Influence of aerobic exercise intensity on myofibrillar and mitochondrial protein synthesis in young men during early and late postexercise recovery

Donato, Danielle M. Di; West, Daniel W. D.; Churchward‐Venne, Tyler A.; Breen, Leigh; Baker, Steven K.; Phillips, Stuart M.

doi:10.1152/ajpendo.00487.2013

Cited by 114 publications

(122 citation statements)

References 36 publications

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“…The HIT protocol was particularly effective for increasing mTOR and rps6 phosphorylation compared with MICT, whereas both protocols similarly increased p70S6K phosphorylation at POST. These data align with evidence that endurance exercise is sufficient to induce anabolic responses in skeletal muscle, including increased mTORC1 signaling and rates of MPS, at least in relatively training-unaccustomed individuals (28,61). For example, mTOR/p70S6K phosphorylation and rates of mixed MPS are increased following 1 h of cycling at 65-70% V O 2 max (61), and high (60% W max for 30 min)-but not low (30% W max for 60 min)-intensity continuous cycling induces sustained (24 -28 h postexercise) increases in myofibrillar MPS (28).…”

Section: Discussionsupporting

confidence: 84%

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Fyfe

Bishop

Zacharewicz

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Fyfe JJ, Bishop DJ, Zacharewicz E, Russell AP, Stepto NK. Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol 310: R1297-R1311, 2016. First published April 13, 2016 doi:10.1152/ajpregu.00479.2015.-We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mechanistic target of rapamycin complex 1 (mTORC1) signaling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean Ϯ SD: age, 27 Ϯ 4 yr; V O2 peak, 45.7 Ϯ 9 ml·kg Ϫ1 ·min Ϫ1 ) performed three experimental trials in a randomized order: 1) RE (8 ϫ 5 leg press repetitions at 80% 1-repetition maximum) performed alone and RE preceded by either 2) HIT cycling [10 ϫ 2 min at 120% lactate threshold (LT); HIT ϩ RE] or 3) work-matched MICT cycling (30 min at 80% LT; MICT ϩ RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise and ϩ1 h (RE ϩ 1 h) and ϩ3 h (RE ϩ 3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACC Ser79 and p70S6K Thr389 phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTOR Ser2448 and rps6 Ser235/236 phosphorylation at POST. REinduced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE ϩ 1 h for MICT ϩ RE vs. both HIT ϩ RE and RE. Expression of miR-133a, miR-378, and miR-486 was reduced at RE ϩ 1 h for HIT ϩ RE vs. both MICT ϩ RE and RE. Postexercise mTORC1 signaling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces postexercise expression of miRNAs implicated in skeletal muscle adaptation to RE. concurrent training; interference; exercise intensity; high-intensity interval training; continuous training INCORPORATING BOTH RESISTANCE (RE) and endurance exercise into a periodized training program is termed concurrent training (56). Compared with undertaking RE alone, concurrent training attenuates skeletal muscle hypertrophy and maximal strength development in some (10,19,33,48,53), but not all (5,58,63,75,76), studies. Given that skeletal muscle mass plays an important role in overall metabolic health (87), and many athletes require elements of strength and muscle hypertrophy, concomitantly with a high aerobic capacity (47), minimizing interference during concurrent training has implications for optimizing both health and performance outcomes.

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Section: Discussionsupporting

confidence: 84%

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Fyfe

Bishop

Zacharewicz

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In a number of studies, activation of AMPK (Rasmussen & Winder 1997, Fujii et al 2000, Chen et al 2003, Sriwijitkamol et al 2007, Egan et al 2010, CaMKII (Rose et al 2006, Egan et al 2010, and stress-inducible p38 MAPK (Di Donato et al 2014) positively associated with the intensity of exercise were shown in human skeletal muscle, while in one study (Egan et al 2010) such association for p38 MAPK was not observed. We found that in endurance-trained human skeletal muscle, the canonical promoter PGC-1a is constitutively expressed at rest and after exercise.…”

