How VO₂ Max Compares to Other Fitness Metrics

Is it more useful than heart rate, steps, or strength? Yes. But here’s the nuance.

Everyone’s tracking something.

Steps. Sleep. HRV. Calories. Heart rate zones. Readiness scores.

The noise is endless. The clarity? Rare.

So what should you track? What actually matters?

That depends on what you’re after.

If you want to know how hard you worked, wearables work.

If you want to know how well you’re recovering, HRV helps.

But if you want to know how long and how well you’ll live—start with VO₂ Max.

Let’s break down how it compares to other popular metrics—and when it makes sense to combine them.

Jump to Section:

• VO₂ Max vs. Resting Heart Rate: Ceiling vs. Idle

• VO₂ Max vs. METs: The Misunderstood Conversion

• VO₂ Max vs. Wearable Estimates: Directional, Not Diagnostic

• VO₂ Max vs. Strength and Power: Two Types of Reserve

• VO₂ Max vs. Step Count and Calorie Burn: Quantity ≠ Capacity

• VO₂ Max vs. HRV: Engine vs. Gearbox

• Which Metrics Actually Predict Mortality?

• The Real Picture: Triangulate with Precision

VO₂ Max vs. Resting Heart Rate: Ceiling vs. Idle

Resting heart rate (RHR) is the number of times your heart beats per minute while fully at rest—typically measured during sleep.

It’s easy to track and inversely related to aerobic fitness.

Lower = generally better.

But RHR is highly reactive. It jumps with stress, caffeine, alcohol, poor sleep, illness, even room temperature.

VO₂ Max, on the other hand, changes slowly—and only through sustained aerobic adaptation. It’s harder to manipulate, and that’s a feature, not a bug.

• RHR shows how calm your engine is at idle
  

• VO₂ Max shows how powerful your engine is at redline
  

Guess which matters more when life demands performance?

VO₂ Max vs. METs: The Misunderstood Conversion

You may have seen the term METs—especially on treadmill reports or cardiac rehab paperwork.

MET stands for Metabolic Equivalent of Task.

1 MET = the estimated amount of oxygen your body uses at rest.

By definition: 1 MET = 3.5 ml/kg/min of VO₂

So if your VO₂ Max is 35 ml/kg/min, you’re said to have a capacity of 10 METs.

Helpful? Somewhat.

But METs are population-based estimates, not personal measures. They assume a resting VO₂ of 3.5 across all people. And they’re often inferred without gas exchange, meaning the number may not reflect your actual physiological reality.

Bottom line: METs are a ballpark.

VO₂ Max is the scan.

VO₂ Max vs. Wearable Estimates: Directional, Not Diagnostic

Most people reading this may already have a “VO₂ Max number.”

It’s tucked into your Apple Watch, Garmin, Whoop, or Oura.

It updates automatically. It moves up or down. And it likely feels scientific.

But here’s the thing: it’s not actually VO₂ Max.

Wearables don’t measure oxygen consumption or carbon dioxide production.

They estimate fitness using heart rate during submaximal exercise—usually walking or running—and compare that to population models based on age, pace, and recovery patterns.

What you get is:

• A prediction, not a measurement
  

• Often 15–30% off from lab-tested VO₂ Max values—especially in highly fit or undertrained individuals [1]
  

• Sensitive to altitude, illness, sleep, hydration, stress, and even temperature
  

It’s like estimating the structural integrity of a building based on how the windows rattle in the wind. You might be close—but you don’t really know.

The Wearable Reality

Wearables may be useful.

If they keep you moving more than you otherwise would, encourage smarter rest, or create awareness around long-term trends, they’re likely directionally helpful.

But if you’re using the number to:

• Set your training thresholds
  

• Evaluate longevity risk
  

• Track aerobic progress over time
  

• Compare yourself to a population or peer group
  

…you’ll need something more precise.

True VO₂ Max is measured, not inferred.

It requires a ramped effort protocol, gas exchange analysis, and trained supervision. It reflects not just your heart and lungs, but how well your blood, cells, and mitochondria actually use oxygen under maximum load.

So if your watch says 42 and your friend’s says 39—and you both feel equally fit—who’s right?

Possibly neither.

