Your VO2 max, a measure of aerobic fitness that refers to the maximum rate at which you can deliver oxygen for use by your exercising muscles, is an important number—if not for racing, then for health. It’s an excellent predictor of longevity: better, in some respects, than how much exercise you get. The American Heart Association recently argued that VO2 max should be considered a new “vital sign” for doctors to regularly measure.
So what determines your VO2 max? Intuitively, we often think of the lungs and heart. And the heart is undoubtedly important: When you train, your heart gets bigger and stronger, capable of pumping more oxygen-rich blood with each beat to the farthest reaches of the body.
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But it’s not the only possible bottleneck. Blood flow through your arteries and veins is also a factor, as is the diffusion of oxygen from tiny capillaries into the muscles. And in the muscles themselves, how fast can your mitochondria, the cellular “powerhouses” that fuel aerobic exercise, make use of oxygen?
A presentation at last month’s American College of Sports Medicine conference delves into this topic, trying to understand why VO2 max declines as we get older. Is it just because our hearts get weaker? Or do also we get worse at delivering and using oxygen?
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The researchers, from a team at the University of Utah led by Jayson Gifford, compared a group of young (average age of 26) and old (average age of 75) volunteers. Importantly, the subjects (though untrained) were matched for physical activity levels and body mass index, so the differences weren’t just the result of being sedentary.
They did two maximal tests: one “whole body” test, cycling, which tested the limits of every part of the system; and one localized test, of simply extending their knee over and over. The latter test, since it involves only a few muscles, doesn’t tax the heart, so it’s a way of checking whether there are bottlenecks in the leg muscles.
As expected, the older subjects had a lower whole-body VO2 max than the younger ones by 38 percent. Interestingly, they were also 27 percent lower in single-leg VO2 max, suggesting that peripheral factors like blood circulation and diffusion had declined.
One trait that didn’t decline was the ability of their muscles to use oxygen. Using muscle biopsies, the researchers calculated the VO2 max of the mitochondria in the subjects’ leg muscles, and it was basically the same in both groups of subjects. This result, Gifford says, suggests that oxygen-processing capacity in the muscles “is primarily driven by physical activity, not age.”
That insight gels with the findings of a similar experiment that Gifford and his colleagues published last year. In that study, they compared trained and untrained volunteers, and found that mitochondria was a limiting factor in the untrained group, but not in the trained group, whose mitochondria had lots of spare capacity even when the rest of the system was maxed out.
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In theory, all this excess mitochondrial capacity seems like a waste—or even a violation of the principle of “symmorphosis,” which argues that “the size of the parts of the system must be matched to the overall functional demand.” In this view, there’s no single bottleneck that determines VO2 max. Instead, all the parts of the cascade—the heart, the arteries, the capillaries, the mitochondria—are just the right size for your needs, and together they dictate VO2 max.
So why do endurance athletes develop excess mitochondrial capacity? The authors argue that “it is doubtful that this reserve capacity serves no purpose.” They discuss a few theories, such as the idea that excess mitochondrial capacity might assist in fat burning, which would enhance actual endurance performance without changing VO2 max. There’s also some evidence that it may buffer oxidative stress and reduce cell damage.
What does this all mean? The overall message is pretty obvious: You should keep training like an endurance athlete in order to (at least partly) ward off age-related decline in VO2 max. In doing so, you’ll be keeping your whole system functioning optimally, not just your heart.
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It’s interesting to consider whether these findings also suggest any more specific training insights. If capillarization—the network of tiny vessels that distribute blood throughout your muscles—is an increasingly significant bottleneck as you age, are there particular types of training that target it? There’s some evidence that the patterns of capillarization induced by interval training and steady endurance training are somewhat different and specific to the demands of each form of exercise, which is perhaps yet another argument for having a diverse exercise program rather than doing the same thing every day.
In the end, though, I’m wary of overselling the practical training insights from a study like this. Gifford does point out that understanding more about the limits that contribute to age-related decline in VO2 max can eventually help target exercise or drug therapies. But mostly, it’s just neat to get a better sense of how the body works, and to learn a new word like symmorphosis.
This article originally appeared on Runner’s World
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