Key result
Long COVID was associated with reduced anaerobic threshold (13.2 vs. 15.6 mL/kg/min, p<0.001) and lower skeletal muscle oxidative capacity compared to healthy controls.
Why the study?
The pathogenesis of exercise intolerance and persistent fatigue following SARS-CoV-2 infection (long COVID) is not fully understood.
Does long COVID reduce exercise performance and skeletal muscle oxidative capacity in adults compared to healthy controls?
Case-Control (n=51)
No
Does long COVID reduce exercise performance and skeletal muscle oxidative capacity in adults compared to healthy controls?
Absolute Event Rate: 13.2% vs 15.6%
p-value: p=<0.001
Exercise intolerance in long COVID is associated with reduced skeletal muscle oxidative capacity and autonomic dysregulation, suggesting mitochondrial pathology rather than microvascular dysfunction.
Skeletal muscle impairment may underlie long COVID exercise intolerance; hypothesis-generating for muscle-targeted therapies in larger prospective studies.
The pathogenesis of exercise intolerance and persistent fatigue which can follow an infection with the SARS-CoV-2 virus ("long COVID") is not fully understood. Cases were recruited from a long COVID clinic (N = 32; 44 ± 12 years; 10 (31%) men), and age-/sex-matched healthy controls (HC) (N = 19; 40 ± 13 years; 6 (32%) men) from University College London staff and students. We assessed exercise performance, lung and cardiac function, vascular health, skeletal muscle oxidative capacity, and autonomic nervous system (ANS) function. Key outcome measures for each physiological system were compared between groups using potential outcome means (95% confidence intervals) adjusted for potential confounders. Long COVID participant outcomes were compared to normative values. When compared to HC, cases exhibited reduced oxygen uptake efficiency slope (1847 (1679, 2016) vs. 2176 (1978, 2373) mL/min, p = 0.002) and anaerobic threshold (13.2 (12.2, 14.3) vs. 15.6 (14.4, 17.2) mL/kg/min, p < 0.001), and lower oxidative capacity, measured using near infrared spectroscopy (τ: 38.7 (31.9, 45.6) vs. 24.6 (19.1, 30.1) s, p = 0.001). In cases, ANS measures fell below normal limits in 39%. Long COVID is associated with reduced measures of exercise performance and skeletal muscle oxidative capacity in the absence of evidence of microvascular dysfunction, suggesting mitochondrial pathology. There was evidence of attendant ANS dysregulation in a significant proportion. These multisystem factors might contribute to impaired exercise tolerance in long COVID sufferers.
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Jamieson et al. (2024) conducted a case-control in Long COVID (n=51). Long COVID vs. Healthy controls was evaluated on Anaerobic threshold (mL/kg/min) (p=<0.001). Long COVID was associated with reduced anaerobic threshold (13.2 vs. 15.6 mL/kg/min, p<0.001) and lower skeletal muscle oxidative capacity compared to healthy controls.
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