I think what mavros is trying to say is that acute adaptations like protein synthesis cannot accurately predict long term muscular adaptations. And this is very true in any field or with any acute adaptation.

But I think in the case of protein synthesis, there is data to show that these acute adaptation can predict muscular adaptations. I think 2 studies which stand out int his regard is the milk and soy and the exercise induced hormone study. Both showed favorable acute adaptations and prompted the researcher to carry out long term studies which came out to support their hypothesis. So most good researchers if they are doing an acute studies, do mention if there is any data to support the that these acute adaptations are consistent with long term changes.

acute adaptations like protein synthesis cannot accurately predict long term muscular adaptations. And this is very true in any field or with any acute adaptation.

Yep…I think we’re all in furious agreement now.

it’s interesting to speculate on what happens when trainees’ gains become less and less as time goes by and eventually reach the point where more growth is almost impossible. Something interesting is definitely going on there

Agreed.  The broader explanation is fairly straightforward - evolutionary pressures on sustaining larger body mass selected for genetic limitations on size - hence the difficulty in eliciting net positive MPS above a certain threshold.

I suppose this is another reason why I keep banging on about homeostasis (in the context of acute versus chronic adaptations) - the body really does have an immensely powerful range of compensatory responses to acute changes, all in service of returning the body to homeostasis (e.g. insulin in response to blood sugar rises, increased thermogenesis and other NEAT in response to calorie excess, kidney response to acid-base irregularities etc.). 

Cheers
Mav

I am curious to know what happens biologically when you hit genetic limits. Does the muscle get resistant to damage or mechanical tension or the muscle is still sensitive but the protein synthetic machinery isn’t responding or both?

anoopbal - 01 August 2010 03:11 PM

I am curious to know what happens biologically when you hit genetic limits. Does the muscle get resistant to damage or mechanical tension or the muscle is still sensitive but the protein synthetic machinery isn’t responding or both?

If we going back to this thread
http://www.exercisebiology.com/index.php/forums/viewthread/263/

and suppose that damage is occurs only if energetic resources of muscle cell is depleted we have a simple explanation to “genetic limit” situation. With training we improve the energetic abilities of muscles - therefor there is hard to make energetic deficit and damage the fibers.
So SD have its logical explanation - by resting for 10-14 days we lower the energetic abilities of muscle and new cycle might damage them more.
I’m sorry if this theory sound lame or retarded, I’m lack of deep biochemistry knowledge

Well, if energetic depletion was the only stimulus for hypertrophy that would be a good theory, but it probably isn’t.

Karky - 02 August 2010 10:40 AM

Well, if energetic depletion was the only stimulus for hypertrophy that would be a good theory, but it probably isn’t.

energetic depletion->muscle damage->hypertrophy

Since we improve an energetic ability with training it’s harder and harder to damage muscle fibers.

What about tension -> muscle damage -> hypertrophy? or just tension ->  increase in MPS -> hypertrophy?

I’ve never seen any evidence suggesting that energetic depletion causes muscle damage. I’ve seen the thread here about the rigor mortis hypothesis, that low ATP levels would cause rigor and thus muscle damage, but as far as I know that’s never been tested, and ATP levels don’t even get close to 0 when you exercise. Also, that muscle damage is necessary for hypertrophy has never been proved as far as I know. We don’t know if the increases in MGF, etc that we see in muscle after exercise is the result of damage or something else.

Karky - 02 August 2010 04:29 PM

What about tension -> muscle damage -> hypertrophy? or just tension ->  increase in MPS -> hypertrophy?

Sounds about right.
But the first step is unclear to me.
How exactly tension causes damage? Is any tension causes damage?
Why RBE effect doesn’t eliminates damage completely after 10-20 workouts?
How fatigue plays it’s role in this process?

Karky - 02 August 2010 04:29 PM

I’ve never seen any evidence suggesting that energetic depletion causes muscle damage. I’ve seen the thread here about the rigor mortis hypothesis, that low ATP levels would cause rigor and thus muscle damage, but as far as I know that’s never been tested, and ATP levels don’t even get close to 0 when you exercise.

Yes. But may be it not suppose to drop to 0 to make a damage

Karky - 02 August 2010 04:29 PM

Also, that muscle damage is necessary for hypertrophy has never been proved as far as I know. We don’t know if the increases in MGF, etc that we see in muscle after exercise is the result of damage or something else.

Exactly. Some experiments on rats shows hypertrophy without damage and fatigue
Occlusion studies shows hypertrophy without damage. Although I think it mostly sarcoplasmic one, not miofibriaal

How exercise causes muscle damage is actually not known. Could be directly by rupturing membranes, or it could be that intracellular stuff like filaments rupture. One cool hypothesis is that as you stretch muscle, specially under load, the actin filaments will be pulled far from the myosinfilaments and when the muscle returns to it’s original length the actin filaments might slide into a different “slot” than they are supposed to and then causes further disturbances that lead to damage. There are also hypothesis that say free radicals produced during exercise can cause muscle damage or make the damage created by one of the previous mechanisms worse. And damage might not be needed. Tension could be sensed in something called focal adhesion complexes, which are molecules that go from the inside of the cell to the outside and attach the cell to the extracellular matrix. Some believe that stretching of these could cause phosphorylation of different proteins inside the muscles and that this leads to the signaling behind MPS (mTOR, PKB, etc)

Doesn’t the repeated bout effect get rid of muscle damage? If you do the same workout with the same weights for several bouts I’m pretty sure you get less and less damage. If you increase the weight, however, you’ll get more tension than the body is used to again.

ATP might not have to drop to 0 to stick some filaments in rigor, but it would have to get pretty close. Also, I’ve never seen this mentioned anywhere in the scientific literature. Of course that doesn’t mean that it can’t happen, but I seriously doubt that this is the cause of muscle damage and/or hypertrophy.

I wonder if we can determine whatever particular training method will lead to muscle damage or not.
I mean we know that heavy eccentric movements leads to damage, and occlusion training not.
Is it function of load only?

Well, since we don’t know yet what actually causes muscle damage we can’t. I think tension and stretch plays a large role, so if you do heavy full ROM exercises, you should get some damage. But the ROM you’re accustomed to probably also plays a role, so if you increase your ROM you should get some damage and when you’re used to full ROM exercises they might not produce damage anymore