Insight into RBE or rather PS in the trained state

dkm1987

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<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> J Physiol. 2008 Aug 1;586(Pt 15):3701-17. Epub 2008 Jun 12. Links
Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle.Wilkinson SB, Phillips SM, Atherton PJ, Patel R, Yarasheski KE, Tarnopolsky MA, Rennie MJ.
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1.

Resistance (RE) and endurance (EE) exercise stimulate mixed skeletal muscle protein synthesis. The phenotypes induced by RE (myofibrillar protein accretion) and EE (mitochondrial expansion) training must result from differential stimulation of myofibrillar and mitochondrial protein synthesis. We measured the synthetic rates of myofibrillar and mitochondrial proteins and the activation of signalling proteins (Akt-mTOR-p70S6K) at rest and after an acute bout of RE or EE in the untrained state and after 10 weeks of RE or EE training in young healthy men. While untrained, RE stimulated both myofibrillar and mitochondrial protein synthesis, 67% and 69% (P &lt; 0.02), respectively. After training, only myofibrillar protein synthesis increased with RE (36%, P = 0.05). EE stimulated mitochondrial protein synthesis in both the untrained, 154%, and trained, 105% (both P &lt; 0.05), but not myofibrillar protein synthesis. Acute RE and EE increased the phosphorylation of proteins in the Akt-mTOR-p70S6K pathway with comparatively minor differences between two exercise stimuli. Phosphorylation of Akt-mTOR-p70S6K proteins was increased after 10 weeks of RE training but not by EE training. Chronic RE or EE training modifies the protein synthetic response of functional protein fractions, with a shift toward exercise phenotype-specific responses, without an obvious explanatory change in the phosphorylation of regulatory signalling pathway proteins.</div>

I found this interesting because it indicates what other research has begun to show as well. In which the idea that PS elevations drop with prolonged training may be true but when looking strictly at myofibrillar PS it doesn't stop completely. Albeit it definately reduces by about half, yet mitochondrial PS virtually stops increasing post work out in the trained state.

For those who are concerned about RBE you can rest assured that myofibrillar PS is still occurring even after training for a while, just not at the same level as an untrained person.
 
This puts the veteran lifter in a difficult situation. This study and others like it demonstrate that not only does protein synthesis shrink in magnitude, but also in duration after a workout in veteran lifters. To me, this may indicate a benefit for more frequent bouts...but...

This, however, poses its own set of problems. As a lifter adapts to years of training, they become considerably stronger than the average person. This means that at any given percentage of his/her 1RM, the veteran lifter is using considerably more weight. This additional weight poses higher risks to connective tissue (tendons, ligaments) in the veteran lifter. Increasing the frequency in training decreases the time allowed for this soft tissue to recover between bouts...often leading to chronic inflammatory problems.
 
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(Bryan Haycock @ Oct. 09 2008,1:18)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">This study and others like it demonstrate that not only does protein synthesis shrink in magnitude, but also in duration after a workout in veteran lifters.</div>
Since this is a discussion thread this is one area in the literature that I feel lacks support especially in the realm of specific fractions of PS. We can see that in this paper there is an obvious response difference as one becomes accustomed but it is most notably seen in sarcoplasmic protein synthethic rates.

In the earlier work you are referring too I don't recall them looking at various fractions (and I could be off there as it's been a while since I looked at that paper) and instead chose to look at total muscle protein synthesis. So to say that the reduction seen in duration would hold true in myofibrillar may not be seen. Unfortunately with the slower turnover of myofibrillar protein the time needed to actually see the change may need a complete shift in testing measures which would cause them to think out of the box for a change.

In Tang et al. they also missed the mark (but did a little better) in that they did measure fractional synthesis rates but chose to measure it in the post training period (one week after last workout bout) with an intensity that was below the maximum acheived.

So if we are lucky perhaps the academics will begin to look a little closer in the near future.

Diverging thoughts are of course welcome.
 
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