Athletes have become increasingly familiar with the concepts of VO2max training over the past couple years. The basic conversation level I’ve been hearing recently is incredibly nuanced compared to when I started learning about the physiology behind VO2max and aerobic performance.
Athletes are able to choose from a wide selection of workout platforms and protocols, to find the training practices that work best for them individually. Without as much need for lab testing or standard boilerplate training plans.
The research of course lags the best practices used by athletes and coaches in real-world training environments. More recent protocols including hard-start and intermittent intervals are starting to find their way into popular training plans and research, because they have worked in the field first.
Now it’s up to us to figure out why and how exactly these workouts work! What are the mechanisms that contribute to improved performances? And how can we continue to optimize individualized interval prescription.
My understanding about the physiological underpinnings of ‘VO2max’ has progressed. So here are some of my current thoughts and questions on the topic of VO2max trainability, time near VO2max, hard-start and intermittent intervals, and adaptations toward capacity and efficiency.
Physiological Limiters to VO2max
The classic view of aerobic capacity is that VO2max is primarily limited by central cardiovascular factors that constrain oxygen (O2) delivery (Lundby et al, 2017). This will be a brief summary of the literature and physiology that premises one of the underlying assumptions to most of the current interval training research.
The potential factors that contribute to VO2max can be conceptualized with the deceptively simple Fick equation.
Fick Equation
V̇O2 = Q̇ · (Ca-vO2)
Q̇ = HR · SV
V̇O2 = HR · SV · (Ca-vO2)
• V̇O2 – maximal rate of oxygen uptake; maximal aerobic capacity
• Q̇ – cardiac output, the product of heart rate (HR) and stroke volume (SV); how fast the heart beats and how much it pumps on each stroke
• Ca-vO2 – arteriovenous O2 difference; the difference in oxygen content of arterial and mixed venous blood
In the context of VO2max, the components of the Fick equation are interrelated such that the maximal attainable rate of O2 uptake will be most limited by the first of these factors to reach a ceiling.
Think of when you might have tried to perform high intensity intervals when fatigued. Maybe you had difficulty raising your heart rate as high as usual? Something else was probably limiting your metabolic capacity, meaning something else failed first before heart rate could (or needed to) approach max.
Empirical literature suggests that at VO2max, the O2 uptake capacity of muscle mitochondria (mV̇O2) contributing to CvO2 exceeds the O2 delivery capacity determined by Q̇ · CaO2 (Lundby et al, 2017). This is related to why we are able to push more resistance during one-leg exercises, compared to what both legs can do together in equivalent two-leg exercise.
Historically much of the literature suggests that cardiac output, and more specifically stroke volume (SV) is the primary limiting factor, and is often one of the earliest adaptations to occur with introduction of training. While other structural adaptations occur over weeks and months (Lundby et al, 2017).
(Joyner & Dominelli, 2020)
(Lundby et al, 2017)
These findings may be more true for less trained populations. Since well-trained athletes will already have benefited from these initial adaptations. Experienced trainers will continue to accumulate adaptations to both O2 delivery and O2 extraction components over years of training. And it typically takes more and more volume and intensity to realize those marginal gains.
Suffice to say that while the ‘classic view’ is that O2 delivery factors limit VO2max trainability, there is some extent of individual variability in the training response, and it is highly related to your existing training status (Skovereng et al, 2018).
It is also important to note that VO2max doesn’t necessarily limit performance. Once you look at similar athletes within a homogenous fitness group, fractional utilization of VO2max at anaerobic threshold (FTP/CP, etc.), O2 extraction fraction, and cycling economy/gross efficiency are equally if not more important than VO2max.
As the quote goes, often attributed to Dr. Andy Coggan:
A high VO2max is necessary, but not sufficient for endurance performance
What we can say is that improving your own VO2max and your performance will most likely require improving whatever your specific limiters are.
Your specific limiter might be peripheral somewhere in the muscle fibers, or central cardiovascular structure/hemodynamics, as above. That will depend primarily on your prior training history and current physiological fitness (eg. Skovereng et al, 2018), and of course heavily depend genetic and epigenetic/environmental factors, etc.
With that being said, there are some well established correlations between metabolic training stimulus and improvements to VO2max and other performance outcomes.
