A symptom of long COVID may be the reason you feel exhausted after a workout — “long COVID may reduce exercise capacity, measured by how much oxygen your body can use and how your heart and lungs function during exercise.”
In January of 2024, a study found long-COVID patients have muscle abnormalities that resulted in cell death after exercise. “It’s really confirming that there is something inside the body going wrong with the disease,” said Dr Rob Wüst, an author of the study at Vrije Universiteit (Free University) Amsterdam.
In the report Cardiopulmonary Long COVID-19 Symptoms found “exercise capacity was reduced by 4.9 mL/kg/min among individuals with symptoms consistent with LC compared with individuals without symptoms more than 3 months after SARS-CoV-2 infection. Findings among individuals with exertional intolerance suggest that deconditioning, dysfunctional breathing, chronotropic incompetence, and abnormal peripheral oxygen extraction and/or use may contribute to reduced exercise capacity.”
“This decline in oxygen peak rate would roughly translate to a 40-year-old woman with an expected exercise capacity of 9.5 METs, dropping to 8.1 METs, the approximate expected exercise capacity for a 50-year-old woman,” says Dr. Matt Durstenfeld, an author on the study and assistant professor of medicine at the University of California, San Francisco.
The press release “Feeling winded after your workout? Long COVID may claim another symptom” states:
The findings suggest that the long COVID cohort in this subgroup may have reduced oxygen extraction in the muscles, irregular breathing patterns, and a lesser ability to increase heart rate during exercise to match cardiac output. In addition, there was evidence of deconditioning, which occurs to some extent after most physical illnesses that result in inactivity, the researchers noted. Importantly, not all the findings could be attributed to deconditioning.
Exercise tests were conducted at least three months following SARS-CoV-2 infection and involved cardiopulmonary exercise testing (CPET), in which oxygen and carbon dioxide were measured, together with other indices of heart and lung function, while the participant used a treadmill or stationary bike.
Doubles Tennis, Lap Swims May Be Too Strenuous for Those With Long COVID
In comparing exercise tolerance, the researchers found the long COVID group’s peak rate of oxygen was 4.9 ml/kg/min lower than the recovered group. According to first author Matthew S. Durstenfeld, MD, MAS, of the UCSF Department of Medicine and of the Division of Cardiology at Zuckerberg San Francisco General Hospital, this difference is equivalent to 1.4 metabolic equivalent of tasks (METs), a measure of energy consumed during physical activities. “This decline in oxygen peak rate would roughly translate to a 40-year-old woman with an expected exercise capacity of 9.5 METs, dropping to 8.1 METs, the approximate expected exercise capacity for a 50-year-old woman,” he said.
Another way of looking at it, Durstenfeld said, is that a doubles tennis player might need to transition to playing golf with a cart or stretching exercises, and those who swim laps may find that low-impact aerobics is a better match.
The study Muscle abnormalities worsen after post-exertional malaise in long COVID found exercise causes the destruction of muscle cells.
A distinctive symptom of patients with long COVID is post-exertional malaise (malaise is a general feeling of discomfort, illness, or uneasiness whose exact cause is difficult to identify), which is associated with a worsening of fatigue and pain-related symptoms after acute mental or physical exercise, but its underlying pathophysiology is unclear. We show that skeletal muscle structure is associated with a lower exercise capacity in patients, and local and systemic metabolic disturbances, severe exercise-induced myopathy and tissue infiltration of amyloid-containing deposits in skeletal muscles of patients with long COVID worsen after induction of post-exertional malaise.
Patients with long COVID displayed a markedly lower exercise capacity, which related to skeletal muscle metabolic alterations and a shift towards more fast-fatigable fibers. The pathophysiology of post-exertional malaise includes an acute exercise-induced reduction in skeletal muscle mitochondrial enzyme activity, an increased accumulation of amyloid-containing deposits in skeletal muscle, signs of severe muscle tissue damage, together with a blunted exercise-induced T-cell response in skeletal muscle. Collectively, these findings help to decipher the underlying physiology of fatigue and a limited exercise capacity from the development of post-exertional malaise in patients with long COVID.
Viral infections can alter mitochondrial function, and multiple studies have shown that residual SARS-CoV-2 protein presence is associated with long COVID. It is unknown if the full virus is present, or only protein remnants. Because the spike protein is located on the exterior of the virus, this protein may have different proinflammatory/coagulatory effects compared with the nucleocapsid protein. The higher skeletal muscle infiltration of CD68+ macrophages and CD3+ T-cells suggests a locally disturbed immune response in patients with long COVID.
In conclusion, this study reveals that local and systemic metabolic disturbances, severe exercise-induced myopathy, infiltration of amyloid-containing deposits, and immune cells in skeletal muscles of long COVID are key characteristics of post-exertional malaise. While these explain the symptomatology of post-exertional malaise in long COVID, the molecular pathways underlying these alterations in patients suffering from post-exertional malaise remain to be determined.
