Brian, Viscious... DKM....

NWlifter

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Mechanism of work-induced hypertrophy of skeletal muscle.

Goldberg AL, Etlinger JD, Goldspink DF, Jablecki C.

Skeletal muscle can undergo rapid growth in response to a sudden increase in work load. For example, the rat soleus muscle increases in weight by 40% within six days after the tendon of the synergistic gastrocnemius is sectioned. Such growth of the overworked muscle involves an enlargement of muscle fibers and occasional longitudinal splitting. Hypertrophy leads to greater maximal tension development, although decreased contraction time and reduced contractility have also been reported. Unlike normal developmental growth, work-induced hypertrophy can be induced in hypophysectomized or diabetic animals. This process thus appears independent of growth hormone and insulin as well as testosterone and thyroid hormones. Hypertrophy of the soleus can also be induced in fasting animals, in which there is a generalized muscle wasting. Thus muscular activity takes precedence over endocrine influences on muscle size. The increase in muscle weight reflects an increase in protein, especially sarcoplasmic protein, and results from greater protein synthesis and reduced protein breakdown. Within several hours after operation, the hypertrophying soleus shows more rapid uptake of certain amino acids and synthesis of phosphatidyl-inositol. By 8 hours, protein synthesis is enhanced. RNA synthesis also increases, and hypertrophy can be prevented with actinomycin D. Nuclear DNA synthesis also increases on the second day after operation and leads to a greater DNA content. The significance of the increased RNA and DNA synthesis is not clear, since most of it occurs in interstitial and satellite cells. The proliferation of the non-muscle cells seems linked to the growth of the muscle fibers; in addition, factors causing muscle atrophy (e.g. denervation) decrease DNA synthesis by such cells. In order to define more precisely the early events in hypertrophy, the effects of contractile activity were studied in rat muscles in vitro. Electrical stimulation enhanced active transport of certain amino acids within an hour, and the magnitude of this effect depended on the amount of contractile activity. Stimulation or passive stretch of the soleus or diaphragm also retarded protein degradation. Presumably these effects of mechanical activity contribute to the changes occuring during hypertrophy in vivo. However, under the same conditions, or even after more prolonged stimulation, no change in rates of protein synthesis was detected. These findings with passive tension in vitro are particularly interesting, since passive stretch has been reported to retard atrophy or to induce hypertrophy of denervated muscle in vivo. It is suggested that increased tension development (either passive or active) is the critical event in initiating compensatory growth.

Muscle ultrastructural characteristics of elite powerlifters and bodybuilders.

MacDougall JD, Sale DG, Elder GC, Sutton JR.

Muscle ultrastructure of a group of subjects possessing extreme hypertrophy was compared with that of a control group which had undergone 6 months of heavy resistance training. Two needle biopsies were taken from triceps brachii of two international calibre powerlifters and five elite bodybuilders. In addition, samples were taken from five healthy volunteers before and after 6 months of training of the elbow extensors. One biopsy was prepared for electron microscopy and analyzed stereologically, and the other was stained for myosin ATPase activity and photographed under the light microscope. Despite large differences in elbow extension strength and arm girth there was no significant difference in fibre areas or percentages of fibre types between the elite group and the trained controls. This suggests that the elite group possessed a greater total number of muscle fibres than the controls did. Mitochondrial volume density of the elite group was similar to that of the control group following training but significantly less (p less than 0.05) than the pretraining control measurements. Myofibrillar volume density was significantly lower and cytoplasmic volume density significantly higher in the elite group than in the trained controls. There was a considerably higher incidence of structural abnormalities including central nuclei and atrophied fibres in the elite group than in the control group, which might possibly have been associated with the use of anabolic steroids by the elite group.
 
Hmm . . . but isn't the first study from 1975 and the 2nd from 1982? ;)

My understanding is that your body tries to keep an equilibrium between # of myonuclei and cell volume (though Akerfeldt has a wacky way of interpreting this.) Meaning, you can probably increase the cell volume to a degree before you have to induce more mechanical strain. How one is done exclusively of the other in a typical training program, I'm really not sure though.

