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.

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.

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.

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.

Reduced leg blood flow during dynamic exercise in older endurance-trained men

1998 ◽  
Vol 85 (1) ◽  
pp. 68-75 ◽  
Author(s):  
David N. Proctor ◽  
Peter H. Shen ◽  
Niki M. Dietz ◽  
Tamara J. Eickhoff ◽  
Lori A. Lawler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Vein ◽  
Pulmonary Ventilation ◽  
Hemoglobin Concentration ◽  
Older Men ◽  
Dynamic Exercise ◽  
Whole Body ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Ergometer Exercise

It is currently unclear whether aging alters the perfusion of active muscles during large-muscle dynamic exercise in humans. To study this issue, direct measurements of leg blood flow (femoral vein thermodilution) and systemic arterial pressure during submaximal cycle ergometry (70, 140, and 210 W) were compared between six younger (Y; 22–30 yr) and six older (O; 55–68 yr) chronically endurance-trained men. Whole body O2uptake, ventilation, and arterial and femoral venous samples for blood-gas, catecholamine, and lactate determinations were also obtained. Training duration (min/day), estimated leg muscle mass (dual-energy X-ray absorptiometry; Y, 21.5 ± 1.2 vs. O, 19.9 ± 0.9 kg), and blood hemoglobin concentration (Y, 14.9 ± 0.4 vs. O, 14.7 ± 0.2 g/dl) did not significantly differ ( P > 0.05) between groups. Leg blood flow, leg vascular conductance, and femoral venous O2 saturation were ∼20–30% lower in the older men at each work rate (all P < 0.05), despite similar levels of whole body O2 uptake. At 210 W, leg norepinephrine spillover rates and femoral venous lactate concentrations were more than twofold higher in the older men. Pulmonary ventilation was also higher in the older men at 140 (+24%) and 210 (+39%) W. These results indicate that leg blood flow and vascular conductance during cycle ergometer exercise are significantly lower in older endurance-trained men in comparison to their younger counterparts. The mechanisms responsible for this phenomenon and the extent to which they operate in other groups of older subjects deserve further attention.

Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes

1990 ◽  
Vol 69 (2) ◽  
pp. 407-418 ◽  
Author(s):  
L. B. Rowell ◽  
D. S. O'Leary
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Nervous Activity ◽  
Isometric Exercise ◽  
Muscle Afferents ◽  
Operating Point ◽  
Central Command ◽  
Vascular Conductance ◽  
Muscle Chemoreflex ◽  
Vagal Withdrawal

The overall scheme for control is as follows: central command sets basic patterns of cardiovascular effector activity, which is modulated via muscle chemo- and mechanoreflexes and arterial mechanoreflexes (baroreflexes) as appropriate error signals develop. A key question is whether the primary error corrected is a mismatch between blood flow and metabolism (a flow error that accumulates muscle metabolites that activate group III and IV chemosensitive muscle afferents) or a mismatch between cardiac output (CO) and vascular conductance [a blood pressure (BP) error] that activates the arterial baroreflex and raises BP. Reduction in muscle blood flow to a threshold for the muscle chemoreflex raises muscle metabolite concentration and reflexly raises BP by activating chemosensitive muscle afferents. In isometric exercise, sympathetic nervous activity (SNA) is increased mainly by muscle chemoreflex whereas central command raises heart rate (HR) and CO by vagal withdrawal. Cardiovascular control changes for dynamic exercise with large muscles. At exercise onset, central command increases HR by vagal withdrawal and "resets" the baroreflex to a higher BP. As long as vagal withdrawal can raise HR and CO rapidly so that BP rises quickly to its higher operating point, there is no mismatch between CO and vascular conductance (no BP error) and SNA does not increase. Increased SNA occurs at whatever HR (depending on species) exceeds the range of vagal withdrawal; the additional sympathetically mediated rise in CO needed to raise BP to its new operating point is slower and leads to a BP error. Sympathetic vasoconstriction is needed to complete the rise in BP. The baroreflex is essential for BP elevation at onset of exercise and for BP stabilization during mild exercise (subthreshold for chemoreflex), and it can oppose or magnify the chemoreflex when it is activated at higher work rates. Ultimately, when vascular conductance exceeds cardiac pumping capacity in the most severe exercise both chemoreflex and baroreflex must maintain BP by vasoconstricting active muscle.

scholarly journals Effects of mode of exercise recovery on thermoregulatory and cardiovascular responses

2002 ◽  
Vol 93 (6) ◽  
pp. 1918-1924 ◽  
Author(s):  
Robert Carter ◽  
Thad E. Wilson ◽  
Donald E. Watenpaugh ◽  
Michael L. Smith ◽  
Craig G. Crandall
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Heat Dissipation ◽  
Sweat Rate ◽  
Local Heating ◽  
Cardiovascular Responses ◽  
Maximal Heart Rate ◽  
Exercise Recovery ◽  
Active Recovery ◽  
Arterial Blood

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.