Time Near VO2max as a Training Target
Last time I investigated this topic, I started with the ubiquitous assumption that accumulating time around 90% VO2max elicits the greatest improvements to VO2max and aerobic performance outcomes (max aerobic power, TT performance, etc).
I was inspired to go digging on this topic a bit recently. The current paradigm of accumulating time near VO2max is based on important empirical findings that suggest achieving a relatively high metabolic intensity (~75-100% VO2max) is important for eliciting positive adaptations to aerobic capacity.
Well-trained athletes may need to accumulate more time at higher intensity closer to VO2max (Wenger & Bell, 1986; Midgley et al, 2006), related to the diminishing returns of adaptations, as mentioned above.
(Turnes et al, 2016)
(Buchheit & Laursen, 2013)
(Midgley et al, 2006)
(Wenger & Bell, 1986)
This is one of those theories on which much of the current high intensity interval training literature is premised. And for good reason. There are robust and extensive data to support this relationship. However:
The correlation between time near VO2max and performance improvements is far from fully mechanistically elucidated.
The empirical evidence for time near VO2max is robust for ‘traditional VO2max’ interval training. Which might look something like 4x5min severe intensity intervals, somewhere above FTP/CP/”threshold”. What I would precisely call a continuous evenly-paced long interval workout.
In these classic workouts there is usually a tight relationship between mechanical workload (external power output) and metabolic intensity (internal VO2, or relative %VO2max). Meaning workload and intensity cannot be separated, nor is there any particular need to, when considering adaptive benefit.
However as training protocol have progressed recently, allowing us to manipulate workload and intensity semi-independently, we have begun to glimpse how there might be more to tease out in this relationship than just maximizing time near VO2max.
The goal now is to investigate whether mechanical workload and metabolic intensity may be independently related to differences in aerobic adaptation.
Hard-Start and Intermittent Intervals to Maximize Time Near VO2max
The two workout protocol I have been most interested in for manipulating time near VO2max are hard-start (alternately called fast-start or all-out) and intermittent intervals (microburst, Tabata, Billat, or repeat sprint training: RST).
They pose an interesting comparison. Hard-start intervals elicit a higher metabolic intensity at a lower mechanical workload. While intermittent intervals allow a higher mechanical workload and a higher metabolic intensity. Both compared to ‘traditional’ VO2max workouts.
Let’s talk about hard-start intervals first.
Hard-Start VO2max Intervals
Hard-start intervals use an initial hard attack at supra-VO2max workload – meaning a power output above what would be sustainable at VO2max – to rapidly stimulate a rise in oxidative metabolism – faster VO2 onset kinetics – in order to meet the sudden elevated O2 demand (Jones et al, 2008; Bailey et al, 2011; Billat et al, 2013; Lisbôa et al, 2015; Ronnestad et al, 2019).
Hard-start protocol can be applied to either continuous or intermittent interval training. Seen here combined into an ‘iso-effort’ mixed-protocol workout.
The goal of this workout was to maximize the effort during each interval, blinded to any power or HR targets. Additional instructions for the hard-start component was to start each interval harder than the athlete thought they would be able to maintain, to simulate a race breakaway situation. Before settling into the maximal sustainable effort for the remaining interval duration.
As the athlete rapidly approaches VO2max, power will naturally decrease to allow the athlete to maintain an elevated VO2 for the entire remaining interval duration. Getting to VO2max faster means more time accumulated near VO2max for the same interval time, and for the same or lower total work.
(Brock et al, 2018)
The effect of a hard-start on oxygen uptake is well illustrated in this study, with a representative tracing of VO2 in response to different pacing strategies during a self-paced TT. Open circles show VO2 from an evenly-paced condition. Closed circles show VO2 with a 12s all-out start.
(Zadow et al, 2015)
Description of proposed mechanisms behind hard-start effect on metabolic intensity.
In this way, studies investigating hard-start pacing strategies have shown that metabolic intensity (time near VO2max) can be increased independently from a change in average power or mechanical workload within an interval workout (Zadow et al, 2015; Lisbôa et al, 2019).