I'm wary of the 2nd study because it looks like the elite bodybuilders experienced not only hypertrophy, but hyperplasia. Not sure how that messes with the cytoplasmic volume density.

cheers,
Jules
 
[b said:
Quote[/b] (vicious @ May 10 2005,5:53)]Hmm . . . but isn't the first study from 1975 and the 2nd from 1982?  ;)
My understanding is that your body tries to keep an equilibrium between # of myonuclei and cell volume (though Akerfeldt has a wacky way of interpreting this.)  Meaning, you can probably increase the cell volume to a degree before you have to induce more mechanical strain.  How one is done exclusively of the other in a typical training program, I'm really not sure though.
I'm wary of the 2nd study because it looks like the elite bodybuilders experienced not only hypertrophy, but hyperplasia.  Not sure how that messes with the cytoplasmic volume density.
cheers,
Jules
Hey Jules! Cheers dude! :)

Yeah, they are a bit older but I figure some of the good ones are old ;) I'm old! LOL

I also got to wondering, maybe the sarcoplasmic density slowly increases over time to maybe make up for the messed up surface to volume changes?
I noticed on the one study, the weightlifter types also had increased cytoplasm and we know they aren't doing pumper stuff.....

Thanks for posting on this :D

Ron
 
[b said:
Quote[/b] ]I also got to wondering, maybe the sarcoplasmic density slowly increases over time to maybe make up for the messed up surface to volume changes?
I noticed on the one study, the weightlifter types also had increased cytoplasm and we know they aren't doing pumper stuff.....

I think, generally, the argument goes that the myonuclei-to-cytoplasmic ratio is actually a constant maximum.  When there's increased work output, then a portion of that protein synthesis will cause the cytoplasmic volume to increase significantly until it reaches the maximum ratio.  And likewise, when there is an atrophy, the myonuclei number will stay the same but same cytoplasmic volume will drop.  It could be that short-term muscle memory phenomena, in part, is this cytoplasm volume going up and down.  Just pure speculation:  it could very well be that metabolic work or the erk1/2 signal (plus a crap load food) in part enables muscle to reach its ideal ratio, creating this "quality" muscle we're looking for.   That would seem to intuitively fit my experience as well as the studies.  Then, you can look at the entire hypertrophy process as A) increasing  the effective tank size (the potential cytoplasmic volume) by increasing myonuclei number through progressive strain, then B) filling the gas tank by introducing a significant work element.   Akerfeldt was sort of going in this direction with his ABCDE diet, though he did the whole relationship backwards.

Ah, sarcoplasm.  Who ya gonna call?  Ghostbusters!  :D
cheers,
Jules
 
Changes do occur in the C/N but they are held within a tight guideline. I think what Bryan was saying was that once the C/N reaches it's limits, it can't continue increasing, as the older models thought, so in order for the fiber to continue growth additional nuclea must be contributed.

Concomitant increases in myonuclear and satellite cell content in female trapezius muscle following strength training.
Kadi F, Thornell LE.

A skeletal muscle fibre maintains its cytoplasmic volume by means of hundreds of myonuclei distributed along its entire length. Therefore it is hypothesised that changes in fibre size would involve modifications in myonuclear number. In this study, we have examined whether 10 weeks of strength training can induce changes in the number of myonuclei and satellite cells in female trapezius muscles. Biopsies were taken pre- and posttraining from the upper part of the descending trapezius muscle of nine subjects. Muscle samples were analysed for fibre area and myonuclear and satellite cell number using immunohistochemistry. There was a 36% increase in the cross-sectional area of muscle fibres. The hypertrophy of muscle fibres was accompanied by an approximately 70% increase in myonuclear number and a 46% increase in the number of satellite cells. Myonuclei number was positively correlated to satellite cell number indicating that a muscle with an increased concentration of myonuclei will contain a correspondingly higher number of satellite cells. The acquisition of additional myonuclei appears to be required to support the enlargement of multinucleated muscle cells following 10 weeks of strength training. Increased satellite cell content suggests that mitotic divisions of satellite cells produced daughter cells that became satellite cells.

Effects of high-intensity resistance training on untrained older men. II. Muscle fiber characteristics and nucleo-cytoplasmic relationships.
Hikida RS, Staron RS, Hagerman FC, Walsh S, Kaiser E, Shell S, Hervey S.

