Department of Life Sciences, Research Centre for Musculoskeletal Science and Sports Medicine, Manchester Metropolitan University, John Dalton Building, Chester Street, Manchester, M1 5GD, UK.
Lithuanian Sports University, Kaunas, Lithuania.
Eur J Appl Physiol. 2024 Feb;124(2):457-466. doi: 10.1007/s00421-023-05289-y. Epub 2023 Aug 6.
Cigarette smoking is associated with a lower exercise capacity and lower muscle fatigue resistance. This is at least partly attributable to carboxyhaemoglobin (HbCO) in the blood that via reduction in the oxygen-carrying capacity, and the left-shift of the Hb-dissociation curve would reduce tissue oxygenation. On the other hand, a reduced oxygen uptake due to mitochondrial dysfunction would result in improved oxygenation. We used previously collected capillarisation, myoglobin and estimated cellular maximal muscle oxygen consumption data derived from succinate dehydrogenase-stained sections from the vastus lateralis muscle from six smokers and five non-smokers. These data were fed into an expanded Krogh tissue oxygenation model to assess whether an impaired muscle fatigue resistance in smokers is primarily due to HbCO or impaired mitochondrial respiration. The model showed that in smokers with 6% and 20% HbCO (causing a left-shift of the Hb-dissociation curve) average muscle oxygenation was reduced by 1.9% and 7.2%, respectively. Muscle oxygenation was increased by 13.3% when maximal mitochondrial respiration was reduced by 29%. A combination of a 29% reduction in maximal mitochondrial respiration and 20% HbCO led to no significant difference in muscle oxygenation from that in non-smokers. This indicates that while HbCO may explain the reduced exercise capacity after just one smoking session, in chronic smokers impaired mitochondrial respiration appears more important in reducing oxygen extraction and exercise capacity with only a small contribution of the left-shift of the Hb-dissociation curve.
吸烟与运动能力降低和肌肉疲劳抵抗力降低有关。这至少部分归因于血液中的碳氧血红蛋白（HbCO），它通过降低携氧能力和血红蛋白解离曲线的左移，减少组织氧合。另一方面，由于线粒体功能障碍导致的氧气摄取减少，会导致氧合改善。我们使用先前收集的毛细血管化、肌红蛋白和从股外侧肌琥珀酸脱氢酶染色切片估计的细胞最大肌肉氧耗数据，这些数据来自 6 名吸烟者和 5 名不吸烟者。这些数据被输入到扩展的 Krogh 组织氧合模型中，以评估吸烟者肌肉疲劳抵抗力降低主要是由于 HbCO 还是由于线粒体呼吸受损。模型显示，在 HbCO 为 6%和 20%的吸烟者中（导致血红蛋白解离曲线左移），平均肌肉氧合分别降低了 1.9%和 7.2%。当最大线粒体呼吸降低 29%时，肌肉氧合增加了 13.3%。最大线粒体呼吸降低 29%和 HbCO 为 20%的组合导致肌肉氧合与不吸烟者相比没有显著差异。这表明，虽然 HbCO 可能解释了一次吸烟后运动能力的降低，但在慢性吸烟者中，线粒体呼吸受损似乎在降低氧摄取和运动能力方面更为重要，而血红蛋白解离曲线的左移仅起很小的作用。
