Prolonged head-down tilt exposure reduces maximal cutaneous vasodilator and sweating capacity in humans

2003 ◽  
Vol 94 (6) ◽  
pp. 2330-2336 ◽  
Author(s):  
C. G. Crandall ◽  
M. Shibasaki ◽  
T. E. Wilson ◽  
J. Cui ◽  
B. D. Levine
Keyword(s):  
Sweat Gland ◽  
Simulated Microgravity ◽  
Sweat Rate ◽  
Bed Rest ◽  
Exercise Group ◽  
Aerobic Exercise Training ◽  
Before And After ◽  
Rate Maximum ◽  
Gland Function ◽  
Cutaneous Vascular Conductance

Cutaneous vasodilation and sweat rate are reduced during a thermal challenge after simulated and actual microgravity exposure. The effects of microgravity exposure on cutaneous vasodilator capacity and on sweat gland function are unknown. The purpose of this study was to test the hypothesis that simulated microgravity exposure, using the 6° head-down tilt (HDT) bed rest model, reduces maximal forearm cutaneous vascular conductance (FVC) and sweat gland function and that exercise during HDT preserves these responses. To test these hypotheses, 20 subjects were exposed to 14 days of strict HDT bed rest. Twelve of those subjects exercised (supine cycle ergometry) at 75% of pre-bed rest heart rate maximum for 90 min/day throughout HDT bed rest. Before and after HDT bed rest, maximal FVC was measured, via plethysmography, by heating the entire forearm to 42°C for 45 min. Sweat gland function was assessed by administering 1 × 10−6 to 2 M acetylcholine (9 doses) via intradermal microdialysis while simultaneously monitoring sweat rate over the microdialysis membranes. In the nonexercise group, maximal FVC and maximal stimulated sweat rate were significantly reduced after HDT bed rest. In contrast, these responses were unchanged in the exercise group. These data suggest that 14 days of simulated microgravity exposure, using the HDT bed rest model, reduces cutaneous vasodilator and sweating capacity, whereas aerobic exercise training during HDT bed rest preserves these responses.

Pilocarpine-induced sweat gland function in individuals with multiple sclerosis

2005 ◽  
Vol 98 (5) ◽  
pp. 1740-1744 ◽  
Author(s):  
Scott L. Davis ◽  
Thad E. Wilson ◽  
Jamie M. Vener ◽  
Craig G. Crandall ◽  
Jack H. Petajan ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Exercise Training ◽  
Sweat Gland ◽  
Aerobic Training ◽  
Sweat Rate ◽  
Aerobic Exercise Training ◽  
Sweat Glands ◽  
Sudomotor Function ◽  
Sweat Function ◽  
Gland Function

This investigation tested the hypothesis that cholinergic sweat function of individuals with multiple sclerosis (MS) (MS-Con; n = 10) is diminished relative to matched healthy control subjects (Con; n = 10). In addition, cholinergic sweat function was determined before and after 15 wk of aerobic training in a subgroup of individuals with MS (MS-Ex; n = 7). Cholinergic sweating responses were assessed via pilocarpine iontophoresis on ventral forearm skin. A collection disk placed over the stimulated area collected sweat for 15 min. Sweat rate (SR) was calculated by dividing sweat collector volume by collection area and time. Iodine-treated paper was applied to the stimulated area to measure number of activated sweat glands (ASG). Sweat gland output (SGO) was calculated by dividing SR by density of glands under the collector. Sweat gland function was determined in MS-Ex to test the hypothesis that exercise training would increase sweating responses. No differences in ASG were observed between MS-Con and Con. SR and SGO in MS-Con [0.18 mg·cm−2·min−1 (SD 0.08); 1.74 μg·gland−1·min−1 (SD 0.79), respectively] were significantly lower ( P ≤ 0.05) than in Con [0.27 mg·cm−2·min−1 (SD 0.10); 2.43 μg·gland−1·min−1 (SD 0.69)]. Aerobic exercise training significantly ( P ≤ 0.05) increased peak aerobic capacity in MS-Ex [1.86 (SD 0.75) vs. 2.10 (SD 0.67) l/min] with no changes in ASG, SR, and SGO. Sweat gland function in individuals with MS is impaired relative to healthy controls. Fifteen weeks of aerobic training did not increase stimulated sweating responses in individuals with MS. Diminished peripheral sweating responses may be a consequence of impairments in autonomic control of sudomotor function.