Unfortunately as far as I’m aware, this has only been demonstrated in the acute response to a workout. And no studies have yet demonstrated beneficial adaptations to a hard-start training intervention over time. Therefore:
The current recommendation for a hard-start strategy is only indirectly based on the acute response of greater time accumulated near VO2max.
Further research is needed to establish whether a hard-start training intervention will produce the expected adaptations over the long term. I know this is a question many research groups are interested in, and I hope we’ll see some longitudinal studies published in the near future!
Intermittent VO2max Intervals
The second protocol that I am most interested in are intermittent intervals. These workouts split a single VO2max interval into a set of short work/rest microbursts. such as 30/15s popularized by Prof. Rønnestad, or earlier Tabata 20/10s or Billat 30/30s. Similar intermittent sets with shorter work and longer rest intervals (eg. 10/20s or 10/60s) may also be called ‘repeat sprint training‘.
The same hard-start mixed-protocol workout as above.
Note that average power during the intermittent work intervals are greater than the continuous interval, despite all intervals being performed at maximum ‘iso-effort’ relative intensity.
Like hard-starts, intermittent intervals also have the athlete perform supra-VO2max efforts for these short, intense work reps. These are interspersed with equally brief rests that intentionally prevent sufficient recovery, and force VO2 to remain elevated.
The accumulation of these short work intervals can be performed at a power output higher than if the equivalent work duration was performed as a single continuous interval.
This higher workload elicits more rapid VO2 onset kinetics and higher sustainable metabolic intensity. VO2, Q̇, ventilation, etc. remain elevated through the brief rest intervals, meaning the effective training stimulus is sustained for closer to the full set duration, rather than just the work duration.
For example, in Rønnestad’s protocol of 3 sets of 13x 30/15s, the work sets add up to ~29min (3x 13x 30+15s) of total ‘intensity time’, compared to 19.5min (3x 13x 30s) of ‘work time’. Whereas the equivalent ‘classic’ 4x5min workout with 20min of work time, might only add a handful of seconds after each interval to intensity time.
(based on protocol reported in Ronnestad et al, 2020)
Rønnestad’s group in Norway have investigated these ‘short’ intermittent intervals over the past few years in well-trained and elite endurance athletes.
They have demonstrated superior acute responses in short intervals compared to long (continuous 5min) intervals. Not only measured by greater time near VO2max and HRmax, but also from superior blood hormone response, and at least no difference in genetic signalling. Which gives stronger evidence for a positive training effect (Almquist et al, 2020).
It should be pointed out that the interval protocols used in these studies are not work-matched. They are ‘iso-effort‘, or ‘effort-matched’. The subjects in both groups “were instructed to perform intervals with their maximal sustainable work intensity, aiming to perform highest possible average power output during each interval session” (Almquist et al, 2020).
In this way power was an outcome measure for what ended up being equally hard workouts. As the authors note, this better reflects real world training, where an interval workout is typically performed as hard as possible, or close to it.
As you might expect, the intermittent protocol allowed for greater average power and total mechanical work performed over the same work duration, and at the same perceived effort.
These findings show that an intermittent VO2max protocol can acutely prolong performance at higher mechanical workload and elicit greater metabolic intensity, compared to a ‘classic’ continuous VO2max workout.
Critically, they have also demonstrated chronic improvements to performance and physiological outcomes with short intervals over 10 weeks in well-trained cyclists (Ronnestad et al, 2015) and 3 weeks in elite cyclsts (Ronnestad et al, 2020). Dr. Steven Cheung just posted a much more concise review of this recent article over at Pezcyclingnews
In the more recent paper in elite cyclists (VO2max 73 ± 4 mL/kg/min) the short interval (SI) group showed greater improvements in VO2max, Wmax (ie. max aerobic power), submaximal efficiency (power output and fractional utilization of VO2max at 4mmol, a proxy for lactate threshold), and power over a 20min time trial. Compared to the long interval (LI) group.
We could speculate that these elite, experienced athletes would have already accrued much of the early gains from training adaptations. They may have seen the dramatic response shown here due to the novelty of the training protocol, and the ability to accumulate greater training load with no increase in volume. Less experienced athletes may see different results.
With intermittent intervals, we have direct evidence of longitudinal performance improvements compared to traditional continuous intervals in highly trained endurance athletes.
