Organismal aging is classically viewed as a gradual decline of cellular functions and a systemic deterioration of tissues that leads to an increased mortality rate in older individuals. According to the prevailing theory, aging is accompanied by a continuous and progressive decline in mitochondrial metabolic activity in cells. However, the most robust approaches to extending healthy lifespan are frequently linked with reduced energy intake or with lowering of mitochondrial activity. While these observations appear contradictory, recent work and technological advances demonstrate that metabolic deregulation during aging is potentially biphasic. In this Opinion we propose a novel framework where middle-age is accompanied by increased mitochondrial activity that subsequently declines at advanced ages.

传统上，有机体衰老被认为是细胞功能的逐渐下降和组织的系统性退化，导致老年人死亡率增加。根据普遍的理论，衰老伴随着细胞线粒体代谢活性的持续和逐步下降。但是，延长健康寿命的最有效方法通常与减少能量摄入或降低线粒体活性有关。尽管这些观察结果相互矛盾，但最近的工作和技术进步表明，衰老过程中的代谢失调可能是双相的。在此意见中，我们提出了一个新的框架，其中中年伴随着线粒体活动的增加，而线粒体活动随后在高龄时下降。