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

Author:

Layec Gwenael12,Trinity Joel D.12,Hart Corey R.123,Kim Seong-Eun4,Groot H. Jonathan23,Fur Yann Le5,Sorensen Jacob R.23,Jeong Eun-Kee4,Richardson Russell S.123

Affiliation:

1. Division of Geriatrics, Department of Medicine, University of Utah, Salt Lake City, Utah;

2. Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah;

3. Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah;

4. Department of Radiology and Utah Center for Advanced Imaging Research, University of Utah, Salt Lake City, Utah; and

5. Aix-Marseille Université, CNRS, CRMBM UMR 7339, Marseille, France

Abstract

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 31P-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.

Funder

NIH

VA

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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