But if those numbers got you off the couch, outside in sunlight, and doing hard things again… they’ve served a purpose.

Just don’t confuse the estimate for the engine.

If you want to know where you really stand—test it.

VO₂ Max vs. Strength and Power: Two Types of Reserve

Strength is your ability to generate force.

VO₂ Max is your ability to sustain oxygen-powered output over time.

They’re not in competition—they’re complementary.

• Strength protects against falls, fractures, and metabolic decline.
  

• VO₂ Max protects against cardiovascular disease, fatigue, and functional decay.
  

In aging populations, both are powerful mortality predictors.

But where VO₂ Max reflects systemic integration, strength reflects neuromuscular reserve.

Think of it this way:

• VO₂ Max = how far you can go
  

• Strength = how much you can carry
  

Longevity favors both.

VO₂ Max vs. Step Count and Calorie Burn: Quantity ≠ Capacity

Most wearables are built to count:

• Steps

• Calories

• Active minutes

But steps don’t guarantee intensity, and calorie estimates vary wildly based on algorithms, not actual exertion.

You can hit 10,000 steps a day and still have a dangerously low VO₂ Max.

You can burn 700 calories in a workout and see zero mitochondrial adaptation.

That’s because these metrics track movement, not capacity.

• Steps = motion
  

• Calories = estimate
  

• VO₂ Max = adaptation
  

Only one of these reflects a deep biological shift.

VO₂ Max vs. HRV: Engine vs. Gearbox

Heart Rate Variability (HRV) measures the tiny variations in time between each heartbeat. Higher HRV generally signals a more adaptive nervous system.

Here’s how it works:

• When your body is stressed, your sympathetic nervous system dominates → HRV drops
  

• When your body is recovered, parasympathetic tone rises → HRV increases
  

A high HRV = flexibility.

A low HRV = rigidity—often associated with chronic stress, burnout, or illness [2].

VO₂ Max tells you what you can do under load.

HRV tells you how well you recover between loads.

They work together.

• VO₂ Max = cardiovascular and metabolic horsepower
  

• HRV = nervous system control and resilience

Which Metrics Actually Predict Mortality?

Let’s draw the line between what’s popular and what’s predictive:

• VO₂ Max – strongest known predictor of cardiovascular and all-cause mortality [3]

• Visceral fat – silent driver of inflammation and chronic disease [4]

• Muscle mass and quality – critical for metabolic health and longevity [5]

• Bone density – fracture resistance and independence, especially post-50 [6]

• Strength – mobility, insulin sensitivity, fall prevention [7]

• HRV – recovery readiness, adaptability, and all-cause mortality [2]

• Gait speed – functional independence predictor [8]

Others—like step count, calorie burn, or sleep score—can be helpful when contextualized, but they don’t hold predictive power on their own.

The Real Picture: Triangulate with Precision

At DexaFit, we don’t guess.

We measure what matters—and use that to build your personalized healthspan blueprint.

Core Diagnostics (Predictive):

Metric	What It Reveals
VO₂ Max	Mitochondrial + cardiovascular horsepower
Visceral Fat	Chronic inflammation and disease risk
Muscle Quality	Functional capacity and metabolic reserve
Bone Density	Structural integrity and fracture resilience
Strength	Neuromuscular power and mobility

---

Complementary Metrics (Contextual):

Metric	What It Reveals
HRV	Nervous system adaptability
Sleep Quality	Recovery, hormone regulation, memory consolidation
Gait Speed	Integration of strength, cognition, and balance

This isn’t fitness vanity.

It’s clinically grounded data—designed to track capacity, resilience, and aging trajectory.

Want to build your true physiological profile?

Start with the most predictive metric of them all.

Book your VO₂ Max test with DexaFit.

