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(QuantumPositron @ Nov. 17 2007,03:41)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Dan,
What about the 'sarcoplasmic hypertrophy' that people mention - glycogen and fluid stores and what not. Is there any research that suggests that higher volume workouts with moderate intensity cause a sort of supercompensation of this tissue? Perhaps by accumulating more glycogen or what not? My question originates from the obvious differences in physique between bodybuilders, lean power lifters, and lean Olympic lifters. My perception is that many bodybuilders still use the high volume approach and have larger, fuller muscles than lean PLs and OLs. I know that much of the strength of the latter two groups comes from CNS and technical training. Am I comparing apples to oranges? There are studies concluding that elite bodybuilders and elite OL's have similar levels of hypertrophy with insignificant differences between groups, but that the bodybuilders still had significantly larger muscles, the reason for which could not be determined (I can fetch this article if you'd like to see it, but its late so I'm moving fast).
I have this crazy idea that once muscle glycogen and/or perhaps liver glycogen is depleted below some threshold (isn't there always a threshold?), that some manner of superaccumulation occurs in the muscle to provide reserves for a possible future bout and that this accumulation contributes to muscle size and shape. It isn't disputed in the running world that carb loading allows you to store more carbs for a short time. Runners use it to carb up for a race. Granted this a distinct mechanism and granted my imagi-reasoning is pseudo-scientific but I've been chewing on it for a while now and wanted to know your thoughts.</div>
QP, not that I'm aware of (speaking of supercomensation in BB). As far as sarcoplasmic hypertrophy, one first must understand that the actual protein fractions, sarcoplasmic versus myofiber, all increase during PS caused by training.
Naturally there are other adaptations as well such as lactate clearance, and such.
I posted a paper on the blog that used an ischemic training model and it clearly stated that the ischemia did cause a much higher glycogen and lactate content in the tissue. Unfortunately they didn't mention how much.
But this isn't quite the same as moderate loading with high rep sets and little rest between sets.
When looking at some competitive lifters I have seen shoulders on some of these guys that BBs would kill for so I think the difference is more owing to the specific movements and body parts that are trained versus the training method itself.
There is some work that shows that the difference in hypertrophy seen may be more owing to the selective hypertrophy of Type II fibers in Weight Lifters. Tesch, many years ago, noted that the percentage of FT fibers was less, mean fiber area was smaller and selective FT fiber hypertrophy was not evident in comparison of BB to WL, Tesch (1982). In some later work by Tesch he notes that bodybuilders in contrast to Olympic weight- and power lifters, display a small increase in number of capillaries per fiber. He also noted that the glycogen storage capacity is increased in OL and PL but enzyme activities reflecting anaerobic metabolism did not increase in response to heavy resistance exercise. When Tesch (1989) dug further into the enzyme changes he noted CS (citrate synthase) activity of ST fibers and MK (myokinase) activity of FT fibers were higher in BB compared to OL/PL. BB displayed greater fiber size than OL/PL. FT vs. ST area was greater in OL/PL than BB. indicating that the mode of training did induce specific metabolic adaptations of FT and ST fiber types. When Fry (2004) looked at the impact of relative intensity what he noticed was when comparing competitive lifters, those typically utilizing the heaviest loads, IE weightlifters and powerlifters, exhibited a preferential hypertrophy of type II fibres compared with body builders who appeared to equally hypertrophy both type I and type II fibres. Obviously there is some impact either metabolically or because of recruitment or both that impact the hypertrophy of differing fiber populations now whether or not adding in a brief rest between reps changes these enzymatic reactions I don't know but when looking at MS it's clear that not only do we lift a respectable load, for a respectable amount of work, but we also should be causing a significant recruitment and therefore training of Type II fibers by always trying to lift the concentric portion as fast as possible.
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haha, but i'm guessing you restest your maxes round the end of your cycle or so??
