How To Increase VO2max As A Cyclist
Maximal oxygen uptake (VO2max) is the highest rate at which oxygen can be taken up, delivered to and utilised by the muscles during intensive exercise.
Alongside variables such as the lactate threshold and exercise economy, VO2max is a major performance factor in most cycling disciplines, so seeking to improve it should be a primary focus of most structured training programs.
In this post, we’ll firstly break down the constituent parts that comprise the VO2max, before moving on to look at what kind of training is needed to signal the necessary adaptations for improvement.
Finally, we’ll present 4 workouts that have proven to be effective in our coaching of both professional and amateur cyclists to improve the VO2max, where we’ll also include a little about the rationale behind the designs of each session.
Components of VO2max
The key components of the oxygen transport system can be broadly segmented into “central” factors and “peripheral” factors. Both are important to an athlete’s aerobic capacity and could represent a potential impediment to O2 flux if under-optimised.
“Central” parts of the system refer to the pulmonary diffusion of oxygen from the lungs to the blood and the transport of that oxygenated blood by the heart to the working muscles.
“Peripheral” refers to the parts of the system concerned with oxygen diffusion and the oxidative capacity of the muscles themselves. This includes the capillaries (blood vessels to the muscle fibres) and the mitochondria within the muscle cells (the sites that produce energy aerobically).
There’s debate as to which is the most significant contributor to the VO2max and thus where positive adaptations brought about by training could make the largest difference to an athlete’s aerobic capacity, so let’s take a more in-depth look at each, starting with the central components of VO2max…
Central Factors
The central components at the beginning of the oxygen transport process start with oxygen being breathed in from the atmosphere and entering the lungs, where it then diffuses into the blood ready to be sent to the muscles, where it is used to create energy.The diffusion of oxygen from the lungs to the blood is known as ‘pulmonary diffusion’ and is one key factor that influences VO2max.
The transport of oxygenated blood to the muscles is facilitated by the beating of the heart muscle, where ‘cardiac output’, meaning the volume of blood pumped through the circulatory system in one minute, is a product of both stroke volume (amount of blood output by the left ventricle in a single beat) and heart rate (beats per minute).
By achieving a higher maximal stroke volume, greater amounts of blood can be transported to the working muscles, thus creating the potential for more of the oxygen being carried in the blood to be used by the mitochondria for energy production.
Studies appear to show that when an untrained person commences endurance training, it is changes in stroke volume that contribute the greatest to improvements in aerobic capacity. In contrast, the aforementioned pulmonary diffusion and maximum heart rate do not appear to change considerably with training.
Once an athlete becomes more highly trained, and the heart’s stroke volume is close to its maximum potential, research suggests that cardiac output does not change appreciably, and it is then adaptations in peripheral factors that appear to allow VO2max to continue increasing.
Let’s look at the peripheral factors next…
Peripheral Factors
The peripheral factors that affect the athlete’s VO2max are principally the density of capillaries (the location of oxygen exchange between the blood and muscle fibres) and the quantity and function of the mitochondria in the muscle cells.
The good news is that both capillary and mitochondrial density can be greatly improved via a well-designed training program.
When a greater amount of capillaries are formed around the muscle fibres as a result of training, there is a greater surface area for diffusion of oxygen as well as a slowing down of the blood flow through these vessels, the latter of which results in a greater amount of time for this diffusion of oxygen to take place.
With an increased number of mitochondria in the muscles (and where the function the mitochondria themselves are improved) more of the diffused oxygen from the capillaries has the potential to be used for aerobic energy production and the task of doing so can be shared across more mitochondria.
In summary, the more oxygen that can get to and be processed by the mitochondria, the more ATP (adenosine triphosphate a.k.a. the energy currency of the body) can be created aerobically to power the muscles involved in cycling power output. The oxygen-processing power of each mitochondria far exceeds that which maximal cardiac output can deliver, so it is a case of getting as much O2 to them as possible.
UPDATE: We just wanted to add a quick update to this latter point to explain a little further… For someone with very low mitochondrial density, this could in principle pose a limiter to VO2max due to a limit on the processing capacity of mitochondria themselves. However, this would be a very rare scenario. It's thought that mitochondrial density mainly poses a potential limitation on VO2max in its effect on O2 extraction from the capillaries. So a higher mitochondrial density seems to be linked with better O2 extraction from muscle capillaries (Bassett & Howley, 2000).
Overall, capillary density is probably the greatest peripheral VO2max limiter in most athletes. In contrast, mitochondrial density seems to play a bigger role in improving things like substrate utilisation, the location of the first and second lactate thresholds, and endurance (Bassett & Howley, 2000). This is because it's thought that a higher mitochondrial density allows for the oxygen-processing demand to be shared across a greater number of mitochondrial sites, allowing for more energy to be produced via the less efficient process of fat oxidation, rather than carbohydrate oxidation (thus resulting in lowered lactate levels for a given power output, and better glycogen sparing).
VO2max Adaptations
Now that we know a bit more about the components that make up the VO2max, we can get to the practical training details of eliciting positive adaptations.
We’ll start by looking at methods to improve the cardiac output firstly…
Central Adaptations
Since it’s clear that the delivery of large volumes of oxygenated blood via a high cardiac output is critical to cycling performance, we need to ensure that training targets improvements in this area throughout the majority of the training cycle.
By and large, the key goal when designing workouts to elicit these improvements is to achieve heart rates close to maximal levels and maintain around 90-95% heart rate max for the longest duration possible.
