Influences of gender on sympathetic nerve responses to static exercise

1996 ◽  
Vol 80 (1) ◽  
pp. 245-251 ◽  
Author(s):  
S. M. Ettinger ◽  
D. H. Silber ◽  
B. G. Collins ◽  
K. S. Gray ◽  
G. Sutliff ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Voluntary Contraction ◽  
Gender Effect ◽  
Static Exercise ◽  
Nerve Activity ◽  
Level Of Training ◽  
Spectroscopy Studies

We compared reflex responses to static handgrip at 30% maximal voluntary contraction (MVC) in 26 untrained men (mean age 35 +/- 3 yr) and 23 untrained women (mean age 39 +/- 4 yr). Women demonstrated attenuated increases in blood pressure and muscle sympathetic nerve activity (MSNA; by microneurography) compared with men. This difference was also observed during a period of posthandgrip circulatory arrest. 31P-nuclear magnetic resonance (NMR) spectroscopy studies demonstrated attenuations in the production of diprotonated phosphate and the development of cellular acidosis in women compared with men. Subjects also performed ischemic handgrip to fatigue. During this paradigm, MSNA responses were similar in the two groups, suggesting that freely perfused conditions are necessary for the full expression of the gender effect. Finally, we examined MSNA responses to adductor pollicus exercise in 7 men (26 +/- 1 yr) and 6 women (25 +/- 2 yr). MVC values and times to fatigue were similar in the two groups (MVC: men, 4.3 +/- 0.4 kg; women, 4.0 +/- 0.3 kg; not significant. Time to fatigue: men, 209 +/- 16 s; women, 287 +/- 50 s; not significant). At periods of end exercise and postexercise circulatory arrest, MSNA responses were attenuated in the women compared with the men. We conclude that, during nonischemic static exercise, sympathetic neural outflow is less in women compared with men. This response is due to an attenuated metaboreflex in women. Finally, on the basis of the adductor pollicus experiments, this effect appears independent of muscle mass, workload, and the level of training.

Sympathetic nerve activity related to local fatigue sensation during static contraction

1989 ◽  
Vol 67 (3) ◽  
pp. 980-984 ◽  
Author(s):  
M. Saito ◽  
T. Mano ◽  
S. Iwase
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Direct Method ◽  
Muscle Sympathetic Nerve Activity ◽  
Nervous Activity ◽  
Total Activity ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Nerve Activity ◽  
Activity Burst

The relationship between autonomic nervous activity and psychophysical responses was studied during static exercise in humans. Muscle sympathetic nerve activity (MSNA) recorded by a direct method of microneurography and the intensity of fatigue sensation in working muscles [levels of fatigue sensation (LFS) scale 0–10] were analyzed in 11 male subjects during static handgrip (SHG). SHG was exerted at a tension of 25% of maximal voluntary contraction until the given tension could no longer be sustained. MSNA, represented as total activity (burst number x mean burst amplitude), and LFS increased in a time-dependent process till the end of the SHG. At the termination of the static exercise MSNA had increased an average of 480% of the resting value. In the simple exponential curve, Y = A expBX, where X was LFS and Y was MSNA. The constants A and B estimated from the total experiments were 84.5 and 0.161, respectively. The correlation between LFS and MSNA was statistically significant. There was a large difference in the value of constant B (0.089–0.278) among the subjects, and a relatively small difference in the value of constant A (37.5–133.8). The increases in both MSNA and LFS during SHG may be mainly related to the same afferent volley from working skeletal muscles. The results indicate that the response of the muscle sympathetic nerve to SHG relates to the psychological feelings of fatigue in the working muscles.

Dichloroacetate reduces sympathetic nerve responses to static exercise

1991 ◽  
Vol 261 (5) ◽  
pp. H1653-H1658 ◽  
Author(s):  
S. Ettinger ◽  
K. Gray ◽  
S. Whisler ◽  
L. Sinoway
Keyword(s):  
Lactic Acid ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Lactic Acid Production ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Exercise Protocol ◽  
Forearm Exercise

Lactic acid is thought to be a stimulant of muscle metaboreceptors. The goal of the present study was to determine if inhibition of lactic acid production by dichloroacetate (DCA) would attenuate muscle sympathetic nerve activity (MSNA) during static forearm exercise. DCA increases pyruvate dehydrogenase levels. Thus, for a given amount of pyruvate produced, less lactic acid is formed. Seven subjects performed static forearm exercise at 20% maximal voluntary contraction until fatigue followed by posthandgrip circulatory arrest (PHG-CA) (trial.1). Subjects then received DCA (35 mg/kg) and repeated the exercise protocol (trial 2). We observed an attenuated rise in forearm venous lactate and MSNA. The trial 2 MSNA value during PHG-CA was 51 +/- 11% less than the value during trial 1 (P less than 0.01). In seven control subjects, two bouts of static forearm exercise were performed with an intervening saline infusion. This intervention had no effect on lactate or MSNA responses to exercise. We conclude that DCA attenuates lactate responses to static exercise, and this is associated with a blunted MSNA response.

