Maximal oxidative capacity during exercise is associated with muscle power output in patients with long coronavirus disease 2019 (COVID-19) syndrome. A moderation analysis

The study titled “Maximal oxidative capacity during exercise is associated with muscle power output in patients with long coronavirus disease 2019 (COVID-19) syndrome” explores the relationship between long COVID syndrome (LCS) and skeletal muscle energy metabolism, focusing on the impact of muscle power output.

Here’s a detailed summary:

Background and Aims:

  • The study examines skeletal muscle energy metabolism in LCS patients compared to healthy controls, investigating if muscle power output mediates the relationship between COVID-19 and skeletal muscle energy metabolism​​.


  • Conducted as a cross-sectional study, it enrolled 71 LCS patients and 63 healthy controls.
  • Assessments included clinical characteristics like body composition, physical activity, and muscle strength.
  • Cardiopulmonary exercise testing was used to evaluate substrate oxidation rates during graded exercise​​.

Key Findings:

  1. Characteristics of Participants: The study cohort consisted of 71 LCS patients (62% women) and 63 healthy controls (54% women), assessed approximately 123 days post-first COVID-19 symptoms. LCS patients had higher body mass, body fat mass, and visceral adipose tissue compared to healthy controls​​.
  2. Lower Oxidative Capacity in LCS Patients: LCS patients showed significantly lower maximal fatty acid oxidation (MFO), carbohydrate oxidation (CHox), and oxygen uptake during peak fat oxidation compared to controls. This suggests compromised mitochondrial bioenergetics and muscle function in LCS patients​​.
  3. Muscle Power Output as a Mediating Factor: Muscle power output significantly influenced the relationship between LCS and reduced peak fat oxidation. Particularly, when muscle power output was below 388 W, the effect of LCS on MFO was significant, highlighting the role of muscle power in this relationship​​.
  4. Physiopathology of Exercise Intolerance in LCS: The study indicates that metabolic and functional impairments of muscle in LCS patients contribute to exercise intolerance. This is evidenced by the decreased oxidative capacity during exercise​​.


  • LCS patients exhibited lower MFO during exercise compared to healthy controls, indicating potential mitochondrial dysfunction.
  • The relationship between MFO and LCS seems to be predominantly mediated by muscle power output in lower body strength.
  • The study suggests the need for further research into the mechanisms of mitochondrial dynamics and muscle function in LCS to improve therapeutic interventions​​.

This research highlights the significant impact of LCS on skeletal muscle energy metabolism and the importance of muscle power output in mediating these effects, providing valuable insights into the physiopathology of LCS.

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