VO2max: Why This One Number May Say More About Your Life Expectancy Than Your Blood Pressure

My starting point

At check-ups we measure blood pressure, cholesterol and blood sugar. We almost never measure how much oxygen your body can actually use under load. Yet that is the very value most closely linked to life expectancy in large cohorts.

1. The staircase that suddenly feels too steep

You come out of the underground. Four flights of stairs. At the top you have to pause for a moment, because your breathing is faster than you expected. Nothing dramatic. Just that brief moment where you notice: this was different three years ago.

I hear that sentence very often. And it is almost always followed by: But everything was normal at the doctor's. Blood pressure fine. Blood count unremarkable. Resting ECG without findings. Everything normal, and yet something does not match the way your own body feels to you.

A pattern many people describe

Not ill, but no longer capable in the way you were

Picture a situation I meet in conversations all the time. Someone has felt heavier, more sluggish and quicker to run out of breath for the past one or two years. The check-up says: unremarkable. The advice is: move more. But nobody has ever measured how much load this system can actually carry.

"I am not ill. I am just no longer the person I used to be."

What is missing here is not another blood value. What is missing is a value that captures the reserve. Resting measurements show whether your system is currently stable. They do not show what happens when you demand something of it. That is exactly the gap maximal oxygen uptake fills.

And now you know why an unremarkable check-up and a poor sense of your own body need not contradict each other.

2. What VO2max actually measures

VO2max is the largest amount of oxygen your body can take up, transport and burn in the cells per minute. It is expressed in millilitres of oxygen per kilogram of body weight per minute.

Picture a supply chain. At the beginning stand the lungs as the port. Then comes the heart as the cargo ship. Then the blood as the container, with haemoglobin as the loading surface. Then the capillaries as the road network reaching into every last corner. And right at the end sit the mitochondria as the factories that turn oxygen into energy in the first place. VO2max measures the capacity of that entire chain, not of any single link.

Lungs

Oxygen passes from the air you breathe into the blood. In healthy people this step is rarely the bottleneck.

Heart and stroke volume

How much blood is ejected per heartbeat is often the real bottleneck in untrained people. This is exactly where training can have the clearest effect.

Blood and iron

Haemoglobin carries the oxygen. A functional iron deficiency can shrink this loading surface, often long before anaemia becomes visible in a blood count.

Capillaries

The finest distribution within the muscle. Easy endurance training can raise capillary density over a period of weeks.

Mitochondria

The power plants of the cell. Their number and their respiratory capacity determine how much oxygen is genuinely used in the end.

The first change of perspective

VO2max is not an athletic number. It is a systems number. That is why it carries so much information. It can hardly be shifted by a single good day or a single tablet. It reflects how well your entire oxygen supply chain has been working over the past months.

And now you know why a single value can capture so many levels at once.

3. What the mortality data show

This is where it gets uncomfortable and hopeful at the same time. The evidence on cardiorespiratory fitness is among the most consistent in preventive medicine. I will tell you about three of these studies rather than simply list them.

Cleveland Clinic, 122,007 exercise testsCohort

A group around Kyle Mandsager analysed every treadmill exercise test performed at a large US hospital between 1991 and 2014, covering 122,007 people and more than a million person years of observation. They sorted participants into five groups by age and sex adjusted fitness.

What was observed: risk adjusted all cause mortality fell continuously as fitness rose, with no discernible upper limit of benefit. The difference between the lowest and the highest group was larger than the difference made by coronary heart disease, smoking or diabetes in the same analysis.

What this means for you: if you move your fitness up by one band, you are shifting a variable that in this cohort was more strongly linked to survival than the classical risk factors. Causality cannot be derived from an observational study, but the magnitude is remarkable.

Mandsager K et al. JAMA Netw Open. 2018;1(6):e183605. DOI: 10.1001/jamanetworkopen.2018.3605

Meta-analysis across 33 cohortsMeta-analysis

Satoru Kodama and colleagues pooled 33 observational studies in JAMA in 2009, with 102,980 participants for all cause mortality.

