Bones, Muscles, Skin, and Glands

TL;DR. Your skeleton is not scaffolding but living tissue that is completely rebuilt roughly every decade, and it doubles as a calcium bank and a blood cell factory. Your muscle is about a third of your body mass, is your largest glucose sink, and shrinks by 3 to 8 percent per decade after 30 unless you actively resist. Your skin is your largest organ, replaces itself monthly, and is the barrier that makes everything else possible. And a handful of glands weighing a few grams in total set your metabolic rate, your stress response, your growth, and your fertility using messages measured in billionths of a gram. The theme of this chapter is use it or lose it: bone and muscle are the two tissues in your body whose maintenance is directly commanded by mechanical load, which means the instruction to keep them is something you send yourself.

Key takeaways

  • Bone is rebuilt continuously, with the whole skeleton replaced roughly every 10 years. It responds directly to load, which is why weightlessness and bed rest cause rapid loss.
  • Peak bone mass is reached by the late twenties and everything afterwards is decline from that peak, which is why what you do at 20 matters at 75.
  • Muscle is lost at 3 to 8 percent per decade after 30, accelerating after 60, and resistance training reverses a large part of it at any age, including in the nineties.
  • Muscle is your largest glucose sink. Losing it worsens blood sugar control independently of anything else, which links this chapter directly to diabetes.
  • Skin is a barrier, a thermostat, an immune organ, and a vitamin factory, and its outermost layer is entirely dead cells.
  • Hormones work at concentrations of parts per billion, which is why a gland weighing 25 grams can control your whole metabolic rate.

Bone

In short: Living, constantly rebuilt tissue that responds to mechanical load, stores 99 percent of your calcium, and manufactures your blood.

What it actually is

Bone is roughly two-thirds mineral (calcium phosphate crystals, providing stiffness) and one-third protein (mostly collagen, providing tensile strength and preventing shattering). That composite is why bone is both hard and slightly flexible: mineral alone would be brittle like chalk, collagen alone would be rubbery.

Two forms:

  • Cortical (compact) bone: the dense outer shell, about 80 percent of skeletal mass. Strong, slow to turn over.
  • Trabecular (spongy) bone: an internal honeycomb, about 20 percent of mass but with far more surface area, and therefore metabolically much more active. It is lost first in osteoporosis, which is why the spine, hip, and wrist, which are trabecular-rich, are the classic fracture sites (Chapter 50).

It is rebuilt constantly

Two cell types work in opposition, continuously, at millions of microscopic sites:

  • Osteoclasts dissolve old bone.
  • Osteoblasts lay down new bone.

The whole skeleton is replaced roughly every ten years. Every osteoporosis drug acts on this balance: bisphosphonates and denosumab suppress the demolition crew, while teriparatide and romosozumab stimulate the building crew.

It responds directly to load

Bone adapts to the forces placed on it, laying down more material where stress is highest. The consequences are dramatic in both directions:

  • Astronauts lose 1 to 2 percent of bone mass per month in weightlessness, which is one of the hardest problems for long-duration spaceflight.
  • Extended bed rest causes comparable loss.
  • The racquet arm of a lifelong tennis player has measurably thicker, denser bone than the other arm, in the same person with the same genes and the same diet.

Which is why the exercise recommendation for bone is specific: impact and resistance, not swimming or cycling. Bone responds to force, and the forces that matter are ground impact and muscle pulling on bone.

The timeline that matters

AgeWhat is happening
Childhood and adolescenceRapid accumulation. Roughly 40 percent of adult bone mass is laid down during the pubertal growth spurt
Late twentiesPeak bone mass reached
30s to menopauseSlow loss, roughly 0.5 to 1 percent a year
Menopause and the following 5 to 10 yearsRapid loss, up to 2 to 3 percent a year, as oestrogen withdrawal releases the brake on osteoclasts
Later lifeContinued slower loss, plus falls risk

The practical implication is unusual in medicine: the most effective intervention for osteoporosis happens fifty years before the disease. Building a higher peak in adolescence and early adulthood, through nutrition, calcium, vitamin D, and above all weight-bearing activity, raises the ceiling from which the rest of life descends.