scholarly journals Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

2009 ◽  
Vol 297 (4) ◽  
pp. R1082-R1085 ◽  
Author(s):  
Michael J. Buono ◽  
Travis R. Numan ◽  
Ryan M. Claros ◽  
Stephanie K. Brodine ◽  
Fred W. Kolkhorst
Keyword(s):  
Sweat Gland ◽  
Sweat Rate ◽  
Heat Acclimation ◽  
Whole Body ◽  
Moderate Intensity ◽  
Sweat Glands ◽  
Exercise Heart Rate ◽  
Sweat Production ◽  
Gland Function ◽  
Pilocarpine Iontophoresis

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35°C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 ± 22 vs. 138 ± 17 beats/min; P = 0.0001) and rectal temperature (38.2 ± 0.3 vs. 37.9 ± 0.3°C; P = 0.0003) and increased whole body sweat rate (0.70 ± 0.29 vs. 1.06 ± 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days ( P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 ± 0.20 vs. 0.66 ± 0.22 mg·cm−2·min−1). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 ± 0.21 mg·cm−2·min−1 ( P = 0.021) but decreased 52% to 0.32 ± 0.18 mg·cm−2·min−1 ( P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.

scholarly journals Pain and Vertebral Dysfunction in Dry Immersion: A Model of Microgravity Simulation Different from Bed Rest Studies

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
L. Treffel ◽  
N. Massabuau ◽  
K. Zuj ◽  
M.-A. Custaud ◽  
G. Gauquelin-Koch ◽  
...  
Keyword(s):  
Back Pain ◽  
Simulated Microgravity ◽  
Simulation Models ◽  
Bed Rest ◽  
Dry Immersion ◽  
Somatic Dysfunction ◽  
Clinical Methods ◽  
Microgravity Simulation ◽  
Before And After ◽  
Manual Palpation

Background. Astronauts frequently experience back pain during and after spaceflight. The aim of this study was to utilize clinical methods to identify potential vertebral somatic dysfunction (VD) in subjects exposed to dry immersion (DI), a model of microgravity simulation. Method. The experiment was performed in a space research clinic, respecting all the ethical rules, with subjects completing three days of dry immersion (n=11). Assessments of VD, spine height, and back pain were made before and after simulated microgravity. Results. Back pain was present in DI with great global discomfort during the entire protocol. A low positive correlation was found (Pearson r=0.44; P<0.001) between VD before DI and pain developed in the DI experiment. Conclusions. There is a specific location of pain in both models of simulation. Our analysis leads to relativizing constraints on musculoskeletal system in function of simulation models. This study was the first to examine manual palpation of the spine in a space experience. Additionally, osteopathic view may be used to select those individuals who have less risk of developing back pain.

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.

WISE-2005: Countermeasures to prevent muscle deconditioning during bed rest in women

2014 ◽  
Vol 116 (6) ◽  
pp. 654-667 ◽  
Author(s):  
Stuart M. C. Lee ◽  
Suzanne M. Schneider ◽  
Alan H. Feiveson ◽  
Brandon R. Macias ◽  
Scott M. Smith ◽  
...  
Keyword(s):  
Lean Mass ◽  
Lower Body Negative Pressure ◽  
Knee Extensor ◽  
Bed Rest ◽  
Protein Supplementation ◽  
Aerobic Exercise Training ◽  
Tissue Mass ◽  
Leg Press ◽  
Mass Losses ◽  
Before And After