During growth and repair of skeletal muscle fibers, satellite cells become activated, undergo mitosis, and a daughter nucleus becomes incorporated into the muscle fiber to increase myonuclear numbers. An increase in myonuclei appears to be required for this postnatal growth. This study examined whether muscle fibers of elderly men can hypertrophy with strength training and, if so, whether they have the capacity to incorporate nuclei into the fibers. The sarcoplasmic area associated with each myonucleus was calculated in nine elderly men before and after 16 weeks of strength training, and compared to nine elderly control men. Muscle fiber type changes and myosin heavy chain composition were also compared. All major fiber types (I, IIA, IIB) became significantly larger after training, and a transition of type IIB fibers to IIA occurred with training. The area occupied by each fiber type correlated with myosin heavy chain percentage, and both of these changed similarly with strength training. The cytoplasm-to-myonucleus ratio increased, but not significantly (p = .07), with muscle fiber hypertrophy. Number of myonuclei per fiber and myonuclei per unit length of muscle fiber increased, but not significantly. Cross-sectional areas of the muscle fibers in untrained elderly men were much smaller than in untrained young men (when compared with our earlier studies). Training increased the sizes of the elderly muscle fibers to that of the untrained young men. This hypertrophy of muscle fibers by 30% with training resulted in no change in the cytoplasm-to-myonucleus ratio. This suggests that the myonuclear population continues to adapt to growth stimuli in the elderly muscles.

Myonuclear domains in muscle adaptation and disease.
Allen DL, Roy RR, Edgerton VR.

Myonuclear domain size varies along the lengths of maturing skeletal muscle fibers.
Rosser BW, Dean MS, Bandman E.

Skeletal muscle adaptation and cell cycle regulation.
Yan Z.

Plasticity of myonuclear number in hypertrophied and atrophied mammalian skeletal muscle fibers.
Allen DL, Monke SR, Talmadge RJ, Roy RR, Edgerton VR.

Ron, I now take you back to the calcium signalling events, AGAIN. I thought we were done with that, guess not.
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Cell fusion in skeletal muscle--central role of NFATC2 in regulating muscle cell size.
Pavlath GK, Horsley V.

BTW, check this out.

http://www.genome.jp/dbget-b....o=04020

Bet you thought I had given up, huh?
 
Hey good insights, I do beleive your right. That fits everything really well. This is good, I'm really glad you guys posted that info. I was completely convinced sarcoplasmic hypertrophy was a myth, then I spotted those studies, but it still didn't sit right. I knew you guys would have some good answers :D

*Now one more question to you guys?
Some people speak of gaining 'fluid and glycogen' from pumping the muscles, The only place this gain could happen would be within the fibers, so that would BE sarcoplasmic hypertrophy. This rules that out then correct?
(Temporary yes, but not long term continual adding of the fluids aka cytoplasm)

DKM - Whoa cool, where did you find that? Man, that's the whole thing right there! I gotta check that out good, thanks :)
 
[b said:
Quote[/b] (NWlifter @ May 11 2005,10:18)]DKM - Whoa cool, where did you find that? Man, that's the whole thing right there! I gotta check that out good, thanks :)
Just browsing during one of my hypertrophy manhunts, the cool thing is, when you click on a green box, it tells what the gene is, and if you click on the "Alternate Process" boxes, the rounded rectangles, it goes to that flowchart. Needless to say this just made my day when I found it. If you go back to Organism List it shows a list of other pathways that can be explored via the same method.
 
Man, that's just freaken cool to be able to do that. I can't beleive someone went through all the trouble to make that. Good job finding it!

Hey you still do those hypertrophy hunts too eh?
What would we do without pubmed and JAP? LOL

Ron
 
[b said:
Quote[/b] (NWlifter @ May 11 2005,5:32)]What would we do without pubmed and JAP? LOL
Well, I wouldn't be Da Pubmed Pimp fo sho. ;)
 
Doesn't this mean the ratio of sarcoplasm to fibrils does change?

Also, it's the opposite of what most say, sarcoplasmic proteins atrophy slower than myofibrills do!


Time course of the response of myofibrillar and sarcoplasmic protein metabolism to unweighting of the soleus muscle.

Munoz KA, Satarug S, Tischler ME.

Department of Biochemistry, University of Arizona Health Sciences Center, Tucson.

