Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle

Craig Porter, Paul T. Reidy, Nisha Bhattarai, Labros S. Sidossis, Blake Rasmussen

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Introduction Loss of mitochondrial competency is associated with several chronic illnesses. Therefore, strategies that maintain or increase mitochondrial function will likely be of benefit in numerous clinical settings. Endurance exercise has long been known to increase mitochondrial function in the skeletal muscle. Comparatively little is known regarding the effect of resistance exercise training (RET) on skeletal muscle mitochondrial respiratory function. Purpose The purpose of the current study was to determine the effect of chronic resistance training on skeletal muscle mitochondrial respiratory capacity and function. Methods Here, we studied the effect of a 12-wk RET program on skeletal muscle mitochondrial function in 11 young healthy men. Muscle biopsies were collected before and after the 12-wk training program, and mitochondrial respiratory capacity was determined in permeabilized myofibers by high-resolution respirometry. Results RET increased lean body mass and quadriceps muscle strength by 4% and 15%, respectively (P < 0.001). Coupled mitochondrial respiration supported by complex I, and complex I and II supstrates increased by 2-and 1.4-fold, respectively (P < 0.01). The ratio of coupled complex I-supported respiration to maximal respiration increased with RET (P < 0.05), as did complex I protein abundance (P < 0.05), whereas the supstrate control ratio for succinate was reduced after RET (P < 0.001). Transcripts responsible for proteins critical to electron transfer and NAD<sup>+</sup> production increased with training (P < 0.05), whereas transcripts involved in mitochondrial biogenesis were unaltered. Conclusions Collectively, 12 wk of RET resulted in qualitative and quantitative changes in skeletal muscle mitochondrial respiration. This adaptation was accompanied by modest changes in mitochondrial proteins and transcript expression. RET seems to be a means to augment the respiratory capacity and intrinsic function of skeletal muscle mitochondria.

Original languageEnglish (US)
Pages (from-to)1922-1931
Number of pages10
JournalMedicine and Science in Sports and Exercise
Volume47
Issue number9
DOIs
StatePublished - Sep 18 2015

Fingerprint

Resistance Training
Skeletal Muscle
Exercise
Muscle Mitochondrion
Education
Mitochondrial Proteins
Quadriceps Muscle
Muscle Strength
Organelle Biogenesis
Respiration
Chronic Disease
Biopsy
Muscles

Keywords

  • BIOENERGETICS
  • MITOCHONDRIA
  • RESISTANCE TRAINING
  • SKELETAL MUSCLE

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle. / Porter, Craig; Reidy, Paul T.; Bhattarai, Nisha; Sidossis, Labros S.; Rasmussen, Blake.

In: Medicine and Science in Sports and Exercise, Vol. 47, No. 9, 18.09.2015, p. 1922-1931.

Research output: Contribution to journalArticle

Porter, Craig ; Reidy, Paul T. ; Bhattarai, Nisha ; Sidossis, Labros S. ; Rasmussen, Blake. / Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle. In: Medicine and Science in Sports and Exercise. 2015 ; Vol. 47, No. 9. pp. 1922-1931.
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abstract = "Introduction Loss of mitochondrial competency is associated with several chronic illnesses. Therefore, strategies that maintain or increase mitochondrial function will likely be of benefit in numerous clinical settings. Endurance exercise has long been known to increase mitochondrial function in the skeletal muscle. Comparatively little is known regarding the effect of resistance exercise training (RET) on skeletal muscle mitochondrial respiratory function. Purpose The purpose of the current study was to determine the effect of chronic resistance training on skeletal muscle mitochondrial respiratory capacity and function. Methods Here, we studied the effect of a 12-wk RET program on skeletal muscle mitochondrial function in 11 young healthy men. Muscle biopsies were collected before and after the 12-wk training program, and mitochondrial respiratory capacity was determined in permeabilized myofibers by high-resolution respirometry. Results RET increased lean body mass and quadriceps muscle strength by 4{\%} and 15{\%}, respectively (P < 0.001). Coupled mitochondrial respiration supported by complex I, and complex I and II supstrates increased by 2-and 1.4-fold, respectively (P < 0.01). The ratio of coupled complex I-supported respiration to maximal respiration increased with RET (P < 0.05), as did complex I protein abundance (P < 0.05), whereas the supstrate control ratio for succinate was reduced after RET (P < 0.001). Transcripts responsible for proteins critical to electron transfer and NAD+ production increased with training (P < 0.05), whereas transcripts involved in mitochondrial biogenesis were unaltered. Conclusions Collectively, 12 wk of RET resulted in qualitative and quantitative changes in skeletal muscle mitochondrial respiration. This adaptation was accompanied by modest changes in mitochondrial proteins and transcript expression. RET seems to be a means to augment the respiratory capacity and intrinsic function of skeletal muscle mitochondria.",
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