Sat, May-06-06, 16:19
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Registered Member
Posts: 1,582
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Plan: antivegan,was subzerocarb
Stats: 200/187/175
BF:27%/19%/12%
Progress: 52%
Location: Flyover Zone
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Quote:
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Originally Posted by Klein
A study about muscle fuel under different training intensity:
http://jp.physoc.org/cgi/content/full/536/1/295
The subjects followed a high carb low fat eating protocol. They speculate that the "measured" relative decrease of FFA oxidation when training intensity passed a certain level is related to decreased levels of free carnitine. Fatty acid availability did not decrease. Maybe free carnitine levels are more easily maintained in a keto adapted person. Speculation upon speculation... |
Wonderful article, Klein. This is the sort of "black box busting" study we need on this thread!
Of course, WAY BACK in post #324 I asked Bear about this VERY thing!
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Originally Posted by PaleoDeano
I am confused as to this glycogen use during activity. What I have heard is glycogen stores in the muscle are ALWAYS used if a burst of energy is needed, like to sprint real hard, or to lift something very heavy. It is an "on demand" energy source. Glycogen is also used at first when one begins an activity, say walking. Then there will be a mix of glucose and fat for energy, and the longer the activity, the higher the percentage of fat will be in that mix. Also, I have heard that in the morning if you exercise before eating, you will be able to use up your glycogen stores quickly, and then start using fat for fuel, because the glycogen stores will be low due to metabolic use during sleep (with no dietary replacement). Is this all just some myth or misinformation? Could someone please explain how this works?... at least how they understand it. It seems as though there are different schools of thought on this for sure.
Thanks. I really want to understand how this works... and the different points of view (and the reasons behind these views).
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BTW... although they mentioned the substantial increase in lactate levels after exercise became more intense, especially during high-intensity exercise (because the flux through the glycolytic pathway and the pyruvate dehydrogenase complex reaction would greatly exceed the flux through the TCA cycle... in other words, anearobic respiration).
Perhaps there may be an adaptation to higher cytosolic concentration of carnitine in an FFA-adapted individual? However, how would this ever obviate the need for the glycolytic pathway (using glucose) to get involved, under anearobic conditions?
Look deep into the black-box..... 
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