Aerobic Glycolysis and the Protective Effects and Mechanisms of Exercise on Cancer Cachexia

Glycolysis is the primary pathway for ATP synthesis in tumor cells even in aerobic status,this process is called aerobic glycolysis(Warburg Effect).The aerobic glycolysis consumes more substrates but generates less energy, which leading to irreversible cancer cachexia. Cancer cachexia is characterized as skeletal muscle wasting, white adipose browning, and liver Cori cycle overactivation. As a metabolite during tumor aerobic glycolysis, lactate is involved in regulating the growth of tumor simultaneously, which contributing to cancer cachexia ultimately. Exercise has extensive positive effects on anti-tumor, however, the increase of lactate level, muscle protein catabolism, adipose tissue browning and liver Cori cycle over-activating are contradictory with the defense of cancer cachexia from exercise. Exercise-induced physiological stress is substantially different from the pathological manifestations of cancer cachexia, which can inhibit tumorigenesis by breaking the tumor abnormal metabolism.In this review,the cell signal regulation of aerobic glycolysis and the contradictions in exercise anti-tumor are discussed. It is speculated that the response of exercise stress in tumor cells varies from it in normal cells, exercise-induced physiological stressis the possible mechanism forexercise anti-tumor.