Cardiac and Cancer-Associated Cachexia: Role of Exercise Training, Non-coding RNAs, and Future Perspectives

Sarcopenia has been defined as the loss of skeletal muscle mass and strength that occurs with advancing age and has also been related to many metabolic diseases. In late stages, sarcopenia precedes cachexia, defined as a multifactorial syndrome characterized by an ongoing skeletal muscle wasting, with or without loss of fat mass, associated with poor prognosis in diseases, worsening quality of life and survival. Heart failure and cancer-associated cachexia represents a progressive involuntary weight loss and is mainly the result of an imbalance in the muscle protein synthesis and degradation, inflammation, and oxidative stress, causing muscle wasting. Importantly, both diseases are still the main causes of death worldwide and the molecular basis of cachexia is still poorly understood. Recently, non-coding RNAs have been described to regulate the cardiac and cancer-associated cachexia. On the other hand, exercise training is a promising ally in slowing down cachexia and improving the quality of life of patients. New studies demonstrate that exercise training, acting through non-coding RNAs, may be able to mitigate muscle wasting, as protein turnover, mitochondrial biogenesis, and antioxidant capacity improvement. This review will therefore discuss the molecular mechanisms associated with the muscle wasting in both cardiac and cancer cachexia, as well as highlighting the effects of exercise training in attenuating the loss of muscle mass in these specific conditions.