The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (e.g. imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial Unfolded Protein Response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of Aerobic Exercise Training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 mo.) and aged (24 mo.) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals.

中文翻译：

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有氧运动训练在老年小鼠骨骼肌中引起线粒体失衡和UPRTt

线粒体功能受损是衰老的标志。在衰老期间，存在两种与线粒体完整性严格相关的机制的下调，包括线粒体失衡（例如，线粒体与核编码的线粒体蛋白质的失衡）和线粒体未折叠蛋白反应（UPRmt）。在这里，我们评估了有氧运动对老年小鼠骨骼肌线粒体失衡和UPRmt标记的影响。我们结合了生理学测试，分子和生物信息学分析，评估了有氧运动训练4周对C57BL / 6J小鼠（2个月龄）和24个月龄（24个月龄）小鼠骨骼肌中微核不平衡和UPRmt标记的影响。最初，我们发现衰老减少了腓肠肌的几个线粒体基因，并伴有低水平的UPRmt标记，包括Yme11l和Clpp mRNA。不出所料，体育锻炼改善了衰老小鼠的全身代谢和身体机能。有氧运动增加了老年小鼠骨骼肌中与线粒体编码基因（mtNd1，mtCytB和mtD-Loop）相关的线粒体生物发生/功能的关键蛋白（VDAC和SIRT1）。有趣的是，有氧运动引起了小核的不平衡，增加了骨骼肌的MTCO1 / ATP5a比值和UPRmt标记，包括老年小鼠腓肠肌中的HSP60，Lonp1和Yme1L1蛋白水平。这些数据表明，有氧运动训练在衰老过程中会引起骨骼肌线粒体失衡和UPRTt。