What was observed: for every additional metabolic equivalent of capacity, which corresponds roughly to one kilometre per hour more running speed, the risk of all cause mortality was 13 per cent lower. People with low fitness had a 70 per cent higher risk of death compared with people with high fitness.

What this means for you: this is not about elite numbers. Even one step upwards out of the lower range may shift a great deal statistically.

Kodama S et al. JAMA. 2009;301(19):2024-2035. DOI: 10.1001/jama.2009.681

Copenhagen, 46 years of follow-upLong-term cohort

In the Copenhagen Male Study, 5,107 middle aged men without cardiovascular disease were tested on a bicycle ergometer in 1970 and 1971 and then followed through registries for 46 years.

What was observed: men in the highest fitness group lived on average 4.9 years longer than those in the lowest. Each additional unit of estimated oxygen uptake was linked to roughly 45 extra days of life. The association persisted even when all deaths in the first ten years were excluded.

What this means for you: the fitness you build at 45 may still matter at 80. That is a very long lever.

Clausen JSR et al. J Am Coll Cardiol. 2018;72(9):987-995. DOI: 10.1016/j.jacc.2018.06.045

13 %lower risk of death per additional metabolic equivalent (meta-analysis, 102,980 people)

4.9years longer mean life expectancy between the highest and lowest fitness group (46 years of follow-up)

11.6 %lower all cause mortality per metabolic equivalent when oxygen uptake is measured directly

The last figure comes from a study of 4,137 healthy adults in whom oxygen uptake was not estimated but measured directly by cardiopulmonary exercise testing. Across an average of 24 years of follow-up, each additional metabolic equivalent was linked to 11.6 per cent lower all cause mortality, 16.1 per cent lower cardiovascular mortality and 14.0 per cent lower cancer mortality.

How to read the markers I mark the level of evidence directly on each study. Green stands for randomised trials and meta-analyses in humans. Teal stands for observational and cohort studies in humans. Observational data show associations, not causes. Intervention studies show what changes when you deliberately intervene. Only together do the two produce a picture.

And now you know why I consider this the most underrated marker in preventive care.

4. More than blood pressure: what that actually means

The title of this article is deliberately pointed, so let me place it properly. I am not claiming blood pressure does not matter. High blood pressure remains one of the most important treatable risk factors we have, and blood pressure therapy has prevented countless strokes. What I am saying is something different.

Blood pressure is a risk factor. VO2max is a system performance. A risk factor tells you what could go wrong. A system performance tells you how much reserve you have when something does go wrong.

In 2016 the American Heart Association published a scientific statement making exactly this point. The author group around Robert Ross concludes that cardiorespiratory fitness may be a stronger predictor of mortality than established risk factors such as smoking, high blood pressure, high cholesterol and type 2 diabetes. And that adding fitness to the classical factors can markedly improve risk assessment. The statement proposes treating fitness as a clinical vital sign.

AHA Scientific Statement 2016Review

The professional society appraised the available epidemiological and clinical evidence on cardiorespiratory fitness.

What was observed: low fitness is consistently linked to high risk of cardiovascular disease, all cause mortality and several cancer mortality endpoints. Adding fitness to risk models markedly improved risk reclassification.

What this means for you: if you know your fitness, you know a part of your risk profile that is usually not captured at all in routine care.

Ross R et al. Circulation. 2016;134(24):e653-e699. DOI: 10.1161/CIR.0000000000000461

What has to be said honestly here

Nearly all mortality data on VO2max come from observational studies. They show associations, not a proven cause and effect relationship. It is conceivable that poor fitness is partly a consequence of illness and not only a cause. That is exactly why the Copenhagen analysis is so valuable: even after excluding all deaths in the first ten years, the association remained, which argues against pure reverse causation.

What is established: training can raise VO2max. What follows from that for an individual life expectancy is a reasoned probability, not a guarantee.

And now you know why I do not play this value off against blood pressure but place it alongside.

5. The bridge to heart, brain and metabolism

Why should oxygen uptake of all things be connected to things as different as dementia, cancer and heart attack? Because it does not reflect an isolated organ but the quality of your energy production. And energy is the shared currency of all four KPNI levels.

