Both enzymatic, proteomic, and gene expression studies (see earlier) have suggested declines in glycolytic and glycogenolytic enzymatic activities, as well as decreases in enzymes involved in citric acid cycle and oxidative phosphorylation (Carmeli et al., 2002; Giresi et al., 2005; Piec et al., 2005). Accompanying the decreases in the mitochondrial enzymes involved in citric acid cycle and electron transport is an overall decrease in mitochon-drial protein synthesis. The net effect of the decline in mitochondrial enzyme levels is an age-related decline in the mitochondrial ATP production rate and a decline in ATP stores (Short et al., 2005). The decline in mitochondrial function correlates with the decline in maximal aerobic capacity (VO2 max) during exercise.
An area of uncertainty is the extent to which the observed metabolic changes relate to the aging of muscle versus the physical inactivity frequently seen in older people (Russ and Kent-Braun, 2004). Carefully conducted studies that correct for the activity level of the young and older participants have suggested that the metabolic changes during aging are fairly minimal with regard to in vitro or in vivo oxidative capacity of muscle. Additionally, physical activity has been shown to be associated with higher levels of mitochondrial proteins involved in electron transport and the citric acid cycle (Russ and Kent-Braun 2004; Greenlund and Nair, 2003).
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