The Sixth Vital Sign: What Your Walking Speed Reveals About How You’re Ageing (And the Molecule Your Muscles Run Low On)

Chapter 1

Four Metres and a Stopwatch

Picture two men, both 75 years old, standing at the start of a short, taped-off line on a clinic floor. Same birthday decade, same city, similar medical files. Each is asked to do something that takes less time than reading this sentence: walk to the other end at his normal pace.

One covers the distance briskly. The other takes noticeably longer.

Here is the unsettling part. Researchers who pooled data from nine large studies found that, at age 75, a man’s predicted chance of being alive ten years later ranged from roughly 19% to 87% depending largely on how fast he walked. For women of the same age, the range was about 35% to 91%.

That is not a fringe finding. It is one of the most robust patterns in the science of ageing, and it is the reason a growing number of geriatric specialists now treat walking speed the way your GP treats blood pressure.

Section 1

The Study That Put Walking Speed on the Map

In 2011, a team led by Dr Stephanie Studenski published an analysis in JAMA that combined individual records from nine cohort studies and 34,485 community-dwelling adults aged 65 and over, followed for between 6 and 21 years.

Every participant had done the same simple thing at the start: a timed walk over a short course at their usual pace. The researchers then asked how well that single number predicted survival.

The answer was striking. For every 0.1 metres per second faster a person walked, the risk of death over the follow-up period was about 12% lower (hazard ratio 0.88). The average walking speed in the group was 0.92 m/s, a little under one metre each second.

To put 0.1 m/s in human terms: over a 4-metre course it is the difference between finishing in about 4.3 seconds and about 4.8 seconds. Barely perceptible to the walker. Highly informative to the scientist.

Four metres, one stopwatch: among the simplest tests in medicine, and one of the most informative.

Section 2

Why Physiotherapists Call It a Vital Sign

Your traditional vital signs are temperature, pulse, breathing rate and blood pressure. Pain is often counted as the fifth. In 2009, two physical therapists, Stacy Fritz and Michelle Lusardi, published a short paper with a deliberately provocative title: walking speed, they argued, deserves to be called “the sixth vital sign.”

Their reasoning was practical. Walking is never just about legs. To walk quickly and steadily, your heart and lungs must deliver oxygen, your nervous system must coordinate dozens of muscles in sequence, your inner ear and eyes must keep you balanced, and your muscles must produce force, stride after stride, without tiring.

When any one of these systems starts to falter, walking speed tends to quietly slip. It is a summary statistic for the whole body.

Section 3

Association, Not Destiny

Before we go further, one honest caveat that matters for everything that follows.

These are observational findings. They show that walking speed and survival travel together. They do not prove that forcing yourself to walk faster on the day of a test would change your future, any more than nudging a thermometer changes a fever.

What they do show is that walking speed is a sensitive read-out of what is happening underneath. And that raises the more interesting question, the one that occupies the rest of this article:

What is actually changing inside an ageing muscle, and is any of it within our control?

Keep that number. We will come back to it in Chapter 4.

Chapter 2

Inside the Ageing Muscle

If walking speed is the dashboard warning light, the obvious next step is to open the bonnet. In muscle science, that means a biopsy: a tiny core of tissue, usually from the thigh, analysed molecule by molecule.

Over the past few years, several research groups have done exactly that in older adults, comparing people whose muscles were holding up well with people whose strength and mobility were declining. One molecule kept appearing near the top of the list of differences.

Its name is NAD+ (nicotinamide adenine dinucleotide).

Section 1

What the Biopsies Found

In 2019, an international team published a study in Nature Communications that analysed muscle samples from 119 older men in Singapore, the United Kingdom and Jamaica. Some had sarcopenia, the age-related loss of muscle mass and strength. Others, of similar age, did not.

The muscles of the men with sarcopenia had lower levels of NAD+. They also showed reduced activity in the pathways that make and recycle NAD+, fewer mitochondria, and lower capacity to use oxygen for energy.

A second study, published in Nature Aging in 2022, compared muscle from young adults with muscle from three groups of older adults: those who trained regularly, those who were normally active, and those who were physically impaired. NAD+ stood out as one of the metabolites most clearly lower in older muscle, and lowest of all in the physically impaired group.