Ideas about control of skeletal and cardiac muscle blood flow (1876–2003): cycles of revision and new vision

2004 ◽  
Vol 97 (1) ◽  
pp. 384-392 ◽  
Author(s):  
Loring B. Rowell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Muscle ◽  
Neural Control ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Site Of Action ◽  
New Vision ◽  
Muscle Chemoreflex

This perspective examines origins of some key ideas central to major issues to be addressed in five subsequent mini-reviews related to Skeletal and Cardiac Muscle Blood Flow. The questions discussed are as follows. 1) What causes vasodilation in skeletal and cardiac muscle and 2) might the mechanisms be the same in both? 3) How important is muscle's mechanical contribution (via muscle pumping) to muscle blood flow, including its effect on cardiac output? 4) Is neural (vasoconstrictor) control of muscle vascular conductance and muscle blood flow significantly blunted in exercise by muscle metabolites and what might be a dominant site of action? 5) What reflexes initiate neural control of muscle vascular conductance so as to maintain arterial pressure at its baroreflex operating point during dynamic exercise, or is muscle blood flow regulated so as to prevent accumulation of metabolites and an ensuing muscle chemoreflex or both?

Leg crossing with muscle tensing, a physical counter-manoeuvre to prevent syncope, enhances leg blood flow

2007 ◽  
Vol 112 (3) ◽  
pp. 193-201 ◽  
Author(s):  
Jan T. Groothuis ◽  
Nynke van Dijk ◽  
Walter ter Woerds ◽  
Wouter Wieling ◽  
Maria T. E. Hopman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Orthostatic Intolerance ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Head Up Tilt

In patients with orthostatic intolerance, the mechanisms to maintain BP (blood pressure) fail. A physical counter-manoeuvre to postpone or even prevent orthostatic intolerance in these patients is leg crossing combined with muscle tensing. Although the central haemodynamic effects of physical counter-manoeuvres are well documented, not much is known about the peripheral haemodynamic events. Therefore the purpose of the present study was to examine the peripheral haemodynamic effects of leg crossing combined with muscle tensing during 70° head-up tilt. Healthy subjects (n=13) were monitored for 10 min in the supine position followed by 10 min in 70° head-up tilt and, finally, for 2 min of leg crossing with muscle tensing in 70° head-up tilt. MAP (mean arterial BP), heart rate, stroke volume, cardiac output and total peripheral resistance were measured continuously by Portapres. Leg blood flow was measured using Doppler ultrasound. Leg vascular conductance was calculated as leg blood flow/MAP. A significant increase in MAP (13 mmHg), stroke volume (27%) and cardiac output (18%), a significant decrease in heart rate (−5 beats/min) and no change in total peripheral resistance during the physical counter-manoeuvre were observed when compared with baseline 70° head-up tilt. A significant increase in leg blood flow (325 ml/min) and leg vascular conductance (2.9 arbitrary units) were seen during the physical counter-manoeuvre when compared with baseline 70° head-up tilt. In conclusion, the present study indicates that the physical counter-manoeuvre of leg crossing combined with muscle tensing clearly enhances leg blood flow and, at the same time, elevates MAP.

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

2002 ◽  
Vol 93 (4) ◽  
pp. 1215-1221 ◽  
Author(s):  
D. L. Kellogg ◽  
Y. Liu ◽  
K. McAllister ◽  
C. Friel ◽  
P. E. Pérgola
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Receptor Antagonist ◽  
Healthy Subjects ◽  
Ringer Solution ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Hoe 140 ◽  
Control Body ◽  
Cutaneous Vascular Conductance

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 μM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P < 0.01) and untreated sites (65 ± 2% maximal CVC, P < 0.01). These responses did not differ between sites ( P > 0.05). Because the bradykinin B2-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

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