High-intensity interval training (HIIT) is a type of exercise characterized by short periods of time, high intensity, and short intervals of rest or recovery. Compared with aerobic exercise and resistance exercise, HIIT is more convenient and time-saving to regulate skeletal muscle mass and function, so it has attracted people’s attention. Current studies have shown that long-term HIIT can up-regulate or delay the reduction of skeletal muscle mass in different age groups. However, to obtain accurate results, future detection needs to pay attention to whether it is the site of exercise, the level of subjects’ training and the combined use of detection instruments. It is worth noting that it is difficult to simulate the movement mode of HIIT on cells, and the gene knockout mice have not been reported in the field of HIIT. Therefore, if we want to further study the specific mechanism of HIIT, the gene knockout mice may be the breakthrough point. Studies have shown that HIIT may activate satellite cell proliferation independent of muscle fiber hypertrophy and subsequently mediate remodeling of cell repair, whereas the effect on myocyte nuclei may depend on the state of the subject. In addition, HIIT can up-regulate PGC-1α, and our group has previously demonstrated that PGC-1α can up-regulate the expression of MOTS-C, which has recently been reported to be closely related to the transformation of fast to slow muscles. This may be a new mechanism for the transformation of HIIT fibers. HIIT can promote skeletal muscle angiogenesis and blood perfusion, but its regulation effect on oxygenation index is still contradictory. The effect of HIIT on mitochondrial morphology and function is mediated by multiple pathways. It is still questionable to evaluate the effectiveness of training based on the change of single marker. Different intensity and duration of HIIT have different order of influence on mitochondrial function and function in skeletal muscle. HIIT may be an effective way to improve the strength of exercise-sensitive people, and its mechanism may be around muscle growth, anti-atrophy, increasing sensitivity to calcium ions, and upregulation of the tensile strength of extracellular matrix. But its strength gain is limited by where it is exercised. HIIT supplementation with protein effectively promoted muscle synthesis independent of upregulated mitochondrial function, although this conclusion remains to be confirmed since only sprint interval training (SIT) has been reported. This article reviews the relationship between HIIT and skeletal muscle mass and function, in order to provide theoretical basis and application strategies for HIIT to prevent and improve muscle loss and function decline.