scholarly journals Modulation of muscle sympathetic nerve activity to muscle heating during dynamic exercise

2009 ◽  
Vol 296 (5) ◽  
pp. R1439-R1444 ◽  
Author(s):  
Jonathan S. Cook ◽  
Chester A. Ray
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Interactive Effect ◽  
Total Activity ◽  
Muscle Temperature ◽  
Isometric Handgrip ◽  
Burst Frequency ◽  
Nerve Activity

Previous studies from our laboratory have demonstrated that altering muscle temperature of the exercising forearm can elicit changes in muscle sympathetic nerve activity (MSNA) during ischemic isometric handgrip. The purpose of the current study was to determine the interactive effect of muscle temperature and blood flow on MSNA responses during dynamic handgrip (DHG). Eight subjects performed two bouts of graded DHG to fatigue followed by 2 min of postexercise muscle ischemia (PEMI). Local heating of the forearm increased muscle temperature from 33.6 ± 0.3 to 38.3 ± 0.5°C ( P < 0.05). Mean arterial pressure and heart rate increased in a linear fashion during graded DHG ( P < 0.05) but were not affected by muscle temperature. MSNA (burst frequency and total activity) at fatigue and PEMI were elevated in all conditions ( P < 0.05). However, MSNA responses were not different between temperature conditions. To ascertain the effect of blood flow, eight additional subjects completed two trials of ischemic DHG under control or warm conditions followed by 2 min of PEMI. MSNA, expressed as burst frequency and total activity, was significantly greater in warm compared with the control trial (Δ14 ± 3 and Δ9 ± 2 bursts/30 s, and Δ1,234 ± 260 and Δ751 ± 199 units/30 s, respectively). This finding supports the concept that muscle heating sensitizes skeletal muscle afferents during muscle contractions and augments MSNA in humans. However, on the basis of these findings, we conclude that muscle blood flow modulates the effect of muscle temperature on MSNA during exercise.

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.

scholarly journals Gender-related differences in the sympathetic vasoconstrictor drive of normal subjects

2007 ◽  
Vol 112 (6) ◽  
pp. 353-361 ◽  
Author(s):  
Andrew J. Hogarth ◽  
Alan F. Mackintosh ◽  
David A. S. G. Mary
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor ◽  
Normal Subjects ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Vasoconstrictor Response ◽  
Baroreceptor Reflex Sensitivity

The risk of cardiovascular disease has been linked to sympathetic activation and its incidence is known to be lower in women than in men. However, the effect of gender on the sympathetic vasoconstrictor drive has not yet been established. In the present study, we investigated whether there is a gender difference in MSNA (muscle sympathetic nerve activity) and blood flow, and to determine the mechanisms involved. We examined 68 normal subjects, 34 women and 34 men, matched for age, BMI (body mass index) and waist circumference. MSNA was measured as the mean frequency of single units (s-MSNA) and as multi-unit bursts (m-MSNA) from the peroneal nerve simultaneously with its supplied muscle CBF (calf blood flow). Women had lower (P=0.0007) s-MSNA (24±2.0 impulses/100 cardiac beats) than men (34±2.3 impulses/100 cardiac beats), and a greater baroreceptor reflex sensitivity controlling efferent sympathetic nerve activity than men. The sympathetic activity was inversely and directly correlated respectively, with CBF (P=0.03) and CVR (calf vascular resistance; P=0.01) in men only. The responses of an increase in CVR to cold pressor and isometric handgrip tests were significantly smaller in women (P=0.002) than in men, despite similar increases in efferent sympathetic nerve activity. Women had a lower central sympathetic neural output to the periphery, the mechanism of which involved differences in central and reflex control, as well as a lower vasoconstrictor response to this neural output. It is suggested that this may partly explain the observed lower incidence of cardiovascular events in women compared with men.

Endurance exercise training is associated with elevated basal sympathetic nerve activity in healthy older humans

1994 ◽  
Vol 77 (3) ◽  
pp. 1366-1374 ◽  
Author(s):  
A. V. Ng ◽  
R. Callister ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Acute Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Control Subjects