Older, weaker muscle tends to carry fewer active mitochondria and less NAD+, according to human biopsy studies.

Section 2

The Trained 70-Year-Old

The same Nature Aging study contained a detail that deserves its own headline.

In the older adults who exercised regularly, muscle NAD+ levels were close to those of the young participants. Age alone did not decide the outcome. How the muscle had been used seemed to matter a great deal.

That is a genuinely hopeful finding, and it reframes the whole question. Muscle NAD+ is not simply a countdown clock. It looks more like a level that responds to what we do, which is exactly why understanding how it is maintained is so useful.

One caution, again: these are cross-sectional snapshots. People who train may differ from those who do not in many other ways. But the direction of the evidence is consistent, and as we will see in Chapter 3, there is experimental work that points the same way.

Section 3

NAD+ in Plain Language

So what does NAD+ actually do?

NAD+ is a coenzyme, a helper molecule that hundreds of enzymes need in order to work. Inside the mitochondria, it shuttles electrons in the chemical reactions that turn food into usable cellular energy. It is also consumed by enzymes involved in DNA repair and in cellular stress responses.

Two features make it especially relevant to muscle:

First, muscle is one of the most energy-demanding tissues you have, especially when you move. Second, NAD+ is not made once and kept. It is used, broken down and rebuilt continuously, mostly through a recycling route biochemists call the salvage pathway.

Picture it as a busy recycling loop running all day in every muscle cell. Used NAD+ is broken down to a simpler molecule, nicotinamide, which is then rebuilt into fresh NAD+. The loop only works if every step keeps pace.

And one step in that loop is far slower than the others.

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Chapter 3

The Bottleneck Step

Every production line has one station that sets the pace for all the others. Speed up the fast stations and nothing changes. Widen the slowest one and the whole line moves faster. Engineers call it the bottleneck.

In the NAD+ salvage pathway, the bottleneck has a name: an enzyme called NAMPT (nicotinamide phosphoribosyltransferase).

NAMPT takes nicotinamide, the leftover piece of used NAD+, and converts it into a molecule called nicotinamide mononucleotide, better known as NMN. A second, faster step then turns NMN back into NAD+.

The salvage loop runs all day, but its pace is set by one narrow gateway: the enzyme NAMPT.

Hold on to that detail. It turns out to connect the two most practical things this article has to offer.

Section 1

What Exercise Actually Changes

If muscle NAD+ is higher in trained older adults, the natural question is how. Part of the answer appears to sit right at the bottleneck.

In a 2010 study, researchers measured NAMPT in the muscle of sedentary adults before and after three weeks of exercise training. NAMPT protein rose by 127%. Trained athletes in the same research had roughly twice as much NAMPT as sedentary people.

Crucially for our readers, this does not only happen in the young. In a 2019 study, adults over 55 who completed 12 weeks of training increased muscle NAMPT by about 28% with aerobic training and about 30% with resistance training. In the same study, NAMPT levels declined with age, and the best predictor of a person’s NAMPT was their aerobic fitness.

A 2023 meta-analysis pooling five studies concluded that exercise training reliably raises this enzyme in human muscle, by roughly one-and-a-half-fold on average.

In other words, when you train, you appear to widen the bottleneck. It is one of the clearest, best-replicated links between everyday behaviour and the NAD+ machinery inside our cells.

Section 2

NMN: The Molecule That Comes Out of the Bottleneck

Now return to the detail we asked you to hold on to. The enzyme that exercise increases, NAMPT, exists to make NMN.

That is why NMN became one of the most studied molecules in longevity research. Supplementing NMN supplies the product of the slowest step directly, so the cell can convert it to NAD+ in the next, faster step.

Does it work in people? On one point, the human evidence is consistent: NMN taken by mouth raises NAD+ levels in the blood.

In a 2022 Japanese trial, older men taking 250 mg of NMN daily for 12 weeks had significantly higher blood NAD+ and related metabolites than men on placebo. In a 60-day trial of 80 adults aged 40 to 65, published in 2023, blood NAD+ rose at all three doses tested (300, 600 and 900 mg per day), with 600 mg producing results similar to 900 mg. A 2023 US trial using 2 g per day for four weeks also reported a substantial rise in NAD+ metabolites.

