Introduction:
Prior exercise, also known as “priming”, is suspected to affect the cardiovascular as well as muscular system (Jones, Koppo, & Burnley, 2003; Layec et al., 2009; Poole, Barstow, McDonough, & Jones, 2008). Many previous studies investigated metabolic processes that are affected by priming. But only a few studies referred prior exercise to muscular fatigue due to difficulties in inducing and measuring muscular fatigue with respect to the cardiovascular system (Maturana, Peyrard, Temesi, Millet, & Murias, 2017). It is supposed that improving local oxygen availability and utilization by prior exercise might improve the resistance against muscular fatigue (DiMenna et al., 2010). Therefore, the aim of this study was to assess (1) the effect of prior exercise on muscle oxygenation and (2) its influence on muscular fatigue after an all-out knee extension protocol.
Methods:
In a randomized cross-over design, 15 healthy males performed two times an all-out knee extension protocol in a motor driven, isokinetic dynamometer (D. & R. Ferstl GmbH, Hemau, Germany). After an unspecific warm-up, peak torque of maximum voluntary contraction (MVC), maximum voluntary activation level (MVA) and potentiated twitch torque were determined as baseline using the interpolated twitch technique (Gandevia, 2001). While 15 min passive rest were set in the control condition, priming exercise, clocked box jumps (30 cm high, 60 s, 80 bpm), and further fatigue measurements (MVC combined with ITT) were executed in the priming condition. To evolve the priming effects participants recovered for 15 min. After the resting phase, the participants performed 60 s of dynamic, all-out knee extension (concentric – eccentric) in both conditions. Immediately after the all-out exercise, the participants fulfilled the final interpolated twitch measurement to receive information about possible effects of priming exercise on muscular fatigue.
Torque measurement, electromyography (Myon AG, Schwarzenberg Swiss) and near-infrared spectroscopy (NIRS, Artinis Medical Systems B.V., Elst, Netherlands) were used during the knee extension protocol to understand muscle activation and oxygenation. In this context, relative changes in deoxygenated hemoglobin (HHb) describe the dynamic balance between muscle oxygen consumption and availability (A. M. Jones, Koppo, & Burnley, 2003; Layec et al., 2009; Poole, Barstow, McDonough, & Jones, 2008). Muscle oxygenation response kinetics were fitted using a mono-exponential model regarding baseline, amplitude, time delay and time constant.
Results:
Central and peripheral fatigue after the knee extension exercise was not affected by priming box jumps and therefore no significant effect between the conditions was shown. While MVA level remained constant during the whole experiment, peak MVC as well as potentiated twitch torque decreased significantly between baseline, after priming and after all out exercise measurement (Fig. 2 A). Muscle oxygenation kinetics during the all-out exercise did not differ between both conditions nether in modeled output nor in average time course of HHb (Fig. 2 B). Angular momentum as well as muscle activation frequency declined in both conditions, while integrated EMG decreased only in non-primed control condition.
Discussion:
It was shown that priming exercise did not affect neither muscular fatigue nor muscle oxygenation. As one of the first studies, fatigue was induced and measured in a highly standardized but also isolated setup. Improvements in primed oxygen delivery, e.g. vasodilation and increased oxygen dissociation (A. M. Jones et al., 2003), might be compensated by high muscular pressure and thus occlusion of smaller vessels induced by all-out muscle activation. With limited oxidative glycolysis and maximum muscle activation a high amount of anaerobic metabolism, i.e. phosphocreatine (PCr) breakdown and anaerobic glycolysis, the all-out intensity itself inhibits priming effects on muscle fatigue (Broxterman, Layec, Hureau, Amann, & Richardson, 2017). Although PCr was not directly measured, almost the same MVC peak torque as well as potentiated twitch torques indicate that PCr breakdown might be identical in both conditions (Fig. 2). Consequently, prior exercise should aim to increase phosphocreatine storage and improve oxidative ATP synthesis (Layec et al., 2009).
In this study, the combination of prior exercise, recovery duration and intensity of fatiguing task might depress possible effects, which must be adapted in further research. Intermittent, maximum intensity exercise or submaximal (e.g. 30% MVC), continuous exercise might allow possible priming effects in microvascular oxygen supply and thus increase aerobic metabolism to save high energy phosphates i.e. PCr. Furthermore, the onset of muscle deoxygenation response was difficult to model with the mono-exponential function that is used in many studies investigating onset kinetics. Because the time delay was determined by the fit and was not supposed to be a constant like in VO2 modelling, the primary response is overestimated in some participants.