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Pain arising from exercise potentiates fatigue and impairs the performance of endurance exercise. We assessed neurophysiological and perceptual responses to endurance exercise performed under experimentally induced muscle pain by a model that separates muscle pain from muscle fatigue. After a series of pilot studies investigating different hypertonic saline volumes, 17 healthy males performed a preliminary VO 2PEAK test before performing a familiarization of the cycling time-to-exhaustion exercise (80% of the peak power output in the VO 2PEAK test). Participants, performed a baseline exercise session before the sessions with hypertonic and isotonic saline injections in the vastus lateralis of both legs, in a crossover and counterbalanced design. Neurophysiological and perceptual responses such as electroencephalography (EEG) in frontal, prefrontal, parietal, and motor cortex, electromyography (EMG) of the vastus lateralis and biceps femoris muscles, ratings of perceived exertion (RPE), pain sensation, and affective valence were measured at rest and during exercise. The hypertonic injection reduced the resting EEG alpha-beta ratio in the frontal and prefrontal cortex. When compared to exercise performed after the isotonic injection (430.5 ± 152.6 s), hypertonic injection shortened the time-to-exhaustion (357.5 ± 173.0 s), reduced the EMG of the assessed muscles, and increased the muscle co-contraction during exercise. The hypertonic injection also reduced the EEG alpha-beta ratio in the prefrontal and parietal cortex, increased RPE and pain sensation, and reduced affective valence during exercise. This proof-of-concept study showed that hypertonic injection-induced muscle pain reduced endurance performance, promoting centrally mediated alterations in motor command and cortical activation, as well as an interplay of perceptual responses., (© 2021 Society for Psychophysiological Research.)

The central and peripheral effects of caffeine remain debatable. We verified whether increases in endurance performance after caffeine ingestion occurred together with changes in primary motor cortex (MC) and prefrontal cortex (PFC) activation, neuromuscular efficiency (NME), and electroencephalography-electromyography coherence (EEG-EMG coherence). Twelve participants performed a time-to-task failure isometric contraction at 70% of the maximal voluntary contraction after ingesting 5 mg/kg of caffeine (CAF) or placebo (PLA), in a crossover and counterbalanced design. MC (Cz) and PFC (Fp1) EEG alpha wave and vastus lateralis (VL) muscle EMG were recorded throughout the exercise. EEG-EMG coherence was calculated through the magnitude squared coherence analysis in MC EEG gamma-wave (CI > 0.0058). Moreover, NME was obtained as the force-VL EMG ratio. When compared to PLA, CAF improved the time to task failure ( p = 0.003, d = 0.75), but reduced activation in MC and PFC throughout the exercise ( p = 0.027, d = 1.01 and p = 0.045, d = 0.95, respectively). Neither NME ( p = 0.802, d = 0.34) nor EEG-EMG coherence ( p = 0.628, d = 0.21) was different between CAF and PLA. The results suggest that CAF improved muscular performance through a modified central nervous system (CNS) response rather than through alterations in peripheral muscle or central-peripheral coupling.