Bone's other two jobs

It is the calcium bank. Blood calcium must stay within a narrow range for nerves and muscle to work at all, and the body will dissolve bone without hesitation to maintain it. Parathyroid hormone commands that withdrawal. This is why chronic kidney disease, which disturbs calcium and phosphate handling, destroys bone (Chapter 23).

It makes your blood. Red marrow in the pelvis, spine, ribs, sternum, and the ends of long bones produces about 2 million red cells per second plus all white cells and platelets. This is what leukaemia disrupts, what chemotherapy suppresses, and what a bone marrow transplant replaces.

Care and durability

What damages bone: inactivity, smoking, excess alcohol, low body weight, corticosteroids (the commonest medical cause), oestrogen or testosterone deficiency, low calcium and vitamin D, coeliac disease, hyperthyroidism, and chronic kidney disease.

What protects it: weight-bearing and resistance exercise, adequate calcium (roughly 700 to 1,200 mg a day, ideally from food) and vitamin D, not smoking, moderate alcohol, and, after a fragility fracture, actual treatment, which most people who fracture never receive (Chapter 50).

Joints

In short: Cartilage-lined bearings lubricated by fluid, with no blood supply and therefore almost no capacity to repair.

A synovial joint has cartilage caps on the bone ends, a capsule enclosing a small volume of synovial fluid, and ligaments holding it together. The system is remarkable: the friction coefficient of healthy cartilage on cartilage is lower than ice on ice.

Cartilage has no blood supply and no nerves. It is fed by fluid moving in and out as the joint is loaded and unloaded, which is a genuine reason movement maintains joint health rather than consuming it. It also means:

  • Cartilage heals very poorly. A defect does not fill in with cartilage; it fills with inferior fibrous tissue or not at all.
  • Cartilage damage is painless, because there are no nerves in it. Osteoarthritis pain comes from the bone underneath, the joint lining, and the capsule, which is why X-ray appearance and pain correlate so weakly (Chapter 50).

Don't be confused: exercise does not wear out your joints. The intuition that joints are like car tyres with a fixed mileage is wrong. Cartilage requires cyclical loading to be nourished, and long-term studies of recreational runners find lower, not higher, rates of knee osteoarthritis than in sedentary people. What does damage joints is a specific injury, particularly a ligament rupture, obesity, and occupational loads involving repetitive kneeling and heavy lifting.

Muscle

In short: A third of your body mass, your largest glucose sink, and the tissue whose decline with age is both the most consequential and the most reversible.

Three kinds

TypeControlWhereNotes
SkeletalVoluntaryAttached to bone, over 600 muscles30 to 40 percent of body mass
CardiacInvoluntaryHeart onlyGenerates its own rhythm; does not regenerate
SmoothInvoluntaryGut, blood vessels, airways, bladder, uterusThe target of many drugs: bronchodilators, calcium channel blockers

How contraction works

Muscle fibres contain interleaved filaments of two proteins, actin and myosin. Myosin heads grab actin, pivot, release, and grab again, sliding the filaments past each other. Each cycle consumes one molecule of ATP. Calcium released inside the fibre is the trigger that exposes the binding sites.

Two clinically important facts fall out. Rigor mortis occurs because ATP is required to release the myosin head, so without it muscle locks. And calcium's central role is why disturbed blood calcium, potassium, and magnesium cause cramps, weakness, and, at the extreme, cardiac arrest.

Fibre types

TypeContractsFatiguesFuelGrows with
Type I (slow)SlowlyVery slowlyMostly fat, aerobic; mitochondria-richEndurance training
Type II (fast)Quickly, more forcefullyQuicklyMostly glucose, largely anaerobicHeavy resistance and sprint training

Type II fibres are lost preferentially with age, which is why older people lose power (the ability to produce force quickly) faster than they lose strength, and why the ability to catch yourself when stumbling declines before the ability to lift a bag. This is a direct argument for including some fast, powerful movement in training rather than only slow strength work.

