate, total peripheral resistance, and mean arterial pressure (MAP) were measured at baseline, at end-exercise, and at 2, 5, 12, 20, and every 10 min thereafter until the end of recovery. MAP and stroke volume were maintained during supine recovery to a greater extent relative to an upright seated recovery following HIE (p ≤ 0.05) and were paralleled by an elevated CVC and sweat rate response (p ≤ 0.05). A significantly lower esophageal temperature was subsequently observed when supine throughout recovery (p ≤ 0.05). Although we observed a reflex bradycardia and increased stoke volume with supine recovery following LIE, no differences were observed for MAP, CVC, sweat rate or esophageal temperature. Supine recovery attenuates the post-exercise reductions in MAP, CVC, and sweat rate in a manner dependent directly on exercise intensity. This effect is likely attributable to a non-thermal baroreceptor mechanism.

Do metaboreceptors alter heat loss responses following dynamic exercise?

2014 ◽  
Vol 306 (1) ◽  
pp. R82-R89 ◽  
Author(s):  
Ryan McGinn ◽  
Brendan Swift ◽  
Konrad Binder ◽  
Daniel Gagnon ◽  
Glen P. Kenny
Keyword(s):  
Heat Loss ◽  
Lower Body Negative Pressure ◽  
Sweat Rate ◽  
Dynamic Exercise ◽  
Treadmill Running ◽  
Isometric Handgrip ◽  
Before And After ◽  
Isometric Handgrip Exercise ◽  
Cutaneous Vascular Conductance ◽  
Cutaneous Blood

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.

Effect of voluntary hypocapnic hyperventilation on the relationship between core temperature and heat loss responses in exercising humans

2014 ◽  
Vol 117 (11) ◽  
pp. 1317-1324 ◽  
Author(s):  
Naoto Fujii ◽  
Yasushi Honda ◽  
Ken Komura ◽  
Bun Tsuji ◽  
Akira Sugihara ◽  
...  
Keyword(s):  
Core Temperature ◽  
Sweat Rate ◽  
Critical Threshold ◽  
Temperature Threshold ◽  
Esophageal Temperature ◽  
Vascular Conductance ◽  
Voluntary Hyperventilation ◽  
Arterial Blood ◽  
Thermoregulatory Responses ◽  
Cutaneous Vascular Conductance

Two thermolytic thermoregulatory responses, cutaneous vasodilation and sweating, begin when core temperature reaches a critical threshold, after which response magnitudes increase linearly with increasing core temperature; thus the slope indicates response sensitivity. We evaluated the influence of hypocapnia induced by voluntary hyperventilation on the core temperature threshold and sensitivity of thermoregulatory responses. Ten healthy males performed 15 min of cycling at 117 W (29.5°C, 50% RH) under three breathing conditions: 1) spontaneous ventilation, 2) voluntary normocapnic hyperventilation, and 3) voluntary hypocapnic hyperventilation. In the hypocapnic hyperventilation trial, end-tidal CO2 pressure was reduced throughout the exercise, whereas it was maintained around the normocapnic level in the other two trials. Cutaneous vascular conductances at the forearm and forehead were evaluated as laser-Doppler signal/mean arterial blood pressure, and the forearm sweat rate was measured using the ventilated capsule method. Esophageal temperature threshold was higher for the increase in cutaneous vascular conductance in the hypocapnic than normocapnic hyperventilation trial at the forearm (36.88 ± 0.36 vs. 36.68 ± 0.34°C, P < 0.05) and forehead (36.89 ± 0.31 vs. 36.75 ± 0.31°C, P < 0.05). The slope relating esophageal temperature to cutaneous vascular conductance was decreased in the hypocapnic than normocapnic hyperventilation trial at the forearm (302 ± 177 vs. 420 ± 178% baseline/°C, P < 0.05) and forehead (236 ± 164 vs. 358 ± 221% baseline/°C, P < 0.05). Neither the threshold nor the slope for the forearm sweat rate differed significantly between the hypocapnic or normocapnic hyperventilation trials. These findings indicate that in exercising humans, hypocapnia induced by voluntary hyperventilation does not influence sweating, but it attenuates the cutaneous vasodilatory response by increasing its threshold and reducing its sensitivity.

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise

2004 ◽  
Vol 96 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Thad E. Wilson ◽  
Robert Carter ◽  
Michael J. Cutler ◽  
Jian Cui ◽  
Michael L. Smith ◽  
...  
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Sweat Rate ◽  
Venous Pressure ◽  
Thoracic Impedance ◽  
Active Recovery ◽  
Central Venous ◽  
Cycle Exercise ◽  
Vascular Conductance ◽  
Cutaneous Vascular Conductance

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.

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.

scholarly journals Nitric oxide and cutaneous active vasodilation during heat stress in humans

1998 ◽  
Vol 85 (3) ◽  
pp. 824-829 ◽  
Author(s):  
D. L. Kellogg ◽  
C. G. Crandall ◽  
Y. Liu ◽  
N. Charkoudian ◽  
J. M. Johnson
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Laser Doppler Flowmetry ◽  
Sweat Rate ◽  
Ringer Solution ◽  
No Synthase ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vascular Conductance

Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laser-Doppler flowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions,l-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38–38.5°C, internal temperature rose from 36.66 ± 0.10 to 37.34 ± 0.06°C ( P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 ± 2 to 44 ± 5% of maximum, but only rose from 13 ± 2 to 30 ± 5% of maximum at l-NAME-treated sites ( P < 0.05 between sites) during heat stress. l-NAME had no effect on sweat rate ( P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.

