Insufficient sleep causes muscle fatigue, impacting performance. The mechanism of brain–muscle signaling remains uncertain. In this study, we examined the impact of sleep deprivation on muscle endurance during isometric contractions and explored the changes in brain–muscle connectivity. Methods: The research involved 35 right-handed male participants who took part in an exercise test that included isometric contractions of the left and right biceps in both sleep-deprived and well-rested states. Muscle contraction duration and electroencephalogram (EEG) and electromyography (EMG) signals were recorded. Functional connectivity between brain regions was assessed using the phase locking value (PLV), while partial directed coherence (PDC) was used to analyze signal directionality between motor centers and muscles. Results: The connectivity strength between Brodmann areas (BAs) 1-5 and the right BA6, 8 regions was significantly decreased in the isometric contractions after sleep deprivation. Insufficient sleep enhanced the PDC signals from the motor center of the right brain to the left biceps, and it decreased the PDC signals from both biceps to their opposite motor centers. Conclusions: Sleep deprivation shortened muscle isometric contraction duration by affecting the interaction between the somatosensory motor cortex and the right premotor cortex, reducing biceps feedback signal connectivity to the contralateral motor center in the brain.

This study investigated the effects of dietary restriction (DR) combined with aerobic exercise training (ET) on high-fat diet (HFD)-induced obesity and associated skeletal muscle impairment in male Sprague-Dawley rats, as well as the underlying mechanisms. An 8-week DR + ET intervention effectively increased the cross-sectional area and protein content of the soleus muscle. Both DR and ET alone promoted the activation of the IGF-1/Akt/mTOR signaling pathway and reduced the protein expression of peroxisome proliferator-activated receptor γ (PPARγ), a target of miR-130 in adipocytes, in HFD-induced obese rats. However, no additional benefit was observed with combined DR + ET treatment. Consistent with these findings, miR-130 expression was upregulated in the skeletal muscle of obese rats compared with those fed a normal diet, and this increase was significantly attenuated by DR, ET, or DR + ET, with DR + ET showing the strongest inhibitory effect. To further explore the role of miR-130 in skeletal muscle cells, L6 and C2C12 cells were transfected with miR-130 mimics. Overexpression of miR-130 markedly suppressed proliferation and differentiation in these cells, accompanied by reduced creatine kinase activity and decreased myogenin expression—both key markers of myogenic differentiation. Moreover, miR-130 overexpression inhibited the luciferase activity of a reporter vector containing the PPARγ-3′-UTR, and this inhibition was abolished by mutation of the PPARγ-3′-UTR, indicating a direct regulatory mechanism affecting protein synthesis in skeletal muscle. In summary, DR and ET each alleviated obesity-related skeletal muscle impairment by activating IGF-1/Akt/mTOR signaling and suppressing miR-130 expression, but their combination did not produce synergistic effects.