Myostatin inhibition enhances the effects of exercise on performance and metabolic outcomes in aged mice
Abstract
The objective of this study was to examine the effects of short-term exercise training, myostatin inhibition (PF-354), and exercise+PF-354, all relative to a vehicle control, on performance and metabolic measures in 24-month-old mice. At study termination, PF-354-treated mice exhibited significantly greater muscle weights. Performance measures revealed that exercise+PF-354 increased treadmill running time and distance to exhaustion (more than twofold) and increased habitual activity. Measures of strength were not different; however, all treatment groups demonstrated more than 30% reductions in muscle fatigue. Metabolic measures showed that basal metabolic rates were higher in PF-354- and exercise+PF-354-treated mice, and exercise and exercise+PF-354 groups exhibited significantly greater insulin sensitivity. PF-354 was associated with decreased Smad3 phosphorylation and increased peroxisome proliferator-activated receptor gamma coactivator-1alpha expression and, similar to exercise, decreased MuRF-1. The data suggest that the combination of exercise training and myostatin blockade may significantly improve physical function and whole-body metabolism in older individuals.
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PGC-1α binds to FOXO and inhibits its transcriptional activity.
“PGC-1α in turn binds to FOXO and inhibits its transcriptional activity (Lebrasseur et al., 2009).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Lebrasseur et al., 2009
The results section reports increased PGC-1α in treated aged mice, while the Discussion describes FoxO1 as a transcription factor involved in MuRF-1 regulation. Neither passage says PGC-1α binds FoxO or inhibits its transcriptional activity. Searches for the claimed interaction and its effect found no supporting passage in our copy. (LLM, conf=0.74)
Experimental — accuracy not yet measuredInhibition of myostatin signaling increases PGC1α and mitochondrial biogenesis.
“Importantly, the inhibition of myostatin signaling increases PGC1α and mitochondrial biogenesis 145, while mice deficient for myostatin show an improved metabolic phenotype and a resistance to HFD 146, 147.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [145]
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- Authors
- LeBrasseur, N. K., Schelhorn, T. M., Bernardo, B. L., Cosgrove, P. G., Loria, P. M., & Brown, T. A.
- Affiliations
- Pfizer (United States) (US)
- Venue
- The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-05-29
- Volume
- 64A
- Issue
- 9
- Pages
- 940-948
- ISSN
- 1079-5006 (ISSN-L)
- 1758-535X
- OpenAlex
- W2165995731
- Cited by
- 180
- References
- 42
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 10 · 2023: 8 · 2022: 12 · 2021: 7 · 2020: 9 · 2019: 9 · 2018: 12 · 2017: 14 · 2016: 17 · 2015: 13 · 2014: 17 · 2013: 16 · 2012: 10
- FWCI
- 4.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journals of Gerontology Series A (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- myostatin inhibition, exercise training, aging, muscle atrophy, muscle fatigue, endurance performance, insulin sensitivity, basal metabolic rate, Smad3 phosphorylation, PGC-1α, MuRF1, muscle strength, treadmill running
- MeSH terms
- Aging, Animals, Energy Metabolism, Insulin Resistance, Male, Mice, Inbred C57BL, Phosphorylation, Physical Conditioning, Animal, Muscle, Skeletal, Mice, Smad3 Protein, Muscle Strength, Myostatin
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