ArticleThe Journal of physiology2003
Insulin-like growth factor-1 prevents age-related decrease in specific force and intracellular Ca2+ in single intact muscle fibres from transgenic mice.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 99 citations in OpenAlex.
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- The mediating role of inflammaging between mitochondrial dysfunction and sarcopenia in aging: a review.American journal of clinical and experimental immunology · 2023Review
- Role of oxidation of excitation-contraction coupling machinery in age-dependent loss of muscle function ineLife · 2022Article
- Assessing the Potential of Nutraceuticals as Geroprotectors on Muscle Performance and Cognition in Aging Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Muscle hypertrophy and muscle strength: dependent or independent variables? A provocative review.European journal of translational myology · 2020Article
- Mechanisms of altered skeletal muscle action potentials in the R6/2 mouse model of Huntington's disease.American journal of physiology. Cell physiology · 2020Article
- Improved Calcium Homeostasis and Force by Selenium Treatment and Training in Aged Mouse Skeletal Muscle.Scientific reports · 2020Article
- Sarcopenia: Aging-Related Loss of Muscle Mass and Function.Physiological reviews · 2019 · on this mapReview
- Development of a high-throughput method for real-time assessment of cellular metabolism in intact long skeletal muscle fibre bundles.The Journal of physiology · 2016Article
- Top-Down Targeted Proteomics Reveals Decrease in Myosin Regulatory Light-Chain Phosphorylation That Contributes to Sarcopenic Muscle Dysfunction.Journal of proteome research · 2016Article
- Length-dependent Ca2+ activation in skeletal muscle fibers from mammalians.American journal of physiology. Cell physiology · 2016Article
- Role of the JP45-Calsequestrin Complex on Calcium Entry in Slow Twitch Skeletal Muscles.The Journal of biological chemistry · 2016Article
- Calpain inhibition rescues troponin T3 fragmentation, increases Cav1.1, and enhances skeletal muscle force in aging sedentary mice.Aging cell · 2016Article
- CUG-BP1 regulates RyR1 ASI alternative splicing in skeletal muscle atrophy.Scientific reports · 2015Article
- Sod1 gene ablation in adult mice leads to physiological changes at the neuromuscular junction similar to changes that occur in old wild-type mice.Free radical biology & medicine · 2015Article
- The effects of testosterone and insulin-like growth factor 1 on motor system form and function.Experimental gerontology · 2015Review
- Role of Mitofusin-2 in mitochondrial localization and calcium uptake in skeletal muscle.Cell calcium · 2015Article
- Oxidative stress, mitochondrial damage, and cores in muscle from calsequestrin-1 knockout mice.Skeletal muscle · 2015Article
- Age affects the contraction-induced mitochondrial redox response in skeletal muscle.Frontiers in physiology · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In the present work we test the hypothesis that sustained transgenic overexpression of insulin-like growth factor-1 (IGF-1) in skeletal muscle prevents age-related decreases in myoplasmic Ca2+ concentration and consequently in specific force in single intact fibres from the flexor digitorum brevis (FDB) muscle from the mouse. Measurements of IGF-1 concentration in FDB muscle showed higher levels in transgenic than in wild-type mice at all ages. The specific tetanic force decreased significantly in single muscle fibres from old (286 +/- 22 kPa) compared to young wild-type (455 +/- 28 kPa), young transgenic (423 +/- 43 kPa), and old transgenic mice (386 +/- 15 kPa) (P < 0.05). These results are consistent with measurements in whole FDB muscles. The peak Ca2+ concentration values in response to prolonged stimulation were: 1.47 +/- 0.15, 1.70 +/- 0.29, 0.97 +/- 0.13 and 1.7 +/- 0.22 microM, in fibres from young wild-type, young transgenic, old wild-type and old transgenic mice, respectively. The effects of caffeine on FDB fibres support the conclusion that the age-related decline in peak myoplasmic Ca2+ and specific force is not explained by sarcoplasmic reticulum Ca2+ depletion. Immunohistochemistry in muscle cross-sections was performed to determine whether age and/or IGF-1 overexpression induce changes in fibre type composition. The relative percentages of type IIa, IIx and I myosin heavy chain (MHC) isoforms did not change significantly with age or genotype. Therefore, IGF-1 prevents age-related decline in peak intracellular Ca2+ and specific force in a muscle that does not exhibit changes in fibre type composition with senescence.
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