Train for Longevity

Nobody dies of weak muscles

Most people read a cause-of-death chart as an explanation of why people die, and that usually leads them to train for the wrong things.

An older man holding a loaded barbell at his shoulders in a gym
Photo: Snappa

Pull up any chart of what people die from. Circulatory disease takes a large block. Cancer takes another. Infections, injuries, and respiratory disease each take a slice. Musculoskeletal disease is a sliver you can barely see, often a line so thin it needs its own color key.

Now look at what health advice spends its time on: muscle, strength, mobility, loading the skeleton.

That looks like a mismatch, and plenty of people treat it as one. If almost nobody dies of musculoskeletal disease, why does everyone talk about muscle?

The mismatch comes from how the chart is built, and it matters because the same misreading shapes what people decide to train.

What the chart’s own caption admits

I was recently reading a large Swedish registry study of young adults with type 1 diabetes and matched controls (Rawshani et al. 2018). One figure breaks deaths into color-coded causes by age group, the way most of these charts do.

In the caption, the authors note that only the primary cause of death was assessed, so cardiovascular disease may be a significant contributor to deaths filed under “Endocrine causes.”

So one of the biggest blocks in their chart is partly heart disease that got filed somewhere else. That’s a limit of the data, and the authors were upfront about it.

A death certificate requires a single underlying cause. The person completing it must pick one, and the picks must sum to 100%. In math terms, that makes the chart a partition: a whole split into pieces that don’t overlap. That’s great for bookkeeping and poor for explaining why someone died.

That’s great for bookkeeping and poor for explaining why someone died.

Real causes overlap

Epidemiologists think about cause differently. An outcome happens when a complete set of contributing causes is present at once. Any one piece is usually not enough on its own, yet remove it and that particular route to the outcome closes (Rothman 1976; VanderWeele 2017). The philosopher J. L. Mackie worked out the same logic in 1965.

Because each death can be credited to every piece of the set that produced it, the shares attributed to different causes routinely add up to more than 100% (Rowe et al. 2004). A death certificate can’t do that. Its categories have to add up to exactly 100%.

So when you read “musculoskeletal disease: 1% of deaths,” you have not learned that muscle does 1% of the causal work. You have learned that in 1% of cases, someone judged a musculoskeletal condition to be the single best label for the final event. Those are different claims, and only one of them is in the data.

The labeling is also noisier than most people assume. When pathologists compared 272 Connecticut autopsies with the death certificates, 29% of deaths moved to a different major disease category, and in another 26% the category held but the specific disease changed (Kircher et al. 1985). In 450 autopsies at a Japanese geriatric hospital, the certificate matched the autopsy 48% of the time overall, and just 9% of the time for pneumonia (Mieno et al. 2016), the label that absorbs many end-of-cascade deaths.

How a fall becomes “Infections”

Here’s one path that ends up in the “Infections” block.

Someone loses muscle mass and power over two decades, slowly, without noticing. Their margin for error narrows. One day they trip, and where a stronger version of them would have caught themselves, they fall and break a hip. That means surgery and weeks of barely moving. Lying in bed sets up pneumonia, and the pneumonia is what kills them.

Every step in that chain happened, but only the last one gets recorded.

Only the last step gets recorded

A common path from lost strength to a death filed under infections.

  1. Muscle and power fadeover decades
  2. A tripmargin too thin to recover
  3. A fall
  4. Hip fracture
  5. Surgery and bed restreserve drains faster
  6. Pneumonia
  7. Death certificate“Infections”

Happened, never recordedThe only link the chart counts

Figure: Hoch Health and Wellness.

The numbers on this path are large. About one in five older adults dies within a year of a hip fracture (Downey et al. 2019). In the first three months, the risk of death runs five to eight times that of peers the same age and sex, and it never fully returns to their level (Haentjens et al. 2010). In a Korean national cohort of nearly 15,000 hip-fracture patients over 65, those who developed pneumonia in the hospital had two to three times the mortality of those who didn’t (Jang et al. 2020). This is one of the most common ways a long decline in physical capacity turns into a death certificate that never mentions physical capacity.

