Impact of age on exercise-induced ATP supply during supramaximal plantar flexion in humans

Currently, the physiological factors responsible for exercise intolerance and bioenergetic alterations with age are poorly understood due, at least in art, to the confounding effect of reduced physical activity in the elderly. Thus, in 40 healthy young (22 ± 2 yr) and old (74 ± 8 yr) activity-matche...

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Published inAmerican journal of physiology. Regulatory, integrative and comparative physiology Vol. 309; no. 4; pp. R378 - R388
Main Authors Layec, Gwenael, Trinity, Joel D., Hart, Corey R., Kim, Seong-Eun, Groot, H. Jonathan, Fur, Yann Le, Sorensen, Jacob R., Jeong, Eun-Kee, Richardson, Russell S.
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 15.08.2015
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Summary:Currently, the physiological factors responsible for exercise intolerance and bioenergetic alterations with age are poorly understood due, at least in art, to the confounding effect of reduced physical activity in the elderly. Thus, in 40 healthy young (22 ± 2 yr) and old (74 ± 8 yr) activity-matched subjects, we assessed the impact of age on: 1) the relative contribution of the three major pathways of ATP synthesis (oxidative ATP synthesis, glycolysis, and the creatine kinase reaction) and 2) the ATP cost of contraction during high-intensity exercise. Specifically, during supramaximal plantar flexion (120% of maximal aerobic power), to stress the functional limits of the skeletal muscle energy systems, we used 31 P-labeled magnetic resonance spectroscopy to assess metabolism. Although glycolytic activation was delayed in the old, ATP synthesis from the main energy pathways was not significantly different between groups. Similarly, the inferred peak rate of mitochondrial ATP synthesis was not significantly different between the young (25 ± 8 mM/min) and old (24 ± 6 mM/min). In contrast, the ATP cost of contraction was significantly elevated in the old compared with the young (5.1 ± 2.0 and 3.7 ± 1.7 mM·min −1 ·W −1 , respectively; P < 0.05). Overall, these findings suggest that, when young and old subjects are activity matched, there is no evidence of age-related mitochondrial and glycolytic dysfunction. However, this study does confirm an abnormal elevation in exercise-induced skeletal muscle metabolic demand in the old that may contribute to the decline in exercise capacity with advancing age.
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ISSN:0363-6119
1522-1490
1522-1490
DOI:10.1152/ajpregu.00522.2014