The reason we need to raise and hold the heart rate at close to these maximal levels is to facilitate adaptations in stroke volume via:
Improvement in the volume and wall thickness of the left ventricle
Greater stretch from this increased volume, resulting in greater elastic recoil
We essentially want to ‘stretch’ the heart muscle by filling it with lots of blood, so that it can increase in capacity and improve its contractile strength to deliver more blood with each beat.
Since heart rate tracks closely to VO2, we can use heart rate during a workout as a good indication of what % of VO2max is reached during high intensity efforts and whether this is sufficiently high to stimulate the desired response.
Training to spend large amounts of training time around 90-95% heart rate max can be applied as one sustained effort or through the use of interval training (i.e. alternating bouts of work and rest), where the latter is the most common method used. In addition, there’s considerable build up of lactate and associated fatiguing metabolites with these efforts, so the rest periods become important to allow the clearance of these fatiguing metabolites before the next effort.
This is where the use of both a power meter to pace the intervals but also a heart rate monitor that helps indicate the level of VO2 reached is crucial, despite common belief that heart rate is of limited value during shorter effort durations and that power output is the primary metric to use.
In the workouts section, we’ll highlight a novel VO2max session where HR is the primary metric rather than wattage.
Peripheral Adaptations
Training to elicit improvements in capillary density as well as mitochondrial content and function involve a few different training methods, and highlights why both lower and higher intensity training is necessary for cyclists seeking to improve aerobic capacity.
Longer duration, lower intensity training is arguably one of the best yet least stressful training methods to build mitochondrial and capillary density due to the facilitation of many muscle contractions, particularly by efficient slow twitch (Type I) but also the ‘malleable’ Type IIa muscle fibres, where these contractions play a key role in the signalling of mitochondrial biogenesis.
By keeping the training intensity to a level where glycolysis (anaerobic energy production via the breaking down of glycogen, the body’s storage form of carbohydrates) is minimised and mitochondrial respiration and the combustion of fat is maximised, mitochondrial growth and capillary density is also enhanced.
In addition to large amounts of lower intensity training, very high intensity workouts (e.g. 4-7x 30 second all-out sprints) have also been shown to improve mitochondrial growth and function, though the sustainability of performing these very stressful, anaerobically-dominant workouts several times per week for many weeks on end should be carefully considered.
Finally, building greater capillary and mitochondrial density within and around higher-power muscle fibres involves designing workouts that sufficiently activate the target fibres.
Slow twitch muscle fibres need very little stimulation for this activation to occur compared to fast twitch fibres (especially the Type IIb fibres, which require a load that both the Type I and Type IIa fibres cannot wholly carry). Adaptations in capillary and mitochondrial density are therefore stimulated by riding at different intensities that are intense enough to stimulate the target fibres, where in one case a longer aerobic ride is appropriate (to activate Type I fibres) and in another 10 second large gear sprints would be ideal (for the recruitment of Type IIb fibres).
VO2max Workouts
Below are 4 effective and scientifically-based workout designs that can be used to stimulate adaptations in both the central and peripheral factors presented above and positively alter the aerobic capacity:
4-min Constant Power Intervals
These relatively short duration intervals (though long enough not to be dominated by the CP and glycolytic anaerobic energy systems) use a high intensity target to stimulate a rapid heart rate response, improving stroke volume as well as the mitochondrial function (efficiency) within the muscle cells. Adding in initial bursts of even higher power (e.g. ~130%) to speed up the rise in heart rate (and VO2) can be applied when the athlete becomes more accustomed to this workout protocol.
6-8-min Variable Power Output Intervals
The longer duration of these “Billat” intervals is facilitated by varying the power output in real-time after the initial increase in heart rate (which acts as a proxy for VO2) where the minimum power output that keeps the heart rate elevated between 90-95% heart rate max is used. In some cases, this can see power output drop close to that associated with the lactate threshold/FTP, but in any case is constantly fluctuated throughout each 6-8 minute interval to maintain this elevated heart rate.
Microburst Interval Blocks
Microburst intervals using a 2:1 work-rest ratio (e.g. 30’ on/15’ off as shown above, or the popular 40’ on/20’ off) raise HR rapidly due to a combination of the high intensity “on” work bouts and short “off” recovery bouts, which facilitate the “drifting” upwards of the heart rate towards maximal levels throughout each block. The inclusion of “micro-recovery” in each block however allows for reasonably long duration blocks to be achieved, leading to greater total time spend at a high % of heart rate max. Some very recent research also suggests that microburst intervals are also an effective design for improving mitochondrial efficiency.
Long Duration, Lower Intensity Rides
Long duration, lower intensity “Zone 2” rides that keep the contribution of glycolysis to minimal levels build capillary density around the efficient Type I muscle fibres and encourage mitochondrial biogenesis within these fibres. Depending on your training goals, shorter duration steady rides (e.g. 1.5-2H) can be performed with restricted carbohydrate availability to specifically target improved fat oxidation ability, which may be helpful if you are looking to develop threshold power and fractional utilisation.
Free Workout Guide
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References
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Raleigh, J. P., Giles, M. D., Islam, H., Nelms, M., Bentley, R. F., Jones, J. H., ... & Tschakovsky, M. E. (2018). Contribution of central and peripheral adaptations to changes in maximal oxygen uptake following 4 weeks of sprint interval training. Applied Physiology, Nutrition, and Metabolism, 43(10), 1059-1068.
Rønnestad, B. R., & Hansen, J. (2016). Optimizing interval training at power output associated with peak oxygen uptake in well-trained cyclists. The Journal of Strength & Conditioning Research, 30(4), 999-1006.
