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Published on: July 27, 2015
Heavy-Intensity Priming Exercise Attenuates the Rate of Quadriceps Muscle Fatigue and Improves Time-to-Task Failure
Keenan B MacDougall1, Saied J Aboodarda, Austin B Wickenberg
1Faculty of Kinesiology, University of Calgary, Calgary, CANADA.
Background:
Prior high-intensity exercise (priming) has been shown to accelerate the oxygen uptake (V̇O 2 ) kinetics, as well as improve exercise tolerance during subsequent high-intensity exercise, yet the mechanisms underpinning the performance changes are unclear. In theory, a reduced reliance on non-oxidative energy input afforded by the faster V̇O 2 response may improve subsequent performance by delaying muscle fatigue; however, this effect has yet to be conclusively shown.
Purpose:
Our purpose was to explore the impact of priming exercise on the energetic response, exercise tolerance, and the kinetics of muscle fatigue during severe-intensity cycling exercise.
Methods:
Fourteen participants completed constant power cycling trials in the severe domain, preceded by either a bout of heavy intensity or an equivalent duration cycling at 20 W. Muscle fatigue was assessed in real time via femoral nerve stimulation while pedaling, and energetic contributions were assessed via V̇O 2 and changes in blood lactate concentration. Quadriceps oxygenation and surface electromyography (EMG) were also measured.
Results:
Priming improved time-to-task failure (450 ± 74 s) compared with control (391 ± 92 s) ( P = 0.008). Relative oxidative contributions increased following priming ( P = 0.001), whereas the non-oxidative glycolytic contribution was reduced ( P < 0.0001), and this was accompanied by a reduction in the rate of quadriceps twitch force decline ( P = 0.041). Vastus lateralis EMG root mean square amplitude and M-wave amplitude increased across the trial similarly in both conditions, but priming resulted in a relative "downshift" in both measures ( P ≤ 0.027).
Conclusions:
Priming exercise resulted in an improvement in exercise tolerance, attenuation in muscle fatigue, and reduction in EMG and M-wave amplitude. We speculate that these effects may arise in part from the interaction between a reduction in metabolite accumulation and altered sarcolemmal excitability.
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