Section 3

What Happened in Ageing Mice (Clearly Labelled)

Much of the excitement around NMN began in animal research, and it is worth knowing what was found, as long as we are clear that mice are not people.

In a 2016 study in Cell Metabolism, mice were given NMN in their drinking water for 12 months during normal ageing. Compared with untreated mice, they showed less age-related weight gain, better energy metabolism, more physical activity and better insulin sensitivity, without obvious toxicity.

Animal results like these explain why scientists moved on to human trials. They do not tell us what will happen in a 60-year-old person. For that, we need to look at the human data directly, including the parts that are less flattering.

Chapter 4

What the Human Trials Really Show

It would be easy to end the story here: muscle NAD+ falls with age, NMN raises NAD+, therefore NMN makes you walk faster. Plenty of websites do exactly that.

We are not going to, because the people who trust us with their health deserve the whole picture. So here is what happened when scientists actually measured walking, grip and stamina in NMN trials.

Section 1

The Encouraging Results

The 6-minute walk. In the 2023 trial of 80 adults aged 40 to 65, everyone taking NMN (300, 600 or 900 mg daily for 60 days) walked significantly farther in a 6-minute walk test than the placebo group. The trial was funded by the manufacturer of the NMN used, and the test was done on a treadmill.

Gait speed in older men. In the 2022 Japanese trial, men over 65 taking 250 mg daily showed improvements in walking speed and in left-hand grip strength. The authors were careful to call these exploratory findings that need confirmation, and a supplier error meant only 20 men had full 12-week data.

A faster short walk. In a 2024 trial of 60 older Japanese adults, 250 mg daily for 12 weeks did not improve the study’s main outcome, a stepping test, but the NMN group did complete a 4-metre walk faster than the placebo group, and the improvement tracked the rise in blood NAD+.

Endurance, pooled. A 2026 network meta-analysis of NAD+ precursor trials found a possible benefit of NMN on endurance-type performance at medium and higher doses, but not on muscle strength.

Section 2

The Results We Won’t Hide

Now the other side of the ledger.

In a 2022 trial of 108 older adults taking 250 mg in the morning or evening for 12 weeks, chair-rise speed improved in every group, including placebo, and grip strength and walking speed did not change. In a small 24-week trial of very old men with diabetes (average age 81), NMN was safe but did not improve grip or walking speed. A 2023 trial using 2 g daily for four weeks found no change in strength or aerobic capacity.

And the most rigorous pooled review so far, published in 2025, combined the randomised trials of NMN in adults with an average age above 60. Its conclusion: no significant improvement in muscle mass, grip strength, gait speed or chair-rise time.

Weighing the evidence honestly: some trials lean positive, the pooled analyses mostly sit on the line.

Two further facts complete the picture. First, NMN has a reassuring short-term safety record: a 2022 trial found 1,250 mg daily for four weeks well tolerated, and a 2026 pooled safety review of trials lasting up to 24 weeks (250 to 2,000 mg daily) found no increase in side effects. Second, the strongest, best-replicated lever on the muscle’s NAD+ machinery remains the one you already have: movement.

Section 3

Putting It Together: The Two-Part Plan

So where does that leave a health-literate reader who wants to protect their sixth vital sign for the decades ahead? We think the evidence supports a clear, honest plan with two parts that work at different points of the same system.

If you are taking prescription medication, are pregnant or breastfeeding, or have a medical condition, speak to your doctor before starting any supplement.

The most remarkable thing about the sixth vital sign is not that it predicts so much. It is that, unlike your birthday, it is a number you can influence. The trained 70-year-olds in that biopsy study are the proof that the muscle you will have at 75 is still being built today.

Four metres. One stopwatch. Write your number down.

Complete Reference List

Walking speed and grip strength

Muscle NAD+ and ageing

Exercise and NAMPT

NMN in humans: NAD+ and physical performance

Pooled analyses and safety

Animal research