Exercise-rest cycles do not alter local and whole body heat loss responses

2011 ◽  
Vol 300 (4) ◽  
pp. R958-R968 ◽  
Author(s):  
Daniel Gagnon ◽  
Glen P. Kenny
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Intermittent Exercise ◽  
Sweat Rate ◽  
Heat Content ◽  
Whole Body ◽  
Evaporative Heat Loss ◽  
Esophageal Temperature ◽  
Direct Calorimetry ◽  
Body Heat

Previous studies have suggested that greater core temperatures during intermittent exercise (Ex) are due to attenuated sweating [upper back sweat rate (SR)] and skin blood flow (SkBF) responses. We evaluated the hypothesis that heat loss is not altered during exercise-rest cycles (ER). Ten male participants randomly performed four 120-min trials: 1) 60-min Ex and 60-min recovery (60ER); 2) 3 × 20-min Ex separated by 20-min recoveries (20ER); 3) 6 × 10-min Ex separated by 10-min recoveries (10ER), or 4) 12 × 5-min Ex separated by 5-min recoveries (5ER). Exercise was performed at a workload of 130 W at 35°C. Whole body heat exchange was determined by direct calorimetry. Core temperature, SR (by ventilated capsule), and SkBF (by laser-doppler) were measured continuously. Evaporative heat loss (EHL) progressively increased with each ER, such that it was significantly greater ( P ≤ 0.05) at the end of the last compared with the first Ex for 5ER (299 ± 39 vs. 440 ± 41 W), 10ER (425 ± 51 vs. 519 ± 45 W), and 20ER (515 ± 63 vs. 575 ± 74 W). The slope of the EHL response against esophageal temperature significantly increased from the first to the last Ex within the 10ER (376 ± 56 vs. 445 ± 89 W/°C, P ≤ 0.05) and 20ER (535 ± 85 vs. 588 ± 28 W/°C, P ≤ 0.05) conditions, but not during 5ER (296 ± 96 W/°C vs. 278 ± 95 W/°C, P = 0.237). In contrast, the slope of the SkBF response against esophageal temperature did not significantly change from the first to the last Ex (5ER: 51 ± 23 vs. 54 ± 19%/°C, P = 0.848; 10ER: 53 ± 8 vs. 56 ± 21%/°C, P = 0.786; 20ER: 44 ± 20 vs. 50 ± 27%/°C, P = 0.432). Overall, no differences in body heat content and core temperature were observed. These results suggest that altered local and whole body heat loss responses do not explain the previously observed greater core temperatures during intermittent exercise.

scholarly journals K+ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of KCa, KATP, and KV channels?

2016 ◽  
Vol 311 (3) ◽  
pp. R600-R606 ◽  
Author(s):  
Naoto Fujii ◽  
Jeffrey C. Louie ◽  
Brendan D. McNeely ◽  
Sarah Yan Zhang ◽  
My-An Tran ◽  
...  
Keyword(s):  
Young Adults ◽  
Channel Blocker ◽  
Sweat Rate ◽  
K Channel ◽  
Cholinergic Nerves ◽  
Vascular Conductance ◽  
Voltage Gated ◽  
Kv Channels ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

Acetylcholine released from cholinergic nerves is involved in heat loss responses of cutaneous vasodilation and sweating. K+ channels are thought to play a role in regulating cholinergic cutaneous vasodilation and sweating, though which K+ channels are involved in their regulation remains unclear. We evaluated the hypotheses that 1) Ca2+-activated K+ (KCa), ATP-sensitive K+ (KATP), and voltage-gated K+ (KV) channels all contribute to cholinergic cutaneous vasodilation; and 2) KV channels, but not KCa and KATP channels, contribute to cholinergic sweating. In 13 young adults (24 ± 5 years), cutaneous vascular conductance (CVC) and sweat rate were evaluated at intradermal microdialysis sites that were continuously perfused with: 1) lactated Ringer (Control), 2) 50 mM tetraethylammonium (KCa channel blocker), 3) 5 mM glybenclamide (KATP channel blocker), and 4) 10 mM 4-aminopyridine (KV channel blocker). At all sites, cholinergic cutaneous vasodilation and sweating were induced by coadministration of methacholine (0.0125, 0.25, 5, 100, and 2,000 mM, each for 25 min). The methacholine-induced increase in CVC was lower with the KCa channel blocker relative to Control at 0.0125 (1 ± 1 vs. 9 ± 6%max) and 5 (2 ± 5 vs. 17 ± 14%max) mM methacholine, whereas it was lower in the presence of KATP (69 ± 7%max) and KV (57 ± 14%max) channel blocker compared with Control (79 ± 6%max) at 100 mM methacholine. Furthermore, methacholine-induced sweating was lower at the KV channel blocker site (0.42 ± 0.17 mg·min−1·cm−2) compared with Control (0.58 ± 0.15 mg·min−1·cm−2) at 2,000 mM methacholine. In conclusion, we show that KCa, KATP, and KV channels play a role in cholinergic cutaneous vasodilation, whereas only KV channels contribute to cholinergic sweating in normothermic resting humans.

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