Université Clermont Auvergne, Laboratoire des Adaptations Métaboliques à l'Exercice en conditions Physiologiques et Pathologiques (AME2P, EA 3533), F-63000, Clermont-Ferrand, France.
Centre for Exercise and Sports Science Research, School of Exercise and Health Sciences, Edith Cowan University, Joondalup, Perth, WA, Australia.
Sports Med. 2017 Aug;47(8):1477-1485. doi: 10.1007/s40279-016-0671-1.
It is well acknowledged that prepubertal children have smaller body dimensions and a poorer mechanical (movement) efficiency, and thus a lower work capacity than adults. However, the scientific evidence indicates that prepubertal children have a greater net contribution of energy derived from aerobic metabolism in exercising muscle and reduced susceptibility to muscular fatigue, which makes them metabolically comparable to well-trained adult endurance athletes. For example, the relative energy contribution from oxidative and non-oxidative (i.e. anaerobic) sources during moderate-to-intense exercise, the work output for a given anaerobic energy contribution and the rate of acceleration of aerobic metabolic machinery in response to submaximal exercise are similar between prepubertal children and well-trained adult endurance athletes. Similar conclusions can be drawn on the basis of experimental data derived from intra-muscular measurements such as type I fibre percentage, succinate dehydrogenase enzyme activity, mitochondrial volume density, post-exercise phosphocreatine re-synthesis rate and muscle by-product clearance rates (i.e. H ions). On a more practical level, prepubertal children also experience similar decrements in peak power output as well-trained adult endurance athletes during repeated maximal exercise bouts. Therefore, prepubertal children have a comparable relative oxidative contribution to well-trained adult endurance athletes, but a decrease in this relative contribution occurs from childhood through to early adulthood. In a clinical context, this understanding may prove central to the development of exercise-based strategies for the prevention and treatment of many metabolic diseases related to mitochondrial oxidative dysfunction (e.g. in obese, insulin-resistant and diabetic patients), which are often accompanied by muscular deconditioning during adolescence and adulthood.
众所周知,青春期前的儿童身体尺寸较小,机械(运动)效率较差,因此工作能力低于成年人。然而,科学证据表明,青春期前的儿童在运动肌肉中,来自有氧代谢的净能量贡献更大,肌肉疲劳的易感性降低,这使他们在代谢上与经过良好训练的成年耐力运动员相当。例如,在适度到剧烈运动中,来自氧化和非氧化(即无氧)来源的相对能量贡献、给定无氧能量贡献的工作输出以及对亚最大运动的有氧代谢机制的加速率,在青春期前儿童和经过良好训练的成年耐力运动员之间是相似的。从肌肉内测量(如 I 型纤维百分比、琥珀酸脱氢酶酶活性、线粒体体积密度、运动后磷酸肌酸再合成率和肌肉副产物清除率(即 H 离子))得出的实验数据也可以得出类似的结论。在更实际的层面上,青春期前的儿童在重复的最大运动中,与经过良好训练的成年耐力运动员一样,峰值功率输出也会出现类似的下降。因此,青春期前的儿童与经过良好训练的成年耐力运动员相比,相对氧化贡献相当,但这种相对贡献从儿童期到成年早期逐渐下降。在临床背景下,这种理解可能对基于运动的策略的发展至关重要,这些策略可预防和治疗与线粒体氧化功能障碍相关的许多代谢疾病(例如肥胖、胰岛素抵抗和糖尿病患者),这些疾病在青少年和成年期间经常伴随着肌肉功能下降。