Skeletal Muscle Mitochondrial Adaptations to Maximal Strength Training in Older Adults

Author:

Berg Ole Kristian1ORCID,Kwon Oh Sung2,Hureau Thomas J34,Clifton Heather L34,Thurston Taylor S345,Le Fur Yann6,Jeong Eun-Kee7,Trinity Joel D345,Richardson Russell S345,Wang Eivind138,Layec Gwenael345910

Affiliation:

1. Faculty of Health and Social Sciences, Molde University College, Norway

2. Department of Kinesiology, University of Connecticut, Storrs

3. Department of Internal Medicine, Division of Geriatrics, University of Utah, Salt Lake City

4. Geriatric Research, Education, and Clinical Center, George E. Whalen VA Medical Center, Salt Lake City, Utah

5. Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City

6. CRMBM, Aix-Marseille Universite, CNRS 7339, France

7. Department of Radiology, Utah Center for Advanced Imaging Research, University of Utah, Salt Lake City

8. Department of Medicine, Norwegian University of Science and Technology, Trondheim, Norway

9. Department of Kinesiology, University of Massachusetts, Amherst

10. Institute for Applied Life Sciences, University of Massachusetts, Amherst

Abstract

Abstract Maximal strength training (MST) results in robust improvements in skeletal muscle force production, efficiency, and mass. However, the effects of MST on muscle mitochondria are still unknown. Accordingly, the purpose of this study was to examine, from the molecular level to whole-muscle, mitochondrial adaptations induced by 8 weeks of knee-extension MST in the quadriceps of 10 older adults using immunoblotting, spectrophotometry, high-resolution respirometry in permeabilized muscle fibers, in vivo 31P magnetic resonance spectroscopy (31P-MRS), and gas exchange. As anticipated, MST resulted in an increased isometric knee-extensor force from 133 ± 36 to 147 ± 49 Nm (p < .05) and quadriceps muscle volume from 1,410 ± 103 to 1,555 ± 455 cm3 (p < .05). Mitochondrial complex (I–V) protein abundance and citrate synthase activity were not significantly altered by MST. Assessed ex vivo, maximal ADP-stimulated respiration (state 3CI+CII, PRE: 23 ± 6 and POST: 14 ± 5 ρM·mg−1·s−1, p < .05), was decreased by MST, predominantly, as a result of a decline in complex I-linked respiration (p < .05). Additionally, state 3 free-fatty acid linked respiration was decreased following MST (PRE: 19 ± 5 and POST: 14 ± 3 ρM·mg−1·s−1, p < .05). Assessed in vivo, MST slowed the PCr recovery time constant (PRE: 49 ± 13 and POST: 57 ± 16 seconds, p < .05) and lowered, by ~20% (p = .055), the quadriceps peak rate of oxidative ATP synthesis, but did not significantly alter the oxidation of lipid. Although these, likely qualitative, mitochondrial adaptations are potentially negative in terms of skeletal muscle energetic capacity, they need to be considered in light of the many improvements in muscle function that MST affords older adults.

Funder

Flight Attendant Medical Research Institute

National Institutes of Health

National Heart, Lung, and Blood Institute

VA Merit Awards

VA SPiRe Award

Career Development award

American Heart Association

Norwegian University of Science and Technology

Publisher

Oxford University Press (OUP)

Subject

Geriatrics and Gerontology,Ageing

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