Nervous system

Endurance training can shift autonomic balance away from permanent sympathetic drive. A higher stroke volume allows a lower resting heart rate. The body can do the same work with less internal alarm.

Immune system

Silent inflammation disturbs mitochondrial respiration. Conversely, regular movement can dampen inflammatory signalling pathways. Anyone with chronic inflammation is training against a headwind they cannot see.

Metabolism

More mitochondria and more capillaries mean better fat utilisation at low intensity and higher insulin sensitivity. That is the direct bridge from VO2max to blood sugar and body composition.

Hormonal system

Thyroid hormones govern mitochondrial activity, cortisol governs recovery. A functional iron deficiency can reduce oxygen loading. Without this level, training often stays less effective than expected.

I find the data on the brain particularly striking. The brain weighs about two per cent of your body weight and consumes roughly twenty per cent of your oxygen. That makes it the organ most sensitive to a faltering supply chain.

HUNT study Norway, 30,375 adultsCohort

Atefe Tari and colleagues used a Norwegian population study in which estimated fitness was recorded twice, ten years apart, and linked it to dementia registries.

What was observed: people who stayed fit across those ten years had a 40 per cent lower risk of a dementia diagnosis than those who were unfit at both time points. Those who moved from unfit to fit were 48 per cent lower. This group gained on average 2.2 dementia free years and 2.7 years of life.

What this means for you: the change counts, not only the starting value. Whoever is at the bottom today has statistically the most to gain.

Tari AR et al. Lancet Public Health. 2019;4(11):e565-e574. DOI: 10.1016/S2468-2667(19)30183-5

Endurance is not the ability to run for a long time. Endurance is the ability to stay capable of acting for a long time.

That is the point where this becomes bigger than a training topic for me. It is not about a number on a watch. It is about whether at seventy you still decide for yourself which hill you walk up. Reserve is freedom.

And now you know why I take VO2max just as seriously in conversations about ageing as in conversations about sport.

6. Not a genetic fate, but not automatic either

The most common objection I hear is: I am simply not the endurance type. Behind it sits the assumption that VO2max is genetically fixed. That assumption is half right, and the wrong half costs people years.

HERITAGE Family Study, 481 adultsTraining study

Claude Bouchard and his team trained 481 previously inactive adults from 98 families for twenty weeks using a standardised protocol and measured oxygen uptake twice before and twice after.

What was observed: the mean increase was around 400 millilitres per minute. The spread, however, was enormous, with some gaining almost nothing and others more than a litre. Variance between families was 2.5 times greater than within families, and the estimated heritability of the training response was about 47 per cent.

What this means for you: your genes influence how strongly you respond to training. They do not decide whether you respond.

Bouchard C et al. J Appl Physiol. 1999;87(3):1003-1008. DOI: 10.1152/jappl.1999.87.3.1003

The second change of perspective

A large share of the so called non-responders in training studies were simply not challenged enough. A meta-analysis of 37 interval studies with 334 participants found a mean increase of 0.51 litres of oxygen per minute. In a subgroup of nine studies using longer, harder intervals the increase was around 0.8 to 0.9 litres, and there practically every person showed a response.

So if you believe you belong to the group for whom endurance training does nothing: it is possible you have simply trained genuinely hard too rarely so far.

The other side of this evidence is less comfortable. Without a stimulus the value falls, and not in a linear way. In the Baltimore Longitudinal Study of Aging, 810 heart healthy people between 21 and 87 years were measured repeatedly on a treadmill over a median of eight years. The decline in peak oxygen uptake was around three to six per cent per decade in the twenties and thirties. From the seventies onwards it exceeded twenty per cent per decade. So the curve gets steeper the later you start.

Why this is good news If the age related decline sits at roughly ten per cent per decade in midlife, and well structured training can produce a five to ten per cent increase in twelve weeks, then a consistent year of training arithmetically buys you back several biological years. That is not rejuvenation. But it is a shift of the curve, and you may feel it in everyday life.

And now you know why I turn down the sentence "I am not the endurance type" kindly but firmly.

