Autonomic responses to exercise: Cortical and subcortical responses during post-exercise ischaemia and muscle pain

Macefield, Vaughan G.; Henderson, Luke A.

doi:10.1016/j.autneu.2014.10.021

Cited by 21 publications

(23 citation statements)

References 57 publications

(76 reference statements)

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“…The observed increase in MAP after I/R resembles previous reports in other models of ischemic insult 13,14,52,55,56 . However, this is the first report where unilaterally targeting a neurotrophic factor or its receptor, prevented the development of exacerbated EPRs post injury.…”

Section: Discussionsupporting

confidence: 89%

A dual role for peripheral GDNF signaling in nociception and cardiovascular reflexes

Queme

Weyler

Cohen

et al. 2019

Preprint

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Group III/IV muscle afferents transduce nociceptive signals and modulate exercise pressor reflexes (EPR).However, the mechanisms governing afferent responsiveness to dually modulate these processes are not well characterized. We and others have shown that ischemic injury can induce both nociception-related behaviors and exacerbated EPRs in the same mice. This correlated with primary muscle afferent sensitization and increased expression of glial cell line-derived neurotrophic factor (GDNF) in injured muscle and increased expression of GDNF family receptor α1 (GFRα1) in DRGs. Here we report that increased GDNF/GFR1 signaling to sensory neurons from ischemia/reperfusion affected muscle modulated nociceptive-like behaviors, increased EPRs, and group III/IV muscle afferent sensitization. This appeared to have taken effect through increased CREB/CREB-binding protein mediated expression of the purinergic receptor P2X5 in the DRGs.Muscle GDNF signaling to neurons may play an important dual role in nociception and sympathetic reflexes and could provide a novel therapeutic target for treating complications from ischemic injuries.

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Section: Discussionsupporting

confidence: 89%

A dual role for peripheral GDNF signaling in nociception and cardiovascular reflexes

Queme

Weyler

Cohen

et al. 2019

Preprint

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“…A sustained metaboreflex-mediated increased in MSNA to the non-contracting muscle and mean arterial pressure, but not heart rate, during post-exercise ischaemia was observed in the present study and has been well documented (Mitchell et al 1980;Victor et al 1988;Ray et al 1992;Macefield & Henderson, 2015). However, MSNA to the contracting muscle was not affected by post-exercise ischaemia, returning to pre-contraction levels within 1 min of the cessation of contraction, and indicating that the metaboreflex was not expressed to the contracting muscle.…”

Section: Effect Of Ischaemia On Msna During and After Contractionsupporting

confidence: 69%

“…; Ray et al . ; Macefield & Henderson, ). However, MSNA to the contracting muscle was not affected by post‐exercise ischaemia, returning to pre‐contraction levels within 1 min of the cessation of contraction, and indicating that the metaboreflex was not expressed to the contracting muscle.…”

Section: Discussionmentioning

confidence: 99%

The metaboreflex does not contribute to the increase in muscle sympathetic nerve activity to contracting muscle during static exercise in humans

Boulton

Taylor

Green

et al. 2018

The Journal of Physiology

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Both central command and metaboreflex inputs from contracting muscles increase muscle sympathetic nerve activity (MSNA) to non-contracting muscle during sustained isometric exercise. We recently showed that MSNA to contracting muscle also increases in an intensity-dependent manner, although whether this can be sustained by the metaboreflex is unknown. MSNA was recorded from the left common peroneal nerve and individual spikes of MSNA extracted from the nerve signal. Eleven subjects performed a series of 4 min dorsiflexions of the left ankle at 10% of maximum voluntary contraction under three conditions: without ischaemia, with 6 min of post-exercise ischaemia, and with ischaemia during and after exercise; these were repeated in the right leg. Compared with pre-contraction values, MSNA to the contracting muscles increased and plateaued in the first minute of contraction (50 ± 18 vs. 34 ± 10 spikes min , P = 0.01), returned to pre-contraction levels within 1 min of the contraction ending and was not influenced by ischaemia during or after contraction. Conversely, MSNA to the non-contracting muscles was not different from pre-contraction levels in the first minute of contraction (34 ± 9 vs. 32 ± 5 spikes min , P = 0.48), whereas it increased each minute and was significantly greater by the second minute (44 ± 8 spikes min , P = 0.01). Ischaemia augmented the MSNA response to contraction (63 ± 25 spikes min after 4 min, P < 0.05) and post-exercise ischaemia (63 ± 27 spikes min after 6 min, P < 0.01) for the non-contracting muscles only. These findings support our conclusion that the metaboreflex is not expressed in the contracting muscle during sustained static exercise.

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“…), although not tested specifically in skeletal muscle. Notwithstanding that PECO procedures can also activate central pain pathways (Macefield and Henderson ), SHG at 30% MVC has been shown consistently to increase MSNA during the second minute of contraction coincident with increased metabolite accumulation (a more rapid response as compared to prolonged ischemia), which is maintained during isolation of the metaboreflex with PECO (Mitchell et al. ; Victor et al.…”

Section: Discussionmentioning

confidence: 99%

Ischemic preconditioning does not alter muscle sympathetic responses to static handgrip and metaboreflex activation in young healthy men

et al. 2017

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Ischemic preconditioning (IPC) has been hypothesized to elicit ergogenic effects by reducing feedback from metabolically sensitive group III/IV muscle afferents during exercise. If so, reflex efferent neural outflow should be attenuated. We investigated the effects of IPC on muscle sympathetic nerve activity (MSNA) during static handgrip (SHG) and used post‐exercise circulatory occlusion (PECO) to isolate for the muscle metaboreflex. Thirty‐seven healthy men (age: 24 ± 5 years [mean ± SD]) were randomized to receive sham (n = 16) or IPC (n = 21) interventions. Blood pressure, heart rate, and MSNA (microneurography; sham n = 11 and IPC n = 18) were collected at rest and during 2 min of SHG (30% maximal voluntary contraction) and 3 min of PECO before (PRE) and after (POST) sham or IPC treatment (3 × 5 min 20 mmHg or 200 mmHg unilateral upper arm cuff inflation). Resting mean arterial pressure was higher following sham (79 ± 7 vs. 83 ± 6 mmHg, P < 0.01) but not IPC (81 ± 6 vs. 82 ± 6 mmHg, P > 0.05), while resting MSNA burst frequency was unchanged (P > 0.05) with sham (18 ± 7 vs. 19 ± 9 bursts/min) or IPC (17 ± 7 vs. 19 ± 7 bursts/min). Mean arterial pressure, heart rate, stroke volume, cardiac output, and total vascular conductance responses during SHG and PECO were comparable PRE and POST following sham and IPC (All P > 0.05). Similarly, MSNA burst frequency, burst incidence, and total MSNA responses during SHG and PECO were comparable PRE and POST with sham and IPC (All P > 0.05). These findings demonstrate that IPC does not reduce hemodynamic responses or central sympathetic outflow directed toward the skeletal muscle during activation of the muscle metaboreflex using static exercise or subsequent PECO.

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Autonomic responses to exercise: Cortical and subcortical responses during post-exercise ischaemia and muscle pain

Cited by 21 publications

References 57 publications

A dual role for peripheral GDNF signaling in nociception and cardiovascular reflexes

A dual role for peripheral GDNF signaling in nociception and cardiovascular reflexes

The metaboreflex does not contribute to the increase in muscle sympathetic nerve activity to contracting muscle during static exercise in humans

Ischemic preconditioning does not alter muscle sympathetic responses to static handgrip and metaboreflex activation in young healthy men

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