The capacity itself drains faster than people expect. When healthy, moderately active adults around 67 years old spent 10 days in bed, a shorter stay than many hospitalizations, they lost about a kilogram of leg muscle and their rate of muscle protein synthesis fell by about 30% (Kortebein et al. 2007). Knee strength dropped 13%, stair-climbing power 14%, and aerobic capacity 12% (Kortebein et al. 2008). And none of them were sick going in.

Save this for later. It’s a 9-minute read. We’ll email it to you so you can finish it later, sources included.

Three ways to name the mistake

Scientists and philosophers have described this mistake in a few different ways, and each one adds something.

Proximate versus distal causation. Death certificates are built to capture the final event. Everything upstream is invisible, because the form has no box for it.

The seen and the unseen. Prevention leaves no trace. The fall that didn’t happen, because someone could catch themselves, generates no code, no bar segment, no data point. Anything whose job is to keep you out of a category will look unimportant when you only count what’s inside the categories.

Mistaking the label for the thing. The ICD code is a filing decision someone makes under time pressure, and reading “Infections, 12%” as a description of biology confuses the index card with the patient.

Death isn’t the only outcome that matters

There’s a simpler problem, too: death may be the wrong outcome to look at.

Musculoskeletal conditions sit near the bottom of mortality tables and near the top of disability tables. Low back pain alone is the leading cause of years lived with disability worldwide: about 619 million people affected and 69 million years of healthy life lost to disability in 2020 (GBD 2021 Low Back Pain Collaborators 2023). It kills almost no one, but it takes away a huge number of good years.

If your question is “how long until I’m dead,” mortality share is the right thing to look at. If your question is “how many years can I live in a body that does what I ask it to,” it isn’t.

What the chart can’t show: reserve

The idea tying all of this together is physiological reserve, the gap between what your systems can do at maximum and what daily life demands of them. Reserve absorbs shocks. It’s why two people with the same illness have different outcomes, and why the same fall is an embarrassment at 40 and a terminal event at 80.

Reserve never appears on a death certificate, because it decides whether you enter a diagnostic category, not which one you land in. It shows up clearly in data that follow people forward in time, though.

In the PURE study, which followed nearly 140,000 adults in 17 countries, each 5 kg lower grip strength was associated with about a 16% higher risk of death from any cause and a 17% higher risk of cardiovascular death. Grip strength predicted death better than systolic blood pressure did (Leong et al. 2015). Grip strength doesn’t cause those deaths; it’s a quick way to read how much reserve someone has.

Among 122,007 adults who completed a treadmill test, higher fitness meant lower long-term mortality with no observed upper limit. The least fit group carried about five times the risk of the fittest, a gap larger than the one attached to smoking, diabetes, or coronary artery disease in the same patients (Mandsager et al. 2018).

Low fitness carried more risk than smoking or diabetes

Adjusted hazard ratio for death from any cause among 122,007 adults after a treadmill test. 1× means no extra risk.

Show as a table (with 95% confidence intervals)
ComparisonHazard ratio95% CI
Least fit vs elite5.044.10–6.20
Least fit vs high3.903.67–4.14
Least fit vs above average2.752.61–2.89
Least fit vs below average1.951.86–2.04
End-stage kidney disease2.782.53–3.05
Smoking1.411.36–1.46
Diabetes1.401.34–1.46
Coronary artery disease1.291.24–1.35
High blood pressure1.211.16–1.25
Figure: adapted from Mandsager et al. (2018), JAMA Network Open, Figure 2C, CC BY 4.0. Redrawn by Hoch Health and Wellness; values unchanged.

On evidence like this, the American Heart Association argued in 2016 that fitness should be treated as a clinical vital sign, because adding it to traditional risk factors improves how well doctors sort patients by risk (Ross et al. 2016).

None of these measurements show up on a cause-of-death chart, yet all of them predict what ends up on one.

Training the reserve, without overselling it

I want to be careful here, because this is where arguments like this one usually get oversold.

