Started Measuring VO₂ Max on Every Cardiac Patient.  
What I Found Changed How I Practice Medicine. 

For most of my career, I practiced cardiology the way we are all trained to practice it. 

I checked blood pressure, LDL cholesterol, and blood sugar, looked for blockages, and treated risk factors. 

And I believed I was preventing heart disease. But over time, I began to realize something uncomfortable: many of my patients who looked “fine” on paper were not actually fine. Their reports were normal. Their stress tests were acceptable. Their cholesterol was controlled. And yet, a few years later, some of them would return with serious heart problems. 

Something was missing. 

That is when I started paying attention to a number that, surprisingly, most of medicine still ignores, VO₂ max, or maximal oxygen uptake. 

If you look at the cardiovascular and longevity literature, VO₂ max is one of the strongest predictors of long-term survival we have. Not blood pressure. Not LDL. Not smoking. Not diabetes. Cardiorespiratory fitness. 

I know that sounds like something from a fitness magazine, not a cardiology clinic. But the data behind VO₂ max is not new, and it is not fringe science. It is decades old, well replicated, and published in some of the most respected medical journals. 

One of the largest studies, published in Mayo Clinic Proceedings, followed more than 120,000 patients for over two decades. What they found was remarkable: low cardiorespiratory fitness was a stronger predictor of mortality than smoking, hypertension, diabetes, and even chronic kidney disease. 

In simple terms, being unfit was more dangerous than being a smoker. 

Another study showed that for every 1 MET increase in exercise capacity, mortality risk drops by about 13 percent. Not 1 percent. Thirteen percent. And the benefit continues across the entire fitness spectrum. There is no point at which getting fitter stops helping you live longer.  

When you see numbers like that, you start asking a very uncomfortable question as a doctor: Why are we not measuring this on every patient? 

So I started doing exactly that. I began measuring VO₂ max as part of comprehensive cardiac evaluations.  

What I found changed how I think about heart disease.

I started seeing patients who looked very healthy by traditional standards but had very poor cardiorespiratory fitness. And I started seeing others who had decent endurance but poor muscle mass, high visceral fat, and poor metabolic health. They were “fit” in one sense, but not in the way that protects you from heart disease and early mortality. 

One patient, a marathon runner in his early fifties, had a good VO₂ max on paper. But when we looked deeper, his body composition showed high visceral fat and low muscle mass. He had endurance, but not metabolic fitness. And metabolic fitness is deeply connected to insulin resistance, inflammation, and long-term cardiovascular risk. 

Another patient, a woman in her mid-fifties, had been told for years that her heart was “normal.” Her echocardiogram was normal. Her basic blood work was normal. She had no major symptoms. But when we measured her VO₂ max, she fell into a very low percentile for her age. The literature is very clear about what that means: significantly higher risk of cardiovascular events and all-cause mortality over time.

She wasn’t sick in the way we usually define sickness. She was functioning, working, living her life. But physiologically, she was aging faster than she needed to. 

And no one had ever measured the one number that would have shown that clearly. 

This is where I think medicine often gets exercise wrong. We tell patients to “exercise more,” the same way we tell them to “eat better” or “reduce stress.” It’s good advice, but it’s vague, and vague advice rarely changes behavior. 

If I prescribe a medication, I don’t say, “Take some medicine.” I write the exact drug, the exact dose, and I review the response after a specific period of time. 

I believe fitness should be treated the same way. 

At Pulse Perfect, when we measure VO₂ max properly, we can also identify ventilatory thresholds, the points that define aerobic and anaerobic training zones. This allows us to prescribe exercise with surprising precision: a specific heart rate range, a specific duration, a specific number of sessions per week, and then we re-measure after a few months to see if the physiology has actually improved. 

Exercise has just changed from being a suggestion to a prescription that needs to be monitored for results. Over time, VO₂ max for me has changed from being a fitness metric to a clinical vital sign. It tells me how well the heart, lungs, blood vessels, and muscles work together as a system. It reflects mitochondrial function, metabolic health, and cardiovascular reserve. In many ways, it is a window into how well the body is actually ageing. 

 My evaluation of patients has transformed. I look beyond cholesterol, blood pressure, or whether there is a blockage. I examine a bigger picture: plaque, lipids, inflammation, visceral fat, metabolic health, and cardiorespiratory fitness. Because heart disease does not result from one abnormal number. It comes from a system that has been under stress for years. 

The old model of cardiology was reactive. We waited for symptoms, waited for blockages, waited for heart attacks, and then we treated them. 

The model we are trying to build now is different. We measure earlier. We look deeper. We find risk earlier. And we track whether our interventions are actually working. 

In that model, VO₂ max becomes a very important number, not because it makes you a better athlete, but because it strongly predicts whether you are likely to live longer and stay independent as you age. 

So the question I now ask many of my patients is very simple: 

Do you know your VO₂ max? 

Because if you don’t, you may be missing one of the most important numbers for your long-term health.  

And as a cardiologist, I can tell you this: We should not wait for the first heart attack to find out how strong the heart really is. 

Data Sources :  

📚 EVIDENCE BASE 

Ross et al., Mayo Clin Proc 2016 (n=122,007): CRF was the strongest predictor of mortality, exceeding smoking, hypertension, T2DM, and ESRD. Kokkinos & Myers, Circulation 2010: Each 1-MET increase = 13% mortality reduction. Mandsager et al., JAMA Network Open 2018: Elite CRF conferred a 5× lower mortality risk vs. low fitness; the survival benefit was linear across the entire fitness spectrum — there is no ceiling. 

📚 EVIDENCE BASE 

Iaia & Bangsbo, Scand J Med Sci Sports 2010: Zone 2 (polarized training) maximizes mitochondrial adaptations and oxidative enzyme activity. Poggio et al., JACC 2015: VO₂ max improvement of even 3–5 mL/kg/min is associated with meaningful reduction in cardiovascular event rates. Hood et al., J Appl Physiol 2011: Mitochondrial biogenesis is the primary cardiovascular adaptation mechanism driven by sustained Zone 2 training.