SARS-CoV-2 infection decreases cardiorespiratory fitness and time-trial performance even two months after returning to regular training, 2024, Deng+

[SNT Gatchaman]

SARS-CoV-2 infection decreases cardiorespiratory fitness and time-trial performance even two months after returning to regular training — Insights from a longitudinal case series of well-trained kayak athletes
Deng; Yin; Chen; Deng; Wang; Li; Lyu; Zhang; Zhu; Hu; Nassis; Li

OBJECTIVES
The aims of this study were to examine the effect of SARS-CoV-2 infection on cardiorespiratory fitness (CRF) and time-trial performance in vaccinated well-trained young kayak athletes.

METHODS
This is a longitudinal observational study. Sixteen (7 male, 9 female) vaccinated kayakers underwent body composition assessment, maximal graded exercise test, and 1000-m time-trial tests 21.9 ± 1.7 days before and 66.0 ± 2.2 days after the SARS-CoV-2 infection. The perception of training load was quantified with Borg's CR-10 scale before and after the infection return to sport period.

RESULTS
There were significant decreases in peak oxygen uptake (−9.7 %; effect size [ES] = 1.38), peak oxygen pulse (−5.7 %; ES = 0.96), and peak heart rate (−1.9 %; ES = 0.61). Peak minute ventilation, and minute ventilation/carbon dioxide production slope were unchanged after infection compared to the pre-infection values. In the entire 1000-m, the impaired tendencies were found in completion time, mean power, and mean speed (−2.4 to 1.2 %; small ESs = -0.40 to 0.47) as well as significant changes in stroke rate and stroke length (−4.5 to 3.7 %; ESs = -0.60 to 0.73).

CONCLUSIONS
SARS-CoV-2 infection decreased CRF and time-trial performance even two months after return to regular training in vaccinated athletes.

Link | PDF (Journal of Exercise Science & Fitness)

 

[Hutan]

Chinese study

Current studies presented significant methodological limitations such as high heterogeneity,3, 4, 5, 6 lack of longitudinal data, the long interval between the tests (i.e., different training phases), and the absence of training load data before and after infection.4,5 Strictly, the available results to support the causality of ARinf's potential effect on CRF in athletes should be interpreted and generalized with considerable caution due to the aforementioned limitations.3, 4, 5, 6 Furthermore, we recently showed that short-term SARS-CoV-2 infection does not decrease neuromuscular and anaerobic performance in well-trained athletes.7 In fact, the effect of ARinf on “sports performance” among athletes including measures or variables of athletic success such as race completion times, changes in kinematics, and reactions/adaptations during the training period has been consistently overlooked.1,2,4

First, just a note about the ethics. It sounds as though the athletes may have been deliberately infected for this study. The authors say the study got ethics approval and the participants were informed. But these are 17 year olds young, who are in a residential facility and trying to become elite athletes. It could potentially be a bit coercive. The impression of this is not helped by the description of the encouragement given to the athletes during the tests:

Each athlete was given powerful and continuous verbal motivation during the GXT by the investigators and coaches.

None of the athletes appear to have had a difficult time with the infection and none had ongoing symptoms at the end of this study, but I do wonder if they would have been looked after if they had developed Long Covid and been unable to continue their sporting career.

 

[Hutan]

It looks to me as though the athletes were back to training very quickly. The mean length of the Covid-19 symptoms was just 3 days.

Training hours were significantly decreased during the post-infection 4 weeks period compared with the pre-infection 2 weeks period (21.02 ± 2.70 vs 14.66 ± 4.54 [h·wk−1]; Δ = −28.66 %; p < 0.001), and no significant changes in other period.

It was interesting to read this, about another study, in the light of claimed incidence rates of Long Covid:

Only 1.2 % of athletes in a large cohort study (n = 3597) had symptoms that persisted >3 weeks.24. However, we did not continuously monitor symptoms during the RTS period, which might present with new exertional symptoms (e.g., exercise intolerance) in some individuals.24

There is the question of whether reduced fitness caused the different results in the pre and post-infection tests in this current study. I think it is possible that it did have an effect - it looks as though training hours and also intensity (as assessed by the athletes) may have been reduced during that first four week period. The second four week period however looks to have been back to normal, if not somewhat more intense. The athletes had more body fat at the second test.

