Related Experiment Video
Updated: Mar 24, 2026
Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans
Published on: February 16, 2017
Protective effect of myostatin gene deletion on aging-related muscle metabolic decline
B Chabi1, M Pauly1, J Carillon2
1INRA, UMR866 Dynamique Musculaire et Métabolisme, Université Montpellier, F-34060, Montpellier, France.
Abstract:
While myostatin gene deletion is a promising therapy to fight muscle loss during aging, this approach induces also skeletal muscle metabolic changes such as mitochondrial deficits, redox alteration and increased fatigability. In the present study, we evaluated the effects of aging on these features in aged wild-type (WT) and mstn knockout (KO) mice. Moreover, to determine whether an enriched-antioxidant diet may be useful to prevent age-related disorders, we orally administered to the two genotypes a melon concentrate rich in superoxide dismutase for 12 weeks. We reported that mitochondrial functional abnormalities persisted (decreased state 3 and 4 of respiration; p<0.05) in skeletal muscle from aged KO mice; however, differences with WT mice were attenuated at old age in line with reduced difference on running endurance between the two genotypes. Interestingly, we showed an increase in glutathione levels, associated with lower lipid peroxidation levels in KO muscle. Enriched antioxidant diet reduced the aging-related negative effects on maximal aerobic velocity and running limit time (p<0.05) in both groups, with systemic adaptations on body weight. The redox status and the hypertrophic phenotype appeared to be beneficial to KO mice, mitigating the effect of aging on the skeletal muscle metabolic remodeling.
Insights
Myostatin gene deletion in mice causes muscle metabolic issues. An antioxidant diet improved endurance and body weight in aging mice, suggesting benefits for muscle health.
Area of Science:
- Muscle physiology
- Aging research
- Nutritional science
Background:
- Myostatin gene deletion shows promise for combating age-related muscle loss.
- However, this approach can lead to skeletal muscle metabolic deficits, including mitochondrial dysfunction, redox imbalances, and increased fatigability.
- Understanding these age-related changes in both wild-type and myostatin knockout models is crucial.
Purpose of the Study:
- To investigate the effects of aging on skeletal muscle mitochondrial function and redox status in wild-type and myostatin knockout mice.
- To determine if an antioxidant-rich diet can mitigate age-related metabolic decline in skeletal muscle.
- To assess the interplay between myostatin deficiency, aging, and antioxidant supplementation.
Main Methods:
- Comparison of aged wild-type (WT) and myostatin knockout (KO) mice.
- Oral administration of a superoxide dismutase-rich melon concentrate for 12 weeks.
- Assessment of mitochondrial respiration, running endurance, glutathione levels, and lipid peroxidation.
- Evaluation of maximal aerobic velocity and running limit time.
Main Results:
- Aged KO mice exhibited persistent mitochondrial functional abnormalities (decreased state 3 and 4 respiration).
- Differences in mitochondrial function and running endurance between WT and KO mice diminished with advanced age.
- KO mice showed increased glutathione levels and reduced lipid peroxidation.
- The antioxidant diet improved maximal aerobic velocity and running time in both genotypes, with positive systemic effects on body weight.
Conclusions:
- While myostatin knockout induces metabolic changes, the hypertrophic phenotype and improved redox status appear beneficial in aging mice.
- Antioxidant supplementation can counteract some age-related declines in skeletal muscle function and endurance.
- These findings suggest potential therapeutic strategies combining genetic approaches with nutritional interventions for age-related muscle disorders.
Related Concept Videos
01:13Formation of Muscle Fibers from Myoblasts
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription...
01:21Satellite Stem Cells and Muscular Dystrophy
01:37Mitochondria