Section: Discussionmentioning

confidence: 99%

Promoter-specific regulation of PPARGC1A gene expression in human skeletal muscle

Popov¹,

Лысенко²,

Vepkhvadze³

et al. 2015

Journal of Molecular Endocrinology

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The goal of this study was to identify unknown transcription start sites of the PPARGC1A (PGC-1a) gene in human skeletal muscle and investigate the promoter-specific regulation of PGC-1a gene expression in human skeletal muscle. Ten amateur endurance-trained athletes performed high-and low-intensity exercise sessions (70 min, 70% or 50% _ V o 2max ). High-throughput RNA sequencing and exon-exon junction mapping were applied to analyse muscle samples obtained at rest and after exercise. PGC-1a promoter-specific expression and activation of regulators of PGC-1a gene expression (AMPK, p38 MAPK, CaMKII, PKA and CREB1) after exercise were evaluated using qPCR and western blot. Our study has demonstrated that during post-exercise recovery, human skeletal muscle expresses the PGC-1a gene via two promoters only. As previously described, the additional exon 7a that contains a stop codon was found in all samples. Importantly, only minor levels of other splice site variants were found (and not in all samples). Constitutive expression PGC-1a gene occurs via the canonical promoter, independent of exercise intensity and exercise-induced increase of AMPK Thr172 phosphorylation level. Expression of PGC-1a gene via the alternative promoter is increased of two orders after exercise. This post-exercise expression is highly dependent on the intensity of exercise. There is an apparent association between expression via the alternative promoter and activation of CREB1.

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“…It is also noteworthy that the increased myofibrillar protein synthetic response to endurance exercise and amino acid ingestion may be the result of a delayed temporal response (i.e. 24-28 h post-exercise) of mitochondrial proteins to endurance exercise (Di Donato et al, 2014). Moreover, in addition to the previously mentioned increase in myosin heavy chain I, protein ingestion with chronic endurance programmes may be required to cause a shift toward mitochondrial-specific responses (Wilkinson et al, 2008).…”

Section: Reduced Energy Availabilitymentioning

confidence: 99%

Effects of skeletal muscle energy availability on protein turnover responses to exercise

Smiles

Hawley

Camera

2016

Journal of Experimental Biology

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Skeletal muscle adaptation to exercise training is a consequence of repeated contraction-induced increases in gene expression that lead to the accumulation of functional proteins whose role is to blunt the homeostatic perturbations generated by escalations in energetic demand and substrate turnover. The development of a specific 'exercise phenotype' is the result of new, augmented steady-state mRNA and protein levels that stem from the training stimulus (i.e. endurance or resistance based). Maintaining appropriate skeletal muscle integrity to meet the demands of training (i.e. increases in myofibrillar and/or mitochondrial protein) is regulated by cyclic phases of synthesis and breakdown, the rate and turnover largely determined by the protein's half-life. Cross-talk among several intracellular systems regulating protein synthesis, breakdown and folding is required to ensure protein equilibrium is maintained. These pathways include both proteasomal and lysosomal degradation systems (ubiquitin-mediated and autophagy, respectively) and the protein translational and folding machinery. The activities of these cellular pathways are bioenergetically expensive and are modified by intracellular energy availability (i.e. macronutrient intake) and the 'training impulse' (i.e. summation of the volume, intensity and frequency). As such, exercisenutrient interactions can modulate signal transduction cascades that converge on these protein regulatory systems, especially in the early post-exercise recovery period. This review focuses on the regulation of muscle protein synthetic response-adaptation processes to divergent exercise stimuli and how intracellular energy availability interacts with contractile activity to impact on muscle remodelling.

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Influence of aerobic exercise intensity on myofibrillar and mitochondrial protein synthesis in young men during early and late postexercise recovery

Cited by 114 publications

References 36 publications

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Promoter-specific regulation of PPARGC1A gene expression in human skeletal muscle

Effects of skeletal muscle energy availability on protein turnover responses to exercise

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