Abstract
Abstract Introduction This study describes macro- and micro- sleep responses to a myotoxic skeletal muscle injury and investigates possible mechanisms. Methods We recorded the electroencephalogram(EEG)/electromyogram(EMG) of 24 wistar rats before and after induction of Tibialis Anterior muscle injury (n=8 per group: control, control +buprenorphine and injured). A top-down analysis of sleep characteristics was processed from total sleep time (TST), sleep stages, sleep stability, spectral-analysis, and spindles. To further investigate the mechanisms involved, we analyzed the protein level of sleep regulatory molecules including TNF-α, IL-1β, IGF-1, BMAL1 in plasma, frontal cortex, hippocampus, and tibialis anterior, collected at Day +2 after injury from non-EEG/EMG implanted rats. Results Muscle injury induces a significant increase in total sleep time at 48 and 72h post-injury, specific to NREM sleep. These increases occur during the dark period and are associated with higher stability of sleep over 24h, without change in the different power/frequency spectral bands of NREM/REM sleep. There was no corresponding sleep increase in slow-wave activity or spindle density, nor were there changes in brain levels of the sleep-regulating proinflammatory cytokine IL-1β, which is otherwise involved in the local response to injury. Conversely, decreased protein levels of brain IGF-1 and muscle BMAL1, a core circadian clock gene, after injury may play a role in increased sleep time. Conclusion Muscle injury induces an increase in total sleep time at 48- and 72-hours post-injury, specific to NREM sleep during the dark period in rats and is associated with higher sleep stability over 24 hours. Support (if any)
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