The Time Course for Elevated Muscle Protein Synthesis Following Heavy Resistance Exercise

MacDougall, J. D.; Gibala, Martin J.; Tarnopolsky, Mark A.; MacDonald, Jay R.; Interisano, Stephen A.; Yarasheski, Kevin E.

doi:10.1139/h95-038

Cited by 198 publications

(137 citation statements)

References 7 publications

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“…Our approach allowed for a detailed time course analysis and demonstrated that addition of nuclei appeared to be most intense 6-9 days after the introduction of overload; this fits previous observations that hypertrophic stimuli initiate satellite cell mitosis before this time period (39)(40)(41). An increase in total protein synthesis (but also in degradation) has already been detected within hours after introducing a hypertrophy stimulus (42)(43)(44)(45), including by hypertrophy models similar to ours (46,47). This has led to speculation that enlargement caused by an increase in synthetic capacity per nucleus precedes addition of nuclei and that nuclei might not be obligatory for hypertrophy.…”

Section: Discussionsupporting

confidence: 80%

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Bruusgaard

Johansen

Egner

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

249

281

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Effects of previous strength training can be long-lived, even after prolonged subsequent inactivity, and retraining is facilitated by a previous training episode. Traditionally, such "muscle memory" has been attributed to neural factors in the absence of any identified local memory mechanism in the muscle tissue. We have used in vivo imaging techniques to study live myonuclei belonging to distinct muscle fibers and observe that new myonuclei are added before any major increase in size during overload. The old and newly acquired nuclei are retained during severe atrophy caused by subsequent denervation lasting for a considerable period of the animal's lifespan. The myonuclei seem to be protected from the high apoptotic activity found in inactive muscle tissue. A hypertrophy episode leading to a lasting elevated number of myonuclei retarded disuse atrophy, and the nuclei could serve as a cell biological substrate for such memory. Because the ability to create myonuclei is impaired in the elderly, individuals may benefit from strength training at an early age, and because anabolic steroids facilitate more myonuclei, nuclear permanency may also have implications for exclusion periods after a doping offense. muscle memory | muscle nuclei | muscle atrophy | muscle hypertrophy | apoptosis

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Section: Discussionsupporting

confidence: 80%

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Bruusgaard

Johansen

Egner

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

249

281

View full text Add to dashboard Cite

show abstract

“…Resistance exercise is important and well known in development of muscle mass (hypertrophy). In humans, resistance exercise increases protein synthesis [97][98][99][100][101][102][103][104][105][106] and improves protein balance during the recovery phase in the skeletal muscle, 8,107,108 but not during acute bouts of resistance exercise. 109 Similar to resistance exercise, low intensity aerobic training 110 causes a significant increase in fractional synthetic rate in the leg muscle.…”

Section: A Correspondence Between Immune and Muscle Cellsmentioning

confidence: 99%

Heat shock response and autophagy—cooperation and control

2015

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Abbreviations: AKT, v-akt murine thymoma viral oncogene homolog 1; AMPK, adenosine monophosphate-activated protein kinase; ATG, autophagy-related; BECN1, Beclin 1, autophagy related; EIF4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; FOXO, forkhead box O; HSF1, heat shock transcription factor 1; HSP, heat shock protein; HSPA8/ HSC70, heat shock 70kDa protein 8; IL, interleukin; LC3, MAP1LC3, microtubule-associated protein 1 light chain 3; MTMR14/ hJumpy, myotubularin related protein 14; MTOR, mechanistic target of rapamycin; NR1D1/Rev-Erb-a, nuclear receptor subfamily 1, group D, member 1; PBMC, peripheral blood mononuclear cell; PPARGC1A/PGC-1a, peroxisome proliferator-activated receptor, gamma, coactivator 1 a; RHEB, Ras homolog enriched in brain; SOD, superoxide dismutase; SQSTM1/p62, sequestosome 1; TPR, translocated promoter region, nuclear basket protein; TSC, tuberous sclerosis complex; ULK1, unc-51 like autophagy activating kinase 1.Protein quality control (proteostasis) depends on constant protein degradation and resynthesis, and is essential for proper homeostasis in systems from single cells to whole organisms. Cells possess several mechanisms and processes to maintain proteostasis. At one end of the spectrum, the heat shock proteins modulate protein folding and repair. At the other end, the proteasome and autophagy as well as other lysosome-dependent systems, function in the degradation of dysfunctional proteins. In this review, we examine how these systems interact to maintain proteostasis. Both the direct cellular data on heat shock control over autophagy and the time course of exercise-associated changes in humans support the model that heat shock response and autophagy are tightly linked. Studying the links between exercise stress and molecular control of proteostasis provides evidence that the heat shock response and autophagy coordinate and undergo sequential activation and downregulation, and that this is essential for proper proteostasis in eukaryotic systems.

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“…The muscle protein synthesis increases within 2-3 h after a single bout of resistance exercise (7) and remains higher for up to 24 h in trained individuals and up to 48 h in untrained subjects (8).…”

Section: Resistance Exercise and Muscle Protein Metabolismmentioning

confidence: 99%