Muscle protein synthesis in response to nutrition and exercise
Philip J. Atherton,Kenneth Smith +1 more
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Analysing distinct subcellular fractions may provide a readout of chronic exercise efficacy in addition to effect size in MPS per se, i.e. while ‘mixed’ MPS increases similarly with endurance and RE, increases in myofibrillar MPS are specific to RE, prophetic of adaptation (i.e., hypertrophy).Abstract:
Muscle protein synthesis (MPS) is the driving force behind adaptive responses to exercise and represents a widely adopted proxy for gauging chronic efficacy of acute interventions, (i.e. exercise/nutrition). Recent findings in this arena have been progressive. Nutrient-driven increases in MPS are of finite duration (∼1.5 h), switching off thereafter despite sustained amino acid availability and intramuscular anabolic signalling. Intriguingly, this ‘muscle-full set-point’ is delayed by resistance exercise (RE) (i.e. the feeding × exercise combination is ‘more anabolic’ than nutrition alone) even ≥24 h beyond a single exercise bout, casting doubt on the importance of nutrient timing vs. sufficiency per se. Studies manipulating exercise intensity/workload have shown that increases in MPS are negligible with RE at 20–40% but maximal at 70–90% of one-repetition maximum when workload is matched (according to load × repetition number). However, low-intensity exercise performed to failure equalises this response. Analysing distinct subcellular fractions (e.g. myofibrillar, sarcoplasmic, mitochondrial) may provide a readout of chronic exercise efficacy in addition to effect size in MPS per se, i.e. while ‘mixed’ MPS increases similarly with endurance and RE, increases in myofibrillar MPS are specific to RE, prophetic of adaptation (i.e. hypertrophy). Finally, the molecular regulation of MPS by exercise and its regulation via ‘anabolic’ hormones (e.g. IGF-1) has been questioned, leading to discovery of alternative mechanosensing–signalling to MPS.read more
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Skeletal muscle wasting in cachexia and sarcopenia: molecular pathophysiology and impact of exercise training
TL;DR: This review will concentrate on specific alterations discussed in the current literature that are present in the skeletal muscle of both muscle wasting disorders, and will focus on exercise training as an intervention strategy.
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Skeletal muscle wasting in cachexia and sarcopenia: molecular pathophysiology and impact of exercise training: Muscle wasting and exercise training
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Interference between Concurrent Resistance and Endurance Exercise: Molecular Bases and the Role of Individual Training Variables
TL;DR: Current evidence for the molecular basis of the specificity of training adaptation and the concurrent interference phenomenon is explored and insights provided by molecular and performance-based concurrent training studies regarding the role of individual training variables are discussed.
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Skeletal Muscle Remodeling in Response to Eccentric vs. Concentric Loading: Morphological, Molecular, and Metabolic Adaptations
TL;DR: It is concluded that, when matched for either maximum load or work, similar increase in muscle size is found between ECC and CON RT, and the molecular mechanisms that may regulate such adaptations are clarified.
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Skeletal muscle aging: influence of oxidative stress and physical exercise.
Mariana Janini Gomes,Paula F. Martinez,Luana Urbano Pagan,Ricardo Luiz Damatto,M. D. M. Cezar,Aline R. R. Lima,Katashi Okoshi,Marina Politi Okoshi +7 more
TL;DR: There has been an increase in information on signaling pathways beneficially modulated by exercise; nonetheless, studies are needed to establish the best type, intensity, and frequency of exercise to prevent or treat age-induced skeletal muscle alterations.
References
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Trevor Stitt,Doreen Drujan,Brian A. Clarke,Frank J. Panaro,Yekatarina Timofeyva,William O. Kline,Michael Gonzalez,George D. Yancopoulos,David J. Glass +8 more
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TL;DR: It is shown that Akt promotes hypertrophy by activating downstream signalling pathways previously implicated in activating protein synthesis: the pathways downstream of mammalian target of rapamycin (mTOR) and the pathway activated by phosphorylating and thereby inhibiting glycogen synthase kinase 3 (GSK3).
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Kirsten A. Burgomaster,Krista R. Howarth,Stuart M. Phillips,Mark Rakobowchuk,Maureen J. MacDonald,Sean L. McGee,Martin J. Gibala +6 more
TL;DR: Given the markedly lower training volume in the SIT group, these data suggest that high‐intensity interval training is a time‐efficient strategy to increase skeletal muscle oxidative capacity and induce specific metabolic adaptations during exercise that are comparable to traditional ET.
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Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle
Daniel J. Cuthbertson,Kenneth Smith,Kenneth Smith,John A. Babraj,Graham P. Leese,T Waddell,Philip J. Atherton,Philip J. Atherton,Henning Wackerhage,Peter M. Taylor,M. J. Rennie,M. J. Rennie +11 more
TL;DR: It is demonstrated that EAA stimulate MPS independently of increased insulin availability, and in the elderly, a deficit in MPS in the basal state is unlikely; and the decreased sensitivity and responsiveness of MPS to EAA, associated with decrements in the expression and activation of components of anabolic signaling pathways, are probably major contributors to the failure of muscle maintenance inThe elderly.
Journal ArticleDOI
AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling.
TL;DR: This is the first investigation to demonstrate changes in translation initiation and skeletal muscle protein synthesis in response to AMPK activation.