Anabolic processes in human skeletal muscle

[dkm1987]

http://www.physsportsmed.com/index.php?article=1814

"Instead, our data indicate that exercise-induced hormonal elevations do not enhance intracellular markers of anabolic signaling or the acute postexercise elevation of myofibrillar protein synthesis. Furthermore, data from our training study demonstrate that exercise-induced increases in GH and testosterone availability are not necessary for and do not enhance strength and hypertrophy adaptations."

 

[grunt11]

Although load does not appear to be a crucial factor in creating an acute anabolic response, we have recently observed that 3 sets of resistance exercise enhance both the intracellular signals and the rate of myofibrillar protein synthesis versus 1 set.40 In other words, certain regulatory anabolic signaling proteins (ie, p70S6K1) appear to remain active for a longer duration following 3 sets versus 1 set of resistance exercise at 70% of 1RM. Specifically, p70S6K1, whose activation is correlated with increases in myofibrillar protein synthesis41 and hypertrophy,42,43 appears to be rejuvenated by protein ingestion 24 hours after exercise, particularly if 3 sets were performed. Thus, it appears that repeat exercise sets may allow for the repeated activation of type II fibers, which may be responsive to either unknown volume-sensitive mechanisms, or may simply require multiple sets to be recruited and anabolically active.

I’m curious under what conditions they tested this and how the spacing of the three sets effect the net length of time that the anabloic signaling proteins remain active. In others words which would create a longer net anabolic effect doing 3 sets per workout every other day or 3 sets spread out AM/PM day one and AM day 2 then AM/PM day 3 etc. . . .

 

[dkm1987]

They did not look at anything but consecutive sets but another study previously looked at divided workouts in rats in which they saw that stacked training, 3 or 4 sets divided by 3hrs between each, showed a somewhat negative response in that many inflammatory signals where more elevated but and IMO most importantly p70S6k was elevated longer and regardless of the lack in phosphorylation state of Akt.

You can also look up the studies by Haddad and Adams (JAP 2002), which have been discussed a multitude of times here on HST, which looked at workouts with 8, 12, and 24 hours between bouts. Albeit and again these were in rats and the human response may be completely different. Unfortunately when they did a follow up in JAP 2005 they only used two bouts separated by 24 hours and instead of voluntary RT they used NMES.

Med Sci Sports Exerc. 2007 Dec;39(12):2135-44. Effect of high-frequency resistance exercise on adaptive responses in skeletal muscle.


J Appl Physiol. 2005 Feb;98(2):482-8. Epub 2004 Oct 1. Time course of molecular responses of human skeletal muscle to acute bouts of resistance exercise.


J Appl Physiol. 2002 Jul;93(1):394-403. Selected contribution: acute cellular and molecular responses to resistance exercise.

 

[anoop]

Here is another one:

http://www.ncbi.nlm.nih.gov/pubmed/20541030

Int J Biochem Cell Biol. 2010 Sep;42(9):1371-5. Epub 2010 Jun 9.
Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process.
West DW, Burd NA, Staples AW, Phillips SM.

Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Canada.
Abstract
Muscle cells (fibres) are post-mitotic and thus undergo changes in phenotype by modifying their existing structure. Hypertrophy is a hallmark change that occurs in response to increased loading and can be achieved in humans through repeated bouts of resistance exercise (i.e., training). In resistance exercise, contractions are initiated by neural drive leading to immediate perturbations such as calcium influx, cross-bridge cycling and tension/stress on the cytoskeleton, sarcolemma and extracellular matrix, as well as more delayed cellular events such as the production/release of potential local growth factors (e.g., IGF-1). Resistance exercise can also elevate the systemic concentration of certain hormones (growth hormone, testosterone, IGF-1) that are hypothesized to drive hypertrophy. However, while these hormones are clearly anabolic during childhood and puberty, or when given at supraphysiological exogenous doses, the transient post-exercise elevations in hormone concentration are of little consequence to the either the acute protein synthetic response or to a hypertrophic phenotype after resistance training. Thus, the acute post-exercise increases in systemic hormones are in no way a proxy marker for anabolism since they do not underpin the capacity of the muscle to hypertrophy in any measurable way. In contrast, the acute activation of intrinsically located signalling proteins such as p70(S6K) and the acute elevation of muscle protein synthesis are more reflective of the potential to increase in muscle mass with resistance training. Ultimately, local mechanisms are activated by the stress imposed by muscle loading and prime the muscle for protein accretion. Membrane-derived molecules and tension-sensing pathways are two intrinsic mechanisms implicated in upregulating the synthesis and incorporation of muscle proteins into the myofibre in response to mechanical stress derived from loaded contractions.

 

[grunt11]

Thanks for those references Dan, I’m checking them out right now. Using general keywords like “frequency” was generating a lot of noise but searching for comments on those studies is exactly what I was looking for.