Against Glycogen Repletion...

[jules]

i do apologise for my drunken ramblings- oh gareth please forgive me, mr 90 pints per week?
and since IL-6 has popped up again, it seems constantly elevated levels would be somewhat deleterious:
Overexpression of Il6 leads to hyperinsulinaemia, liver inflammation and reduced body weight in mice,Diabetologia. 2008 Apr 24

[Gareth83]

Originally Posted by jules

i do apologise for my drunken ramblings- oh gareth please forgive me, mr 90 pints per week?

ha ha

it's just I thought I'd read the whole thread through again the other week and found your original posts confusing and offputting especially to someone who may not have been involved in the thread to begin with. Once you grasped the concept of the thread (clearly your drunkenness must have worn off ) you made some excellent points.

Peace brother

[NU_nutrition_TS]

Originally Posted by jules

i do apologise for my drunken ramblings- oh gareth please forgive me, mr 90 pints per week?
and since IL-6 has popped up again, it seems constantly elevated levels would be somewhat deleterious:
Overexpression of Il6 leads to hyperinsulinaemia, liver inflammation and reduced body weight in mice,Diabetologia. 2008 Apr 24

But - again - is this IL-6 secreted from muscle tissue (myokine) or elsewhere (cytokine)?

Also, mice studies should be approached with caution when applying the results to humans...

Although such models are informative, a recent analysis serves as a reminder that mice are not men...

By examining the Mouse Genome Informatics database and the literature, Liao and Zhang identified 120 genes known to be essential for human survival and found that 22% of these are nonessential in mice.

In independent studies, Kobuke et al. and Bartoli et al. found that a missense mutation responsible for a specific type of muscular dystrophy in humans (an R77C substitution in alpha-sarcoglycan) caused no disease phenotype when introduced into mice.

[jules]

the study examined il6 from skeletal muscle, they extrapolated their findings from the mice to suggest :Thus, the pleiotrophic effects of chronically elevated IL-6 levels preclude any obvious usefulness in treating obesity or its associated metabolic complications in man, despite the fact that weight reduction may be expected.

[NU_nutrition_TS]

Well I stand by my previous post: you can't always extrapolate mouse data to humans.

Also, would allowing post workout myokines to do their job constitute 'chronic elevations of IL-6' if you only trained 3-4 times per week?

[jules]

thats a good point Nu, the researchers hardly define chronic (not from the abstract anyway), i should be able to get a copy of the paper from an endo, to see if it alludes to anything further

postulation is the only thing we can work on - unless we can get Hitler and Hess to run ethics committees, they'd sanction a fair few studies

[NU_nutrition_TS]

Not all studies using mouse models find myokines detrimental:

The BUSM researchers suspect that the beneficial effects of muscle growth seen in the MyoMouse are mediated through the production and secretion of a variety of signaling factors. Walsh and his colleagues are currently identifying the novel proteins in muscle that communicate with other tissues. These new proteins, referred to as "myokines" from the Greek words "muscle" and "motion," may represent new targets for therapies that mimic the benefits of weight training for the treatment of obesity and diabetes as well as muscle wasting disorders.

http://www.sciencedaily.com/releases...0205121740.htm

And then to emphasize how mouse models do not always typify human responses:

Whilst IL-6 appears to play a role in endogenous glucose production (EGP) during muscular activity in humans, its action on the liver is totally dependent on other muscle contraction-induced factors (17). At resting conditions, acute IL-6 administration at physiological concentrations does
not impair whole-body glucose disposal, net leg-glucose uptake, or endogenous glucose production in resting healthy young humans (3; 39; 71). In patients with type 2 diabetes, plasma insulin decreases in response to IL-6 infusion without a corresponding increase of the hepatic glucose
production (3). Recently, we demonstrated that IL-6 may increase glucose infusion rate (11) and glucose oxidation without changes in EGP during a hyperinsulinemic euglycemic clamp in healthy humans. These data are in contrast with observations reported in mice (53), suggesting that the effects of IL-6 on hepatic insulin sensitivity observed in murine models in vivo may not be similar in humans.

Extract from: Role of myokines in exercise and metabolism
Bente Klarlund Pedersen, Thorbjörn C.A. Åkerström, Anders R. Nielsen,
Christian P. Fischer
J Appl Physiol (March 8, 2007). doi:10.1152/japplphysiol.00080.2007

[sendos]

I'm not sure if anythings been said about net protein balance in this thread yet? for example although carbohydrates seem to do nothing to increase protein synthesis, they have been shown to impede the breakdown of protein thus improving net protein balance.

