Original episode & show notes | Raw transcript
The foundation of this discussion is the Fick equation, a fundamental principle in exercise physiology that describes the body’s oxygen consumption (VO2). The equation is expressed as:
VO2 = Cardiac Output (Q) × Arteriovenous Oxygen Difference (a-vO2 difference)
VO2: The volume of oxygen consumed by the body per minute. Your VO2 max is the maximum rate at which your heart, lungs, and muscles can effectively use oxygen during intense exercise.
Cardiac Output (Q): The amount of blood the heart pumps per minute. This is the central focus of this podcast episode.
Arteriovenous Oxygen Difference (a-vO2 difference): This represents how much oxygen the muscles are extracting from the blood. It’s the difference in oxygen concentration between the arterial blood (going to the muscles) and the venous blood (coming from the muscles). The previous podcast episode (Wattstock #20) covered this in detail, concluding that while important, it’s not the primary limiter of VO2 max for most athletes.
Cardiac output is where the most significant potential for VO2 max improvement lies. It is determined by two factors:
Cardiac Output (Q) = Stroke Volume (SV) × Heart Rate (HR)
Heart Rate (HR): The number of times the heart beats per minute (BPM).
Stroke Volume (SV): The volume of blood pumped from the left ventricle of the heart with each beat. This is the key variable for long-term VO2 max adaptation.
The podcast emphasizes that stroke volume is the primary long-term limiter of VO2 max. Just as a larger bike pump can move more air per stroke, a heart with a larger stroke volume can pump more blood—and thus deliver more oxygen—to the working muscles with each beat.
How does an athlete increase their stroke volume? The answer is multifaceted, beginning with blood volume.
A key study discussed is by Ed Coyle, which explored the effects of detraining and blood volume manipulation on VO2 max. The study found:
Detraining led to a decrease in blood volume (mostly plasma), which in turn caused a significant drop in stroke volume and a corresponding decrease in VO2 max.
To compensate for the lower stroke volume during submaximal exercise, the detrained subjects’ heart rates increased to maintain the necessary cardiac output.
Re-infusing plasma into the detrained subjects restored most of their lost stroke volume and VO2 max.
Crucially, infusing extra plasma into the same subjects while they were trained had no effect on their VO2 max.
This leads to a critical insight: simply having more blood isn’t enough. The heart must be able to accommodate and pump that extra volume. This brings us to diastolic filling.
Diastole: The phase of the heartbeat when the heart muscle relaxes and the chambers fill with blood.
Systole: The phase when the heart muscle contracts and pumps blood out.
The amount of blood that fills the ventricles during diastole (end-diastolic volume) is a primary determinant of the subsequent stroke volume. A major question in physiology has been whether diastolic filling, and therefore stroke volume, plateaus as heart rate increases during intense exercise.
A study on cyclists revealed a stark difference:
Untrained Individuals: Their stroke volume increased up to a certain heart rate (around 120 BPM) and then plateaued. They had more time for diastolic filling, but their hearts couldn’t fill faster as the available time decreased.
Trained Endurance Cyclists: Their stroke volume continued to increase almost linearly all the way up to 180 BPM. Their hearts were adapted to fill with more blood in a much shorter amount of time. The diastolic filling rate of the trained cyclists was dramatically higher.
This demonstrates a key adaptation: a trained heart is not just a stronger pump, but a more efficient and rapid-filling chamber.
How does the heart “know” how hard to contract to match the amount of blood filling it? This is explained by the Frank-Starling Law of the Heart.
This law states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the ventricles (the end-diastolic volume). In simple terms: the more the heart muscle is stretched during filling, the more forcefully it contracts.
This is an intrinsic property of the cardiac muscle fibers (cardiomyocytes). When the heart walls are stretched by incoming blood (a condition known as preload), the contractile filaments (actin and myosin) within the muscle cells are positioned at a more optimal length for force generation. This allows the heart to automatically adjust its output to match its input (venous return) on a beat-by-beat basis, ensuring a balanced flow through the pulmonary (lungs) and systemic (body) circuits.
The heart muscle adapts to long-term stress through a process called cardiac remodeling or cardiac hypertrophy (growth). The podcast highlights two distinct types of adaptation, driven by two different kinds of stress:
Concentric Hypertrophy (Afterload-Driven):
Stimulus: High afterload. Afterload is the resistance the heart must overcome to eject blood. Think of it as the pressure the heart has to pump against. This occurs during activities like heavy weightlifting or a track cyclist’s standing start, where intense muscular contraction and the Valsalva maneuver dramatically increase blood pressure.
Adaptation: The heart wall thickens by adding sarcomeres (the contractile units) in parallel. The chamber size does not increase. This is analogous to a skeletal muscle getting thicker and stronger to lift heavier weights. This is a “pressure-overload” adaptation.
Eccentric Hypertrophy (Preload-Driven):
Stimulus: High preload. As discussed, preload is the stretch on the ventricles at the end of diastole, determined by the volume of blood filling them. This is the dominant stress in endurance sports like running, swimming, and cross-country skiing, where rhythmic muscle contractions (the “muscle pump”) continuously return large volumes of blood to the heart.
Adaptation: The heart chambers, particularly the ventricles, enlarge. The heart muscle cells get longer by adding sarcomeres in series. This allows the heart to accommodate a larger filling volume and thus eject a larger stroke volume. This is a “volume-overload” adaptation.
This eccentric, preload-driven hypertrophy is the most crucial adaptation for increasing VO2 max in endurance athletes.
Different sports induce different combinations of these adaptations.
Weightlifting: Almost purely concentric adaptation (high afterload).
Cross-Country Skiing: The most eccentric adaptation (very high preload). The use of both arms and legs as major muscle pumps creates a massive venous return, constantly stretching the heart.
Cycling: Induces a mix of both eccentric and concentric adaptations. While it is a high-preload activity, the fixed, bent-over posture can increase resistance to blood flow at the hips, creating a degree of afterload that isn’t as prevalent in running or skiing.
This leads to the podcast’s central training philosophy: To maximize VO2 max, especially in cyclists, training must be specifically targeted at maximizing preload. The goal is to spend quality time at or near the heart’s maximum diastolic filling volume to create the mechanical stretch that signals the heart to remodel eccentrically.
The podcast argues that for well-trained athletes, simply doing more low-intensity endurance riding is not a sufficient stimulus to drive further eccentric hypertrophy. While it’s effective for beginners by increasing blood plasma volume, a well-trained heart is already operating well within its capacity during such rides.
To trigger further adaptation, the heart must be challenged with maximum preload. This means performing intervals that push the cardiovascular system to its limit, forcing the heart to handle the largest possible volume of blood return. The hypothesis is that spending less time at 100% of VO2 max (and thus 100% of maximum preload) is more effective for stimulating this specific adaptation than spending more time at 90% or 95%. The mechanical tension from the stretch is the key signaling mechanism, and this signal is likely strongest when the stretch is greatest.
Therefore, the most effective VO2 max training involves intervals designed to elicit the highest possible stroke volume for a sustained period, thereby providing the necessary stimulus for the heart to grow larger and more efficient—the “supernormal heart” of an elite endurance athlete.