Abstract

PurposeThis study investigated the effect of ischemic preconditioning (IP) on metaboreflex activation following dynamic leg extension exercise in a group of healthy participants.MethodSeventeen healthy participants were recruited. IP and SHAM treatments (3 × 5 min cuff occlusion at 220 mmHg or 20 mmHg, respectively) were administered in a randomized order to the upper part of exercising leg’s thigh only. Muscle pain intensity (MP) and pain pressure threshold (PPT) were monitored while administrating IP and SHAM treatments. After 3 min of leg extension exercise at 70% of the maximal workload, a post-exercise muscle ischemia (PEMI) was performed to monitor the discharge group III/IV muscle afferents via metaboreflex activation. Hemodynamics were continuously recorded. MP was monitored during exercise and PEMI.ResultsIP significantly reduced mean arterial pressure compared to SHAM during metaboreflex activation (mean ± SD, 109.52 ± 7.25 vs. 102.36 ± 7.89 mmHg) which was probably the consequence of a reduced end diastolic volume (mean ± SD, 113.09 ± 14.25 vs. 102.42 ± 9.38 ml). MP was significantly higher during the IP compared to SHAM treatment, while no significant differences in PPT were found. MP did not change during exercise, but it was significantly lower during the PEMI following IP (5.10 ± 1.29 vs. 4.00 ± 1.54).ConclusionOur study demonstrated that IP reduces hemodynamic response during metaboreflex activation, while no effect on MP and PPT were found. The reduction in hemodynamic response was likely the consequence of a blunted venous return.

Highlights

  • Ischemic preconditioning (IP) is a non-invasive procedure involving three to four bouts of non-lethal ischemia commonly administered via 5 min cycles of circulatory occlusion and reperfusion by inflating and gradually deflating a blood pressure cuff placed around the limb

  • Our experiment shows that ischemic preconditioning reduces hemodynamic response and muscle pain of the knee extensor muscles during metaboreflex activation

  • Our results suggest that the reduction in metaboreflex activation seems to be caused by a blunted cardiac preload rather than a reduction of discharge from group III/IV muscle afferents

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Summary

Introduction

Ischemic preconditioning (IP) is a non-invasive procedure involving three to four bouts of non-lethal ischemia commonly administered via 5 min cycles of circulatory occlusion and reperfusion by inflating and gradually deflating a blood pressure cuff placed around the limb. Experimental studies described IP as a safe method to reduce infarct size and cardiac dysfunction in patients with stable angina during exercise (Kharbanda et al 2002; Crisafulli et al 2004b). Experimental studies reported beneficial effects on cardiac and skeletal muscle following IP administration. IP reduces cardiac tachyarrhythmias (Oxman et al 1997), myocardial infarct size (Kharbanda et al 2002) and ischemia–reperfusion injury in clinical settings (Loukogeorgakis et al 2005). Experimental studies investigating the effect of IP in the muscle reported an increase in PCr production and higher oxygen consumption (Andreas et al 2011), reduced glycogen depletion (Lintz et al 2013), reduced lactate production (Addison et al 2003) and attenuated ischemia-induced mitochondrial dysfunction (Mansour et al 2012)

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