Speculating on Trainability of Capacity, Efficiency, and VLamax
This section might feel a bit scattered. These are some of the ideas currently cycling around my brain. Hopefully they coalesce into something more coherent, and inspire some ideas for you to experiment with!
To pose some final questions, considering what we now know about metabolic intensity and mechanical workload, and what you know about your own performance strengths & limiters:
How would you expect to respond to hard-start or intermittent interval training?
How might aerobic capacity and efficiency respond to each protocol? How might they drive different peripheral or central adaptations? How would VLamax respond? Are all VO2 equal during ‘intensity time’ vs ‘work time’, in terms of representing a specific training stimulus?
Briefly, Ronnestad et al (2020) showed that aerobic capacity (VO2max) and peak power output (Wmax/MAP and 20min power) all improved with intermittent interval training. They also showed improvements to submaximal efficiency with a greater fractional utilization of VO2max (%VO2max) and power output at 4mmol blood lactate (BLa).
This is good evidence that these interval workouts can enhance both capacity and efficiency for these tested outcome measures.
These data may also imply that VLamax was decreased, based on higher power at 4mmol BLa and higher power relative to BLa at both max and submax workloads. [edit: Sebastian Weber of INSCYD suggests in the comments below that the changes at max and submax intensity can be explained by the change in VO2max alone.
Blood lactate accumulation or ‘tolerance’ also seems to have increased, suggesting a combination of mechanisms is at work behind La production and clearance.
Were these improvements due to higher workloads recruiting more muscle fiber mass, greater proportion of faster twitch fibers, and stimulating more peripheral adaptations toward enhanced O2 uptake?
Or were they caused by central adaptations and improved O2 delivery elicited by the enhanced metabolic intensity?? What would efficiency look like in terms of fatigue resistance over longer durations, say at 60min or 3+ hrs?
Hard-start intervals are even less well understood. I would expect the hard-start to recruit more muscle mass (I haven’t even got into EMG signals) and more ‘faster fibers‘ at the start of the interval. Leading to a rapid depletion of ‘anaerobic resources’ in those fibers and accumulation of ‘metabolic milieu’ within the working muscle.
As the workload is decreased in these intervals, are those fatigued fibers still recruited to produce power with whatever aerobic function they have left? Or is the ‘excess’ systemic VO2 we measure during hard-start intervals going toward restoring homeostasis within the working muscle and elsewhere in the body, without actually contributing to mechanical power output and locomotion?
Does that make a difference to the adaptive benefit of time near VO2max?
I might speculate that our central cardiovascular system doesn’t care where the O2 demand is coming from. So perhaps central adaptations in hard-start protocol might persist despite lower workloads. However could this come at the trade-off of diminished peripheral adaptations at the working muscle, with less specific work being performed?
For example, could depleting those anaerobic pathways early in the hard-start interval tend to cause VLamax to increase, as glycolysis will be preferred by faster fibers to rapidly restore homeostasis? Whereas more gradual, progressive fiber recruitment in an evenly-paced interval may allow greater fat oxidation across more fibers as they begin to contribute directly to mechanical locomotion?
Conclusions & Future Research Directions
Hard-start and intermittent intervals give us new ways to explore mechanisms behind individual response to exercise and training adaptations. And a couple of shiny new tools for coaches and athletes to optimize their own training and improve real world performances. This should be our ultimate goal.
I would be interested in seeing future research continue to manipulate metabolic intensity and mechanical workload to optimize the desired training effect.
For example, maybe I can mix my training stimuli by using an intermittent 30/15s workout to hammer the legs early in the week, then hard-start continuous intervals to add extra focus on the cardiovascular system while minimizing additional fatigue on the legs.
I am also more interested to think about and explore the effect of various workout protocol on VLamax and FATmax, and how they relate to aerobic capacity and efficiency. Keep these terms in mind. They will come up again in future articles.
There are a lot of unanswered questions currently on the table. Obviously I’m still thinking through everything and trying to piece together a story of what might be going on behind the scenes, based on the available literature.
And I’m very curious what you think. What are some missing puzzle pieces I’ve overlooked? Let’s keep the discussion going.
