Explaining Fatigue a nd Post-Exertional Malaise in Long COVID and ME/CFS: From Skeletal Mu scle To Exercise Immunology
Following a SARS-SoV-2 infecti on, many individuals recover, however there are some people which hav e symptoms that persist beyond 3 months, leading to a diagnosis of lo ng COVID. Many symptoms of long COVID overlap with another disease, m yalgic encephalomyelitis/chronic fatigue (ME/CFS), where symptoms occ ur after viral or bacterial infections, but are otherwise unexplainab le.
Patients with long COVID and ME/CFS suffer from severe, une xplainable fatigue, muscle pain, and post-exertional malaise (PEM), w hich their symptoms worsen after physical activity (i.e. cycling or w alking) or cognitive exertion (i.e. writing an exam or reading).
< p>The aim of my research was to understand whether changes to muscles of patients could in part explain their fatigue, whether these chang es are due to lack of physical activity or whether they are disease s pecific, and finally whether any changes in the muscle environment ma y partially explain PEM or contribute to PEM onset.In my thesi s I show that both long COVID and ME/CFS patients have lower aerobic exercise capabilities that is not due to heart or lung function neces sarily, but rather changes at the working muscle. Some of these chang es include more fast twitch fibres (known as “sprinting” fibres), smaller slow twitch fibres (known as “endurance fibres”), less c apillaries around the muscle to supply oxygen and nutrients, and poor er mitochondrial function (necessary for producing energy to supply t he working muscle).
Moreover, while long COVID and ME/CFS patie nts may have aerobic capacities similar to individuals that are physi cally inactive, physical inactivity reduces all muscle fibre types eq ually, does not change the proportion of fast and slow fibres, mainta ins the number of capillaries supplying each muscle fibre, and result s in more mitochondrial loss rather than poorer functioning mitochond ria. So, physical inactivity itself cannot fully explain symptoms and reduced aerobic capacity in patients.
More information on the thesis to follow.
DESCRIPTION: Explaining Fatigue and Post-Exertional Malaise in Long CO VID and ME/CFS: From Skeletal Muscle To Exercise Immunology 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 wi th 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 fr om severe, unexplainable fatigue, muscle pain, and post-exertional ma laise (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 thes e changes are due to lack of physical activity or whether they are di sease specific, and finally whether any changes in the muscle environ ment may partially explain PEM or contribute to PEM onset.In my thesi s I show that both long COVID and ME/CFS patients have lower aerobic exercise capabilities that is not due to heart or lung function neces sarily, but rather changes at the working muscle. Some of these chang es include more fast twitch fibres (known as “sprinting” fibres), smaller slow twitch fibres (known as “endurance fibres”), less c apillaries around the muscle to supply oxygen and nutrients, and poor er mitochondrial function (necessary for producing energy to supply t he working muscle).Moreover, while long COVID and ME/CFS patients may have aerobic capacities similar to individuals that are physically i nactive, 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 mo re mitochondrial loss rather than poorer functioning mitochondria. So , physical inactivity itself cannot fully explain symptoms and reduce d aerobic capacity in patients.More information on the thesis to foll ow. END:VEVENT END:VCALENDAR