Increased aerobic exercise capacity, as a result of exercise training, has important health benefits. However, some individuals are resistant to improvements in exercise capacity, probably due to undetermined genetic and environmental factors. Here, we show that exercise-induced improvements in aerobic capacity are blunted and aerobic remodelling of skeletal muscle is impaired in several animal models associated with chronic hyperglycaemia. Our data point to chronic hyperglycaemia as a potential negative regulator of aerobic adaptation, in part, via glucose-mediated modifications of the extracellular matrix, impaired vascularization and aberrant mechanical signalling in muscle. We also observe low exercise capacity and enhanced c-Jun N-terminal kinase activation in response to exercise in humans with impaired glucose tolerance. Our work indicates that current shifts in dietary and metabolic health, associated with increasing incidence of hyperglycaemia, might impair muscular and organismal adaptations to exercise training, including aerobic capacity as one of its key health outcomes.

作为运动训练的结果，增加的有氧运动能力具有重要的健康益处。然而，一些人对运动能力的提高有抵抗力，这可能是由于未确定的遗传和环境因素。在这里，我们表明在与慢性高血糖相关的几种动物模型中，运动引起的有氧能力的改善减弱，骨骼肌的有氧重塑受损。我们的数据表明，慢性高血糖是有氧适应的潜在负调节因子，部分原因是葡萄糖介导的细胞外基质修饰、血管化受损和肌肉中的异常机械信号传导。我们还观察到低运动能力和增强的 c-Jun N 末端激酶激活，以响应葡萄糖耐量受损的人类的运动。