Sarcopenic obesity is becoming a global health concern, owing to the rising older population, causing cardiometabolic morbidity and mortality. Loss of muscle exceeding normal age-related changes has been revealed to be associated with obesity, aggravating each other through complex interactions. Physiological regeneration and proliferation of muscle tissue are achieved through harmonious processes of regulated inflammation, autophagy, muscle satellite cell proliferation, and signaling molecule function. Adipokines and myokines are signaling molecules from adipose tissue and muscle, respectively, that exert autocrine, paracrine, and endocrine effects on fat and muscle tissues. These signaling molecules interact with each other to regulate metabolic homeostasis. However, excessive adiposity creates pro-inflammatory conditions, leading to metabolic disorders and the disorganization of systemic homeostasis. Therefore, obesity impedes muscle tissue regeneration and induces the loss of muscle mass and function. Numerous studies have attempted to demonstrate the pathophysiological interaction between sarcopenia and obesity, but the interwoven matrix of the relationship between myokines and adipokines has made it difficult for researchers to understand them. This review briefly describes updated information about the crosstalk between muscle and adipose tissue.