The objectives of this study were to evaluate the efficacy of two separate countermeasures, exercise and protein supplementation, to prevent muscle strength and lean tissue mass losses during 60 days of bed rest (BR) in women and whether countermeasure efficacy was influenced by pre-BR muscular fitness (strength, endurance, tissue mass). Twenty-four women were assigned to an exercise (EX, n = 8), a no-exercise control (CON, n = 8), or a no-exercise protein supplementation group (PROT, n = 8). EX performed supine treadmill exercise within lower body negative pressure 3–4 days/wk and maximal concentric and eccentric supine leg- and calf-press exercises 2–4 days/wk. PROT consumed a diet with elevated protein content compared with CON and EX (1.6 vs. 1.0 g·kg−1·day−1). Knee and calf isokinetic strength and endurance, isotonic leg-press strength, and leg lean mass were measured before and after BR. Post-BR knee extensor strength and endurance, ankle strength, and leg lean mass were significantly greater and leg-press strength tended to be higher in EX than in CON and PROT. Post-BR measures in PROT were not different than those in CON. Exercise countermeasure efficacy was less, and strength, endurance, and leg lean mass losses in CON and PROT were greater, in subjects who were more fit pre-BR. An exercise protocol combining resistive and aerobic exercise training protects against losses in strength, endurance, and leg lean mass in women during BR, while a nutritional countermeasure without exercise was not effective. Exercise countermeasures may require individualization to protect higher levels of strength and endurance.

Effects of 14 days of head-down tilt bed rest on cutaneous vasoconstrictor responses in humans

2003 ◽  
Vol 94 (6) ◽  
pp. 2113-2118 ◽  
Author(s):  
Thad E. Wilson ◽  
Manabu Shibasaki ◽  
Jian Cui ◽  
Benjamin D. Levine ◽  
Craig G. Crandall
Keyword(s):  
Bed Rest ◽  
Cycle Ergometer ◽  
Exercise Group ◽  
Lower Limbs ◽  
Response Curves ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Rate Maximum ◽  
Forearm Skin ◽  
Cutaneous Vasoconstriction

This study tested the hypothesis that head-down tilt bed rest (HDBR) reduces adrenergic and nonadrenergic cutaneous vasoconstrictor responsiveness. Additionally, an exercise countermeasure group was included to identify whether exercise during bed rest might counteract any vasoconstrictor deficits that arose during HDBR. Twenty-two subjects underwent 14 days of strict 6° HDBR. Eight of these 22 subjects did not exercise during HDBR, while 14 of these subjects exercised on a supine cycle ergometer for 90 min a day at 75% of pre-bed rest heart rate maximum. To assess α-adrenergic vasoconstrictor responsiveness, intradermal microdialysis was used to locally administer norepinephrine (NE), while forearm skin blood flow (SkBF; laser-Doppler flowmetry) was monitored over microdialysis membranes. Nonlinear regression modeling was used to identify the effective drug concentration that caused 50% of the cutaneous vasoconstrictor response (EC50) and minimum values from the SkBF-NE dose-response curves. In addition, the effects of HDBR on nonadrenergic cutaneous vasoconstriction were assessed via the venoarteriolar response of the forearm and leg. HDBR did not alter EC50 or the magnitude of cutaneous vasoconstriction to exogenous NE administration regardless of whether the subjects exercised during HDBR. Moreover, HDBR did not alter the forearm venoarteriolar response in either the control or exercise groups during HDBR. However, HDBR significantly reduced the magnitude of cutaneous vasoconstriction due to the venoarteriolar response in the leg, and this response was similarly reduced in the exercise group. These data suggest that HDBR does not alter cutaneous vasoconstrictor responses to exogenous NE administration, whereas cutaneous vasoconstriction of the leg due to the venoarteriolar response is reduced after HDBR. It remains unclear whether attenuated venoarteriolar responses in the lower limbs contribute to reduced orthostatic tolerance after bed rest and spaceflight.

scholarly journals WISE 2005: Aerobic and resistive countermeasures prevent paraspinal muscle deconditioning during 60-day bed rest in women