References

1. Clausen JSR, Marott JL, Holtermann A, et al. Accuracy of heart rate-based VO₂ max estimation from consumer wearables: Validation against direct measurement. Eur J Prev Cardiol. 2021;28(15):1689–1699. doi:10.1177/2047487320919952
   
   
   

2. Jarczok MN, Koenig J, Mauss D, et al. The association of heart rate variability with all-cause mortality: a meta-analysis. PLoS One. 2014;9(12):e115003. doi:10.1371/journal.pone.0115003
   
   
   

3. Mandsager K, Harb S, Cremer P, et al. Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Netw Open. 2018;1(6):e183605. doi:10.1001/jamanetworkopen.2018.3605
   
   
   

4. Britton KA, Massaro JM, Murabito JM, et al. Body fat distribution, incident cardiovascular disease, cancer, and all-cause mortality. J Am Coll Cardiol. 2013;62(10):921–925. doi:10.1016/j.jacc.2013.06.027
   
   
   

5. Srikanthan P, Karlamangla AS. Muscle mass index as a predictor of longevity in older adults. Am J Med. 2014;127(6):547–553. doi:10.1016/j.amjmed.2014.02.007
   
   
   

6. Looker AC, Melton LJ, Harris TB, et al. Prevalence and trends in low femur bone density among older US adults. J Bone Miner Res. 2010;25(1):64–71. doi:10.1359/jbmr.090706
   
   
   

7. Rantanen T, Volpato S, Ferrucci L, et al. Handgrip strength and cause-specific and total mortality in older disabled women. J Am Geriatr Soc. 2003;51(5):636–641. doi:10.1034/j.1600-0579.2003.00207.x

8. Studenski S, Perera S, Patel K, et al. Gait speed and survival in older adults. JAMA. 2011;305(1):50–58. doi:10.1001/jama.2010.1923

Why VO₂ Max Declines with Age (and What You Can Do About It)

It starts falling in your 30s. But not because it has to.

Most people think aging just “happens.”
But what they call aging is often sedentary decay in disguise. That’s especially true for VO₂ Max.

Although it declines with age, the trajectory isn’t written in your genes—it’s shaped by what you do or don’t do. The difference between an active 60‑year‑old and a sedentary 40‑year‑old can be 30–40% in VO₂ Max—the gap between hiking a hill and needing help up the stairs.

This article explores why VO₂ Max declines, how much is truly inevitable, and what you can do—starting today—to maintain or even reclaim your aerobic reserve.

Jump to Section:

• The Standard Curve: ~10% Decline Per Decade

• What Drives the Decline?

• The Bigger Culprit: Behavioral Aging

• What Slows (or Reverses) the Decline?

• Sunlight, Mitochondria & Circadian Alignment: The Foundation Beneath the Engine

• What VO₂ Max Tells Us About Longevity

• Function Translated: What Your VO₂ Max Means

• Conclusion: Reserve, Not Just Decline

• References

The Standard Curve: ~10% Decline Per Decade

After age 30, VO₂ Max tends to drop around 10% per decade in average adults [1].
Someone with 45 ml/kg/min at 30 may decline to the low 30s by 50, and into the 20s by 70—under the threshold needed for independent mobility [2].

That assumes average behavior: low demand, minimal intensity. But what happens when you don’t send the right signals?

What Drives the Decline?

Several systems degrade in tandem:

• Maximum heart rate declines → lowers cardiac output

• Lean muscle mass shrinks → reduces oxygen demand

• Mitochondrial density drops → less ATP generated per unit O₂

• Capillary networks thin → poorer oxygen delivery

• Pulmonary efficiency decreases → less oxygen uptake

Each piece matters—but most are trainable, even into older age.
The real culprit is disuse.

Myth: Decline is mostly genetic.
Reality: Up to 70% of VO₂ Max loss is modifiable through training, movement, and recovery.

The Bigger Culprit: Behavioral Aging

By your mid-30s, most people stop sprinting. By 40, they avoid hills or fast walking.
The body takes the hint: if the system is never challenged, it adapts downward.

This is called allostatic adaptation—your body rebalances to the demands you place on it.
VO₂ Max declines not simply because you age, but because the signal to maintain it disappears.

What Slows (or Reverses) the Decline?

Some loss is inevitable. But much—possibly most—is avoidable.
The right interventions don’t just slow VO₂ Max decline—they can reverse it, even into your 60s and beyond.

Here are five of the most effective levers:

1. Zone 2 Training

Prolonged low‑to‑moderate intensity movement—like incline walking, cycling, or rucking—enhances mitochondrial density, increases fat oxidation, and builds the aerobic base that all higher-level efforts rely on.

