Reduced athletic performance post-COVID-19 is associated with reduced anaerobic threshold, 2023, Barker-Davies et al.

Reduced athletic performance post-COVID-19 is associated with reduced anaerobic threshold
Robert M Barker-Davies; Peter Ladlow; Rebecca Chamley; Edward Nicol; David A Holdsworth

Detailed characterisation of cardiopulmonary limitations in patients post-COVID-19 is currently limited, particularly in elite athletes. A male elite distance runner in his late 30s experienced chest pain following confirmed COVID-19. He underwent cardiopulmonary exercise testing (CPET) at 5 months postacute illness. Subjective exercise tolerance was reduced compared with normal, he described inability to ‘kick’ (rapidly accelerate).

His CPET was compared with an identical protocol 15 months prior to COVID-19. While supranormal maximal oxygen uptake was maintained (155% of peak predicted V̇O2) anaerobic threshold (AT), a better predictor of endurance performance, reduced from 84% to 71% predicted peak V̇O2 maximum. Likewise, fat oxidation at AT reduced by 21%, from 0.35 to 0.28 g/min. Focusing exclusively on V̇O2 maximum risks missing an impairment of oxidative metabolism. Reduced AT suggests a peripheral disorder of aerobic metabolism.

This finding may result from virally mediated mitochondrial dysfunction beyond normal ‘deconditioning’, associated with impaired fat oxidation.

Link | PDF | PMC (BMJ Case Reports CP)

 

Has this been looked at much/at all in exercise studies of ME/CFS?

 

Media article on this:

Effects of COVID-19 fatigue in elite athlete revealed in new study
https://www.ctvnews.ca/health/coronavirus/effects-of-covid-19-fatigue-in-elite-athlete-revealed-in-new-study-1.6286234

He made a full recovery:
By four months post-infection, he could run up to 16 kilometres without chest pain. By seven months, he'd regained his "kick" and was able to run steeplechase races. And eleven months after contracting COVID-19, the authors wrote, he managed to run 10 kilometres in 33 minutes and three seconds, "a time (one minute) faster than run 17 months prior to his acute illness."

 

When I look at onset/recovery stories like this, coupled with new findings of mitochondrial/metabolic suppression mechanisms in LC (eg [1]), but long-term ME patient findings showing possibly different mechanisms (eg [2]), it makes me wonder if there's two phases to ME illness progression.

Phase 1 would be the initial "sub-acute" viral effects from which some people may develop a PVFS and mostly recover; phase 2 could involve latent viruses using a different metabolic suppression pathway, which is more likely to persist.

I'll try and flesh this idea out in a separate thread.

ETA: thread Do the findings in LC suggest two distinct phases for ME/CFS onset?

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[1] Core mitochondrial genes are down-regulated during SARS-CoV-2 infection of rodent and human hosts (2023)
[2] WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome (2023)