Contributions of altered in vivo protein synthesis and degradation to unweighting atrophy of the soleus muscle in tail-suspended young female rats were analyzed daily for up to 6 days. Specific changes in myofibrillar and sarcoplasmic proteins were also evaluated to assess their contributions to the loss of total protein. Synthesis of myofibrillar and sarcoplasmic proteins was estimated by intramuscular (IM) injection and total protein by intraperitoneal (IP) injection of flooding doses of 3H-phenylalanine. Total protein loss was greatest during the first 3 days following suspension and was a consequence of the loss of myofibrillar rather than sarcoplasmic proteins. However, synthesis of total myofibrillar and sarcoplasmic proteins diminished in parallel beginning in the first 24 hours. Therefore sarcoplasmic proteins must be spared due to a decrease in their degradation. In contrast, myofibrillar protein degradation increased, thus explaining the elevated degradation of the total pool. Following 72 hours of suspension, protein synthesis remained low, but the rate of myofibrillar protein loss diminished, suggesting a slowing of degradation. These various results show (1) acute loss of protein during unweighting atrophy is a consequence of decreased synthesis and increased degradation of myofibrillar proteins, and (2) sarcoplasmic proteins are spared due to slower degradation, likely explaining the sparing of plasma membrane receptors. Based on other published data, we propose that the slowing of atrophy after the initial response may be attributed to an increased effect of insulin.
 
Ron, this seems to coincide with what I have seen from Allen, Booth, Haddad, Fitts, and Baldwin. MHC is impacted the most during atrophy from suspension, zero gravity, Spinal Isolation and so on. Allen really looked at myonucleus number, Baldwin at the changes in MHC and differing isoforms, Fitts at function loss.
 
So you've seen this before too then, man, what do you make of it?

1) So the sarcoplasmic ratios can change a bit then, but not enough for 'big CSA' gains or losses?

2) Weird the sarcoplasm atrophies slower, this means, we need to be more concerned with frequency for myofibrillar gains. Maybe those high set/low frequency programs lean the adaptations towards the sarcoplasm?
(maybe steroids somehow aid in sarcoplasmic increases?)
 
[b said:
Quote[/b] (NWlifter @ May 20 2005,6:32)]So you've seen this before too then, man, what do you make of it?
1) So the sarcoplasmic ratios can change a bit then, but not enough for 'big CSA' gains or losses?
2) Weird the sarcoplasm atrophies slower, this means, we need to be more concerned with frequency for myofibrillar gains. Maybe those high set/low frequency programs lean the adaptations towards the sarcoplasm?
(maybe steroids somehow aid in sarcoplasmic increases?)
1. Yes, they do change. From what I have not enough to make a huge difference.
2. I think steroid treatment has more to do with satellite cell activation and donation of available nuclei plus other things. THis in turn wouldn't change the ration only the number.
See; Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men
Am J Physiol Endocrinol Metab 285: E197–E205, 2003.
If you need it let me know I'll email it.
 
Ah ok, thanks :D

I wonder just how much this is (from abstract I posted above)

cytoplasmic volume density significantly higher in the elite group than in the trained controls
 
Effects of anabolic steroids on the muscle cells of strength-trained athletes.

Kadi F, Eriksson A, Holmner S, Thornell LE.

PURPOSE: Athletes who use anabolic steroids get larger and stronger muscles. How this is reflected at the level of the muscle fibers has not yet been established and was the topic of this investigation. METHODS: Muscle biopsies were obtained from the trapezius muscles of high-level power lifters who have reported the use of anabolic steroids in high doses for several years and from high-level power lifters who have never used these drugs. Enzyme-immunohistochemical investigation was performed to assess muscle fiber types, fiber area, myonuclear number, frequency of satellite cells, and fibers expressing developmental protein isoforms. RESULTS: The overall muscle fiber composition was the same in both groups. The mean area for each fiber type in the reported steroid users was larger than that in the nonsteroid users (P < 0.05). The number of myonuclei and the proportion of central nuclei were also significantly higher in the reported steroid users (P < 0.05). Likewise, the frequency of fibers expressing developmental protein isoforms was significantly higher in the reported steroid users group (P < 0.05). CONCLUSION: Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers. We propose that activation of satellite cells is a key process and is enhanced by the steroid use. The incorporation of the satellite cells into preexisting fibers to maintain a constant nuclear to cytoplasmic ratio seems to be a fundamental mechanism for muscle fiber growth. Although all the subjects in this study have the same level of performance, the possibility of genetic differences between the two groups cannot be completely excluded.
 
SInce I don't have the full study it's hard to say what he's inferring by that last sentence.
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