The science of muscle hypertrophy:

[Guest guest]

The below may be of interest:

The science of muscle hypertrophy: making dietary protein count.

SM.

Proc Nutr Soc. 2010 Nov 22:1-4. [Epub ahead of print]

Abstract

Growing evidence supports the conclusion that consumption of protein in close

temporal proximity to the performance of resistance exercise promotes greater

muscular hypertrophy. We can also state with good certainty that merely

consuming energy, as carbohydrate for example, is also not sufficient to

maximise muscle protein synthesis leading to anabolism and net new muscle

protein accretion. Recent work also indicates that certain types of proteins,

particular those that are rapidly digested and high in leucine content (i.e.

whey protein), appear to be more efficient at stimulating muscle protein

synthesis. Continued practice of consumption of these types or proteins after

exercise should lead to greater hypertrophy.

Reviews of numerous training studies indicate that studies in which milk

proteins and principally whey protein show an advantage of these proteins over

and above isoenergetic carbohydrate and soya protein in promoting hypertrophy.

Thus, the combined evidence suggests a strategic advantage of practising early

post-exercise consumption of whey protein or dairy-based protein to promote

muscle protein synthesis, net muscle protein accretion and ultimately

hypertrophy.

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Resistance exercise enhances mTOR and MAPK signalling in human muscle over that

seen at rest after bolus protein ingestion.

DR, Atherton PJ, Rennie MJ, Tarnopolsky MA, SM.

Acta Physiol (Oxf). 2010 Sep 27. doi: 10.1111/j.1748-1716.2010.02187.x. [Epub

ahead of print]

Abstract

Aim: & #8194; Feeding protein after resistance exercise enhances the magnitude and

duration of myofibrillar protein synthesis (MPS) over that induced by feeding

alone. We hypothesized that the underlying mechanism for this would be a greater

and prolonged phosphorylation of signalling involved in protein translation.

Methods: & #8194; Seven healthy young males performed unilateral resistance

exercise followed immediately by the ingestion of 25 & #8195;g of whey protein to

maximally stimulate MPS in a rested and exercised leg.

Results: & #8194; Phosphorylation of p70 ribosomal protein S6 kinase (p70S6K) was

elevated (P & #8195;< & #8195;0.05) above fasted at 1 & #8195;h at rest whereas it was

elevated at 1, 3 and 5 & #8195;h after exercise with protein ingestion and

displayed a similar post-exercise time course to that shown by MPS.

Extracellular regulated kinase1/2 (ERK1/2) and p90 ribosomal S6 kinase (p90RSK)

phosphorylation were unaltered after protein ingestion at rest but were elevated

(P & #8195;< & #8195;0.05) above fasted early in recovery (1 & #8195;h) and were

greater for the exercised-fed leg than feeding alone (main effect;

P & #8195;< & #8195;0.01). Eukaryotic elongation factor 2 (eEF2) phosphorylation was

also less (main effect; P & #8195;< & #8195;0.05) in the exercised-fed leg than in

the rested leg suggesting greater activity after exercise. Eukaryotic initiation

4E binding protein-1 (4EBP-1) phosphorylation was increased

(P & #8195;< & #8195;0.05) above fasted to the same extent in both conditions.

Conclusion: & #8194; Our data suggest that resistance exercise followed by protein

feeding stimulates MPS over that induced by feeding alone in part by enhancing

the phosphorylation of select proteins within the mammalian target of rapamycin

(p70S6K, eEF2) and by activating proteins within the mitogen-activated protein

kinase (ERK1/2, p90RSK) signalling.

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Nutrient provision increases signalling and protein synthesis in human skeletal

muscle after repeated sprints.

Eur J Appl Physiol. 2010 Dec 17. [Epub ahead of print]

Coffey VG, DR, Burd NA, Rerecich T, Stellingwerff T, Garnham AP,

SM, Hawley JA.

