The best explaination I’ve seen for muscular fatigue (in most cases, obviously all the factors mentioned can have some impact or possibly be the primary mechanism in some cases) is the buildup of K+ ions outside the plasma membrane, thereby decreasing the charge of the membrane and increasing the stimulus required to reach threshold.
The acidity theory just doesn’t seem to work, as muscles submerged in an acidic environment or artifically injected with acidic solution seem to be able to function just fine within the pH created during exercise. Also, substantial amounts of glucose and ATP appear to be present in a muscle cell immediately following exercise (as well as the necessary substrates, again, in most cases), so the energy depletion theory just doesn’t seem to hold either. I can’t pull sources on this right now, as I came to these conclusions discussing the idea with my physiology professor who actively keeps up with the research in the area and with a friend of mine who’s researching fatigue/post workout nutrition, though I could probably hunt them down if anyone’s interested.
Not real sure how one would go about preventing extracellular K+ buildup due to saturated transport mechanisms, though. Genetic engineering so that more Na+/K+ pumps are expressed is the best I can figure.
[quote]buffalokilla wrote:
The acidity theory just doesn’t seem to work, as muscles submerged in an acidic environment or artifically injected with acidic solution seem to be able to function just fine within the pH created during exercise. Also, substantial amounts of glucose and ATP appear to be present in a muscle cell immediately following exercise (as well as the necessary substrates, again, in most cases), so the energy depletion theory just doesn’t seem to hold either. I can’t pull sources on this right now, as I came to these conclusions discussing the idea with my physiology professor who actively keeps up with the research in the area and with a friend of mine who’s researching fatigue/post workout nutrition, though I could probably hunt them down if anyone’s interested.
Not real sure how one would go about preventing extracellular K+ buildup due to saturated transport mechanisms, though. Genetic engineering so that more Na+/K+ pumps are expressed is the best I can figure.
-Dan[/quote]
BK, having researched the Na/K-ATPase for 5 years, I can tell you that it doesn’t initiate fatigue. While Pi and ADP play a role, it seems like the Ryanodine receptor/DHPR is the culprit (this was the other focus of our lab).
BK, having researched the Na/K-ATPase for 5 years, I can tell you that it doesn’t initiate fatigue. While Pi and ADP play a role, it seems like the Ryanodine receptor/DHPR is the culprit (this was the other focus of our lab).
Cheers[/quote]
Intriguing… could you elaborate a little more/point me towards the literature that was published? I’d (and my professor I’m sure) love to take a look at it.
I don’t know much about those little foot proteins yet - are the free H+ ions causing a conformation change that clogs them up, so to speak?
Saw how old this thread is, but wanted to reply that I actually tried the soda loading. Let me tell you, I couldn’t make it 1 lap around the track without going to the bathroom.
I had to do 3 miles that day as it was a pre-race day. Calculate that once and then you’ll know how much that run sucked.