Physiology Friday #266: A New Theory on What Limits Our Maximal Aerobic Capacity

Exercise training doesn't increase maximal heart rate. But why?

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Maximal aerobic capacity is determined by several factors—the ability of the lungs to take in air and oxygenate the blood, the ability of the heart to pump oxygen-rich blood to the rest of the body, and the ability of the muscles to extract oxygen from the blood and turn it into energy in the mitochondria.

If you want to get fitter, one or more of these factors has to increase: You have to get bigger and stronger lungs, a bigger and stronger heart and vascularity, or denser, more efficient mitochondria. These are the determinants of VO2 max, but not all of them are equally limiting.

It’s generally agreed upon that for most people, aerobic capacity is limited by the heart’s ability to deliver blood to working muscles—otherwise known as cardiac output. This is the amount of blood pumped from the heart each minute. When we do endurance training, cardiac output increases. But how?

Cardiac output has two components: heart rate and stroke volume, the latter referring to how much blood the heart pumps with every beat. Multiplied by heart rate, this gives us cardiac output.

But only one of these components increases with endurance training—stroke volume. Our maximal heart rate doesn’t increase when we get fitter, but our pump gets stronger. That’s a bit counterintuitive, as it would seem like the easiest way to pump more blood would be for the heart to “go faster.” But that’s not what happens with training.

Metabolic Mechanisms of Exercise-Induced Cardiac Remodeling

This begs the question: what’s limiting cardiac output in humans?

That’s the question that Ilkka Heinonen (@ileximius on X) delves deeply into in a new review article—detailing the mechanisms restricting maximal cardiac output and proposing a novel perspective on myocardial physiology.¹

While intuitively it might seem beneficial for maximal cardiac output to increase through higher maximal heart rates (a faster beating heart delivers more blood), endurance training paradoxically reduces maximal heart rates. Heinonen clarifies that maximal heart rate remains stable or even decreases post-training due to physiological constraints: higher heart rates diminish diastolic duration (the amount of time our heart spends in the relaxation/filling phase), compromising myocardial blood flow, which predominantly occurs during diastole. The myocardium, already extracting oxygen at high rates even at rest, cannot easily cope with reduced perfusion time. In other words, if heart rate gets too high, cardiac muscle doesn’t have enough time to oxygenate itself, risking ischemia (a lack of blood flow) and hypoxia (oxygen deprivation).

Rather, the primary adaptation of the endurance-trained heart is not a faster beat, but a significantly larger stroke volume—the amount of blood pumped with each beat.

Endurance training causes the heart to grow bigger, and this hypertrophy, primarily eccentric (outward), enlarges cardiac chambers, thus enhancing stroke volume while simultaneously moderating oxygen demand by maintaining lower maximal heart rates—oxygen extraction is optimized in endurance-trained individuals because the blood spends more time in transit in the coronary arteries, even though resting and sub maximal blood flow aren’t enhanced.

What’s putting a constraint on the body’s ability to elevate heart rate above some predetermined max?

The paper introduces an intriguing hypothesis: nerves that communicate from the heart to the rest of the body (cardiac afferent sensory nerves) may serve a protective mechanism by limiting maximal heart rate to prevent myocardial ischemia. These nerves, sensitive to metabolic, mechanical, and oxygen states within the heart muscle, potentially function as a regulatory “ceiling,” preventing the heart from reaching detrimental metabolic states. This protective mechanism explains why elite athletes do not simply develop progressively faster heart rates but instead benefit from structural adaptations that optimize stroke volume.

Heinonen further elaborates that myocardial oxygen supply-demand balance is delicately maintained through structural rather than dunctional adaptations—the efficiency of myocardial oxygen utilization is improved,

What are the implications of this for training?

Exercises optimizing stroke volume—typically rhythmic and dynamic low- to moderate-intensity activities that maximize venous return—are most beneficial. These stretch the heart maximally for extended periods of time.

Heinonen suggests integrating diverse training intensities, tailored to fitness levels, to progressively challenge and improve cardiac function. That means plenty of “zone 2” training but also a balance of high-intensity intervals. While resistance training has plenty of merits, maximizing gains in stroke volume isn’t one of them—hence why lifting weights is a poor way to increase VO2 max.

I found this review to be a brilliant illustration of the incredibly complex way that our body operates—it’s almost as though there’s intentionality behind it. Physiology is smart enough to side step the obvious (to us) solution to a problem and come up with unique (and far superior) ways of accomplishing a goal. Next time you’re out training, think about what’s going on under the hood and appreciate how the body makes us stronger and fitter in ways that, mechanistically, we are only still beginning to understand.

Thanks for reading. See you next Friday.

~Brady~

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1. Heinonen, I. (2025). Cardiac output limits maximal oxygen consumption, but what limits maximal cardiac output? Experimental Physiology, 1–9. https://doi.org/10.1113/EP091594