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(JAMR @ Oct. 31 2006,04:45)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">[/b]In addition, there appeared to be a strong dose response relation between the concentration of insulin and phosphorylation of mTOR and p70 S6 kinase (M. J. Rennie, P. L. Greenhaff, and H. Wackerhage, unpublished results). These results strongly suggest that, in the absence of insulin, AAs are able to signal their presence without involvement of p70 S6 kinase or mTOR, but that the effects of insulin and AAs must share a final common pathway because the effects are maximal in the presence of high physiological insulin concentrations. It is possible that AAs signal through other nutrient-sensing and signaling pathways involving eukaryotic initiation factor 2B and glycogen synthase kinase or hitherto unrecognized pathways involving protein kinase B.
27. Greenhaff PL, Peirce N, Simpson E, Hazell M, Babraj J, Waddell T, Smith K, Rennie M. Dose-response relationship during hyperaminoacidaemia between insulin and leg protein turnover in healthy young men studied by tracer amino acid exchange. J Physiol 2005;558P.</div>
And that is one reason why nutrition response is additive to the response of mechaincal strain. The PI3-K path is involved in insulin response whereas mTOR and P70 can be effected without nutritional intervention. But, as Aaron points out there is no human research indicating that a higher magnitude of insulin is better. In fact Kubica shows that diabetic rats can grow just fine (limited versus non diabetic but still grow significantly) during weight training type exercise.
Barr and Esser showed that P70 and mTOR can be manipulated via strictly mechanical sensing even in the face of fasting.
As Aaron is pointing out the role of insulin is more permissive than causative.
(JAMR @ Oct. 31 2006,04:45)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">[/b]In addition, there appeared to be a strong dose response relation between the concentration of insulin and phosphorylation of mTOR and p70 S6 kinase (M. J. Rennie, P. L. Greenhaff, and H. Wackerhage, unpublished results). These results strongly suggest that, in the absence of insulin, AAs are able to signal their presence without involvement of p70 S6 kinase or mTOR, but that the effects of insulin and AAs must share a final common pathway because the effects are maximal in the presence of high physiological insulin concentrations. It is possible that AAs signal through other nutrient-sensing and signaling pathways involving eukaryotic initiation factor 2B and glycogen synthase kinase or hitherto unrecognized pathways involving protein kinase B.
27. Greenhaff PL, Peirce N, Simpson E, Hazell M, Babraj J, Waddell T, Smith K, Rennie M. Dose-response relationship during hyperaminoacidaemia between insulin and leg protein turnover in healthy young men studied by tracer amino acid exchange. J Physiol 2005;558P.</div>
And that is one reason why nutrition response is additive to the response of mechaincal strain. The PI3-K path is involved in insulin response whereas mTOR and P70 can be effected without nutritional intervention. But, as Aaron points out there is no human research indicating that a higher magnitude of insulin is better. In fact Kubica shows that diabetic rats can grow just fine (limited versus non diabetic but still grow significantly) during weight training type exercise.
Barr and Esser showed that P70 and mTOR can be manipulated via strictly mechanical sensing even in the face of fasting.
As Aaron is pointing out the role of insulin is more permissive than causative.
