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

Ramirez-Velez R; Hospital Universitario de Navarra, Madrid, Spain
Oscoz-Ochandorena S; Garcia-Alonso Y; Garcia-Alonso N;
Legarra-Gorgonon G; Oteiza J; Lorea AE; Izquierdo M; Correa-Rodriguez M

Clinical Nutrition ESPEN. 58:253-262, 2023 Dec.

BACKGROUND & AIMS: Long COVID syndrome (LCS) involves persistent symptoms
experienced by many patients after recovering from coronavirus disease
2019 (COVID-19). We aimed to assess skeletal muscle energy metabolism,
which is closely related to substrate oxidation rates during exercise, in
patients with LCS compared with healthy controls. We also examined whether
muscle power output mediates the relationship between COVID-19 and
skeletal muscle energy metabolism.

METHODS: In this cross-sectional study, we enrolled 71 patients with LCS
and 63 healthy controls. We assessed clinical characteristics such as body
composition, physical activity, and muscle strength. We used
cardiopulmonary exercise testing to evaluate substrate oxidation rates
during graded exercise. We performed statistical analyses to compare group
characteristics and peak fat oxidation differences based on power output.

RESULTS: The two-way analysis of covariance (ANCOVA) results, adjusted
for covariates, showed that the patients with LCS had lower absolute
maximal fatty acid oxidation (MFO), relative MFO/fat free mass (FFM),
absolute carbohydrates oxidation (CHox), relative CHox/FFM, and oxygen
uptake (VO2) at maximum fat oxidation (g min-1) than the healthy controls
(P < 0.05). Moderation analysis indicated that muscle power output
significantly influenced the relationship between LCS and reduced peak fat
oxidation (interaction beta = -0.105 [95% confidence interval -0.174;
-0.036]; P = 0.026). Therefore, when muscle power output was below 388 W,
the effect of the LCS on MFO was significant (62% in our study sample P =
0.010). These findings suggest compromised mitochondrial bioenergetics and
muscle function, represented by lower peak fat oxidation rates, in the
patients with LCS compared with the healthy controls.

CONCLUSION: The patients with LCS had lower peak fat oxidation during
exercise compared with the healthy controls, potentially indicating
impairment in skeletal muscle function. The relationship between peak fat
oxidation and LCS appears to be mediated predominantly by muscle power
output. Additional research should continue investigating LCS pathogenesis
and the functional role of mitochondria.