Omega‐3 fatty acid supplementation attenuates skeletal muscle disuse atrophy during two weeks of unilateral leg immobilization in healthy young women

McGlory, Chris; Gorissen, Stefan H.M.; Kamal, Michael; Bahniwal, Ravninder; Hector, Amy J.; Baker, Steven K.; Chabowski, Adrian; Phillips, Stuart M.

doi:10.1096/fj.201801857rrr

Cited by 102 publications

(125 citation statements)

References 43 publications

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“…We also provide insight that the immobilization-mediated reductions in mitochondrial bioenergetics are rapidly influenced by muscle disuse (as early as 3 d), and an increase in mitochondrial-mediated redox stress may not be required for decrements in mitochondrial content or function during immobilization. In parallel with a previous report in these participants (28), the preserved mitochondrial content, function, and lipid metabolism during immobilization may contribute to maintained muscle mass and strength in response to v-3 supplementation.…”

Section: Discussionsupporting

confidence: 82%

“…Mitochondrial-derived ROS or global oxidative stress is implicated in muscle loss during immobilization in both rodents (18) and humans (7,(9)(10)(11)(12)(13). Although previous work in the same participants as the current study displayed a loss of muscle mass and strength across 14 d of immobilization (28), unlike previous reports in men (10), our data indicate an unaltered propensity for H 2 O 2 emission and 4HNE adducts in skeletal muscle. Although sex differences remain to be investigated, it is possible that the antioxidant influence of 17-b estradiol (33,34) could play a role in preserving the propensity for ROS emission despite a reduction in mitochondrial content; alternatively, this discrepancy may reflect methodological differences between studies (isolated mitochondria vs. permeabilized muscle fibers).…”

Section: Immobilization and Mitochondrial-ros Emissioncontrasting

confidence: 73%

“…Participants consumed supplements containing sunflower oil (control) or v-3 (3 g eicosapentaenoic acid; and 2 g docosahexaenoic acid daily) for 4 wk prior to and throughout the 2 wk single leg immobilization protocol. The present study is part of a larger investigation, and participants were all comparable in age, height, mass, body composition, and activity status, as previously reported in McGlory et al (28).…”

Section: Participants and Skeletal Muscle Biopsymentioning

confidence: 67%

“…Given that long-term muscle disuse or inactivity is occasionally associated with lipid accumulation in parallel with compromised cellular homeostasis (27), it is also possible that v-3 supplementation preserves skeletal muscle health and metabolic parameters during disuse secondary to maintained mitochondrial lipid metabolism. Although we have recently shown that v-3 supplementation attenuated muscle atrophy in a single-leg immobilization model through unclear mechanisms (28), we hypothesized that adaptations in mitochondrial function may contribute. Therefore, we aimed to determine the potential of v-3 supplementation to improve ADP sensitivity and mitigate the detrimental effects of immobilization on mitochondrial bioenergetics and markers of lipid metabolism in young women.…”

mentioning

confidence: 96%

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Supplementation with dietary ω‐3 mitigates immobilization‐induced reductions in skeletal muscle mitochondrial respiration in young women

et al. 2019

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Omega‐3 (ω‐3) supplementation attenuates immobilization‐induced atrophy; however, the underlying mechanisms remain unclear. Since mitochondrial dysfunction and oxidative stress have been implicated in muscle atrophy, we examined whether ω‐3 supplementation could mitigate disuse‐mediated mitochondrial dysfunction. Healthy young women (age = 22 ± 3 yr) randomly received control (n = 9) or ω‐3 supplementation (n = 11; 3 g eicosapentaenoic acid, 2 g docosahexaenoic acid) for 4 wk prior to and throughout 2 wk of single‐limb immobilization. Biopsies were performed before and after 3 and 14 d of immobilization for the assessment of mitochondrial respiration, H2O2 emission, and markers of ADP transport/lipid metabolism. In controls, immobilization rapidly (3 d) reduced (∼20%) ADP‐stimulated mitochondrial respiration without altering ADP sensitivity or the abundance of mitochondrial proteins. Extending immobilization to 14 d did not further reduce mitochondrial coupled respiration; however, unlike following 3 d, mitochondrial proteins were reduced ∼20%. In contrast, ω‐3 supplementation prevented immobilization‐induced reductions in mitochondrial content and respiration throughout the immobilization period. Regardless of dietary supplement, immobilization did not alter mitochondrial H2O2 emission in the presence or absence of ADP, markers of cellular redox state, mitochondrial lipid–supported respiration, or lipid‐related metabolic proteins. These data highlight the rapidity of mitochondrial adaptations in response to muscle disuse, challenge the necessity for increased oxidative stress during inactivity, and establish that ω‐3 supplementation preserves oxidative phosphorylation function and content during immobilization.—Miotto, P. M., McGlory, C., Bahniwal, R., Kamal, M., Phillips, S. M., Holloway, G. P. Supplementation with dietary ω‐3 mitigates immobilization‐induced reductions in skeletal muscle mitochondrial respiration in young women. FASEB J. 33, 8232–8240 (2019). http://www.fasebj.org

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Section: Discussionsupporting

confidence: 82%

Section: Immobilization and Mitochondrial-ros Emissioncontrasting

confidence: 73%

Section: Participants and Skeletal Muscle Biopsymentioning

confidence: 67%

mentioning

confidence: 96%

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Supplementation with dietary ω‐3 mitigates immobilization‐induced reductions in skeletal muscle mitochondrial respiration in young women

et al. 2019

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“…Omega-3 (n-3) polyunsaturated fatty acids (PUFAs) are receiving increasing attention due to their antiinflammatory action in several conditions, such as cancer, diabetes, and metabolic syndrome. The main biological effects come from the presence of docosahexaenoic (DHA) and eicosapentaenoic acid (EPA), which can be incorporated in the sarcolemmal and mitochondrial phospholipidic membranes [25,43], increasing fluidity due to the presence of unsaturated binding in its structural composition. Importantly, omega-3 PUFA supplementation increases mitochondrial ADP sensitivity without alterations in mitochondrial content or oxidative stress markers in healthy humans [25].…”

Section: Nutritionmentioning

confidence: 99%

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

Brunetta

Holwerda

Loon

et al. 2019

J. of SCI. IN SPORT AND EXERCISE

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Sarcopenia, which is characterized by reduction in muscle mass and strength, contributes to several age-related conditions, including insulin resistance and frailty. Despite the importance of maintaining muscle mass for healthy aging, the mechanisms contributing to sarcopenia are not fully elucidated. Nevertheless, mitochondria appear to play a key role in the underlying condition, and importantly, respond robustly to exercise interventions. Mitochondria are intracellular organelles largely attributed to maintaining ATP concentrations, however, the importance of this organelle in overall cellular homeostasis has been expanded in the last decades to include redox signaling, calcium homeostasis, inflammation, and apoptosis. Several lines of evidence suggest that mitochondrial bioenergetics are altered in aged skeletal muscle, resulting in an increase in reactive oxygen species (ROS) production, while conversely genetic/pharmacological approaches that attenuate mitochondrial ROS promote healthy aging and maintenance of muscle mass. These observations suggest that increased free radicals are one of the bases of the aging process and related sarcopenia. Here, we reviewed the current knowledge regarding mitochondrial function and redox balance in aged human skeletal muscle, highlighting the implications of redox unbalance on skeletal muscle mass maintenance and muscle health. Additionally, we describe the benefits of exercise and nutrition interventions in the context of improving mitochondrial bioenergetics and functional outcomes regarding skeletal muscle mass and function.

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