Effect of carbohydrate intake on net muscle protein synthesis during recovery from resistance exercise
Elisabet Børsheim, Melanie G. Cree, Kevin D. Tipton, Tabatha A. Elliott, Asle Aarsland, and Robert R. Wolfe

Department of Surgery, Metabolism Unit, Shriners Hospitals for Children-Galveston, University of Texas Medical Branch, Galveston, Texas 77550

Submitted 3 April 2003 ; accepted in final form 24 October 2003

The purpose of this study was to determine the effect of ingestion of 100 g of carbohydrates on net muscle protein balance (protein synthesis minus protein breakdown) after resistance exercise. Two groups of eight subjects performed a resistance exercise bout (10 sets of 8 repetitions of leg presses at 80% of 1-repetition maximum) before they rested in bed for 4 h. One group (CHO) received a drink consisting of 100 g of carbohydrates 1 h postexercise. The other group (Pla) received a noncaloric placebo drink. Leg amino acid metabolism was determined by infusion of 2H5- or 13C6-labeled phenylalanine, sampling from femoral artery and vein, and muscle biopsies from vastus lateralis. Drink intake did not affect arterial insulin concentration in Pla, whereas insulin increased several times after the drink in CHO (P < 0.05 vs. Pla). Arterial phenylalanine concentration fell slightly after the drink in CHO. Net muscle protein balance between synthesis and breakdown did not change in Pla, whereas it improved in CHO from -17 ± 3 nmol·ml-1·100 ml leg-1 before drink to an average of -4 ± 4 and 0 ± 3 nmol·ml-1·100 ml leg-1 during the second and third hour after the drink, respectively (P < 0.05 vs. Pla during last hour). The improved net balance in CHO was due primarily to a progressive decrease in muscle protein breakdown. We conclude that ingestion of carbohydrates improved net leg protein balance after resistance exercise. However, the effect was minor and delayed compared with the previously reported effect of ingestion of amino acids.

Although it does say at the very end the effect of net balance was minor and delayed when compared to the ingestion of amino acids alone.

[Gareth83]

I posted the following on page 43 which may help answer your query:

Eat smart after exercise
by Jeff S. Volek, Ph.D., R.D., F.A.C.N.
There are many options available for post workout protein beverages. Some are primarily protein while others have varying amounts of carbohydrates or fat. Few studies have directly compared the effects of different combinations of protein and carbohydrate after exercise.

Researchers from the Netherlands addressed the impact of co-ingestion of various amounts of carbohydrates combined with protein on the rate of protein synthesis in healthy young men. On three separate occasions subjects performed a 60-minute resistance exercise workout followed by one of three supplements and further measurements of protein synthesis for 6 hours during recovery. Supplementation over the 6 hour recovery period consisted of 0.3 g/kg of a casein hydrolysate per hour combined with either no carbohydrate, low carbohydrate (0.15 g/kg) or high carbohydrate (0.6 g/kg). For a 180 pound man this equates to about 25g protein per hour, and about 12g and 49g carbohydrate per hour for the low and high carbohydrate trials.

As expected, there was a significant increase in muscle protein synthesis during recovery in the protein-only trial. The co-ingestion of carbohydrate with adequate protein did not further augment protein synthesis. These findings show protein as the most important nutrient to consume after resistance exercise, and further indicate that adding carbohydrates offers little benefit. This is good news if you are trying to lose body fat because it means you can get an optimal anabolic effect from protein alone without adding additional calories from carbohydrate and the accompanying insulin response that will inhibit fat breakdown.

Reference: Am J Physiol Endocrinol Metab. 2007 Sep;293:E833-E842.

[NU_nutrition_TS]

Yes, I have tackled this question - not sure if it was in this thread though - the answer lies in the cellular mechanism known as chaperone mediated autophagy!

Let's pick that study apart:

"The purpose of this study was to determine the effect of ingestion of 100 g of carbohydrates on net muscle protein balance (protein synthesis minus protein breakdown) after resistance exercise."

This method of determining 'net muscle protein balance' is a rather 'blunt tool' - it assumes that the 'protein breakdown products' observed are from the recently trained muscle tissue. This is not necessarily the case. There is always a certain proportion of generalized whole body muscle tissue that is specifically laid down to be re-catabolized into amino acids and is part of the amino acid pool. This process is always going on in cycles, even in sedentary individuals, and is largely determined by the protein content of the diet and the body's need for essential amino acids at any given time (for enzyme/hormone synthesis for example).

The other source is 'junk proteins' such as 'misfolded' proteins or old and damaged proteins such as the aforementioned enzymes/hormones. These are disposed of by means of chaperone mediated autophagy (CMA).

This process is particularly activated when the body is in ketosis - such as after intense resistance exercise.

The 'chaperone' cells 'escort' the damaged proteins to special 'compartments' within each cell where they are 'consumed' - hence 'autophagy'; to 'eat oneself'! It is these protein breakdown products that often give the illusion that protein breakdown is greater than protein synthesis and that a person is in negative nitrogen balance when in fact they may still be synthesizing plenty of muscle tissue.

But when you consume carbs post workout you stop ketosis dead in its tracks which means less or no CMA. Hence, apparently, more protein synthesis than breakdown and a more positive nitrogen balance. But this does not necessarily mean there is more muscle tissue synthesis going on than in the other scenario!

This is why the differences noted were 'minor and delayed'!

Amino Acids are complex chemicals that are the building blocks of protein, which in turn are required for the creation of new muscle tissue, and the repair of existing cells. An Essential Amino Acid can not be synthesised or created by the body, and must come from the diet. Whilst a regular diet is enough to supply most people with all the amino acids that they require, anyone involved in heavy training may require a supplement to ensure enough of the various essential amino acids are consumed to meet the body's needs. Required by the body for building muscle tissue Aids physical recovery after intensive exercise