2016 ◽  
Vol 120 (10) ◽  
pp. 1215-1222 ◽  
Author(s):  
Jacquelyn A. Holt ◽  
Brandon R. Macias ◽  
Suzanne M. Schneider ◽  
Donald E. Watenpaugh ◽  
Stuart M. C. Lee ◽  
...  
Keyword(s):  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Exercise Group ◽  
Erector Spinae ◽  
Paraspinal Muscle ◽  
Control Group ◽  
Cross Sectional ◽  
Before And After ◽  
Spine Function ◽  
Muscle Cross Sectional Area

Microgravity-induced lumbar paraspinal muscle deconditioning may contribute to back pain commonly experienced by astronauts and may increase the risk of postflight injury. We hypothesized that a combined resistive and aerobic exercise countermeasure protocol that included spinal loading would mitigate lumbar paraspinal muscle deconditioning during 60 days of bed rest in women. Sixteen women underwent 60-day, 6° head-down-tilt bed rest (BR) and were randomized into control and exercise groups. During bed rest the control group performed no exercise. The exercise group performed supine treadmill exercise within lower body negative pressure (LBNP) for 3-4 days/wk and flywheel resistive exercise for 2–3 days/wk. Paraspinal muscle cross-sectional area (CSA) was measured using a lumbar spine MRI sequence before and after BR. In addition, isokinetic spinal flexion and extension strengths were measured before and after BR. Data are presented as means ± SD. Total lumbar paraspinal muscle CSA decreased significantly more in controls (10.9 ± 3.4%) than in exercisers (4.3 ± 3.4%; P < 0.05). The erector spinae was the primary contributor (76%) to total lumbar paraspinal muscle loss. Moreover, exercise attenuated isokinetic spinal extension loss (−4.3 ± 4.5%), compared with controls (−16.6 ± 11.2%; P < 0.05). In conclusion, LBNP treadmill and flywheel resistive exercises during simulated microgravity mitigate decrements in lumbar paraspinal muscle structure and spine function. Therefore spaceflight exercise countermeasures that attempt to reproduce spinal loads experienced on Earth may mitigate spinal deconditioning during long-duration space travel.

scholarly journals Cardiovascular adaptation to simulated microgravity and countermeasure efficacy assessed by ballistocardiography and seismocardiography

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jeremy Rabineau ◽  
Amin Hossein ◽  
Federica Landreani ◽  
Benoit Haut ◽  
Edwin Mulder ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Simulated Microgravity ◽  
Cardiac Cycle ◽  
Cardiovascular Effects ◽  
Bed Rest ◽  
Exercise Group ◽  
Control Group ◽  
Resting Heart Rate ◽  
Cardiovascular Deconditioning ◽  
Controlled Breathing

Abstract Head-down bed rest (HDBR) reproduces the cardiovascular effects of microgravity. We tested the hypothesis that regular high-intensity physical exercise (JUMP) could prevent this cardiovascular deconditioning, which could be detected using seismocardiography (SCG) and ballistocardiography (BCG). 23 healthy males were exposed to 60-day HDBR: 12 in a physical exercise group (JUMP), the others in a control group (CTRL). SCG and BCG were measured during supine controlled breathing protocols. From the linear and rotational SCG/BCG signals, the integral of kinetic energy ($$iK$$ iK ) was computed on each dimension over the cardiac cycle. At the end of HDBR, BCG rotational $$iK$$ iK and SCG transversal $$iK$$ iK decreased similarly for all participants (− 40% and − 44%, respectively, p < 0.05), and so did orthostatic tolerance (− 58%, p < 0.01). Resting heart rate decreased in JUMP (− 10%, p < 0.01), but not in CTRL. BCG linear $$iK$$ iK decreased in CTRL (− 50%, p < 0.05), but not in JUMP. The changes in the systolic component of BCG linear iK were correlated to those in stroke volume and VO2 max (R = 0.44 and 0.47, respectively, p < 0.05). JUMP was less affected by cardiovascular deconditioning, which could be detected by BCG in agreement with standard markers of the cardiovascular condition. This shows the potential of BCG to easily monitor cardiac deconditioning.

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