OK, got a little time.

So most of you who went through this in school biology class were probably told that the end product of glycolysis (remember, the initial anaerobic breakdown of glucose or glycogen?) was pyruvate. Pyruvate then enters mitochondria, looses a carbon and a hydrogen, becoming the 2 carbon molecule Acetyl-CoA (with me so far?). Acetyl-CoA enters the Krebs Cycle by combining with the 4 carbon oxaloaccetate to make the 6 carbon citrate and off it goes around Krebs (I doubt it's really a circle <img src="/forums/images/graemlins/lol.gif" alt="" />). If glycolysis goes too fast, the extra pyruvate cannot enter the mitochondria fast enough and so any leftover is converted to lactate and sent out of the cell causing a rise in blood lactate, fatigue and muscle soreness 1-2 days later. Sound OK?

There are three principle problems with this idea;

1. A reduced NAD (NADH) needs to be oxidized back to NAD to be reduced again during the 2nd phase of glycolysis. If this doesn't happen, glycolysis will slow or even stop...that's a problem! The NADH can be oxidized by lactate dehydrogenase by converting pyruvate to lactate at the end of glycolysis, thus re-cycling the NAD. So, lactate must then be the end product of glycolysis if glycolysis is to continue.

2. If pyruvate is the important molecule that enters the mitochondia for further energy production, why would there be lactate shuttle systems embedded in the mitochondiral membrane? If lactate is the end product of glycolysis, there is no pyruvate available to enter the mitochondira. It appears that lactate is in fact shuttled in to the mitochondiral inner membrane space where it is converted back to pyruvate by lactate dehydrogenase and the rest we know. This seems to happen for the sole purpose of oxidizing those NADH's in the cytoplasm so glycolysis can continue. Now, if the lactate shuttles become saturated (i.e. high levels of lactate because glycolysis is going too fast. High intensity exercise for example) then excess lactate is shuttled out of the cell causing a rise in blood lactate levels.

3. Lactate is not a waste product. Actually, it is a source of energy, like glucose. Organs like the brain and heart love to use lactate and the liver converts excess blood lactate back to glycogen for storage and later use. Also, high lactate levels, in blood and muscle, after intense exercise typically return to resting levels within ~15 minutes of rest. So lactate is not a good candidate for causing delayed onset muscle soreness, which occurs 1-2 days after the exercise (there's another theory about that).

Essentially, we produce lactate ALL the time. It only becomes a problem when we produce it faster than we can use it.

A final note about lactic acid and lactate. The true end product of glycolysis is likely lactic acid. However, once formed, lactic acid quickly looses a hydrogen ion and becomes the salt lactate.

That's it in a nutshell. Anyone awake? <img src="/forums/images/graemlins/lol.gif" alt="" />

Clay, why the interest (of which I'm glad)? I though you, Phil and others didn't believe in science <img src="/forums/images/graemlins/cheers.gif" alt="" />


'97 Montero 'LSR' - 4.6 gears & factory rear locker, 33" Procomp muds on 15x8 steelies, 50mm coil spacers, T-bar crank, Airlift, sans rear sway, 50mm rear frame & fuel tank lift, Aisins, ARB front bumper + 10k lb winch, 50mm DIY body lift, rock sliders, cut rear quarter panels...