Abstract
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.
Highlights
Exposing tissue to repeated periods of brief circulatory occlusion, termed ischemic preconditioning (IPC), has been shown to protect the myocardium (Murry et al.1986, 1990) and skeletal muscle (Pang et al 1995; Addison et al 2003) against subsequent ischemia–reperfusion injury
High-quality muscle sympathetic nerve activity (MSNA) recordings were obtained in 29 of 37 participants, while in the remaining eight participants we were unable to locate a recording site. In those with microneurographic recordings (n = 29), the MSNA signal was lost in three participants after PECO before (PRE) and re-established prior to POST
The present study is the first to investigate the effects of Ischemic preconditioning (IPC) on a direct measure of central sympathetic outflow during exercise and isolated muscle metaboreflex activation
Summary
Exposing tissue to repeated periods of brief circulatory occlusion, termed ischemic preconditioning (IPC), has been shown to protect the myocardium (Murry et al.1986, 1990) and skeletal muscle (Pang et al 1995; Addison et al 2003) against subsequent ischemia–reperfusion injury. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. One mechanism hypothesized to account for the observed exercise benefits is reduced stimulation of metabolically sensitive small diameter skeletal muscle afferents (Crisafulli et al 2011; Cruz et al 2016, 2017; Salvador et al 2016). Feedback from thinly myelinated group III/IV muscle afferents can induce central fatigue (Sidhu et al 2014) and inhibit a-motor neuron activation (Gandevia 2001; Amann et al 2015) explaining prior observations of IPC-mediated reductions in ratings of perceived exertion (Bailey et al 2012; Cruz et al 2015) and increases in electromyographic activity (Cruz et al 2015, 2016) during exercise
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