Aerobic training of almost any kind raises VO2max. In a meta-analysis of 28 controlled trials in healthy 18- to 45-year-olds, continuous endurance training improved it by about 4.9 mL/kg/min and high-intensity intervals by about 5.5; head to head, intervals came out ahead by a small margin, about 1.2 mL/kg/min (Milanović et al. 2015). Because VO2max is among the strongest single predictors of all-cause mortality we have, intervals earn a place in your week, especially when time is short.

That doesn’t mean intervals beat everything else at protecting the heart. SAINTEX-CAD randomized 200 people with stable coronary artery disease to interval or continuous training and found equal improvements in exercise capacity and blood-vessel function (Conraads et al. 2015). SMARTEX-HF randomized 261 people with heart failure across three arms and found intervals no better than continuous training at reversing heart enlargement, its primary endpoint (Ellingsen et al. 2017).

No exercise modality has hard-outcome trial evidence approaching what statins, blood pressure control, or quitting smoking have. The evidence is strong enough without stretching it: aerobic training, including intervals, raises a trait that independently predicts how long and how well you live. Strength training works on the other reserve, the one that decides whether a stumble stays a stumble. If you want to see where you stand on each, the sitting-rising test checks the strength-and-balance side and the one-mile walk test estimates the aerobic one.

What to do with this

So instead of asking what kills people, which a cause-of-death chart can’t really answer, ask how big your margin is and whether it’s growing or shrinking. That question has answers you can measure: strength, aerobic capacity, balance, the ability to get off the floor unassisted. Those numbers tell you where you stand today and where you’re headed. If you want the risk-calculator view of the same idea, your heart’s 10- and 30-year odds runs the American Heart Association’s PREVENT equations. A cause-of-death chart can only tell you how the story ended for someone else.

Most people have never measured their own margin, and it only takes a few simple tests.

This article is for general education. It discusses mortality risk in populations, not your personal risk, and creates no medical or other professional relationship. Talk with your physician before starting a new exercise program, and never delay seeking medical advice because of something you read here.

Sources

Every number in this article traces to one of these 19 peer-reviewed sources. In-text citations use the author and year.

