Long COVID, a condition affecting approximately 3% of people in the UK post-COVID-19 infection, manifests in persistent and debilitating symptoms. These encompass a spectrum of health issues, such as extreme fatigue, shortness of breath, muscle pains, and loss of smell. What’s intriguing is that around 50% of long COVID sufferers also demonstrate symptoms aligning with myalgic encephalomyelitis (ME), a neuro-immune disease characterized by depleted energy, muscle weakness, cognitive dysfunction, and dysautonomia impacting blood pressure and heart rate.
A defining characteristic of ME and long COVID is “post-exertional malaise” (PEM) – the aggravation of symptoms 24-48 hours after any form of exertion. This enigmatic feature, particularly in long COVID, might find its explanation in a recent study addressing the structural alterations in the muscles of long COVID patients.
Researchers conducting the study compared muscle biopsies and blood plasma samples from individuals with long COVID and those who had had COVID but did not develop long COVID. The results revealed that individuals with long COVID exhibited diminished muscular strength and lower oxygen uptake during a controlled cycling test. More strikingly, their muscle samples showed a higher proportion of fast-twitch glycolytic muscle fibers with reduced mitochondrial function – a revelation indicating potential damage to the muscle tissue during exercise and a reduced capacity for physical exertion.
Further analysis uncovered lower levels of vital molecules required for glycolysis in long COVID individuals, shedding light on why individuals with long COVID experience exacerbated symptoms following exercise. The study also delved into the presence of “microclots” and immune cells in muscle tissue, uncovering elevated microclots and activated immune cells in long COVID sufferers, possibly leading to mitochondrial dysfunction and tissue damage.
These findings resonate with previous research pointing to significant abnormalities in metabolic, muscular, and immune functions in long COVID and ME patients, hinting at the prospect of targeting mitochondria to alleviate symptoms. Encouragingly, there’s existing research demonstrating the positive impact of compounds like coenzyme Q10 on mitochondrial function, raising the possibility of developing effective therapies. However, cautious rehabilitation strategies tailored to the unique challenges faced by long COVID patients are paramount, as evidenced by this study’s revelations.
In essence, these breakthroughs illustrate the complexity of long COVID, emphasizing the need for tailored rehabilitation approaches and sparking hope for improved therapeutic interventions for this enigmatic condition.