7. How to measure your value or estimate it honestly

Before you train, you need a starting point. Otherwise in three months you will not know whether anything has changed. There are three levels of accuracy, and all three have their place.

Method	Accuracy	Who it suits
Cardiopulmonary exercise testing with gas exchange analysis	Gold standard, direct measurement	If you have symptoms, pre-existing conditions, or want a solid baseline
Field test, for example a 12 minute run or a submaximal step test	Good estimate, very good for tracking change	Healthy people who want to work without a lab and repeat the test identically every eight to twelve weeks
Smartwatch using heart rate and pace	Rough estimate, usable trend	Everyday observation, as long as you do not overrate the absolute figure

Validation of a smartwatch against laboratory testingValidation study

A German research group compared the estimate of a widely used smartwatch with a laboratory measurement by gas exchange analysis in 19 people.

What was observed: the watch estimated a mean of 41.4 millilitres per kilogram per minute, while 45.9 was measured. The mean absolute percentage error was 15.8 per cent and individual reliability was weak. Very fit people tended to be underestimated, less trained people overestimated.

What this means for you: use the number on your watch as an arrow, not as a diagnosis. If the arrow points upwards over eight weeks, you have probably done something right.

Caserman P et al. JMIR Biomed Eng. 2024;9:e59459. DOI: 10.2196/59459

Rough anchors you can orient yourself by

I deliberately avoid naming target scores, because reference tables vary strongly between sources. Two solid anchors exist nonetheless. In the Norwegian HUNT3 study of 4,527 heart healthy adults, directly measured peak oxygen uptake averaged 36.0 millilitres per kilogram per minute in women and 44.4 in men. And in Kodama's large meta-analysis, the range below 7.9 metabolic equivalents, that is roughly 28 millilitres per kilogram per minute, marked the zone with markedly raised mortality.

The more important question

Not: Am I good enough? But: In which direction is my value moving over the next twelve months? In the HUNT dementia analysis it was precisely the change across ten years that was the decisive factor, not the starting value alone.

And now you know why I would rather see two honest measurements three months apart than one perfect one.

8. The polarised model: why the middle delivers least

Now to the practical part. Most people train in the middle intensity range. Not easy enough for real recovery, not hard enough for a strong stimulus. I call it the comfort zone of effort: it feels like training, it costs time, and it changes comparatively little.

The polarised model does the opposite. It pulls the intensities apart: a great deal of easy volume and a small share of genuinely hard work. The middle is deliberately thinned out.

Trondheim 2007, same work, different intensityRCT

Jan Helgerud and colleagues divided 40 moderately trained men into four groups: long slow distance running at 70 per cent of maximum heart rate, lactate threshold training at 85 per cent, 15 second intervals, and the so called 4x4 protocol. Crucially, all four groups performed the same total work, three times a week for eight weeks.

What was observed: only the two interval groups raised maximal oxygen uptake significantly, by 5.5 and 7.2 per cent respectively. The distance and threshold groups showed no comparable gain. In parallel, cardiac stroke volume rose by around ten per cent in the interval groups.

What this means for you: for the same investment of time, the distribution of intensity decides whether your heart gets stronger.

Helgerud J et al. Med Sci Sports Exerc. 2007;39(4):665-671. DOI: 10.1249/mss.0b013e3180304570

Salzburg 2014, four training models comparedRCT

Thomas Stöggl and Billy Sperlich compared four concepts in 48 well trained endurance athletes over nine weeks: high volume, threshold training, pure interval training and polarised training.

What was observed: the polarised group raised peak oxygen uptake most clearly at 11.7 per cent, and time to exhaustion at 17.4 per cent. High volume alone and threshold training produced no further improvements in performance variables in this study.

What this means for you: the combination beats the raw dose. It is not about doing more, but about distributing differently.

Stöggl T, Sperlich B. Front Physiol. 2014;5:33. DOI: 10.3389/fphys.2014.00033

Where I temper the enthusiasm

A recent meta-analysis of 17 studies with 437 people did confirm an advantage of the polarised model for peak oxygen uptake, though with a small effect and only under certain conditions: in interventions shorter than twelve weeks and in highly trained athletes. For time trial performance and threshold performance it was equal to other models, not superior.

