Fatigue is a common symptom of numerous acute and chronic diseases, including myalgic encephalomyelitis/ chronic fatigue syndrome, multiple sclerosis, heart failure, cancer, and many others. In these multi-system diseases the physiological determinants of enhanced fatigue encompass a combination of metabolic, neurological, and myofibrillar adaptations.
Previous research studies have focused on adaptations specific to skeletal muscle and their role in fatigue. However, most have neglected the contribution of physical inactivity in assessing disease syndromes, which, through deconditioning, likely contributes to symptomatic fatigue.
In this commentary, we briefly review disease-related muscle phenotypes in the context of whether they relate to the primary disease or whether they develop secondary to reduced physical activity. Knowledge of the etiology of the skeletal muscle adaptations in these conditions and their contribution o fatigue symptoms is important for understanding the utility of exercise rehabilitation as an intervention to alleviate the physiological precipitants of fatigue.
In conclusion, what one sees with chronic disease is a slide into less functionality, with diminished muscle size, strength, and oxidative capacity. As a bulwark against this slide, exercise becomes particularly important for maintaining/ improving muscle size, contractility and oxidative capacity, all of which help to ameliorate fatigue by reducing the amount of fatiguing stimuli.
Where exercise is tolerated, it is beneficial. The only possible exception is ME/CFS, where, as noted above, restorative rest and careful pacing of one’s activities are foremost among the currently recommended therapeutic approaches.
Discerning Primary and Secondary Factors Responsible for Clinical Fatigue in Multisystem Diseases, by D Maughan & M Toth in Biology (Basel), 22 September 2014.