Interaction of Central and Peripheral Factors during Repeated Sprints at Different Levels of Arterial O2 Saturation

François Billaut,David T Martin,David J Bishop,Ramon F Rodriguez,Jarrod P Kerris,Christopher J Gore,Stephen E Alway

doi:10.1371/journal.pone.0077297

François Billaut, David T Martin + Show 5 more

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https://doi.org/10.1371/journal.pone.0077297

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Abstract

PurposeTo investigate the interaction between the development of peripheral locomotor muscle fatigue, muscle recruitment and performance during repeated-sprint exercise (RSE).MethodIn a single-blind, randomised and cross-over design, ten male team-sport athletes performed two RSE (fifteen 5-s cycling sprints interspersed with 25 s of rest; power self-selected) in normoxia and in acute moderate hypoxia (FIO2 0.138). Mechanical work, total electromyographic intensity (summed quadriceps electromyograms, RMSsum) and muscle (vastus lateralis) and pre-fontal cortex near-infrared spectroscopy (NIRS) parameters were calculated for every sprint. Blood lactate concentration ([Lac-]) was measured throughout the protocol. Peripheral quadriceps fatigue was assessed via changes in potentiated quadriceps twitch force (ΔQtw,pot) pre- versus post-exercise in response to supra-maximal magnetic femoral nerve stimulation. The central activation ratio (QCAR) was used to quantify completeness of quadriceps activation.ResultsCompared with normoxia, hypoxia reduced arterial oxygen saturation (-13.7%, P=0.001), quadriceps RMSsum (-13.7%, P=0.022), QCAR (-3.3%, P=0.041) and total mechanical work (-8.3%, P=0.019). However, the magnitude of quadriceps fatigue induced by RSE was similar in the two conditions (ΔQtw,pot: -53.5% and -55.1%, P=0.71). The lower cycling performance in hypoxia occurred despite similar metabolic (muscle NIRS parameters and blood [Lac-]) and functional (twitch and M-wave) muscle states.ConclusionResults suggest that the central nervous system regulates quadriceps muscle recruitment and, thereby, performance to limit the development of muscle fatigue during intermittent, short sprints. This finding highlights the complex interaction between muscular perturbations and neural adjustments during sprint exercise, and further supports the presence of pacing during intermittent sprint exercise.

Highlights

Arterial hypoxemia influences maximal aerobic power and endurance exercise performance [1,2,3]
It has been shown that the central motor output, as indicated by changes in power output and muscle electromyographic (EMG) activity, is reduced during most of a high-intensity cycling time trial performed in moderate hypoxia, compared with normoxia, but that the amount of peripheral muscle fatigue developed at end-exercise is similar in both conditions [4]
Summary of main findings We examined the interaction of peripheral and central mechanisms during short, intermittent bouts of sprints by investigating the influence of arterial hypoxemia on muscle recruitment, cycling performance and the development of peripheral locomotor muscle fatigue

Summary

Introduction

Arterial hypoxemia influences maximal aerobic power and endurance exercise performance [1,2,3]. It has been shown that the central motor output, as indicated by changes in power output and muscle electromyographic (EMG) activity, is reduced (and performance time is lengthened) during most of a high-intensity cycling time trial performed in moderate hypoxia, compared with normoxia, but that the amount of peripheral muscle fatigue developed at end-exercise (assessed via quadriceps twitch force) is similar in both conditions [4] This muscle de-recruitment by the central nervous system (CNS) in anticipation of the end of the exercise could limit the development of locomotor muscle fatigue, and, presumably, increase the likelihood of optimal performance [7,8,9]. These observations have led to the theoretical proposition that peripheral muscle fatigue may be regulated during whole-body, high-intensity exercise (for review see 10)

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