Translated, that means: polarised is a very good basic framework, particularly for lifting aerobic peak performance. It is not a magic recipe, and for recreational athletes a broader distribution may work similarly well. More important than the perfect model is that hard stimuli occur at all and that the easy sessions really are easy.

The mechanism behind it

Martin MacInnis and Martin Gibala have summarised the physiology of this intensity question in a review. The cellular stress that triggers the formation of new mitochondria depends strongly on intensity. For the same amount of work, intense intervals appear to generate a stronger signal for mitochondrial biogenesis within the same person than moderate continuous training. At whole body level, maximal oxygen uptake rises more with intense intervals for the same training volume.

The easy sessions work at a different point in the chain. They raise blood volume, stroke volume and capillary density, and they do so at very low recovery cost. That is why the zone 2 base is not an accessory. It is the foundation that makes the hard sessions bearable in the first place.

Mayo Clinic 2017, young and old comparedRCT

Matthew Robinson and the team around Sreekumaran Nair compared high intensity interval training, resistance training and a combination of both in younger and older adults over twelve weeks.

What was observed: all forms improved insulin sensitivity and muscle mass. But only interval training and the combination raised aerobic capacity and mitochondrial respiration. In the older participants, interval training shifted the muscle proteome markedly towards a younger pattern, particularly in mitochondrial proteins.

What this means for you: resistance training remains important for muscle and bone. The oxygen chain additionally needs an aerobic stimulus, and that stimulus may still move something at an older age.

Robinson MM et al. Cell Metab. 2017;25(3):581-592. DOI: 10.1016/j.cmet.2017.02.009

And now you know why easy and hard are not opposites but two tools for two different construction sites.

9. A weekly structure that stays realistic

Now to the concrete part. The structure below is not a prescription but a direction, derived from the study protocols described above. It assumes you are healthy. If you have pre-existing cardiovascular conditions, are older than 40 and have been inactive for a long time, or if you notice chest pain, dizziness or breathlessness under load, medical assessment belongs before the first hard stimulus.

Base

2 to 3 easy sessions

40 to 60 minutes each, steady
About 60 to 70 per cent of maximum heart rate
Talk test: full sentences must stay possible
Cycling, rowing, brisk walking or easy running
These sessions may feel almost too easy

Stimulus

1 hard interval session

Following the 4x4 pattern from the Trondheim research
4 blocks of 4 minutes at about 90 to 95 per cent of maximum heart rate
3 minutes of active recovery in between at around 70 per cent
10 minutes warm-up before, 10 minutes cool-down after
At least 48 hours before the next hard session

The most common mistake Easy sessions too fast and hard sessions too slow. If you end up out of breath during your base sessions, you have done middle pace training that costs recovery without setting the strong stimulus. If you can still chat comfortably after the third interval block, it was not an interval.

Realistic timeframes

4 to 6weeks until the first noticeable everyday changes, such as a lower heart rate at the same pace

8 to 12weeks until a measurable increase, which is the typical duration of the studies cited here

6 to 12months until a change that stays clearly visible in the longer trend

In Zoran Milanović's meta-analysis of 28 controlled studies with 723 participants, the mean increase from interval training was 5.5 millilitres per kilogram per minute compared with control groups, and 4.9 from classical endurance training. In direct comparison, interval training was about 1.2 millilitres ahead. Both are relevant magnitudes, given that one metabolic equivalent corresponds to 3.5 millilitres and was linked in the cohort studies to roughly 12 per cent lower mortality.

Three levers you can put in place this week

Record a baseline. A simple, repeatable test is enough: the same route, the same time of day, the same heart rate measurement. Repeat in twelve weeks.
Make one session per week genuinely hard. Four blocks, four minutes, at the edge. That is the stimulus that made the difference in the studies.
Make two sessions per week genuinely slow. Slower than your ego would like. That is precisely where the base lies that makes hard stimuli tolerable.

And now you know why three to four hours a week may change more than six hours at the same unvarying middle pace.

