Diesel, yet again, you’ve sparked another interesting conversation. However, a few bones to pick, per se, with your understanding of physiology.
Muscle hypertrophy is not necessarily dependent upon ATP, but I think I see your point. It’s indirectly related in that the stimulus can’t be presented. Do I understand you correctly? Actually, muscle hypertrophy seems to be a function of protein synthesis and growth factors (i.e. insulin-like growth factor I).
Another thing, Diesel, is to understand that the body is very efficient at providing energy (i.e. ATP) in the absence of oxygen. Through anaerobic pathways (i.e. anaerobic glycolysis and creatine phosphate), immediate energy can be produced within the cytosol itself. Also, I would say that after about 10-15 seconds of repeated maximal/high-intensity efforts, the CP stores of the muscle cell are relatively depleted. Thus, anaerobic glycolysis predominates from this time.
Just for clarification, Diesel, you meant “aerobic” metabolism (both glycolysis and lipolysis) occurs >5 minutes of repeated exercise.
Restless, I’m not sure I understand your take on hypertrophy being dependent upon muscle glycogen stores. Could you expand? Your other points present sound principles and science.
Diesel, could you possibly share that piece of literature. That’s interesting. Also, don’t forget that capillary density would likely be as important, if not more important, than enhanced mitochondrial density in expediting the process of repleneshing ATP and CP stores.
Now, Diesel, when you talk about increased sarcoplasmic hypertrophy, I can’t imagine that increasing mitochondrial density would provide a significant amount of “muscle size.” Mitochondria are tiny, man! Think about it, endurance athletes are jam-packed with mitochondria, yet muscle hypertrophy is, well, not very evident. Sarcoplasmic hypertrophy, therefore, would not be due to increased mitochondrial density; rather, it would be due to increased non-functional/non-contractile tissue.
Actually, lactate is converted to glucose via the Cori Cycle in the liver and really is not related to having “scores of mitochondria.”
As mentioned, all the energy systems contribute. However, at the onset of a marathon, it’s not because of the fact that fast-twitch fibers dominate. No, sir. It’s instead due to the fact that there’s a slight oxygen lag. Fast-twitch fibers don’t likely come into play in long-distance endurance events until the slow-twitch fibers are sufficiently fatigued (i.e. near the end of the marathon).
What book, Diesel?
Yes, Diesel, the heart is very efficient at using both lactate and fatty acids for fuel. However, the heart and other muscle groups do not convert lactate into glycogen, or glucose for that matter. As I mentioned earlier, lactate is converted back to glucose by the liver in a process called the Cori Cycle. Also recall that lactate can be converted to pyruvate and thus enter the Krebs Cycle.
Good discussion and keep throwing out theories and thoughts.