2. Strength Training

Muscle isn’t just about force production—it’s metabolic scaffolding.
Maintaining lean mass supports oxygen demand, improves insulin sensitivity, preserves bone density, and reduces the risk of injury and frailty—all of which reinforce your ability to train and recover effectively.

3. VO₂ Max Intervals (Top-End Work)

Short bursts of high-intensity effort (e.g. 4 x 4 minutes at 90–95% max effort with equal rest) stimulate peak cardiac output and maintain your aerobic ceiling. They’re uncomfortable—but essential.

Note: Zone models vary. Some use 3, 4, 5, or even 8 zones. DexaFit uses a 4-zone model designed for clarity, precision, and clinical applicability.

4. Functional Movement

Stairs. Hills. Weighted carries. Crawls. These patterns train your aerobic and musculoskeletal systems under real-world conditions, forcing your body to adapt dynamically—not just in isolated reps or lab settings.

But what may be the most foundational—and underappreciated—way to preserve VO₂ Max isn’t about reps, intervals, or load.

It’s light.
And the circadian rhythm it entrains.

Let’s look at the engine beneath the engine:
the mitochondrial timing system that determines how—and when—you burn oxygen.

Sunlight, Mitochondria & Circadian Alignment: The Foundation Beneath the Engine

Before your heart beats faster… before your mitochondria burn oxygen… your body first checks the time.

Circadian Rhythm: The System That Sets the System

Your body isn’t one clock—it’s thousands.
Every organ, tissue, and cell contains peripheral clock genes—governing digestion, muscle repair, hormone release, and mitochondrial energy output. But these clocks don’t set themselves.

They rely on a master timekeeper: the suprachiasmatic nucleus (SCN)—a small cluster of neurons behind your eyes that listens to light.

When light enters the retina—especially from the low solar angle of sunrise—it signals the SCN: “Set the master clock. Synchronize the system.”

But what happens when you miss that signal?

Imagine workers across five time zones all scheduling meetings without saying if “2:00” means EST, CST, or PST.
Or a symphony in which every musician follows a different downbeat—while the conductor, drunk and waving his baton erratically, insists everything is fine.

This is what happens in a body with circadian misalignment.
Systems designed to operate in sequence instead crash into each other.
Recovery falters. Hormones mistime. Mitochondria become inefficient.
And VO₂ Max—the output of these inputs—suffers as collateral.

Sunlight’s Influence Doesn’t Stop at the Clock

Circadian rhythm sets the tempo.
But sunlight also feeds and tunes the system throughout the day.

Red and near-infrared light (660–900 nm), most abundant at sunrise and sunset, penetrate tissue and activate cytochrome c oxidase (CCO)—the final enzyme in the mitochondrial electron transport chain [4,5]. This activation:

• Boosts ATP production

• Increases electron flow

• Frees nitric oxide (NO) from binding sites—improving oxygen delivery

Studies show 10–40% increases in mitochondrial ATP output following red/NIR exposure, particularly in aging, stressed, or deconditioned cells [6].

UV Light and Neurovascular Performance

Sunlight’s ultraviolet (UV) spectrum—particularly in the morning and midday—triggers nitric oxide release from skin-based stores, leading to systemic vasodilation and enhanced blood flow [7].
It also stimulates the production of dopamine and serotonin, elevating focus, motivation, and mood—while setting the foundation for nighttime melatonin synthesis.

These neurochemical and vascular effects are not cosmetic.
They directly affect your aerobic economy, motivation to train, sleep quality, recovery capacity, and ultimately, your VO₂ Max trajectory.

Practical Application: Full-Spectrum Exposure Timing

The sun’s angle and spectrum shift throughout the day—each phase offering distinct biological cues. A coherent light strategy builds coherence in your physiology.

• Sunrise (within 30 minutes of waking):
  Full-spectrum light with high red/IR, low blue—entrains the SCN, synchronizes peripheral clocks, raises cortisol, activates mitochondria, and begins dopamine signaling.

• Midmorning to Midday:
  Higher blue and UV content stimulates vitamin D, promotes nitric oxide release, sharpens focus, and supports neurochemical tone. Indoor light doesn’t replicate this.

