scholarly journals Central Command Increases Muscle Sympathetic Nerve Activity More to Contracting than Non‐Contracting Muscle during Unloaded Rhythmic Exercise in Humans

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Chloe E Taylor ◽  
Daniel Boulton ◽  
Erin Howden ◽  
Christoph Siebenmann ◽  
Vaughan G Macefield
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Central Command ◽  
Nerve Activity ◽  
Contracting Muscle ◽  
Rhythmic Exercise ◽  
Exercise In Humans

scholarly journals Central command increases muscle sympathetic nerve activity more to contracting than noncontracting muscle during rhythmic isotonic leg exercise

2019 ◽  
Vol 121 (5) ◽  
pp. 1704-1710 ◽  
Author(s):  
Chloe E. Taylor ◽  
Daniel Boulton ◽  
Erin J. Howden ◽  
Christoph Siebenmann ◽  
Vaughan G. Macefield
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Electromyographic Activity ◽  
Central Command ◽  
Nerve Activity ◽  
Contracting Muscle ◽  
Contraction Phase ◽  
Isotonic Exercise

We have previously shown that the increase in muscle sympathetic nerve activity (MSNA) to contracting muscle during sustained isometric exercise is due primarily to central command and that contracting muscle does not express a metaboreceptor-driven increase in MSNA. Here we tested the hypothesis that MSNA increases to the contracting muscle also during rhythmic isotonic exercise, in which muscle metabolites will not accumulate because the contraction is performed without external load. MSNA was recorded from the common peroneal nerve in 10 participants, and negative-going sympathetic spikes were extracted during 50 cycles of sinusoidal (0.15 Hz) isotonic dorsiflexions of the ipsilateral or contralateral ankle. Electromyographic activity (EMG) was recorded from the tibialis anterior muscle on both sides. Cross-correlation analysis between MSNA and EMG revealed a marked cyclic modulation of MSNA to the contracting (ipsilateral) muscle. This modulation, in which MSNA increased during the contraction phase, was three times greater than that to the noncontracting muscle (modulation index = 27.4 ± 3.2% vs. 9.2 ± 1.5%; P < 0.002). There were no differences in either the intensity or the magnitude of modulation of EMG during ipsilateral and contralateral contractions. We conclude that central command increases MSNA to the contracting muscle during rhythmic isotonic exercise. NEW & NOTEWORTHY Muscle sympathetic nerve activity (MSNA) increases to contracting muscle during isometric exercise, but whether this occurs during rhythmic isotonic exercise is unknown. We recorded MSNA to the pretibial flexors during cyclic dorsiflexion of the ipsilateral or contralateral ankle. MSNA showed a cyclic increase during the contraction phase that was significantly higher to the contracting than the noncontracting muscle, supporting central command as the primary mechanism responsible for increasing MSNA.

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 The Role of Central Command in the Increase in Muscle Sympathetic Nerve Activity to Contracting Muscle During High Intensity Isometric Exercise

2021 ◽  
Vol 15 ◽  
Author(s):  
Daniel Boulton ◽  
Chloe E. Taylor ◽  
Simon Green ◽  
Vaughan G. Macefield
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Dependent Manner ◽  
Nerve Activity ◽  
Contracting Muscle ◽  
Tungsten Microelectrode ◽  
The Right

We previously demonstrated that muscle sympathetic nerve activity (MSNA) increases to contracting muscle as well as to non-contracting muscle, but this was only assessed during isometric exercise at ∼10% of maximum voluntary contraction (MVC). Given that high-intensity isometric contractions will release more metabolites, we tested the hypothesis that the metaboreflex is expressed in the contracting muscle during high-intensity but not low-intensity exercise. MSNA was recorded continuously via a tungsten microelectrode inserted percutaneously into the right common peroneal nerve in 12 participants, performing isometric dorsiflexion of the right ankle at 10, 20, 30, 40, and 50% MVC for 2 min. Contractions were immediately followed by 6 min of post-exercise ischemia (PEI); 6 min of recovery separated contractions. Cross-correlation analysis was performed between the negative-going sympathetic spikes of the raw neurogram and the ECG. MSNA increased as contraction intensity increased, reaching mean values (± SD) of 207 ± 210 spikes/min at 10% MVC (P = 0.04), 270 ± 189 spikes/min at 20% MVC (P &lt; 0.01), 538 ± 329 spikes/min at 30% MVC (P &lt; 0.01), 816 ± 551 spikes/min at 40% MVC (P &lt; 0.01), and 1,097 ± 782 spikes/min at 50% MVC (P &lt; 0.01). Mean arterial pressure also increased in an intensity-dependent manner from 76 ± 3 mmHg at rest to 90 ± 6 mmHg (P &lt; 0.01) during contractions of 50% MVC. At all contraction intensities, blood pressure remained elevated during PEI, but MSNA returned to pre-contraction levels, indicating that the metaboreflex does not contribute to the increase in MSNA to contracting muscle even at these high contraction intensities.

scholarly journals Muscle sympathetic nerve responses to passive and active one-legged cycling: insights into the contributions of central command

2018 ◽  
Vol 314 (1) ◽  
pp. H3-H10 ◽  
Author(s):  
Connor J. Doherty ◽  
Anthony V. Incognito ◽  
Karambir Notay ◽  
Matthew J. Burns ◽  
Joshua T. Slysz ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Central Command ◽  
Arterial Baroreflex ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Low Intensity ◽  
Leg Exercise

The contribution of central command to the peripheral vasoconstrictor response during exercise has been investigated using primarily handgrip exercise. The purpose of the present study was to compare muscle sympathetic nerve activity (MSNA) responses during passive (involuntary) and active (voluntary) zero-load cycling to gain insights into the effects of central command on sympathetic outflow during dynamic exercise. Hemodynamic measurements and contralateral leg MSNA (microneurography) data were collected in 18 young healthy participants at rest and during 2 min of passive and active zero-load one-legged cycling. Arterial baroreflex control of MSNA burst occurrence and burst area were calculated separately in the time domain. Blood pressure and stroke volume increased during exercise ( P < 0.0001) but were not different between passive and active cycling ( P > 0.05). In contrast, heart rate, cardiac output, and total vascular conductance were greater during the first and second minute of active cycling ( P < 0.001). MSNA burst frequency and incidence decreased during passive and active cycling ( P < 0.0001), but no differences were detected between exercise modes ( P > 0.05). Reductions in total MSNA were attenuated during the first ( P < 0.0001) and second ( P = 0.0004) minute of active compared with passive cycling, in concert with increased MSNA burst amplitude ( P = 0.02 and P = 0.005, respectively). The sensitivity of arterial baroreflex control of MSNA burst occurrence was lower during active than passive cycling ( P = 0.01), while control of MSNA burst strength was unchanged ( P > 0.05). These results suggest that central feedforward mechanisms are involved primarily in modulating the strength, but not the occurrence, of a sympathetic burst during low-intensity dynamic leg exercise. NEW & NOTEWORTHY Muscle sympathetic nerve activity burst frequency decreased equally during passive and active cycling, but reductions in total muscle sympathetic nerve activity were attenuated during active cycling. These results suggest that central command primarily regulates the strength, not the occurrence, of a muscle sympathetic burst during low-intensity dynamic leg exercise.

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