<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 < 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 < 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.