View All Posts: Voj

AMH_Power said:
Yeah of course, but please take with a pinch of salt... I'm not a nutritionist or dietitian.
Here is the process as far as I know it (I'm sure people can add to it):
-Muscle, adipose and brain cells require glucose to function (infact, most/all cells do).
Each type of cell has a couple of important features relevant to insulin signalling pathways. The first, is it's ability to hold glucose. Glucose held in adipose is stored as Triglycerides (slow burning energy source), and glucose held in muscle is stored as Glycogen (fast, ready available energy).
-These cells have the ability to shuttle glucose from outside the cell (extracellular) to inside the cell (intracellular). The protein that facilitates this is GLUT4, and is termed a 'glucose transporter'. Each cell also has an insulin receptor, which regulates where/what the GLUT4 is doing. When insulin isn't present, GLUT4 proteins are pretty dormant in an idle area of the cytosol.
-Eat food. Depending on how much this food increases blood sugar, depends on how much insulin will be released (by the beta cells/islets of Langerhans within the pancreas). Food has a score on it's ability to spike blood sugars, and is called its 'Glycemic Index', or simply GI.
-When insulin binds to the insulin receptors of the cell from the outside (the receptors have a foot both intra and extra), it is met by ATP (adenosie TRIphosphate) on the inside. This causes the cell to be in an 'active' state. the ATP releases a phosphagen cell (and becomes ADP; adenosine DIphosphate). This phosphagen cell is the signal for the GLUT4's to kick in to action (this process is called auto phosphorylation), and they start shuttling/recycling back and forth from the cell membrane (pulling in glucose) to inside the cell. (Another point to note, proteins that add phosphate groups to other proteins, like in this case ATP &rt; GLUT4, are called Kinase).
-The storage further utilizes Kinase; and further signals.. in particular RAB proteins and PIP2 molecules.. but this is beyond scope of this post... and I'll start making stuff up through memory failure, I digress.....
-When anaerobic exercise is performed, ATP to ADP combustion is high as part of normal energy pathways. This, causes excessive signalling of GLUT4 (termed translocation) via the same principle above. Actually, there are MANY more functions involved, ATP &rt; AMP &rt; AMPK etc. But what is important, is that GLUT4 activity is VERY high following resistance training.... but ONLY in the muscle cell.
-This means, we have a very, very good environment for shuttling blood sugar almost exclusively to intramuscular cells!
Lets talk through this a minute....
We lift heavy. Glucose transporters (GLUT4) cling to the cell membrane trying to pull in what glucose it can.
We let them, by smashing a bag of haribo directly AFTER training. The GLUT4 pull the glucose into the muscle cells... as GLYCOGEN.
This gives us RAPID recovery, a larger glycogen reserve than what we could store otherwise (Giving a fuller muscle, and enhanced future training sessions).
BUT... there's more. Following the high blood sugar, the beta cells in the pancreas secrete insulin. Our blood sugars are already cleared from the GLUT4 translocation!
What happens next... the same process occurs, a second bout of GLUT4 translocation occurs, but there is f**k all blood sugar. We now have TGLUT clung to both fat cells, and muscle cells as a response to the insulin signal pathway... but with no blood sugar to pull in.
We are now in a mild form of hypoglycaemia (low blood sugar). The liver would now usually secrete glycogen as glucose in to the blood stream as a response to low blood sugar (the liver stores glycogen similar to muscles, and stores a relatively large amount).
however... it's insulin receptor is 'active' due to our insulin spike... the GLUT4's are tied up, there is nothing they can do!
The only solution for the liver, is to produce ketones. Ketones break down tryglycerides (stored fat glucose) into glucose... ready for the GLUT4 proteins we have clinging to the muscle cell to further pull in glycogen as a second bout of glycogen retention.
As you can see, over-storage of muscle glycogen, fat/triglyceride depletion, faster recovery, stronger performance on consecutive sessions.... and a f**king bag of haribo!
vs.... A protein shake.
2015 vs 1975.

Wigan said:Lapikov down to open at 230 on the C&J

Lovchev and the big fella both down at 240

MrSmall said:Did Rasulov get 3rd in 94?

Polovnikov was 2nd overall apparently so I guess Sheyko was 3rd. If only David was a better snatcher, he would be a world fighter.