scholarly journals Whole body heat stress attenuates the pressure response to muscle metaboreceptor stimulation in humans

2016 ◽  
Vol 121 (5) ◽  
pp. 1178-1186 ◽  
Author(s):  
Jian Cui ◽  
Cheryl Blaha ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Whole Body ◽  
Isometric Handgrip ◽  
Whole Body Heat Stress ◽  
Body Heat

The effects of whole body heat stress on sympathetic and cardiovascular responses to stimulation of muscle metaboreceptors and mechanoreceptors remains unclear. We examined the muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate in 14 young healthy subjects during fatiguing isometric handgrip exercise, postexercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed under normothermic and whole body heat stress (increase internal temperature ~0.6°C via a heating suit) conditions. Heat stress increased the resting MSNA and heart rate. Heat stress did not alter the mean blood pressure (MAP), heart rate, and MSNA responses (i.e., changes) to fatiguing exercise. During PECO, whole body heat stress accentuated the heart rate response [change (Δ) of 5.8 ± 1.5 to Δ10.0 ± 2.1 beats/min, P = 0.03], did not alter the MSNA response (Δ16.4 ± 2.8 to Δ17.3 ± 3.8 bursts/min, P = 0.74), and lowered the MAP response (Δ20 ± 2 to Δ12 ± 1 mmHg, P < 0.001). Under normothermic conditions, passive stretch during PECO evoked significant increases in MAP and MSNA (both P < 0.001). Of note, heat stress prevented the MAP and MSNA responses to stretch during PECO (both P > 0.05). These data suggest that whole body heat stress attenuates the pressor response due to metaboreceptor stimulation, and the sympathetic nerve response due to mechanoreceptor stimulation.

scholarly journals Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia

2009 ◽  
Vol 106 (4) ◽  
pp. 1125-1131 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David A. Low ◽  
David M. Keller ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Whole Body Heat Stress ◽  
Body Heat

Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature ∼ 0.7°C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (−4.34 ± 0.40 to −3.57 ± 0.31 units·beat−1·mmHg−1, respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating ( P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation.

scholarly journals Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Controlled Trial ◽  
Whole Body ◽  
Cord Injury ◽  
Whole Body Heat Stress ◽  
Body Heat

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P &lt; .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P &lt; .001) and 5 mm Hg (F6,24 = 5.4, P &lt; .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P &lt; .001) increased in the plasma (58% and 285%, respectively) (P &lt; .05). The HSP72 (F1,12 = 44.7, P &lt; .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

scholarly journals Carotid baroreflex control of heart rate is enhanced during whole‐body heat stress

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Davor Krnjajic ◽  
Cory L Butts ◽  
W Shane Warren ◽  
Mitchel R Samels ◽  
David M Keller
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Whole Body ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Whole Body Heat Stress ◽  
Body Heat

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

1999 ◽  
Vol 277 (6) ◽  
pp. H2348-H2352 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
D. B. Farr
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Whole Body ◽  
Nerve Activity ◽  
Arterial Blood

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

scholarly journals Carotid baroreflex control of heart rate is enhanced, while control of mean arterial pressure is preserved during whole body heat stress in young healthy men

2016 ◽  
Vol 311 (4) ◽  
pp. R735-R741 ◽  
Author(s):  
Davor Krnjajic ◽  
Dustin R. Allen ◽  
Cory L. Butts ◽  
David M. Keller
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Whole Body ◽  
Chamber Pressure ◽  
Carotid Baroreflex ◽  
Whole Body Heat Stress ◽  
Neck Pressure ◽  
Body Heat

Whole body heat stress (WBH) results in numerous cardiovascular alterations that ultimately reduce orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported as a potential reason for this decrement, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in 10 healthy male subjects (age: 26 ± 3; height: 185 ± 7 cm; weight: 82 ± 10 kg; BMI: 24 ± 3 kg/m2; means ± SD) using 5-s trials of neck pressure (+45, +30, and +15 Torr) and neck suction (−20, −40, −60, and −80 Torr) during normothermia (NT) and passive WBH (Δ core temp ∼1°C). Analyses of stimulus response curves (four-parameter logistic model) for CBR control of heart rate (CBR-HR) and mean arterial pressure (CBR-MAP), as well as separate two-way ANOVA of the hypotensive and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure), were performed. For CBR-HR, maximal gain was increased during WBH (−0.73 ± 0.11) compared with NT (−0.39 ± 0.04, mean ± SE, P = 0.03). In addition, the CBR-HR responding range was increased during WBH (33 ± 5) compared with NT (19 ± 2 bpm, P = 0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at −40, −60, and −80 Torr (condition × chamber pressure interaction, P = 0.049) compared with NT. For CBR-MAP, both logistic analysis and separate two-way ANOVA revealed no differences during WBH. Therefore, in response to passive WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well preserved.

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

2002 ◽  
Vol 282 (1) ◽  
pp. R252-R258 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Arterial Blood ◽  
The Relationship

To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature ( P < 0.01), MSNA ( P < 0.01), heart rate ( P< 0.01), and skin blood flow ( P < 0.001), whereas mean arterial blood pressure did not change significantly ( P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (−128.3 ± 13.9 U · beats−1 · mmHg−1) was similar ( P = 0.31) with normothermia (−140.6 ± 21.1 U · beats−1 · mmHg−1). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating.

Sympathetic Nerve Activity and Whole-Body Heat Stress

2008 ◽  
Vol 40 (Supplement) ◽  
pp. S334 ◽  
Author(s):  
David A. Low ◽  
David M. Keller ◽  
Jonathan E. Wingo ◽  
R. Matthew Brothers ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Nerve Activity ◽  
Whole Body Heat Stress ◽  
Body Heat

Baroreflex modulation of muscle sympathetic nerve activity during posthandgrip muscle ischemia in humans

2001 ◽  
Vol 91 (4) ◽  
pp. 1679-1686 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Manabu Shibasaki ◽  
Nicole A. Hodges ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
The Relationship

To identify whether muscle metaboreceptor stimulation alters baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA, beat-by-beat arterial blood pressure (Finapres), and electrocardiogram were recorded in 11 healthy subjects in the supine position. Subjects performed 2 min of isometric handgrip exercise at 40% of maximal voluntary contraction followed by 2.5 min of posthandgrip muscle ischemia. During muscle ischemia, blood pressure was lowered and then raised by intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure was more negative ( P < 0.001) during posthandgrip muscle ischemia (−201.9 ± 20.4 units · beat−1 · mmHg−1) when compared with control conditions (−142.7 ± 17.3 units · beat−1 · mmHg−1). No significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. However, both curves shifted during postexercise ischemia to accommodate the elevation in blood pressure and MSNA that occurs with this condition. These data suggest that the sensitivity of baroreflex modulation of MSNA is elevated by muscle metaboreceptor stimulation, whereas the sensitivity of baroreflex of modulate heart rate is unchanged during posthandgrip muscle ischemia.

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