10. When training alone is not enough

Sometimes someone trains cleanly and consistently for months and the value barely moves. That is the moment where I do not ask for more training but for what might be blocking the stimulus. Here we partly leave the territory of the large studies and enter that of clinical observation, and I say so openly.

Levels I keep in mind in such cases

Iron status. Haemoglobin alone is not enough for me. A functional iron deficiency with low ferritin alongside a still normal haemoglobin can limit oxygen loading. For physically active people I consider a ferritin well above the lower laboratory limit more sensible than a value that sits only just inside the reference range.
Thyroid. Thyroid hormones govern mitochondrial activity. A sluggish thyroid can slow training adaptation.
Silent inflammation. Chronic inflammatory activity disturbs mitochondrial respiration. It may originate in the gut, in chronic infections or in an environmental exposure.
Sleep and recovery. Adaptation does not happen during training but afterwards. Anyone sleeping under six hours long term is training against their own regeneration.
Vitamin D status and nutrient density. Neither is a miracle solution, but both may improve the conditions under which adaptation can take place at all.

What is established and what remains observation

Well established by randomised trials: intensity distribution clearly influences the increase in maximal oxygen uptake. Interval training can improve mitochondrial respiration even at an older age.

Mechanistically plausible, human studies inconsistent: the influence of ferritin in the lower reference range on endurance performance in non-anaemic people. The evidence here is mixed, while the physiology of oxygen transport suggests it may be relevant.

Clinical observation without a strong study base: that when a training response fails to appear, several small brakes are strikingly often present at once rather than one large one. I am describing here what I see, not what is proven.

And now you know why, with stagnating values, I look for the brakes first and only then talk about more throttle.

Frequently asked questions about VO2max

The questions I am asked most often on this topic, answered briefly and honestly.

What is VO2max in simple terms?

VO2max is the largest amount of oxygen your body can take up, transport and use in the muscle cells per minute. It is usually given in millilitres of oxygen per kilogram of body weight per minute.

The value reflects an entire supply chain: lungs, cardiac stroke volume, blood and oxygen transport, capillaries and mitochondria. That is why VO2max is not merely an athletic number but a systems number describing your physical performance reserve. It cannot be flattered by a good day, and no single measure raises it in the short term.

Does VO2max really say more about life expectancy than blood pressure?

A 2016 scientific statement from the American Heart Association concludes that cardiorespiratory fitness may be a stronger predictor of mortality than established risk factors such as smoking, high blood pressure, high cholesterol and type 2 diabetes.

In an analysis of 122,007 exercise tests, the difference between very low and very high fitness was more strongly linked to mortality than coronary heart disease, smoking or diabetes. This does not mean blood pressure is unimportant. Blood pressure therapy remains one of the most effective measures in medicine. It means a single exercise value can reveal a surprising amount about the system as a whole, and it is usually missing from routine care.

Which VO2max value is good for my age?

Population data give more reliable orientation than gut feeling. In the Norwegian HUNT3 study of 4,527 heart healthy adults, the mean directly measured peak oxygen uptake was 36.0 millilitres per kilogram per minute in women and 44.4 in men.

A large meta-analysis used 7.9 metabolic equivalents as the threshold for low fitness, which corresponds to roughly 28 millilitres per kilogram per minute. Below that threshold, mortality risk rose markedly. More important than a single number, however, is the direction of travel across the years, because it was precisely the change that proved decisive in the long term data.

How can I improve my VO2max?

The best supported approach combines a large amount of easy base volume with a small number of genuinely hard intervals. In a randomised study with matched total work, high intensity intervals raised maximal oxygen uptake by 5.5 to 7.2 per cent over eight weeks, while long slow distance running and training at the lactate threshold showed no comparable gain.

A meta-analysis of 28 controlled studies found a mean increase of 5.5 millilitres per kilogram per minute for interval training compared with control groups. Easy sessions remain indispensable because they address blood volume, stroke volume and capillary density, and because they carry the volume that makes hard stimuli tolerable in the first place.

What is zone 2 and how do I find it?

Zone 2 is the easy steady state range in which you can still speak in full sentences and your breathing stays even. Roughly, it sits at about 60 to 70 per cent of maximum heart rate.

