Age-induced oxidative stress: how does it influence skeletal muscle quantity and quality?
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With advancing age, skeletal muscle function declines as a result of strength loss. These strength deficits are largely due to reductions in muscle size (i.e., quantity) and its intrinsic force-producing capacity (i.e., quality). Age-induced reductions in skeletal muscle quantity and quality can be the consequence of several factors, including accumulation of reactive oxygen and nitrogen species (ROS/RNS), also known as oxidative stress. Therefore, the purpose of this mini-review is to highlight the published literature that has demonstrated links between aging, oxidative stress, and skeletal muscle quantity or quality. In particular, we focused on how oxidative stress has the potential to reduce muscle quantity by shifting protein balance in a deficit, and muscle quality by impairing activation at the neuromuscular junction, excitation-contraction (EC) coupling at the ryanodine receptor (RyR), and cross-bridge cycling within the myofibrillar apparatus. Of these, muscle weakness due to EC coupling failure mediated by RyR dysfunction via oxidation and/or nitrosylation appears to be the strongest candidate based on the publications reviewed. However, it is clear that age-associated oxidative stress has the ability to alter strength through several mechanisms and at various locations of the muscle fiber.
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Reactive oxygen species also activate muscle proteases such as caspases and calpains, leading to protein breakdown.
“ROS also activates muscle proteases such as caspases and calpains, leading to protein breakdown [87, 105, 108, 111, 112].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [112]
Elevated reactive oxygen species levels activate the ubiquitin-proteasome system, increasing expression of the muscle-specific ubiquitin ligase MuRF1 and atrogin-1.
“Elevated ROS levels activate the UPS, increasing expression of the muscle-specific ubiquitin ligase MuRF1 (Muscle RING-finger protein-1) and atrogin-1.”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [112]
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- Authors
- Baumann, C. W., Kwak, D., Liu, H. M., & Thompson, L. V.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Thompson, LaDora V.
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2016-11-01
- Volume
- 121
- Issue
- 5
- Pages
- 1047-1052
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- PMC
- PMC5142250
- OpenAlex
- W2406210544
- Cited by
- 169
- References
- 79
- Citations by year
- 2026: 4 · 2025: 21 · 2024: 18 · 2023: 23 · 2022: 28 · 2021: 20 · 2020: 19 · 2019: 16 · 2018: 11 · 2017: 8 · 2016: 1
- FWCI
- 1.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- OpenBU (Boston University) (submittedVersion)
- Funders
- NIA/NIH (T32-AG029796)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- age-related muscle loss, sarcopenia, oxidative stress, skeletal muscle quality, muscle strength, reactive oxygen species, reactive nitrogen species, protein balance, neuromuscular junction, excitation-contraction coupling, ryanodine receptor, nitrosylation
- MeSH terms
- Aging, Animals, Humans, Oxidative Stress, Muscle, Skeletal, Muscle Fibers, Skeletal, Muscle Weakness, Muscle Strength
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