Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK.
Acta Physiol (Oxf). 2010 Aug;199(4):425-39. doi: 10.1111/j.1748-1716.2010.02132.x. Epub 2010 Mar 24.
One of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction. For instance, myocardial improvements may still be observed after exercise training in post-myocardial infarction heart failure. In both health and disease, it is the changes that occur in the individual cardiomyocytes with respect to their ability to contract that by and large drive the exercise training-induced adaptation to the heart. Here, we review the evidence and the mechanisms by which exercise training induces beneficial changes in the mammalian myocardium, as obtained by means of experimental and clinical studies, and argue that these changes ultimately alter the function of the whole heart and contribute to the changes in whole-body function.
有氧运动耐力训练的主要结果之一是最大摄氧量的提高，这对运动训练后工作能力的提高至关重要。最大摄氧量的提高至少部分是因为运动训练增加了心肌产生更大心输出量的能力。在健康受试者中，这一点已经在过去几十年中得到了反复证明。最近发现，在初始心肌功能障碍的情况下，这种情况也可能是真实的。例如，心肌梗死后心力衰竭患者在运动训练后仍可观察到心肌改善。在健康和疾病中，基本上是个体心肌细胞在收缩能力方面的变化推动了运动训练对心脏的适应性改变。在这里，我们通过实验和临床研究回顾了运动训练引起哺乳动物心肌有益变化的证据和机制，并认为这些变化最终改变了整个心脏的功能，并有助于全身功能的改变。
