Department of Clinical and Biological Sciences, University of Turin, Turin, ITALY.
Physical Education and Sport Sciences Department, Tarbiat Modares University, Teheran, IRAN.
Med Sci Sports Exerc. 2019 Jul;51(7):1387-1395. doi: 10.1249/MSS.0000000000001916.
Cancer cachexia is characterized by loss of muscle mass and function. Increased protein catabolism, inflammation, impaired anabolism, and mitochondrial function markedly contribute to the pathogenesis of this syndrome. Physical activity has been suggested as a useful tool to prevent or at least delay the onset and progression of cancer-induced muscle wasting. Two main types of exercise can be adopted, namely, resistance and endurance training. The present study is aimed to investigate the effectiveness of a combined (resistance + endurance) exercise protocol in preventing/reverting cancer-induced muscle wasting.
Mice bearing the C26 colon carcinoma have been used as a model of cancer cachexia. They have been exposed to combined exercise training during 6 wk (4 before tumor implantation, 2 during tumor growth). Climbing a 1-m ladder inclined at 85° has been used for resistance training, while aerobic (endurance) exercise has been carried out on the same day using a motorized wheel.
In C26-bearing mice, both muscle mass and strength are improved by combined training, while just the latter increased in exercised healthy animals. Such a pattern is associated with modulations of two markers of autophagy, namely, LC3B-I/II ratio, increased in sedentary tumor hosts and reduced in exercised C26-bearing mice, and p62, steadily increased in both sedentary and trained tumor-bearing animals. Finally, combined training is not able to modify PGC-1α protein levels, but it improves succinate dehydrogenase activity, both reduced in the muscle of the C26 hosts.
The data reported in the present study show that combined training improves muscle mass and function in the C26 hosts, likely modulating autophagy and improving mitochondrial function; these observations suggest that combined exercise might become part of a multimodal approach to treat cancer cachexia.
癌症恶病质的特征是肌肉质量和功能丧失。蛋白质分解代谢增加、炎症、合成代谢受损和线粒体功能障碍显著促进了该综合征的发病机制。身体活动已被认为是预防或至少延迟癌症引起的肌肉消耗的发生和进展的有用工具。可以采用两种主要类型的运动，即抗阻运动和耐力运动。本研究旨在探讨联合（抗阻+耐力）运动方案预防/逆转癌症引起的肌肉消耗的效果。
C26 结肠癌细胞荷瘤小鼠被用作癌症恶病质的模型。它们在肿瘤植入前 4 周和肿瘤生长期间进行了 6 周的联合运动训练。使用 85°倾斜的 1 米梯进行抗阻训练，而在同一天使用电动轮进行有氧（耐力）运动。
在 C26 荷瘤小鼠中，联合训练可改善肌肉质量和力量，而仅后者在运动健康动物中增加。这种模式与自噬的两个标志物的调节有关，即 LC3B-I/II 比值在静止肿瘤宿主中增加，在运动的 C26 荷瘤小鼠中减少，p62 在静止和训练的肿瘤荷瘤动物中均稳定增加。最后，联合训练不能改变 PGC-1α 蛋白水平，但可以改善琥珀酸脱氢酶活性，在 C26 宿主的肌肉中均降低。
本研究报告的数据表明，联合训练可改善 C26 宿主的肌肉质量和功能，可能通过调节自噬和改善线粒体功能来实现；这些观察结果表明，联合运动可能成为治疗癌症恶病质的多模式方法的一部分。
