24.5 — What Exercise Does to the Body

If exercise were a drug, it would be the most valuable one ever developed.

It reduces all-cause mortality by around 30 percent. It reduces cardiovascular disease, type 2 diabetes, stroke, dementia, depression, several cancers, falls and fractures. It improves sleep, mood, cognition and pain.

No drug does all of that. Nothing comes close.

And it is free.

This page is what is actually happening inside you when you move, because understanding the mechanism makes the recommendations stop being arbitrary.

Where the energy comes from

Three systems, working together, with different time courses.

The phosphagen system — 0 to 10 seconds.

ATP is the cell's energy currency (Chapter 1.6), and muscle holds only a few seconds' worth.

Creatine phosphate regenerates it rapidly. This is what powers a sprint, a heavy lift, a jump.

And it is why creatine supplementation works — it increases the size of that store, allowing a few more repetitions, which over months produces more training stimulus.

Glycolysis — 10 seconds to 2 minutes.

Glucose is broken down without oxygen, producing ATP quickly and lactate as a by-product.

And the lactate story needs correcting, because the version most people learned is wrong.

Lactate does not cause muscle soreness the next day, and it is not a waste product. It is a fuel — shuttled to other muscle fibres, the heart and the liver, and used for energy.

The burning sensation during hard exercise comes from hydrogen ions and other metabolites, not from lactate itself. And it clears within an hour.

The oxidative system — 2 minutes onwards.

In the mitochondria, using oxygen to extract far more energy from glucose and fat (Chapter 1.6).

Slower, and vastly more productive — around 30 ATP per glucose molecule against 2 from glycolysis alone.

This is what powers everything from walking to a marathon.

And the fuel mix shifts with intensity: at low intensity most energy comes from fat; as intensity rises, the proportion from carbohydrate increases. Which is why the "fat burning zone" on gym machines is technically true and practically misleading — you burn a higher percentage of fat at low intensity and more total fat at higher intensity, because you burn more of everything.

What adapts, and how

The heart

The heart is a muscle, and it responds to training like one.

Endurance training increases the size of the left ventricle's chamber, so it holds and ejects more blood per beat — stroke volume rises.

Which is why trained athletes have low resting heart rates. A resting rate of 40 in an endurance athlete is not a problem; it is the same amount of blood delivered in fewer, larger beats.

Maximum cardiac output rises substantially with training — from around 20 litres a minute in an untrained person to 35 or more in an elite endurance athlete.

Resting heart rate falls. Recovery after exertion speeds up. And how fast your heart rate drops in the minute after stopping is itself a marker of fitness and of cardiovascular risk.

Blood vessels

New capillaries grow in trained muscle, shortening the distance oxygen must diffuse.

The endothelium — the lining of blood vessels — improves its ability to produce nitric oxide, which relaxes vessels.

And this is one of the mechanisms by which exercise lowers blood pressure, typically by 5 to 8 mmHg in people with hypertension — comparable to a low-dose medication (Chapter 18.2).

Blood volume increases, and blood becomes slightly less viscous.

Muscle

Mitochondria increase in number and size — mitochondrial biogenesis — which is the central adaptation to endurance training and the reason trained muscle can sustain output.

Aerobic enzymes increase. Myoglobin, which stores oxygen inside muscle, increases. Glycogen storage capacity rises. Fat oxidation improves, sparing glycogen.

And with resistance training: muscle fibres increase in cross-sectional area — hypertrophy — through increased contractile protein.

Plus neural adaptations, which come first. Strength rises substantially in the first weeks of training before any measurable muscle growth, because the nervous system learns to recruit more motor units, fire them faster and coordinate them better (Chapter 6.1).

Fibre types: type I slow-twitch, fatigue-resistant, aerobic; type II fast-twitch, powerful, fatiguing quickly. The proportion is largely genetic, and training shifts characteristics within types considerably.

Bone

Bone responds to load (Chapter 5.1).

Mechanical stress stimulates osteoblasts, so weight-bearing and resistance exercise increase bone density. Swimming and cycling, which are excellent for the heart, do very little for bone, which is a real gap for people whose only exercise is one of those.

And the effect is site-specific — loading the hips and spine is what protects the hips and spine.

The brain

And this is the part that has changed most in the last two decades.

Exercise increases BDNF — brain-derived neurotrophic factor — which supports the survival of neurons and the formation of new connections.

It stimulates neurogenesis in the hippocampus, the region central to memory (Chapter 11.6), and hippocampal volume has been shown to increase with aerobic training in older adults, reversing part of the age-related decline.

It increases blood flow to the brain, and promotes new capillary growth there.

It improves executive function, attention and processing speed.

And it is associated with substantially reduced dementia risk (Chapter 20.4).

On mood: exercise has effect sizes for depression comparable to antidepressants in mild to moderate cases (Chapter 20.7). The mechanisms include BDNF, endocannabinoids — which are a better explanation for the "runner's high" than endorphins, since endorphins cross poorly into the brain — serotonin, reduced inflammation, improved sleep, and the psychological effects of mastery and routine.

Metabolism

Insulin sensitivity improves — and the effect starts immediately.