Abstract

The effect of nutrient availability on the acute molecular responses following

repeated sprint exercise is unknown. The aim of this study was to determine

skeletal muscle cellular and protein synthetic responses following repeated

sprint exercise with nutrient provision. Eight healthy young male subjects

undertook two sprint cycling sessions (10 × 6 s, 0.75 N m torque kg(-1), 54 s

recovery) with either pre-exercise nutrient (24 g whey, 4.8 g leucine, 50 g

maltodextrin) or non-caloric placebo ingestion. Muscle biopsies were taken from

vastus lateralis at rest, and after 15 and 240 min post-exercise recovery to

determine muscle cell signalling responses and protein synthesis by primed

constant infusion of L: -[ring-(13)C(6)] phenylalanine. Peak and mean power

outputs were similar between nutrient and placebo trials. Post-exercise

myofibrillar protein synthetic rate was greater with nutrient ingestion compared

with placebo (~48%, P < 0.05) but the rate of mitochondrial protein synthesis

was similar between treatments. The increased myofibrillar protein synthesis

following sprints with nutrient ingestion was associated with coordinated

increases in Akt-mTOR-S6K-rpS6 phosphorylation 15 min post-exercise (~200-600%,

P < 0.05), while there was no effect on these signalling molecules when exercise

was undertaken in the fasted state.

For the first time we report a beneficial effect of nutrient provision on

anabolic signalling and muscle myofibrillar protein synthesis following repeated

sprint exercise. Ingestion of protein/carbohydrate in close proximity to

high-intensity sprint exercise provides an environment that increases cell

signalling and protein synthesis.

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Nutritional modulation of training-induced skeletal muscle adaptation.

Hawley JA, Burke LM, SM, Spriet LL.

J Appl Physiol. 2010 Oct 28. [Epub ahead of print]

Abstract

Skeletal muscle displays remarkable plasticity enabling substantial adaptive

modifications in its metabolic potential and functional characteristics in

response to external stimuli such as mechanical loading and nutrient

availability. Contraction-induced adaptations are largely determined by the mode

of exercise and the volume, intensity and frequency of the training stimulus.

However, evidence is accumulating that nutrient availability serves as a potent

modulator of many acute responses and chronic adaptations to both endurance and

resistance exercise. Changes in macronutrient intake rapidly alter the

concentration of blood-borne substrates and hormones causing marked

perturbations in the storage profile of skeletal muscle and other

insulin-sensitive tissues. In turn, muscle energy status exerts profound effects

on resting fuel metabolism and patterns of fuel utilization during exercise, as

well as acute regulatory processes underlying gene expression and cell

signalling. As such, these nutrient-exercise interactions have the potential to

activate or inhibit many biochemical pathways with putative roles in training

adaptation.

This review provides a contemporary perspective of our understanding of the

molecular and cellular events that take place in skeletal muscle in response to

both endurance and resistance exercise commenced after acute and/or chronic

alterations in nutrient availability (carbohydrate, fat, protein and several

antioxidants). Emphasis is on the results of human studies and how nutrient

provision (or lack of) interacts with specific contractile stimulus to modulate

many of the acute responses to exercise, thereby potentially promoting or

inhibiting subsequent training adaptation.

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Curr Opin Clin Nutr Metab Care. 2010 Nov;13(6):630-4.

Resistance exercise and appropriate nutrition to counteract muscle wasting and

promote muscle hypertrophy.

Glover EI, SM.

Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

Abstract

PURPOSE OF REVIEW: Loss of skeletal muscle mass is a common feature of a number

of clinical scenarios including limb casting, bed rest, and various disorders

such as HIV-AIDS, sepsis, cancer cachexia, heart failure, and uremia. Commonly,

muscle disuse (hypodynamia) is the sole reason, or a large part, of why muscle

mass is lost. The reduction in strength, or dynapenia, that accompanies these

conditions is also a function of the degree of hypodynamia and is related to

muscle loss.

RECENT FINDINGS: The major and consistent finding in a number of human-based

models of muscle wasting is a decline in the synthesis of new muscle proteins

both in the postabsorptive and fed states. Thus, countermeasures are best suited

to those that augment muscle protein synthesis and not those that attempt to

counteract proteolysis. Our main thesis is that retention of muscle mass in

wasting conditions will be achieved to the greatest extent by focussing on

increased muscle use with moderate-to-high resistance loads as the primary

countermeasure with a secondary countermeasure being to provide adequate

nutritional support. Either intervention alone will alleviate some part of

hypodynamia-induced muscle mass loss and dynapenia; however, together nutrition

and muscular contraction will result in greater mitigation of muscle loss.

SUMMARY: Advances in our understanding of hypodynamia-induced muscle loss, a

condition common to almost all syndromes of muscle wasting, has led to a focus

on reduced basal and feeding-induced elevations in protein synthesis.

Countermeasures for wasting should focus on stimulating anabolism rather than

alleviating catabolism.

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Carruthers

Wakefield, UK