We tested the hypothesis that endurance training is associated with altered basal levels of muscle sympathetic nerve activity (MSNA) and responses to acute stress in healthy older adults. MSNA (peroneal microneurography) and plasma norepinephrine (NE) concentrations were measured during supine rest, a cold pressor test, and isometric handgrip (40% maximal voluntary force to exhaustion) in 16 older masters endurance athletes [10 men, 6 women; 66 +/- 1 (SE) yr] and 15 healthy normotensive untrained control subjects (9 men, 6 women; 65 +/- 1 yr). The athletes had higher levels of estimated daily energy expenditure and maximal oxygen uptake and lower levels of resting heart rate and body fat than the control subjects (all P < 0.05). MSNA during supine rest was elevated in the athletes whether expressed as burst frequency (43 +/- 2 vs. 32 +/- 3 bursts/min, respectively; P < 0.05) or burst incidence (75 +/- 4 vs. 52 +/- 5 bursts/100 heartbeats, respectively; P < 0.01). These whole group differences were due primarily to markedly higher levels of MSNA in the athletic vs. untrained women (48 +/- 4 vs. 25 +/- 3 bursts/min, 82 +/- 3 vs. 38 +/- 3 bursts/100 heartbeats, respectively, P < 0.001). In contrast, basal plasma NE concentrations were not significantly different in the athletes vs. control subjects. The MSNA and plasma NE responses to acute stress tended to be greater in the athletes. These findings indicate that vigorous regular aerobic exercise is associated with an elevated level of MSNA at rest and a tendency for an enhanced response to acute stress in healthy normotensive older humans.

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.

scholarly journals Heart rate variability and muscle sympathetic nerve activity response to acute stress: the effect of breathing

2010 ◽  
Vol 299 (1) ◽  
pp. R80-R91 ◽  
Author(s):  
Lindsay D. DeBeck ◽  
Stewart R. Petersen ◽  
Kelvin E. Jones ◽  
Michael K. Stickland
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Nerve ◽  
Spontaneous Breathing ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Controlled Breathing

Previous research has suggested a relationship between low-frequency power of heart rate variability (HRV; LF in normalized units, LFnu) and muscle sympathetic nerve activity (MSNA). However, investigations have not systematically controlled for breathing, which can modulate both HRV and MSNA. Accordingly, the aims of this experiment were to investigate the possibility of parallel responses in MSNA and HRV (LFnu) to selected acute stressors and the effect of controlled breathing. After data were obtained at rest, 12 healthy males (28 ± 5 yr) performed isometric handgrip exercise (30% maximal voluntary contraction) and the cold pressor test in random order, and were then exposed to hypoxia (inspired fraction of O2 = 0.105) for 7 min, during randomly assigned spontaneous and controlled breathing conditions (20 breaths/min, constant tidal volume, isocapnic). MSNA was recorded from the peroneal nerve, whereas HRV was calculated from ECG. At rest, controlled breathing did not alter MSNA but decreased LFnu ( P < 0.05 for all) relative to spontaneous breathing. MSNA increased in response to all stressors regardless of breathing. LFnu increased with exercise during both breathing conditions. During cold pressor, LFnu decreased when breathing was spontaneous, whereas in the controlled breathing condition, LFnu was unchanged from baseline. Hypoxia elicited increases in LFnu when breathing was controlled, but not during spontaneous breathing. The parallel changes observed during exercise and controlled breathing during hypoxia suggest that LFnu may be an indication of sympathetic outflow in select conditions. However, since MSNA and LFnu did not change in parallel with all stressors, a cautious approach to the use of LFnu as a marker of sympathetic activity is warranted.

scholarly journals Influence of Sex and Age on Muscle Sympathetic Nerve Activity of Healthy Normotensive Adults

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 997-1005 ◽  
Author(s):  
Daniel A. Keir ◽  
Mark B. Badrov ◽  
George Tomlinson ◽  
Catherine F. Notarius ◽  
Derek S. Kimmerly ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Body Mass ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Systematic Change ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Age Related

As with blood pressure, age-related changes in muscle sympathetic nerve activity (MSNA) may differ nonlinearly between sexes. Data acquired from 398 male (age: 39±17; range: 18–78 years [mean±SD]) and 260 female (age: 37±18; range: 18–81 years) normotensive healthy nonmedicated volunteers were analyzed using linear regression models with resting MSNA burst frequency as the outcome and the predictors sex, age, MSNA, blood pressure, and body mass index modelled with natural cubic splines. Age and body mass index contributed 41% and 11%, respectively, of MSNA variance in females and 23% and 1% in males. Overall, changes in MSNA with age were sigmoidal. At age 20, mean MSNA of males and females were similar, then diverged significantly, reaching in women a nadir at age 30. After 30, MSNA increased nonlinearly in both sexes. Both MSNA discharge and blood pressure were lower in females until age 50 (17±9 versus 25±10 bursts·min −1 ; P <1×10 −19 ; 106±11/66±8 versus 116±7/68±9 mm Hg; P <0.01) but converged thereafter (38±11 versus 35±12 bursts·min −1 ; P =0.17; 119±15/71±13 versus 120±13/72±9 mm Hg; P >0.56). Compared with age 30, MSNA burst frequency at age 70 was 57% higher in males but 3-fold greater in females; corresponding increases in systolic blood pressure were 1 (95% CI, −4 to 5) and 12 (95% CI, 6–16) mm Hg. Except for concordance in females beyond age 40, there was no systematic change with age in any resting MSNA-blood pressure relationship. In normotensive adults, MSNA increases after age 30, with ascendance steeper in women.

Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans

2004 ◽  
Vol 287 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Takeshi Ogawa ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Burst Strength

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: −15 and −35 mmHg). At −15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at −35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at −15 mmHg LBNP (vs. CON) and further shifted upward at −35 mmHg LBNP. At −15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at −35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.

Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans

2006 ◽  
Vol 290 (4) ◽  
pp. H1419-H1426 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Time Dependent ◽  
Operating Pressure ◽  
Dependent Manner ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Nerve Activity

We investigated the time-dependent modulation of arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) that occurs during isometric handgrip exercise (IHG). Thirteen healthy subjects performed a 3-min IHG at 30% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). The ABR control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between spontaneous variations in diastolic arterial pressure (DAP) and MSNA during supine rest, at each minute of IHG, and during PEMI. We found that 1) the linear relations between DAP and MSNA variables were shifted progressively rightward until the third minute of IHG (IHG3); 2) 2 min into IHG (IHG2), the DAP-MSNA relations were shifted upward and were shifted further upward at IHG3; 3) the sensitivity of the ABR control of total MSNA was increased at IHG2 and increased further at IHG3; and 4) during PEMI, the ABR operating pressure was slightly higher than at IHG2, and the sensitivity of the control of total MSNA was the same as at IHG2. During PEMI, the DAP-burst strength and DAP-total MSNA relations were shifted downward from the IHG3 level to the IHG2 level, whereas the DAP-burst incidence relation remained at the IHG3 level. These results indicate that during IHG, ABR control of MSNA is modulated in a time-dependent manner. We suggest that this modulation of ABR function is one of the mechanisms underlying the progressive increase in blood pressure and MSNA during the course of isometric exercise.

Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans

2001 ◽  
Vol 280 (3) ◽  
pp. H1383-H1390 ◽  
Author(s):  
P. J. Fadel ◽  
S. Ogoh ◽  
D. E. Watenpaugh ◽  
W. Wasmund ◽  
A. Olivencia-Yurvati ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Dynamic Exercise ◽  
Moderate Intensity ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Arm Cycling ◽  
Carotid Baroreflex ◽  
Neck Pressure

We sought to determine whether carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) was altered during dynamic exercise. In five men and three women, 23.8 ± 0.7 (SE) yr of age, CBR function was evaluated at rest and during 20 min of arm cycling at 50% peak O2uptake using 5-s periods of neck pressure and neck suction. From rest to steady-state arm cycling, mean arterial pressure (MAP) was significantly increased from 90.0 ± 2.7 to 118.7 ± 3.6 mmHg and MSNA burst frequency (microneurography at the peroneal nerve) was elevated by 51 ± 14% ( P < 0.01). However, despite the marked increases in MAP and MSNA during exercise, CBR-Δ%MSNA responses elicited by the application of various levels of neck pressure and neck suction ranging from +45 to −80 Torr were not significantly different from those at rest. Furthermore, estimated baroreflex sensitivity for the control of MSNA at rest was the same as during exercise ( P = 0.74) across the range of neck chamber pressures. Thus CBR control of sympathetic nerve activity appears to be preserved during moderate-intensity dynamic exercise.

scholarly journals Sympathetic nerve activity and whole body heat stress in humans

2011 ◽  
Vol 111 (5) ◽  
pp. 1329-1334 ◽  
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 ◽  
Total Activity ◽  
Whole Body ◽  
Internal Temperature ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Mean Body Temperature ◽  
Arterial Blood

We and others have shown that moderate passive whole body heating (i.e., increased internal temperature ∼0.7°C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature ∼1.3°C, while either MSNA ( n = 8) or SSNA ( n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Δ∼5°C, P < 0.001), internal temperature (Δ∼1.3°C, P < 0.001), mean body temperature (Δ∼2.0°C, P < 0.001), heart rate (Δ∼40 beats/min, P < 0.001), and cutaneous vascular conductance [Δ∼1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained ( P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Δ core temperature 0.63 ± 0.01°C) when expressed as burst frequency (26 ± 14 to 45 ± 16 bursts/min, P = 0.001), burst incidence (39 ± 13 to 48 ± 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 ± 170 to 489 ± 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 ± 15 bursts/min, P = 0.01; burst incidence: 56 ± 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 ± 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 ± 472 to mid heat stress 6,467 ± 5,256 units/min, P = 0.03) and continued to increase until the end of heat stress (11,217 ± 6,684 units/min, P = 0.002 vs. mid-heat stress). These results indicate that both MSNA and SSNA continue to increase as internal temperature is elevated above previously reported values.

Sign in / Sign up

Export Citation Format

Share Document