Show all 19 sources
Rawshani et al. (2018)
The Swedish type 1 diabetes registry study whose cause-of-death figure caption notes that only the primary cause was assessed.
Rawshani A, Sattar N, Franzén S, et al. Excess mortality and cardiovascular disease in young adults with type 1 diabetes in relation to age at onset. Lancet. 2018;392(10146):477–486. [PMID: 30129464]
Rothman (1976)
The sufficient-component cause model: outcomes arise from sets of contributing causes.
Rothman KJ. Causes. Am J Epidemiol. 1976;104(6):587–592. [PMID: 998606]
Mackie (1965)
The philosophical analysis of causes as insufficient but necessary parts of sufficient sets.
Mackie JL. Causes and conditions. Am Philos Q. 1965;2(4):245–264.
VanderWeele (2017)
Why the sufficient-cause model still matters for epidemiology.
VanderWeele TJ. Invited commentary: the continuing need for the sufficient cause model today. Am J Epidemiol. 2017;185(11):1041–1043.
Rowe et al. (2004)
Why attributable fractions for different causes can add up to more than 100%.
Rowe AK, Powell KE, Flanders WD. Why population attributable fractions can sum to more than one. Am J Prev Med. 2004;26(3):243–249. [PMID: 15026106]
Kircher et al. (1985)
272 Connecticut autopsies compared with death certificates: 29% reclassified to a different major disease category.
Kircher T, Nelson J, Burdo H. The autopsy as a measure of accuracy of the death certificate. N Engl J Med. 1985;313(20):1263–1269. [PMID: 4058507]
Mieno et al. (2016)
450 Japanese geriatric autopsies: 48% overall agreement with the certificate, 9% for pneumonia.
Mieno MN, Tanaka N, Arai T, et al. Accuracy of death certificates and assessment of factors for misclassification of underlying cause of death. J Epidemiol. 2016;26(4):191–198. [PMID: 26639750]
Downey et al. (2019)
Systematic review of 1-year mortality after hip fracture: mean 22%.
Downey C, Kelly M, Quinlan JF. Changing trends in the mortality rate at 1-year post hip fracture — a systematic review. World J Orthop. 2019;10(3):166–175. [PMID: 30918799]
Haentjens et al. (2010)
Meta-analysis: death risk 5.75–7.95 times that of peers in the first 3 months after hip fracture, never fully normalising.
Haentjens P, Magaziner J, Colón-Emeric CS, et al. Meta-analysis: excess mortality after hip fracture among older women and men. Ann Intern Med. 2010;152(6):380–390. [PMID: 20231569]
Jang et al. (2020)
Korean national cohort (n = 14,736): in-hospital pneumonia raised mortality 2.3–3.4 times.
Jang SY, Cha Y, Yoo JI, et al. Effect of pneumonia on all-cause mortality after elderly hip fracture: a Korean nationwide cohort study. J Korean Med Sci. 2020;35(2):e9. [PMID: 31920015]
Kortebein et al. (2007)
10 days of bed rest in healthy older adults: ~1 kg leg lean mass lost, muscle protein synthesis down ~30%.
Kortebein P, Ferrando A, Lombeida J, Wolfe R, Evans WJ. Effect of 10 days of bed rest on skeletal muscle in healthy older adults. JAMA. 2007;297(16):1772–1774. [PMID: 17456818]
Kortebein et al. (2008)
Same protocol: knee strength −13%, stair-climb power −14%, VO2max −12%.
Kortebein P, Symons TB, Ferrando A, et al. Functional impact of 10 days of bed rest in healthy older adults. J Gerontol A Biol Sci Med Sci. 2008;63(10):1076–1081. [PMID: 18948558]
GBD 2021 Low Back Pain Collaborators (2023)
Low back pain: 619 million people, 69 million years lived with disability, the leading cause of YLDs worldwide.
GBD 2021 Low Back Pain Collaborators. Global, regional, and national burden of low back pain, 1990–2020, its attributable risk factors, and projections to 2050. Lancet Rheumatol. 2023;5(6):e316–e329. [PMID: 37273833]
Leong et al. (2015)
PURE: each 5 kg lower grip strength → 16% higher all-cause mortality; stronger predictor than systolic blood pressure.
Leong DP, Teo KK, Rangarajan S, et al. Prognostic value of grip strength: findings from the Prospective Urban Rural Epidemiology (PURE) study. Lancet. 2015;386(9990):266–273. [PMID: 25982160]
Mandsager et al. (2018)
122,007 treadmill tests: no upper limit to the benefit of fitness. Source of the adapted figure (CC BY 4.0).
Mandsager K, Harb S, Cremer P, Phelan D, Nissen SE, Jaber W. Association of cardiorespiratory fitness with long-term mortality among adults undergoing exercise treadmill testing. JAMA Netw Open. 2018;1(6):e183605. [PMID: 30646252]
Ross et al. (2016)
AHA scientific statement: fitness as a clinical vital sign.
Ross R, Blair SN, Arena R, et al. Importance of assessing cardiorespiratory fitness in clinical practice: a case for fitness as a clinical vital sign. Circulation. 2016;134(24):e653–e699. [PMID: 27881567]
Milanović et al. (2015)
Meta-analysis of 28 trials: intervals raise VO2max slightly more than continuous training (~1.2 mL/kg/min).
Milanović Z, Sporiš G, Weston M. Effectiveness of high-intensity interval training (HIT) and continuous endurance training for VO2max improvements. Sports Med. 2015;45(10):1469–1481. [PMID: 26243014]
Conraads et al. (2015)
SAINTEX-CAD: interval and continuous training equally improved exercise capacity in coronary disease.
Conraads VM, Pattyn N, De Maeyer C, et al. Aerobic interval training and continuous training equally improve aerobic exercise capacity in patients with coronary artery disease: the SAINTEX-CAD study. Int J Cardiol. 2015;179:203–210. [PMID: 25464446]
Ellingsen et al. (2017)
SMARTEX-HF: intervals not superior to continuous training for heart remodelling in heart failure.
Ellingsen Ø, Halle M, Conraads V, et al. High-intensity interval training in patients with heart failure with reduced ejection fraction. Circulation. 2017;135(9):839–849. [PMID: 28082387]