A single session of exercise increases glucose uptake by muscle for up to 48 hours afterwards, through a mechanism that works independently of insulin, using a different transporter pathway (Chapter 18.7).

Which is why exercise is genuinely a treatment for type 2 diabetes and not merely a preventive.

Also: improved lipid profile, reduced visceral fat specifically, reduced liver fat, and reduced chronic inflammation.

Exercising muscle releases myokines — signalling molecules that act on other organs, including the brain, liver, fat tissue and immune system. Muscle is an endocrine organ, which was not appreciated until recently and explains a lot about why the benefits of exercise are so systemic.

Immune function

Moderate regular exercise improves immune surveillance and reduces the frequency of infections.

Very prolonged intense exercise produces a temporary period of increased susceptibility — the "open window" — though the size of this effect has been debated and is smaller than once claimed.

Measuring fitness

VO2 max — the maximum rate of oxygen consumption. The gold standard measure of aerobic fitness.

And it is one of the strongest predictors of mortality that exists — stronger than smoking, diabetes or hypertension in several large analyses. Which is a remarkable finding and an argument for treating fitness as a vital sign.

It improves by 15 to 25 percent with training in most people, with wide genetic variation in trainability.

And it declines by around 10 percent per decade after 30, which training slows substantially.

Heart rate zones — the maximum heart rate formula of 220 minus age is a rough population average with a standard deviation of around 10 to 12 beats, so it can be well out for an individual.

A more practical guide is the talk test: you can hold a conversation at moderate intensity; you can speak only a few words at a time at vigorous intensity; you cannot speak at maximal intensity.

Grip strength — a simple measure that predicts mortality, disability and cognitive decline remarkably well, because it stands in for overall muscle status.

Recovery, and why it is part of training

Training does not make you fitter. Recovering from training makes you fitter.

The stimulus damages and depletes; the adaptation happens afterwards.

Which is why more is not always better, and why rest days are training days.

Delayed onset muscle soreness — peaking 24 to 72 hours after unaccustomed exercise, particularly eccentric work like running downhill or lowering weights.

Caused by microscopic muscle damage and the inflammatory repair response — not by lactate.

It reduces with repeated exposure — the repeated bout effect — and light activity helps more than complete rest.

Overtraining — persistent fatigue, declining performance, disturbed sleep, low mood, irritability, frequent infections, and loss of motivation. Treated by rest, which is difficult advice for the people most likely to need it.

Sleep is the most important recovery tool (Chapter 24.7). Growth hormone is released during deep sleep, and sleep deprivation measurably impairs recovery and performance.

Getting started safely

Most people can start moderate exercise without medical clearance.

Check with a doctor first if you have: known heart disease; chest pain on exertion; unexplained breathlessness, dizziness or fainting; uncontrolled blood pressure or diabetes; significant joint problems; or if you are over 45 with several cardiovascular risk factors and plan vigorous exercise.

Warning signs to stop and seek help: chest pain or pressure; severe breathlessness out of proportion; dizziness or feeling faint; an irregular heartbeat; and severe or unusual pain.

Start where you actually are, not where you think you should be.

Progress gradually — a common guideline is increasing volume by no more than about 10 percent a week, which is imperfect as a rule and useful as a brake.

And the most important predictor of benefit is not the programme. It is that you are still doing it in a year.

The dose

The evidence-based minimum for adults:

150 to 300 minutes of moderate aerobic activity per week, or 75 to 150 minutes of vigorous, or a combination.

Plus muscle-strengthening activity on two or more days a week.

Plus balance training for older adults.

And two findings worth knowing, because they change how achievable this looks:

The biggest health gain comes from going from nothing to something. The curve is steepest at the start — moving from sedentary to even 60 to 90 minutes a week of moderate activity produces a substantial mortality reduction. Additional benefit continues and with diminishing returns.

And there is no minimum bout length. The old ten-minute rule was removed from guidelines, because short bursts count. Taking the stairs, walking to the shop and carrying shopping all add up.

Step counts: the 10,000-step target came from a Japanese pedometer marketing campaign in the 1960s, not from research. The actual data shows mortality falling steeply up to around 7,000 to 8,000 steps a day, with benefit plateauing after that — and in older adults the plateau comes earlier, around 6,000 to 8,000.

So 7,000 is a well-supported target, and it is considerably more achievable than the number people think they have failed to reach.

Sitting

Prolonged sitting is associated with worse health outcomes partly independently of exercise.

Muscle activity affects lipoprotein lipase, glucose uptake and blood flow, and prolonged inactivity suppresses all three.

And the practical finding: high levels of physical activity substantially attenuate the risk associated with sitting. Around 30 to 40 minutes of moderate activity a day appears to offset the risk of even long sitting hours.

Which makes "sitting is the new smoking" an overstatement, and "break up long periods of sitting and get your activity in" a fair summary.

Break it every 30 to 60 minutes. Stand up. Walk to the kettle. It does not have to be more than that.

What the next page fixes

Chapter 24.6 turns the physiology into a plan — what to actually do, how to train strength, cardio and mobility, and how to build something you will still be doing in a decade.