• Late Afternoon / Sunset:
  Blue light drops. Red and IR dominate again. This second wave supports mitochondrial recovery, helps shift circadian phase, and cues melatonin production—which is blocked by evening exposure to artificial blue light.

These transitions are non-negotiable to the biological systems VO₂ Max depends on.
Energy is not just something you make.
It’s something you make in time.

For those raised to fear the sun—lathering on sunscreen, avoiding outdoor exposure, wearing sunglasses from dawn to dusk—the growing body of evidence may come as a surprise.

One study in particular stands out. In a 20-year prospective analysis of more than 29,000 Swedish women, those with active sun exposure habits had significantly lower all-cause mortality, particularly from cardiovascular and non-cancer causes [8].

Most strikingly, nonsmokers who avoided sunlight had a similar mortality risk to smokers in the highest sunlight exposure group.

Put differently: the absence of sunlight may carry a mortality risk comparable to smoking.

While observational, these findings point to pathways beyond vitamin D—such as nitric oxide release, circadian alignment, and mitochondrial efficiency—that likely contribute to longevity.

Mitochondrial performance, among other factors, is profoundly shaped by sunlight, oxygen, and circadian timing.

VO₂ Max—our best non-invasive proxy for mitochondrial oxidative capacity—captures this system in action. It reflects:

• Mitochondrial density and efficiency

• Vascular function and oxygen delivery

• Circadian coordination of metabolic systems

When you avoid sunlight, you're not just avoiding UV.
You're disrupting the biological infrastructure that determines how well your cells use oxygen.

Though direct trials are needed, these mechanisms suggest sunlight may enhance VO₂ Max—a key driver of resilience.

What VO₂ Max Tells Us About Longevity

This isn’t speculation. VO₂ Max is among the most predictive biomarkers of mortality we have.

In a JAMA study of over 122,000 adults [2]:

• Moving from low (bottom 25%) to below average (25–50%) reduced all-cause mortality risk by ~50%

• Moving to above average (50–75%) reduced it by ~70%

• Those in the elite group (top 2.3%) had an 80% lower risk of death than those in the bottom quartile

Other studies confirm: VO₂ Max correlates strongly with both cardiovascular and all-cause mortality [8].

The higher your VO₂ Max, the more physiological reserve you carry into aging, illness, and recovery.

Function Translated: What Your VO₂ Max Means

VO₂ Max (ml/kg/min)	What You Can Do
>50	Sprint, bike hills, perform intense activity
40–50	Jog, hike, keep pace with active peers
30–40	Climb stairs, walk briskly, do light hiking
20–30	Flat walking only, fatigue with exertion
<20	Limited function, high frailty risk

Above 35 = long-term independence
Below 20 = elevated risk of hospitalization and dependency

Conclusion: Reserve, Not Just Decline

Some decline is inevitable.
But the rate and magnitude are negotiable.

VO₂ Max is the physiological reserve your body draws from when life gets hard.
Every small gain buys you protection. Every improvement buys you time.

Start now.
The sooner you build it, the longer you’ll keep it.

References

1. Fleg JL, et al. Accelerated longitudinal decline of aerobic capacity in healthy older adults. Circulation. 2005;112(5):674–682.
   

2. Mandsager K, et al. Cardiorespiratory fitness and mortality. JAMA Netw Open. 2018;1(6):e183605.
   

3. Carskadon MA, et al. Circadian rhythms and exercise. NIH Circadian Review. 2023.
   

4. Hamblin MR. Photobiomodulation mechanisms. AIMS Biophys. 2017;4(3):337–361.
   

5. Passarella S, Karu T. Visible/NIR absorption in mitochondria. J Photochem Photobiol B. 2014;140:344–358.
   

6. Chung H, et al. PBM and mitochondrial bioenergetics. Ann Biomed Eng. 2012;40(2):516–533.
   

7. Liu D, et al. UVA triggers systemic NO release. J Invest Dermatol. 2014;134(7):1839–1846.
   

8. Lindqvist PG, et al. Avoidance of sun exposure as a risk factor for major causes of death. J Intern Med. 2016;280(4):375–387. doi:10.1111/joim.12496