DOMs and Inflammation

Good answer Dan :D

The way I look at it, is if we have too low of blood amino levels, especially right after training, we might be asking for trouble. mTOR is very AA sensitive, especially during a rebound from a workout. If blood AA is low, and insulin is low there could be a good amount of supression.

Ron
 
This is a back-to-basics question I guess...

MPD - is this term used to describe the proteins being broken down due to mechanical strain - the way anything will be under enough tension...or is it used to describe MP being used as an energy source..?
 
Ok, so, obviously I have had a lot of experience in losing muscle while trying to get lean, but I never considered that the workout alone might be responsible.  Is that what we are saying?  If my protein stays high, and my calories are at maintenance or slightly below, I might still be losing muscle through my workouts (it seems like Bryan has always said not to change your training just because you are trying to cut rather than bulk -- you need the stimulus to maintain as much mass as possible)?

I also lost you, DKM, in some of the abbreviations. I think I got the gist, though.
 
For the guys who got lost in abbreviations, here ya go:

PSMF - Protein Sparing Modified Fast
MHC - Myosin Heavy Chain
FSR - Fractional Synthesis Rate
FBR - Fractional Breakdown Rate
MPS - Muscle Protein Synthesis
MPD - Muscle Protein Degradation

Regards,
-JV
 
[b said:
Quote[/b] ]MPD - is this term used to describe the proteins being broken down due to mechanical strain - the way anything will be under enough tension...or is it used to describe MP being used as an energy source..?
Click to expand...
MPD is increased protein breakdown which can actually be the result of many things, not just due to mechanical strain of the workout - for example, fasting (early only; prolonged fasting tends to gradually decrease protein breakdown as the body adapts to the environment of little food available) and denervation.
 
[b said:
Quote[/b] (semajes @ Oct. 10 2005,1:00)]Ok, so, obviously I have had a lot of experience in losing muscle while trying to get lean, but I never considered that the workout alone might be responsible.  Is that what we are saying?  If my protein stays high, and my calories are at maintenance or slightly below, I might still be losing muscle through my workouts (it seems like Bryan has always said not to change your training just because you are trying to cut rather than bulk -- you need the stimulus to maintain as much mass as possible)?

I also lost you, DKM, in some of the abbreviations.  I think I got the gist, though.
Click to expand...
Which is why Bryan says this. The decrease in breakdown which occurs during periods of training helps reduce the catabolic effect of dieting.

So in other simpler words;

Dieting alone=catabolism with FBR
Dieting with reduced protein=catabolism with more FBR
Dieting with Exercise=catabolism with less FBR
Dieting with exercise with adquate protein=catabolism with less FBR than dieting with exercise alone.

JV, good job and thanks for defining the abbreviations
 
And more than MPD during the workout, the majority actually happens during the days after the workout. It's part of the remodeling process. All those macrophages in the immune system, ect.
 
So, take a subject who fits under the general "healthy" status, is exercising with heavy-ish weights (5s range) has a sufficient protein intake, caloric intake is in surplus - accounting for exercise - ...why does MPD occur?
 
I would assume that MPD always occurs as part of the remodeling process. Under the conditions described (heavy weights, adequate calories), I would guess that synthesis simply outweighs degradation.

Am I close?
 
Yes.
But again, it's not just that. MPD occurs thanks to a lot of other things:

-Fasting (Early)
-Acidosis: Diabetes mellitus (Uncontrolled)
-Paraneoplastic
-Metabolic: Uremia; Sepsis; Burns; Hyperthyroid
-Inactivity: Denervation; Disuse
-Glucocorticoids: Inhibited by insulin
-Cytokines
      --Interferon-Y (IFN-Y - induces proteasome activator (PA28)
             20S core proteasome subunits)
      -- Protein cleavage

These arent stuff bodybuilders aren't interested in, most of these aren't even connected in anyway to hypertophy. MPD is a natural thing. The broken down muscle protein results in free amino acids (obviously) which is then used for hepatic gluconeogenesis, energy generation in muscles (BCAA's), or lost in urine (specifically the 3-methylhistidine from myofibrillar proteins, actin & myosin).

The important thing is not stopping MPD as I doubt that is possible, but rather raising MPS over MPD levels, which is what proper weightlifting and diet achieve: more protein FSR than FBR, so in the end we get a net gain.
 
Right on the money with all that info.
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MHC's have a half life of about 14 days, so that shows just how much breakdown is going on. It's like a building with a wrecking crew taking stuff apart while another crew is using most of the left overs to put things back together again. on and on....
 
[b said:
Quote[/b] (dkm1987 @ Oct. 11 2005,2:27)]Which is why Bryan says this. The decrease in breakdown which occurs during periods of training helps reduce the catabolic effect of dieting.
So in other simpler words;
Dieting alone=catabolism with FBR
Dieting with reduced protein=catabolism with more FBR
Dieting with Exercise=catabolism with less FBR
Dieting with exercise with adquate protein=catabolism with less FBR than dieting with exercise alone.
Click to expand...
Im guessing you mean MPB rather than FBR as one has a time component :) and the other is a more generic term with no set time component.
 
For interests sake, a couple of charts to show the 'differences' between measurement of FSR and MPS (it also shows MPB in this - FBR is a similar concept to FSR)

One has a time component in the measurement as a requirement. The other just has a time component for utilities sake (they can measure MPS all day if needed, but it has a IV into the leg so most people may not like it.)
 
Do you want it on a silver platter :D

copied from one of the papers.

[b said:
Quote[/b] ]The three-pool model enables the calculation of the rate of amino acid delivery to the leg (Fin), the rate at which amino acids leave the leg (Fout), the rate of inward (FM,A) and outward (FV,M) muscle transmembrane transport, the rate at which they are shunted from the artery to the vein without entering the intracellular space (FV,A), the rate of intracellular appearance (FM,0) of the amino acids (from protein breakdown when phenylalanine is used), and the rate of amino acid utilization (F0,M; for protein synthesis for phenylalanine, because it is not oxidized in muscle).
Click to expand...

[b said:
Quote[/b] ]Additionally, we determined the FSR of muscle proteins by measuring the incorporation rate of L-[ring-2H5]phenylalanine into the proteins with the precursor-product model (10).

FSR 5 (DEP/t)/[(EM(1) 1 EM(2))/2] · 60 · 100 (10)

where DEP is the increment of protein bound phenylalanine
enrichment between two sequential biopsies, t is the time
interval between the two sequential biopsies, and EM(1) and
EM(2) are the phenylalanine enrichments expressed as tracerto-tracee ratio in the free muscle pool in the two subsequent biopsies. The results are expressed in percent per hour.
Click to expand...
 
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