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57; Fig. 5) that corresponds to independent analyses (0.6; Whipp & Wasserman, 1969), as shown by the dashed line in Fig. 5. This correspondence means that two independent methods for determining mitochondrial efficiency [one from phosphorylation capacity of mitochondria (ATPmax/Vv[mt,f]; GPX4 eqn 8) and the other from the ratio of exercise to contractile efficiency (?D/?C)] reveal that the metabolic efficiency of mitochondria is compromised with age both at the limit of function and during submaximal exercise. This agreement between independent methods validates, for this analysis, the combination of measurements made during submaximal and maximal conditions. The ?D/?C ratio also predicts reduced mitochondrial-coupling efficiency in the elderly subjects (0.43 �� 0.03). Independent evidence for a decline in mitochondrial-coupling efficiency is the substantially lower phosphorylation capacity of mitochondria (ATPmax/Vv[mt,f]) in the elderly versus the adult group (Fig. 5). Conversion of ATPmax/Vv[mt,f] into values for mitochondrial-coupling efficiency (0.57) and mitochondrial coupling (P/O = 2.23) yielded values Alectinib solubility dmso in close agreement with the theoretical value for mitochondrial-coupling efficiency (?M= 0.6) and coupling (P/O = 2.3�C2.5; eqn 9; Brand, 2005). Published studies confirm these P/O values in adults, as follows: healthy recreationally active subjects during exercise in vivo, P/O = 2.3�C2.5 (Flatt et al. 1984); resting vastus lateralis muscle of active subjects in vivo, P/O = 2.3 (Conley et al. 2012); and in vitro measurements on isolated mitochondria for assay conditions emulating moderate to maximal exercise conditions, P/O = 2.4�C2.5, respectively (Mogensen et al. 2006). Thus, two independent methods for estimating the coupling state of mitochondria in this study agree and are consistent with published determinations. Taken together, these results demonstrate that mitochondria are well coupled in adults and operate close to the theoretical efficiency for mitochondria. The lower ATPmax/Vv[mt,f] values in the elderly, when converted into efficiency result in an ?M selleck chemicals that corresponds to the lower mitochondrial-coupling efficiency in the elderly evident from ?D/?C (Fig. 5). This agreement in the decline in mitochondrial-coupling efficiency by two methods demonstrates a key role of mitochondrial dysfunction in the lower exercise efficiency of elderly subjects. It also suggests that non-metabolic factors, including biomechanical changes, muscle fibre type and muscle coactivation, do not contribute significantly to the drop in exercise efficiency as measured in the ergometer test used in this study.
