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Many of you have performed a VO2max test at some point to test your maximal aerobic capacity. Many also understand that this is a test of aerobic potential and has a large genetic determination. Through intense training (starting from no training) one can realistically expect to increase VO2max by 9-17%. What VO2max measures is the maximal ability of your skeletal muscle to use oxygen in the mitochondria to create ATP, and consequently work. There are many steps in that process from breathing oxygen into the lungs to exchanging oxygen from the air into red blood cells, distributing that oxygenated blood to the rest of the body by the heart and blood vessels, dumping the oxygen off at the tissues (in this case skeletal muscle), and finally, oxygen making its way into the tissue and then into the mitochondria where it can accept an electron to drive the making of ATP (our form of usable potential energy). A question that has intrigued some scientists for years is what step in that process is limiting? It has largely been determined that the ability to breath in oxygen is not the problem (which always makes me look at someone funny when their lungs were the problem during a hard effort), but there has been much debate over whether it is the ability of the heart to deliver oxygen to the tissues or the ability of muscle to use it. What is the weak link in the system?
Many studies have attempted to answer this question with some interesting approaches. For example, if you are doing leg exercise and reach a max, and then add arm exercise to the legs and your VO2max goes up, that would indicate that the heart had the ability to deliver more oxygen, but the legs were maxed out in their ability to use it since adding different muscle increased oxygen use. Recently, a very competent research group from Spain took a slightly different approach and asked what causes failure during an incremental exercise test? Anyone that has ever done a VO2max test knows that it ends in failure, so what causes that failure? The study was done with an interesting combination of incremental exercise tests that included normal air or hypoxia (low oxygen), with or without blood occlusion at exhaustion to “capture” anything that might be in the blood at that point, a quick muscle biopsy to look in the muscle, and then another all out sprint to see if there was a decrement in peak power generation.
From this unique study, here is what information was learned. First, at the end of an incremental exercise to exhaustion, the muscles still have the ability to generate power, even at a level far above the power at which failure occurred. What this means then is that your muscles have not actually failed. Second, the point of exhaustion is not due to lactate accumulation or the associated muscle acidification, and muscle lactate accumulation may actually facilitate early recovery after the exercise bout. This evidence is just another nail in coffin of the outdated concept that lactate causes fatigue. Please, don’t be that person that talks about lactic acid and fatigue – it just makes you look uninformed. Finally, the ability to make ATP in the muscle at a high enough rate to match the work still exists at fatigue. This last piece of information indicates that failure during an incremental test to exhaustion depends more on central than peripheral mechanisms. Therefore, it is the cardiovascular system (the ability to deliver blood) that is the culprit when you fail during a VO2max test.
There is a subtle distinction that I want to point out here so these data are not misinterpreted. This study does not indicate that improving heart function is the key to improving performance. During submaximal efforts (what we do 90% of the time) the ability of the mitochondria to use oxygen efficiently is the key to performance. This study only shows that during a maximal exercise test, like you do during a VO2max test, the ability of the heart to deliver oxygen is the limiting factor to a higher VO2max. Again, this is strongly indicative of genetic links to VO2max because just like hand size is a function of genetics, so is heart size. To read the full article, I have provided the web link.
http://www.ncbi.nlm.nih.gov/pubmed?term=26250346