Modulation of sympathetic nerve activity during posthandgrip muscle ischemia in humans

1994 ◽  
Vol 266 (1) ◽  
pp. H79-H83 ◽  
Author(s):  
C. A. Ray ◽  
N. H. Secher ◽  
A. L. Mark
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sensory Nerve ◽  
Vascular Occlusion ◽  
Voluntary Contraction ◽  
Central Command ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

To evaluate modulation of muscle sympathetic nerve activity (MSNA) during posthandgrip muscle ischemia (PHGMI), subjects performed 2 min of isometric handgrip at 33% of maximal voluntary contraction (MVC) followed by 2 min of PHGMI produced by forearm vascular occlusion. The response to PHGMI was studied in the absence and again during the addition of contralateral rhythmic handgrip (RHG; 40 times/min) at 15% (n = 6) and 30% (n = 10) MVC during the second minute of the PHGMI. Additionally, to isolate the effect of central command, response to PHGMI was studied during attempted RHG after sensory nerve blockade (n = 5). RHG for 2 min at 15 and 30% MVC and attempted RHG for 2 min did not increase MSNA. Isometric handgrip elicited an 130 +/- 48% increase in MSNA (P < 0.05), which was maintained during PHGMI. RHG at 15 and 30% MVC elicited an attenuation of MSNA (-10 +/- 7% and -14 +/- 6%, respectively) when performed during the second minute of PHGMI (P < 0.05). In contrast, attempted RHG did not significantly affect MSNA during PHGMI. The findings demonstrate modulation of MSNA during activation of the muscle metaboreflex. The attenuation of metaboreceptor-mediated increases in MSNA appear to be the result of mechanosensitive muscle afferents and not central command.

Naloxone does not affect the cardiovascular and sympathetic adjustments to static exercise in humans

1994 ◽  
Vol 77 (1) ◽  
pp. 231-235 ◽  
Author(s):  
C. A. Ray ◽  
J. A. Pawelczyk
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Static Exercise ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Double Blind ◽  
Endogenous Opiates ◽  
Muscle Ischemia

Previous studies suggested that endogenous opiates may attenuate the cardiovascular and sympathetic adjustments to static exercise. We tested whether this effect originates from exercising skeletal muscle. Eight men performed 2 min of static handgrip (30% maximum) followed by 2 min of posthandgrip muscle ischemia after three interventions: 1) control, 2) intra-arterial injection of naloxone HCl (60 micrograms) or vehicle (saline) in the exercising arm, and 3) systemic infusion of naloxone (4 mg) or vehicle. Naloxone and vehicle trials were performed double blind on separate days. Preexercise baseline muscle sympathetic nerve activity (burst frequency), heart rate, and blood pressure were similar across interventions on either day. During static handgrip, control, intra-arterial, and systemic administration of vehicle and naloxone elicited similar increases in total muscle sympathetic nerve activity (58 +/- 24 vs. 68 +/- 26, 146 +/- 49 vs. 132 +/- 42, 137 +/- 54 vs. 164 +/- 44%, respectively), heart rate (9 +/- 2 vs. 8 +/- 3, 16 +/- 3 vs. 16 +/- 2, 20 +/- 4 vs. 19 +/- 3 beats/min, respectively), and mean arterial pressure (22 +/- 4 vs. 21 +/- 4, 29 +/- 5 vs. 26 +/- 3, 28 +/- 4 vs. 27 +/- 4 mmHg, respectively). Additionally, there were no differences between vehicle and naloxone trials during posthandgrip muscle ischemia. Thus, contrary to previous reports, we conclude that the endogenous opiate peptide system does not modulate cardiovascular and sympathetic responses to brief periods of static exercise or muscle ischemia in humans.

Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating

1997 ◽  
Vol 82 (6) ◽  
pp. 1719-1733 ◽  
Author(s):  
Chester A. Ray ◽  
Kathryn H. Gracey
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Local Heating ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
Muscle Temperature ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Exercise Induced

Ray, Chester A., and Kathryn H. Gracey. Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating. J. Appl. Physiol. 82(6): 1719–1725, 1997.—The muscle metabo- and mechanoreflexes have been shown to increase muscle sympathetic nerve activity (MSNA) during exercise. Group III and IV muscle afferents, which are believed to mediate this response, have been shown to be thermosensitive in animals. The purpose of the present study was to evaluate the effect of muscle temperature on MSNA responses during exercise. Eleven subjects performed ischemic isometric handgrip at 30% of maximal voluntary contraction to fatigue, followed by 2 min of postexercise muscle ischemia (PEMI), with and without local heating of the forearm. Local heating of the forearm increased forearm muscle temperature from 34.4 ± 0.2 to 38.9 ± 0.3°C ( P = 0.001). Diastolic and mean arterial pressures were augmented during exercise in the heat. MSNA responses were greater during ischemic handgrip with local heating compared with control (no heating) after the first 30 s. MSNA responses at fatigue were greater during local heating. MSNA increased by 16 ± 2 and 20 ± 2 bursts per 30 s for control and heating, respectively ( P = 0.03). When expressed as a percent change in total activity (total burst amplitude), MSNA increased 531 ± 159 and 941 ± 237% for control and heating, respectively ( P = 0.001). However, MSNA was not different during PEMI between trials. This finding suggests that the augmentation of MSNA during exercise with heat was due to the stimulation of mechanically sensitive muscle afferents. These results suggest that heat sensitizes skeletal muscle afferents during muscle contraction in humans and may play a role in the regulation of MSNA during exercise.

Muscle sympathetic nerve responses to static leg exercise

1992 ◽  
Vol 73 (4) ◽  
pp. 1523-1529 ◽  
Author(s):  
C. A. Ray ◽  
R. F. Rea ◽  
M. P. Clary ◽  
A. L. Mark
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Knee Extension ◽  
Voluntary Contraction ◽  
Leg Exercise

Previous studies of muscle sympathetic nerve activity (MSNA) during static exercise have employed predominantly the arms. These studies have revealed striking increases in arm and leg MSNA during static handgrip (SHG) and postexercise circulatory arrest (PECA). The purpose of this study was to examine MSNA during static leg exercise (SLE) at intensities and duration commonly used during SHG followed by PECA. During 2 min of SLE (static knee extension) at 10% of maximal voluntary contraction (MVC; n = 18) in the sitting position, mean arterial pressure and heart rate increased significantly. Surprisingly, MSNA in the contralateral leg did not increase above control levels during SLE but rather decreased (23 +/- 5%; P < 0.05) during the 1st min of SLE at 10% MVC. We compared MSNA responses to SHG and SLE (n = 8) at 30% MVC. SHG and SLE elicited comparable increases (P < 0.05) in arterial pressure and heart rate, but SHG elicited significant increases in MSNA, whereas SLE did not. During PECA after SHG and SLE, mean arterial pressure remained significantly above control. However, MSNA was unchanged during PECA after SLE but was significantly greater than control during PECA after SHG. Because previous studies have indicated differences in MSNA responses to the arm and leg, we measured arm and leg MSNA simultaneously in six subjects during SLE at 20% MVC and PECA. During SLE and PECA, MSNA in the contralateral arm and leg did not differ significantly from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

GABAA receptor activation modulates the muscle sympathetic nerve activity responses at the onset of static exercise in humans

2021 ◽  
Author(s):  
André L. Teixeira ◽  
Igor A. Fernandes ◽  
Philip J. Millar ◽  
Lauro C. Vianna
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stroke Volume ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Receptor Activation ◽  
Static Exercise ◽  
Nerve Activity ◽  
Exercise Onset

