PhD defense B.T. Charlton

Following a SARS-SoV-2 infection, many individuals recover, however there are some people which have symptoms that persist beyond 3 months, leading to a diagnosis of long COVID. Many symptoms of long COVID overlap with another disease, myalgic encephalomyelitis/chronic fatigue (ME/CFS), where symptoms occur after viral or bacterial infections, but are otherwise unexplainable.

Patients with long COVID and ME/CFS suffer from severe, unexplainable fatigue, muscle pain, and post-exertional malaise (PEM), which their symptoms worsen after physical activity (i.e. cycling or walking) or cognitive exertion (i.e. writing an exam or reading).

The aim of my research was to understand whether changes to muscles of patients could in part explain their fatigue, whether these changes are due to lack of physical activity or whether they are disease specific, and finally whether any changes in the muscle environment may partially explain PEM or contribute to PEM onset.

In my thesis I show that both long COVID and ME/CFS patients have lower aerobic exercise capabilities that is not due to heart or lung function necessarily, but rather changes at the working muscle. Some of these changes include more fast twitch fibres (known as “sprinting” fibres), smaller slow twitch fibres (known as “endurance fibres”), less capillaries around the muscle to supply oxygen and nutrients, and poorer mitochondrial function (necessary for producing energy to supply the working muscle).

Moreover, while long COVID and ME/CFS patients may have aerobic capacities similar to individuals that are physically inactive, physical inactivity reduces all muscle fibre types equally, does not change the proportion of fast and slow fibres, maintains the number of capillaries supplying each muscle fibre, and results in more mitochondrial loss rather than poorer functioning mitochondria. So, physical inactivity itself cannot fully explain symptoms and reduced aerobic capacity in patients.

More information on the thesis to follow.