During maximal exercise, skeletal muscle metabolism and oxygen consumption remain elevated despite precipitous declines in power. Presently, it is unclear whether these responses are caused by an increased ATP cost of force generation (ATP COST) or mitochondrial uncoupling; a process that reduces the efficiency of oxidative ATP synthesis (ATP OX). r To address this gap, we used 31-phosphorus magnetic resonance spectroscopy to measure changes in ATP COST and ATP OX in human quadriceps during repeated trials of maximal intensity knee extensions lasting up to 4 min. r ATP COST remained unchanged. In contrast, ATP OX plateaued by ß2 min and then declined (ß15%) over the final 2 min. The maximal capacity for ATP OX (V max), as well as ADP-specific rates of ATP OX , were also significantly diminished. r Collectively, these results suggest that mitochondrial uncoupling, and not increased ATP COST , is responsible for altering the regulation of skeletal muscle metabolism and oxygen consumption during maximal exercise.

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https://mc06.manuscriptcentral.com/apnm-pubs Applied Physiology, Nutrition, and Metabolism D r a f t 2 ABSTRACTDespite intensive efforts to understand the extent to which skeletal muscle mitochondrial capacity changes in older humans, the answer to this important question remains unclear. To determine what the preponderance of evidence from in vivo studies suggests, we conducted a systematic review and meta-analysis of the effects of age on muscle oxidative capacity as measured noninvasively by magnetic resonance spectroscopy. A secondary aim was to examine potential moderators contributing to differences in results across studies, including: muscle group, physical activity status, and sex. Candidate papers were identified from PubMed searches (n=3,561 papers) and the reference lists of relevant papers. Standardized effects (Hedges' g) were calculated for age and each moderator using data from the 22 studies that met the inclusion criteria (n=28 effects). Effects were coded as positive when older (≥55 years) adults had higher muscle oxidative capacity than younger (20-45 years) adults. The overall effect of age on oxidative capacity was positive (g=0.171, p<0.001), indicating modestly greater oxidative capacity in old. Notably, there was significant heterogeneity in this result (Q=245.8, p<0.001; I 2 ~70-90%). Muscle group, physical activity, and sex were all significant moderators of oxidative capacity (p≤0.029). This analysis indicates that the current body of literature does not support a de facto decrease of in vivo muscle oxidative capacity in old age. The heterogeneity of study results and identification of significant moderators provide clarity regarding apparent discrepancies in the literature, and indicate the importance of accounting for these variables when examining purported age-related differences in muscle oxidative capacity.

In practice, the EVS and GPPAQ may not identify ∼50% of patients who should be advised to increase their PA. Therefore, physicians should advocate that all of their patients adopt an active lifestyle, including the achievement of ≥150 min of MVPA per week.

Because of the fundamental dependence of mammalian life on adequate mitochondrial function, the question of how and why mitochondria change in old age is the target of intense study. Given the importance of skeletal muscle for the support of mobility and health, this question extends to the need to understand mitochondrial changes in the muscle of older adults, as well. We and others have focused on clarifying the age-related changes in human skeletal muscle mitochondrial function in vivo. These changes include both the maximal capacity for oxidative production of energy (ATP), as well as the relative use of mitochondrial ATP production for powering muscular activity. It has been known for nearly 50 yr that muscle mitochondrial content is highly plastic; exercise training can induce an ∼2-fold increase in mitochondrial content, while disuse has the opposite effect. Here, we suggest that a portion of the age-related changes in mitochondrial function that have been reported are likely the result of behavioral effects, as physical activity influences have not always been accounted for. Further, there is emerging evidence that various muscles may be affected differently by age-related changes in physical activity and movement patterns. In this review, we will focus on age-related changes in oxidative capacity and flux measured in vivo in human skeletal muscle.