As a vital locomotor organ in the human body, skeletal muscle plays a crucial role in sustaining life, and the maintenance of its homeostasis is fundamental to the proper execution of various physiological functions. Exercise influences skeletal muscle through multiple mechanisms, notably by regulating muscle protein synthesis and degradation, and by modulating metabolic balance, thereby contributing significantly to the maintenance of skeletal muscle homeostasis. However, the specific mechanisms by which exercise maintains skeletal muscle homeostasis have not yet been fully elucidated. Notably, high-intensity exercise promotes glycolysis within skeletal muscle, resulting in lactate production. Recent studies, however, have revealed a new perspective: lactate can serve as a donor for protein lactylation, modifying both histone and non-histone proteins. This modification plays a critical role in various physiological activities within skeletal muscle. In this context, this review summarizes recent research on lactate and lactylation, exploring their roles and potential mechanisms in maintaining skeletal muscle homeostasis, with the aim of providing novel insights and therapeutic targets for preventing and treating skeletal muscle-associated diseases through exercise.