Exercise is a well-known sympathoexcitatory stimulus. However, muscle sympathetic nerve activity (MSNA) can decrease during the onset of muscle contraction. Yet, the underlying mechanisms and neurotransmitters involved in the sympathetic responses at the onset of exercise remain unknown. Herein, we tested the hypothesis that GABAA receptors may contribute to the MSNA responses at the onset of static handgrip in humans. Thirteen young, healthy individuals (4 females) performed 30 s of ischemic static handgrip at 30% of maximum volitional contraction before and following oral administration of either placebo or diazepam (10 mg), a benzodiazepine that enhances GABAA activity. MSNA (microneurography), beat-to-beat blood pressure (finger photopletysmography), heart rate (electrocardiogram) and stroke volume (ModelFlow) were continuously measured. Cardiac output (CO = stroke volume x heart rate) and total vascular conductance (TVC = CO / mean blood pressure) were subsequently calculated. At rest, MSNA was reduced while hemodynamic variables were unchanged after diazepam administration. Before diazepam, static handgrip elicited a significant decrease in MSNA burst frequency (∆-7±2 bursts/min, P<0.01 vs. baseline) and MSNA burst incidence (∆-16±2 bursts/100 heart beats, P<0.01 vs. baseline); however, these responses were attenuated following diazepam administration (∆-1±2 bursts/min and ∆-7±2 bursts/100 heart beats, respectively; P<0.01 vs. before diazepam). Diazepam did not affect the increases in heart rate, blood pressure, CO and TVC at the exercise onset. Importantly, the placebo had no effect on any variable at rest or exercise onset. These findings suggest that GABAA receptor activation modulates the MSNA responses at the onset of static exercise in young, healthy humans.

Forearm compression during exercise increases sympathetic nerve traffic

1994 ◽  
Vol 77 (6) ◽  
pp. 2612-2617 ◽  
Author(s):  
J. McClain ◽  
J. C. Hardy ◽  
L. I. Sinoway
Keyword(s):  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Voluntary Contraction ◽  
Venous Congestion ◽  
Static Exercise ◽  
Interstitial Pressure ◽  
Hemodynamic Variables ◽  
Arterial Blood ◽  
Before And After

Previously, we showed that forearm venous congestion augmented muscle sympathetic nerve activity (MSNA) during static exercise. We postulated that venous congestion increased interstitial pressure, sensitizing mechanoreceptor afferents that led to a greater sympathoexcitation during exercise. In this study, we tested the hypothesis that forearm compression (FC) would increase interstitial pressure and selectively stimulate mechanically sensitive afferents. We measured MSNA during 2 min of ischemic static exercise (40% maximal voluntary contraction) and 2 min of posthandgrip circulatory arrest. Exercise was performed again after 5 min of FC induced by inflation of a forearm cuff to 90 mmHg (n = 6) and 110 mmHg (n = 7). FC without exercise had no effect on any of the hemodynamic variables. MSNA and mean arterial blood pressure responses were not augmented when exercise was performed with FC at 90 mmHg. However, static exercise coupled with FC at 110 mmHg did augment the reflex responses to static exercise (changes in MSNA before and after FC were 277 +/- 58 and 503 +/- 82 arbitrary units, respectively, P < 0.02; changes in mean arterial pressure before and after FC were 35 +/- 4 and 41 +/- 5 mmHg, respectively, P < 0.003). These responses were probably not due to greater metaboreceptor stimulation, since posthandgrip circulatory arrest responses were unaffected by FC. We postulate that FC sensitizes mechanoreceptors, leading to greater sympathoexcitation during exercise.

Isometric handgrip training reduces arterial pressure at rest without changes in sympathetic nerve activity

2000 ◽  
Vol 279 (1) ◽  
pp. H245-H249 ◽  
Author(s):  
Chester A. Ray ◽  
Dario I. Carrasco
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

The purpose of this study was to determine whether isometric handgrip (IHG) training reduces arterial pressure and whether reductions in muscle sympathetic nerve activity (MSNA) mediate this drop in arterial pressure. Normotensive subjects were assigned to training ( n = 9), sham training ( n = 7), or control ( n = 8) groups. The training protocol consisted of four 3-min bouts of IHG exercise at 30% of maximal voluntary contraction (MVC) separated by 5-min rest periods. Training was performed four times per week for 5 wk. Subjects' resting arterial pressure and heart rate were measured three times on 3 consecutive days before and after training, with resting MSNA (peroneal nerve) recorded on the third day. Additionally, subjects performed IHG exercise at 30% of MVC to fatigue followed by muscle ischemia. In the trained group, resting diastolic (67 ± 1 to 62 ± 1 mmHg) and mean arterial pressure (86 ± 1 to 82 ± 1 mmHg) significantly decreased, whereas systolic arterial pressure (116 ± 3 to 113 ± 2 mmHg), heart rate (67 ± 4 to 66 ± 4 beats/min), and MSNA (14 ± 2 to 15 ± 2 bursts/min) did not significantly change following training. MSNA and cardiovascular responses to exercise and postexercise muscle ischemia were unchanged by training. There were no significant changes in any variables for the sham training and control groups. The results indicate that IHG training is an effective nonpharmacological intervention in lowering arterial pressure.

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