Julian wrote: On any given day, your muscles can use far more oxygen than is delivered. Race-day limiter is the delivery system, not the cell’s ability to put O2 to work.
Good, someone got my point! I ramble so much that I wasn’t sure if I were getting it across.
However, we are probably on opposite poles of the continuum.
I maintain it IS local cellular conditions that limit muscle function, not the cardiovascular oxygen delivery system. If by “delivery system” you are including oxygen field theory, mitochondrial enzyme functions, local energy substrate availabilty, etc., in other words…LOCAL oxygen delivery system functions, then we would be on the same end of the arguement.
Consider this experiment…take an isolated muscle (a frog leg muscle hooked up to a strain gauge is easy enough), hook it’s femoral artery up to a blood flow system that provides normal blood flow rates at normal oxygen concentrations with glucose at normal levels, and stimulate the muscle electrically over and over. Use the strain guage to measure the forces the muscle produces. It generally contracts harder and harder the first few stimulations, peaks, then gradually contracts with less and less force over time.
Repeat the experiment with 1.5 times greater than normal blood flow. Guess what you’ll find…almost exactly the same forces generated. It may improve performance slightly, but that’s all. The arguement is this…why did performance improve? More oxygen delivered? More waste products removed? More energy substrate available? Why did performance decrease with the higher blood flow in some frog’s legs? Either way, there isn’t much difference in performance between the two groups.
If the experiment is continued to exhaustion of the muscle, there is very little difference in time to exhaustion, even at DOUBLE the blood flow.
I’ve done this experiment.
Here’s the experiment I’d like to do…take this same setup as above with one change…also include a hip flexor muscle. There are a couple of interesting ways to experiment with this setup.
Test one: run the test with the same intensity and rate of stimulation as before, but with the hip flexor also stimulated. Observe the forces recorded. My bet is that the forces will be higher when the added hip flexor muscle is included.
Test two: Decrease the intensity of stimulation to this dual muscle system (probably have to do this by making the stimulation shorter, as skeletal muscle has an “all or none” approach to contraction) to the point that the total peak force is the same as the total peak force of the non-hip flexor model. Observe the forces recorded. My bet is that the hip flexor inclusive model will contract for a longer time before exhaustion than the non-hip flexor model.
(These two tests could be done without any extracorporeal blood oxygenation/delivery device hooked up to the femoral artery in order to simplify it.)
Anyway, these experiments will demonstrate that it isn’t systemic oxygen delivery that is THE limiter to muscle function, and that using accessory muscles DO make contractions more forceful and/or able to continue for longer periods of time compared to not using accessory muscles.
Furthermore, the experiments that I would really like to see done, would be to train the muscles for a time, and see what differences can be trained into the muscles. Lot’s of frog volunteers would be required, though! Of course, this would be better done in rats, but much more expensive.