I’m curious how aerobic training helps in a sport like freediving where oxygen is the limiting factor.
I know exercise increases your lung capacity, strength of your heart and diaphragm, increases stroke volume and potential for peak heart rate, maybe shift oxygen dissociation curve etc. That’s all geared to maximize delivery and consumption of oxygen, which is seldom an issue when you’re above water.
But what happens if you’re only allowed one breath of air? If you’re well trained, are your muscles somehow able to perform activity more efficiently and consume less oxygen?
Can good muscles store more oxygen? Or is the benefit of training mostly limited to increasing the size of that one gulp of air, and a slower resting heart rate?
Aerobic capacity includes factors such as oxygen uptake efficiency, total V0[sub]2[/sub] capacity (i.e the oxygen storing capacity of blood), and lactic acid threshold (the point at which you give up due to pain from lactic acid increase.
Something like free diving requires aerobic training to increase the capacity of the blood to hold oxygen - it isn’t just a single breath, it is all the breaths leading up to the last one.
Aerobic efficiency is about the metabolic system feeding all that oxygen to the muscles without wasting any energy to get the diver to the target depth, and the muscles using all of the available oxygen when it is there.
Once the oxygen runs out, the body shifts to anaerobic activity, and has two further mechanisms to fight - increasing C0[sub]2[/sub] levels in the blood stream requiring additional oxygen intake, and increasing lactic acid in the muscles and bloodstream causing fatigue and pain. High aerobic fitness delays the onset of these, and aerobic fitness that pushes into anaerobic fitness is used to prepare the body to endure these events and continue to function under duress.
Also not an exercise physiologist but do have a moderately strong interest. I pretty much agree with si_blakely.
Yes, training results in your muscles able to perform the activity more efficiently and consume less oxygen, therefore able to produce more energy aerobically without producing the acid and CO2 that is usually activity limiting. We actually have only a weak hypoxic drive; the need to take another breath is more driven by the fact that we need to exhale more CO2 than the one tidal volume allowed. And more.
Let’s take some of the adaptations one at a time. The goal is to have more oxygen carried by the system (mainly in RBCs), to have it last longer, and most importantly produce less CO2 and acid. More O2 on board is a large part of that as aerobic metabolism is so much more efficient.
Mild impact of an increased ability to clear lactate I think as, despite the standard phrase “lactate threshold” (or for that matter “anaerobic threshold”) not being quite precise as neither lactate build-up or low oxygen levels in the muscles are likely actually the immediate limiting factors.
Decreased vascular resistance in the muscles in response to demand. Likely a major part of aerobic conditioning. A broader network of capillaries and more vasodilation of arterioles means a lot less work for the heart to do, and more blood flow to the muscles, both meaning much less CO2 produced.
Increased parasympathetic tone. Parasympathetic tone is metabolic braking. High parasympathetic tone is a large part of why endurance athletes have low resting heart rates and what allows the heart rate to recover quickly from high demands. Of course that big stroke volume also means both slower heart rate for unit of blood pushed through and less CO2 produced by the heart as well.
Increased oxygen carrying capacity and other RBC differences. Interestingly many highly trained endurance athletes will actually have a lowish hematocrit (amount of RBC volume per unit blood volume) but they have significantly more total plasma volume. Thus total RBC volume is still increased. They both destroy RBCs more in the process of exercise and produce more. A result is that the average RBC is younger, and younger RBCs work better. In particular they are more flexible squeezing through capillaries with less force. That flexibility and increased total volume means not only increased carrying capacity but less viscosity and thus less work for the heart to do.
Increased tolerance to a given level of lactate, CO2, and acid level. I’d guess occurs at a brain level and I’d guess altering the CO2 drive set point is likely the major item that can be modified. But that is less with aerobic conditioning than with doing freedives I’d think.
The big gulp of air? Possibly training can decrease functional residual capacity, and/or otherwise increase vital capacity but if it does occur then I’d guess the impact would be less for more O2 than to allow for more of a slow exhalation volume continuing to get rid of CO2 a bit longer.
https://www.unm.edu/~lkravitz/Article%20folder/optimizeendurance.html
"The reduced lactate production, at the same given workload, following endurance training can be attributed to increased mitochondria size, mitochondrial numbers, and mitochondrial enzymes (Holloszy & Coyle 1984; Honig, Connett, & Gayeski 1992). The combined result of these training adaptations is an enhanced ability to generate energy through mitochondrial respiration, thus lowering the amount of lactate production at a given workload.
In addition, endurance training appears to cause an increase in lactate utilization by muscles, leading to a greater capacity for lactate removal from circulation (Gladden 2000). Consequently, despite the heightened lactate production rates occurring at high levels of exercise intensity, blood lactate levels will be lower. It should be noted that endurance training may also improve capillary density around the muscles, especially the slow-twitch muscles. This adaptation improves blood flow to and from exercising muscles, which will enhance the clearance of lactate and acidosis (Roberts & Robergs 1997)."