Abstract
Introduction: Sarcopenia can lead to physical disability and lower quality of life, but increasing muscle protein synthesis in older adults may reduce its effects. Dose-response curves may be used to determine the optimal protein dose in rested and exercised muscle to elicit maximal muscle protein synthesis. Methods: A literature review was conducted to explore and summarize the findings on the following topics: the mechanisms of muscle protein synthesis, anabolic resistance, and the dose-responses of muscle protein synthesis to anabolic stimuli in both younger and older individuals. Results: Reduced phosphorylation in downstream targets of the mammalian target of rapamycin complex 1 pathway is characteristic of muscle protein synthesis in older muscle. Compared to younger muscle, older muscle can elicit a similar maximal muscle protein synthesis response, but is less sensitive to lower doses of protein ingestion. With ingestion of 40g of whey protein, the fractional synthetic rate in older muscle is similar to that of younger muscle with 20g of whey protein ingestion. Marked increases in amino acid oxidation are also observed. Discussion: Anabolic resistance can be biochemically explained by reduced phosphorylation in the mammalian target of rapamycin complex 1 pathway. Due to this phenomenon, older individuals require greater anabolic stimuli to achieve maximal muscle protein synthesis. However, the most effective protein dose for maximal muscle protein synthesis in older muscle is not well-established. Conclusion: The muscle protein synthesis dose-response curve for older individuals reveals blunted responses to stimuli due to anabolic resistance. Further research is warranted to determine the optimal protein dose for maximal muscle protein synthesis in older adults.
Highlights
Sarcopenia can lead to physical disability and lower quality of life, but increasing muscle protein synthesis in older adults may reduce its effects
muscle protein synthesis (MPS) is activated and regulated through the mammalian target of rapamycin complex 1, a complex commonly associated with tissue growth and MPS [8,9,10,11,12]. mTORC1 acts as a control center receiving inputs from anabolic stimulants, and upon phosphorylation by mTORC1 kinase, leads to a pathway of downstream targets that upregulate translation of mRNA into protein [9, 12]
The phosphorylation of mTORC1 triggers the phosphorylation of two key sets of substrates, eukaryotic initiation factor 4E binding proteins 1 and 2 (4E-BP1/2) and ribosomal S6 kinases 1 and 2 (S6K1/2) [8,9,10,11,12,13]
Summary
Sarcopenia can lead to physical disability and lower quality of life, but increasing muscle protein synthesis in older adults may reduce its effects. Discussion: Anabolic resistance can be biochemically explained by reduced phosphorylation in the mammalian target of rapamycin complex 1 pathway Due to this phenomenon, older individuals require greater anabolic stimuli to achieve maximal muscle protein synthesis. Sarcopenia, defined as muscle loss with increasing age, has severe implications on frailty and overall mobility [1] These negative effects can decrease an individual’s quality of life and loss of strength could impede everyday functions, such as walking. This gradual phenomenon is accelerated at and past the fifth decade of life [2], and is evident in middleaged and elderly adults It is characterized by lower muscle protein synthesis (MPS) than breakdown, which together govern overall skeletal muscle mass. This effect is much more prominent in older populations, blunting the sensitivity to stimulate MPS [5]
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