The severe fatigue and exercise-related issues experienced by people with post COVID and ME/CFS cannot be explained simply by a lack of physical activity. Specific changes can be observed in the muscles of these patients that may affect their exercise capacity. This is the finding of research conducted by pathophysiologist Braeden Charlton. The results raise questions about standard rehabilitation programs that focus primarily on physical exercise.
While many people recover after a SARS-CoV-2 infection, some continue to experience symptoms for more than three months. Individuals with post COVID often report symptoms similar to those seen in ME/CFS- a condition that can develop following a viral or bacterial infection, among other triggers. Common symptoms include severe fatigue, muscle pain, and post-exertional malaise (PEM). In the case of PEM, symptoms can worsen following physical exertion- such as walking or cycling- as well as after cognitive effort, such as reading or taking an exam.
Charlton investigated whether changes in the muscles might help explain why people with post COVID and ME/CFS become fatigued so quickly. Both patient groups were found to have a lower aerobic exercise capacity. These findings point not only to the heart and lungs but also to the muscles themselves.
In the muscle tissue, Charlton observed, among other things, a relatively higher proportion of fast-twitch muscle fibers- which are primarily suited for short, powerful bursts of activity - and smaller slow-twitch muscle fibers, which are essential for endurance. Furthermore, there are fewer capillaries surrounding the muscle fibers to supply oxygen and nutrients, and the mitochondria- the cell’s energy producers - function less effectively.
Not the same as a loss of physical conditioning
An important question was whether these abnormalities simply arise because patients move less due to their symptoms. Charlton shows that physical inactivity has different effects on muscles. For instance, during periods of inactivity, all muscle fibres shrink to a similar degree, while the ratio between fast-twitch and slow-twitch fibers remains unchanged. Furthermore, the number of capillaries per muscle fiber is preserved.
Consequently, the study suggests that a lack of physical activity cannot fully explain why these patients have a reduced exercise capacity.
These findings are also relevant to treatment. Physical exercise is often used as part of rehabilitation for a wide range of conditions. In the context of ME/CFS and post COVID, it has also been- or remains- a common belief that patients can improve their exercise tolerance through increased training. However, Charlton discovered that these patients also have fewer cells involved in the growth and repair of muscle tissue. This suggests that their muscles may respond to training differently than those of healthy individuals.
Charlton’s research therefore underscores the need for caution when applying a standardized approach to physical exercise. Rehabilitation strategies that are effective for other patient groups may not work in the same way for people with post COVID or ME/CFS. These findings could contribute to the development of rehabilitation strategies that better account for the physiological changes associated with these conditions.