VO2 max

VO2 max is the point during progressively harder exercise at which oxygen uptake stops rising even though the workload keeps increasing. Because it is usually divided by body weight, it allows people of different sizes to be compared on one scale. Fitness is also reported in METs, where 1 MET is the oxygen used while sitting quietly. In research on exercise intensity, moderate activity begins at about 3 METs and vigorous activity at about 6 METs [7]. One MET of fitness corresponds to a running or jogging speed about 1 km/h faster [1].

In physiological terms, oxygen uptake is described by the Fick principle: it equals cardiac output (heart rate multiplied by stroke volume, the volume of blood pumped per beat) multiplied by the arteriovenous oxygen difference (the amount of oxygen the tissues extract from each litre of blood). VO2 max therefore depends on a chain of systems: pulmonary gas exchange, the pumping capacity of the heart, the oxygen-carrying capacity of the blood, capillary density in muscle, and the mitochondrial capacity of muscle fibres. A limitation at any point lowers the maximum, which is one reason VO2 max reflects the state of several organ systems at once.

The reference method is a graded exercise test on a treadmill or cycle ergometer. The workload rises in stages until the person can no longer continue, while a mask or mouthpiece measures the oxygen breathed in and the carbon dioxide breathed out. The test requires laboratory equipment and a maximal effort, so it is rarely performed outside research and sports medicine.

Most large studies of fitness and mortality used a standard clinical treadmill test instead, in which fitness is estimated in METs from the peak speed and incline reached, without gas analysis. Both the study of 122,007 patients at a US academic medical centre and the study of 750,302 US veterans classified fitness this way, by peak estimated METs [2, 3]. The HERITAGE Family Study measured VO2 max directly on a cycle ergometer, twice per participant [6].

Consumer fitness watches estimate VO2 max from heart rate at a given running or walking speed. These estimates rest on assumptions about maximum heart rate and movement efficiency, and none of the mortality figures on this page were derived from wearable readings.

Aerobic capacity declines with age in all adults, and the decline accelerates. In the Baltimore Longitudinal Study of Aging, peak treadmill oxygen uptake was measured repeatedly in 375 women and 435 men aged 21 to 87 who were free of heart disease, over a median of 7.9 years. The decline was about 3 to 6% per decade in the 20s and 30s and more than 20% per decade in the 70s and beyond, and from the 40s onward it was larger in men than in women [4].

The same study found that earlier cross-sectional estimates, which compared different age groups at one point in time, had understated the decline by assuming a constant rate. The rate was similar across all quarters of self-reported leisure-time activity. Most of the fall tracked a decline in oxygen pulse (the oxygen used per heartbeat), while maximum heart rate fell only about 4 to 6% per decade [4].

Because the decline occurs regardless of activity level, a higher starting level delays the age at which everyday tasks such as climbing stairs or walking briskly approach maximal effort. This reserve connects aerobic fitness with functional fitness and with the loss of muscle described under sarcopenia.

Studies of fitness and death usually report a hazard ratio or risk ratio (the risk in one group relative to another; 0.80 means 20% lower). The largest pooled analysis combined 33 observational studies of healthy adults with fitness measured by exercise testing: 102,980 participants and 6,910 deaths. Each 1-MET higher fitness level was associated with 13% lower all-cause mortality (risk ratio 0.87, 95% CI 0.84 to 0.90) and 15% fewer coronary heart disease or cardiovascular events (0.85, 0.82 to 0.88). Adults with low fitness (under 7.9 METs) had 70% higher all-cause mortality than those with high fitness (10.9 METs or more; 1.70, 1.51 to 1.92) and 40% higher than those with intermediate fitness (1.40, 1.32 to 1.48) [1].

Individual studies show the size of the gap at the extremes. Among 122,007 patients referred for treadmill testing at one US medical centre and followed for a median of 8.4 years (13,637 deaths), those in the lowest quarter of fitness for their age and sex had 5.04 times the mortality of elite performers, the top 2.3% (95% CI 4.10 to 6.20). Below-average compared with above-average fitness carried a hazard ratio of 1.41 (1.34 to 1.49), the same as smoking (1.41) and similar to diabetes (1.40) in the same patients. Elite fitness remained associated with lower mortality than high fitness in patients aged 70 or older, and no upper limit of benefit was observed [2].

Among 750,302 US veterans aged 30 to 95, followed for a median of 10.2 years with 174,807 deaths, risk fell steadily with fitness across age groups, sexes and races. Mortality was lowest at about 14 METs for both men (hazard ratio 0.24) and women (0.23), and there was no increase in risk at extremely high fitness. The least fit fifth had about four times the risk of the extremely fit (4.09, 3.90 to 4.20), and being unfit carried greater risk than any cardiac risk factor examined [3].

A 2014 meta-analysis of 10 prospective studies that measured both fitness and body mass index (BMI) examined their joint association with all-cause mortality. Compared with fit adults of normal weight, unfit adults had about twice the risk of death regardless of BMI, while fit adults who were overweight or obese had mortality similar to fit adults of normal weight [5]. The authors concluded that fitness-based approaches deserve more emphasis than weight loss alone for lowering mortality risk. The finding describes mortality only and does not mean excess body fat carries no other health risks.

Part of the variation in VO2 max between people is inherited. The HERITAGE Family Study measured VO2 max twice on a cycle ergometer in 429 sedentary people (170 parents and 259 of their children, aged 16 to 65 in all) from 86 families. Spouse, sibling and parent-child correlations were all significant, and the maximal heritability was estimated at 50% or more, a figure the authors noted is inflated to an unknown degree by non-genetic factors that families share. A maternal component, possibly related in part to mitochondrial inheritance, was estimated at about 30% [6].

VO2 max also rises with training. An umbrella review of 24 meta-analyses covering 429 trials and 12,967 participants found that high-intensity interval training increased VO2 max by 3.25 to 5.5 mL/kg/min compared with no exercise, and by a further 0.52 to 3.76 mL/kg/min compared with moderate continuous training, although most of the included reviews were rated of moderate to critically low methodological quality [8]. Training methods are described under high-intensity interval training and Zone 2 training.

Nearly all evidence linking VO2 max to mortality is observational. Because fitness is partly inherited, some of the survival advantage of fit people may reflect genetic factors that favour both fitness and longevity [6].

Reverse causation is a second limitation: undiagnosed heart failure, lung disease, anaemia or cancer lower exercise capacity before diagnosis, so low fitness can be a consequence of disease as well as a cause. The 122,007-patient study consisted of people referred for a clinical exercise test, many of whom had a medical reason for the referral [2]. Statistical adjustment can account for recorded diagnoses but not for undetected illness.

No randomised trial has assigned people to raise their VO2 max and measured the effect on lifespan. The closest test, the five-year Generation 100 trial of supervised exercise in 1,567 adults aged 70 to 77, found no statistically significant difference in mortality between groups [9]; it is described under high-intensity interval training. The association between fitness and survival is large, consistent and biologically plausible, but the number of years gained per unit of VO2 max has not been established.