The simplest everyday check is the talk test. If you could hold a conversation without gasping, you are probably in the right place. Most people run their easy sessions too fast and their hard ones too slow. Precisely this blurring may dilute the training stimulus, because it costs recovery without setting a strong stimulus.

What is the 4x4 interval protocol?

The so called Norwegian 4x4 protocol consists of four work blocks of four minutes each at around 90 to 95 per cent of maximum heart rate, separated by three minutes of active recovery at about 70 per cent.

In the original study with 40 moderately trained men, maximal oxygen uptake rose by 7.2 per cent over eight weeks, and cardiac stroke volume increased by around ten per cent in parallel. The protocol comes from research and does not replace individual medical assessment. Particularly with pre-existing cardiovascular conditions, an assessment belongs before the first hard stimulus.

How long does it take for VO2max to rise?

Most controlled training studies run for six to thirteen weeks and see measurable gains within that window. In a meta-analysis of 37 interval studies, the mean increase was 0.51 litres of oxygen per minute, and around 0.8 to 0.9 litres in programmes using longer intervals.

Realistically that means: first noticeable everyday changes after four to six weeks, a solid new baseline after roughly three months, and a stably shifted level after six to twelve months. Anyone who stops after two weeks will see nothing.

Is VO2max genetically determined?

Partly. In the HERITAGE study of 481 previously untrained adults from 98 families, the mean increase after 20 weeks was about 400 millilitres per minute, but the spread was enormous.

Variability between families was 2.5 times greater than within families, and the estimated heritability of trainability was around 47 per cent. Genetics therefore explains roughly half of how strongly you respond, not whether you respond at all. In studies using longer, harder intervals, practically all participants showed a gain.

How accurate is my smartwatch VO2max estimate?

Useful as a trend indicator, to be treated with caution as an absolute figure. In a validation study of 19 people, a widely used smartwatch estimated a mean of 41.4 millilitres per kilogram per minute, while laboratory testing measured 45.9.

The mean absolute percentage error was just under 16 per cent and individual reliability was weak. Very fit people tend to be underestimated, less trained people overestimated. For tracking your own trend on your wrist, that is often still enough, as long as you read the number as an arrow and not as a diagnosis.

Can I still raise my VO2max beyond 60?

Yes, and that is precisely where the lever may matter most. In a study of younger and older adults, twelve weeks of high intensity interval training improved aerobic capacity and mitochondrial respiration in both age groups. In the older participants the shift in the muscle proteome was even more pronounced.

In people with heart failure after myocardial infarction, peak oxygen uptake rose by 46 per cent under supervised interval training in a randomised study, compared with 14 per cent with moderate continuous training. Medical assessment before starting matters, rather than giving up on intensity.

How often per week should I train?

In the studies cited here, frequency was mostly three sessions per week over eight to twelve weeks. A workable everyday pattern is three to four sessions: two to three easy base sessions and one hard interval session.

At least 48 hours should sit between hard stimuli. More hard sessions do not automatically deliver more, because recovery is the limiting factor. If you sleep poorly or catch infections easily, it is better to reduce the hard share than to raise it.

Does resistance training replace endurance training for VO2max?

No, the two stimuli address different systems. In the Mayo study over twelve weeks, both resistance training and interval training improved insulin sensitivity and muscle mass. But only interval training and the combination raised aerobic capacity and mitochondrial respiration.

Resistance training remains indispensable for muscle, bone and metabolism, particularly with increasing age. The oxygen chain additionally needs an aerobic stimulus. In my view the combination of both is the most sensible foundation.

Sources

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Transparency note: The associations between cardiorespiratory fitness and mortality come predominantly from large observational studies. They show robust associations but no proven cause and effect relationship. The training effects on maximal oxygen uptake come from randomised intervention studies and are well established. What follows from all this for your personal life expectancy is a reasoned probability, not a promise. Training recommendations in this text are general orientation and do not replace individual medical assessment, particularly not with pre-existing cardiovascular conditions, with symptoms under load, or after a longer period of inactivity.