Heavy Intensity Priming Exercise Attenuates the Rate of Quadriceps Muscle Fatigue and Improves Time-to-Task Failure during Severe Intensity Cycling.

Background: Prior high-intensity exercise (priming) has been shown to accelerate the V̇O2 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 V̇O2 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 V̇O2 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 to control (391 ± 92 s) (P = 0.008). Relative oxidative contributions increased following priming (P = 0.001), while 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.