Academic Department of Military Rehabilitation, Loughborough, UK.
Oxford University Hospitals NHS Trust, Oxford, UK.
BMJ Case Rep. 2023 Feb 17;16(2):e250191. doi: 10.1136/bcr-2022-250191.
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 V̇O) anaerobic threshold (AT), a better predictor of endurance performance, reduced from 84% to 71% predicted peak V̇O maximum. Likewise, fat oxidation at AT reduced by 21%, from 0.35 to 0.28 g/min. Focusing exclusively on V̇O 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.
目前,对 COVID-19 后患者心肺功能限制的详细描述非常有限,特别是在精英运动员中。一名 30 多岁的男性精英长跑运动员在确诊 COVID-19 后出现胸痛。他在急性疾病后 5 个月进行了心肺运动测试(CPET)。与正常相比,他的主观运动耐量降低,他描述说无法“冲刺”(快速加速)。他的 CPET 与 COVID-19 前 15 个月相同的方案进行了比较。虽然保持了超正常的最大摄氧量(峰值预测 V̇O 的 155%),但作为耐力表现更好的预测指标的无氧阈(AT)从峰值 V̇O 的 84%降至 71%。同样,AT 时的脂肪氧化减少了 21%,从 0.35 降至 0.28 g/min。仅关注 V̇O 最大值可能会忽略氧化代谢的损害。AT 降低提示有氧代谢的外周障碍。这种发现可能是由病毒介导的线粒体功能障碍引起的,超出了正常的“去适应”,与脂肪氧化受损有关。