Molecular and Cellular Aspects of Sarcopenia, Muscle Healthy Aging and Physical Conditioning in the Elderly

During aging,the skeletal muscle tissue is one of the most affected,undergoing loss of mass and function,a process defined as sarcopenia.This age-related muscle mass and function decline,dependent on many factors,predispose individuals to decreased mobility,reduced muscle power and increased risk of falls.Several factors at the cellular and molecular level affect muscle aging,synergizing with each other.At present,it is broadly accepted that Reactive Oxygen Species(ROS)play a primary role in the aging process,especially in those tissues like skeletal muscle,where the generation of free radicals is more pronounced as a consequence of the high consumption of oxygen.Recently,several studies have highlighted the involvement of muscle stem cells(satellite cells,SCs)in the progression of sarcopenia,showing a concomitant regression of activity and number of these cells.At a sub-cellular level,the main processes correlated with sarcopenia are the alteration of protein synthesis and mitochondrial dysfunction.Attempts to slow down or revert sarcopenia are essentially based on three approaches:use of supplements,pharmaceutical therapies and physical activity.In brief,it seems that appropriate physical exercise training protocols could be capable of slowing down and sometimes reversing the sarcopenic process.This finding is the consequence of a beneficial action of physical exercise on mitochondria and/or on the regenerative process led by SCs with different effects on the basis of training characteristics.Furthermore,according to a recent hypothesis,early strength training should be considered as public health advice.

Muscle mitochondria and oxidative metabolism as targets against cancer cachexia

Cancer cachexia is a debilitating syndrome mainly characterized by muscle and fat wasting, leading to the progressive loss of body weight and complicating the management of cancer patient. In particular, the loss of muscle weight is a negative prognostic factor, being associated with chemotherapy toxicity and reduced survival. Increased inflammation and protein dysmetabolism are some of the impairments that lead to muscle wasting in cancer patients. Together with these alterations, tumor growth and chemotherapy administration may affect mitochondrial function, impinging on the muscle energy metabolism. Indeed, therapeutic approaches poised to correct both hypercatabolism and mitochondrial alterations could be effective in preventing cancer-induced muscle wasting. Among the non-pharmacological approaches, exercise training is one of the best modulator of muscle physiology able to impinge on both protein and energy metabolism. However, the wasting phenotype that characterizes cancer patients could be not compatible with physical training, prompting the development of different strategies to improve muscle metabolism. The aim of this mini-review is to discuss both the beneficial effects and the limitations of exercise training in cancer cachexia and the adoption of drugs able to modulate exercise-induced pathways.