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Previous evidence suggests that though N-acetylcysteine (NAC) supplementation following eccentric exercise-induced muscle damage disrupts the skeletal muscle's repair and remodelling process at 8 days of recovery, it attenuates substantially the decline of skeletal muscle performance during the first 48 hours of recovery. The enhanced performance capacity during the first phase of recovery in response to NAC supplementation might be attributed to the altered redox status in skeletal muscle as a consequence of the NAC-mediated elevation of reduced glutathione (GSH) levels. The rise in GSH results in a redox-dependent attenuation of immune cell mobilisation and reduction of oxidative stress response, leading to a blunted rise of muscle damage and inflammatory markers during the first 2-3 days of recovery. However, following exercise-induced muscle damage, protein synthesis increases in ske
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