Abstract

To determine whether task failure during incremental exercise to exhaustion (IE) is principally due to reduced neural drive and increased metaboreflex activation eleven men (22 ± 2 years) performed a 10 s control isokinetic sprint (IS; 80 rpm) after a short warm-up. This was immediately followed by an IE in normoxia (Nx, PIO2:143 mmHg) and hypoxia (Hyp, PIO2:73 mmHg) in random order, separated by a 120 min resting period. At exhaustion, the circulation of both legs was occluded instantaneously (300 mmHg) during 10 or 60 s to impede recovery and increase metaboreflex activation. This was immediately followed by an IS with open circulation. Electromyographic recordings were obtained from the vastus medialis and lateralis. Muscle biopsies and blood gases were obtained in separate experiments. During the last 10 s of the IE, pulmonary ventilation, VO2, power output and muscle activation were lower in hypoxia than in normoxia, while pedaling rate was similar. Compared to the control sprint, performance (IS-Wpeak) was reduced to a greater extent after the IE-Nx (11% lower P < 0.05) than IE-Hyp. The root mean square (EMGRMS) was reduced by 38 and 27% during IS performed after IE-Nx and IE-Hyp, respectively (Nx vs. Hyp: P < 0.05). Post-ischemia IS-EMGRMS values were higher than during the last 10 s of IE. Sprint exercise mean (IS-MPF) and median (IS-MdPF) power frequencies, and burst duration, were more reduced after IE-Nx than IE-Hyp (P < 0.05). Despite increased muscle lactate accumulation, acidification, and metaboreflex activation from 10 to 60 s of ischemia, IS-Wmean (+23%) and burst duration (+10%) increased, while IS-EMGRMS decreased (−24%, P < 0.05), with IS-MPF and IS-MdPF remaining unchanged. In conclusion, close to task failure, muscle activation is lower in hypoxia than in normoxia. Task failure is predominantly caused by central mechanisms, which recover to great extent within 1 min even when the legs remain ischemic. There is dissociation between the recovery of EMGRMS and performance. The reduction of surface electromyogram MPF, MdPF and burst duration due to fatigue is associated but not caused by muscle acidification and lactate accumulation. Despite metaboreflex stimulation, muscle activation and power output recovers partly in ischemia indicating that metaboreflex activation has a minor impact on sprint performance.

Highlights

  • Muscle fatigue has been defined as “any exercise-induced reduction in the ability to exert muscle force or power, regardless of whether the task can be sustained (BiglandRitchie and Woods, 1984), that can be reversed by rest” (Gandevia, 2001)

  • From the 10th to 60th s of ischemia muscle lactate was increased by 24.0 ± 20.7 and 21.6 ± 24.5 mmol kg d.w.−1, and muscle pH reduced by 0.102 ± 0.040 and 0.109 ± 0.041 units, after the Incremental exercise to exhaustion (IE) in normoxia and hypoxia, respectively (ANOVA time effect: P < 0.01). This investigation confirms, in agreement with previous studies using constant intensity (Marcora and Staiano, 2010) and incremental exercise to exhaustion in normoxia (Coelho et al, 2015), that task failure during incremental exercise in normoxia is not caused by muscle fatigue

  • The present study extends these findings to whole-body incremental exercise in severe hypoxia

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Summary

Introduction

Muscle fatigue has been defined as “any exercise-induced reduction in the ability to exert muscle force or power, regardless of whether the task can be sustained (BiglandRitchie and Woods, 1984), that can be reversed by rest” (Gandevia, 2001). During constantintensity or incremental exercise to exhaustion in severe hypoxia (PIO2 ≈ 75 mmHg), muscle fatigue is swiftly relieved by mild hyperoxic gas or room air (Kayser et al, 1994; Calbet et al, 2003a,b; Amann et al, 2007). These findings led to the concept that during incremental exercise to exhaustion in normoxia, task

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