Adiponectin (ADPN) was initially thought to be a factor secreted by adipocytes. However, with the development of research and technology, it has been found that skeletal muscle is an important organ for the synthesis of ADPN, and its biological function can be effectively regulated by ADPN. Current studies have shown that ADPN can up-regulate the expression of slow-twitch muscle fiber and aerobic energy-related genes and proteins, and down-regulate the expression of fast-twitch muscle fiber and glycolysis energy-related genes and proteins. Our research group has previously proved that ADPN can up-regulate the expression of MOTS-C, and MOTS-C has recently been reported to be closely related to the conversion of fast muscle to slow-twitch muscle. This may be a new mechanism of ADPN-mediated myofiber conversion type. ADPN can significantly up-regulate mitochondrial number, inhibit autophagy, reduce membrane potential depolarization, and promote fatty acid β oxidation. However, the current reports are limited to the intervention of ADPN and its receptor, and its mechanism should be further explored in cells, in downstream factor knockout animals, and by omics. ADPN and its receptor activators can increase insulin sensitivity and promote blood glucose uptake, in which sex hormones may play an important role. However, long-term intervention of ADPN and its receptor activator may lead to abnormal tricarboxylic acid cycle and thus eliminate this effect. Although no study has directly proved the relationship between ADPN and muscle contractility, combined with current reports, it is speculated that the possible connection mechanism is calcium regulation. Considering the conversion of fiber type, endurance and strength should be taken into account in selecting indicators for measuring contractility in the future. ADPN plays an important role in skeletal muscle remodeling. However, it may not act directly on muscle cells but indirectly regulate the growth of undifferentiated myogenic or satellite cells to accelerate the remodeling. AdipoR1 agonist significantly improved the activity of skeletal muscle cells, and AdipoR1 expression was not affected by various muscle-related diseases, suggesting that AdipoR1 may be an effective therapeutic agent. Skeletal muscle, as an organ that is both regulated and accomplished by movement, is closely related to movement. However, the regulation effect of different forms and intensities of exercise on serum and skeletal muscle ADPN is still controversial. Serum experiments show that the change of ADPN after a single exercise is related to exercise duration, while long-term aerobic exercise up-regulates the expression of ADPN in pathological state. Skeletal muscle experiments show that exercise only seems to modulate fast muscle ADPN levels. In addition, the time of sample collection and measurement of ADPN subtypes are points that need to be considered in future studies. This paper reviews the new functions of ADPN in skeletal muscle and the exact effects of exercise on the expression of ADPN in skeletal muscle, in order to provide new ideas for the treatment of skeletal muscle related diseases.