The authors however discount the idea of deconditioning.

Our data demonstrated that SARS-CoV-2 infection decreased VO2peak by ∼10 % (Table 2). The VO2peak of the infected athletes could be influenced by main three factors including ventilatory/pulmonary, central, and peripheral factors.6,31 Firstly, the present longitudinal studies indicated that athletes' pulmonary function by spirometry (e.g., forced vital capacity [FVC] and forced expiratory volume in 1 s [FEV1]) did not decline compared to pre-infection data.32,33 There is also no current evidence that lung diffusing capacity is negatively affected in athletes after SARS-CoV-2 infection.32,34Moreover, symptoms of lower respiratory restriction (shortness of breath and chest pain) were minimal in our previous study.7 The VEpeak and VE/VCO2 slope did not significantly change after infection in our case series (Table 2), which is in accordance with previous studies.32,35 Therefore, in the athletic population, pulmonary/ventilation function might not be the primary limitation of low VO2peak and exercise intolerance in the long term,5,6 or these factors could be gradually recovered over time.32,36

Regarding the central factors, our results showed that Peak O2 pulse and HRpeak significantly decreased as well as increases in PETCO2peak after infection (Table 2). The Peak O2 pulse was calculated at this stage of VO2/HR and used to estimate stroke volume (SV).6,31 According to Fick's equation, the cardiac output (CO) was equal to SV × HR.31 Due to the previous studies that have examined the positive correlation between PETCO2peak and CO at peak exercise,37 we hypothesized that in our case series, CO and SV did not decline and may have even been super-normal.38 Furthermore, deconditioning (usually accelerated HR response) cannot serve as the simple explanation for the low CRF.6,30,39 There was some evidence that demonstrated the significant decrease in HRpeak even after 7 months to >1 year post-infection in the athletic and general population.35,40,41 We speculated that this might be due to chronic autonomic dysfunction blunting the HR response to exercise,41,42 which leads to a sub-optimal distribution of supernormal CO in the exercising musculature.38 Reassuringly, most studies have shown reversibility of CO, SV, and O2 pulse after 3–6 months post-infection.6,36,40

They note that there is some evidence that decreased peak heart rate can continue for more than a year in athletic and general populations, and they speculate that this might be due to 'chronic autonomic dysfunction blunting the heart rate response to exercise', with this leading to 'sub-optimal distribution of supernormal CO in the exercising musculature'. (CO is 'cardiac output'; I'm not clear on quite what they are saying there.). Reference 38 there investigates exercise pathophysiology in a set of patients with acute Covid-19.

Muscle O2 extraction was demonstrated to be more important than central factors (VO2peak, CO, and SV) in kayaking performance (i.e., upper-body exercise mode).43 Previous studies suggest that SARS-CoV-2 might lead to systemic microvascular dysfunction39,41 and small-fiber neuropathy that induces peripheral shunting.44 Additionally, recent studies have shown that SARS-CoV-2 disrupts mitochondria as the primary O2 organelles leading to impaired mitochondrial function.45 Reduced mitochondrial O2 sensing, amount of mitochondrial in muscle cells, and impaired oxidative stress-related thrombocyte function may contribute to oxidative phosphorylation compromise,45 which might be related to the prolonged anaerobic fatigue (i.e., greater glycolytic metabolism) presented by the larger RERpeak in our results (Table 2).46 We speculated that since no sustained cardiac or pulmonary impairment was observed (which might have been recovered), the VO2peak tested by the upper-body GXT significantly decreased (∼10 %) in our well-trained endurance-type athlete's case series might be related to the impaired ability of O2 delivery/extraction6,30,38,39 However, more studies (e.g., invasive cardiopulmonary exercise testing) are needed to demonstrate the above-postulated mechanisms causing low CRF in athletes after infection.

They speculate that the reduction in VO2max might be due to impaired oxygen delivery or extraction by muscles.