Sarcopenia: the decline that matters most

Muscle mass declines by roughly 3 to 8 percent per decade after 30, accelerating after 60, and strength declines faster than mass because fibre quality and neural drive also decline.

The consequences reach much further than appearance:

ConsequenceWhy
Falls and fracturesWeak legs and slow reactions cause the fall; weak bone determines the fracture (Chapter 50)
Worse blood sugarMuscle is the largest disposal site for glucose. Less muscle means less capacity, worsening insulin resistance (Chapter 18)
Loss of independenceThe ability to rise from a chair or a toilet unaided is a specific strength threshold
Worse outcomes from any illnessMuscle is a protein reserve drawn on during illness. Low reserve predicts worse recovery from surgery, cancer treatment, and hospital admission
Higher mortalityGrip strength, a simple proxy for total muscle, is a consistent predictor of death across large cohorts

And it is substantially reversible. Resistance training produces measurable gains in strength and mass in people in their eighties and nineties, including in nursing home residents. The adaptation machinery does not switch off with age; it becomes less sensitive, which means the stimulus needs to be adequate and the protein intake needs to be a little higher (Chapter 2).

Care and durability

What damages muscle: disuse (the largest single factor, and bed rest can cost several percent of mass in a week), inadequate protein, corticosteroids, some cholesterol drugs in a minority, chronic inflammatory disease, and rapid weight loss without resistance training, which is a real concern with GLP-1 drugs (Chapter 66).

What protects it: resistance training two or three times a week, adequate protein spread across meals, and staying out of bed during illness wherever safely possible. Early mobilisation after surgery and in intensive care is a treatment for exactly this reason.

Skin

In short: The largest organ, a barrier that replaces itself monthly, and simultaneously a thermostat, an immune organ, a sensor, and a vitamin factory.

The structure

LayerWhat it isJob
EpidermisTop layer, no blood supply. Its outermost part (stratum corneum) is dead, flattened, keratin-filled cells in a lipid matrixThe barrier. Keeps water in and pathogens, chemicals, and UV out
DermisCollagen and elastin, with blood vessels, nerves, hair follicles, sweat and oil glandsStrength, elasticity, sensation, temperature control
Subcutaneous fatFat and connective tissueInsulation, padding, energy store

The outermost layer being dead is the point. Dead, keratin-packed cells embedded in lipid form a waterproof, chemically resistant sheet. When that lipid matrix is disrupted, as in eczema, water escapes and allergens get in, which is why moisturisers are a treatment rather than a cosmetic and why infant eczema is a route to food allergy (Chapter 46).

Skin covers about 1.5 to 2 square metres, weighs 3 to 5 kg, and the epidermis is completely replaced roughly every 4 to 6 weeks.

Its five jobs

  1. Barrier, as above.
  2. Temperature control. Blood vessels dilate to dump heat and constrict to conserve it, and 2 to 4 million sweat glands can produce over a litre an hour in the heat. Evaporation is the only mechanism that works when air temperature exceeds body temperature, which is why humidity makes heat dangerous (Chapter 60).
  3. Sensation. Distinct receptors for light touch, pressure, vibration, temperature, and pain.
  4. Immunity. Resident immune cells sample everything crossing the surface, which is why skin is where many allergies begin.
  5. Vitamin D synthesis. UVB converts a cholesterol derivative in the skin into vitamin D precursor. This is why deficiency tracks latitude, season, skin pigmentation, clothing, and indoor living, and why supplementation is recommended in many countries during winter.

Care and durability

What ages skin: ultraviolet light does most of it. Compare sun-exposed forearm skin to skin on the same person's buttock at 70 and the difference is almost entirely UV, not time. Photoageing degrades collagen and elastin, producing wrinkling, thinning, irregular pigmentation, and, cumulatively, skin cancer. Smoking adds substantially.

What protects it: sun protection (shade, clothing, and sunscreen, applied at the quantity people almost never actually use), not smoking, and treating the barrier with emollients if it is compromised.

What to watch: a new or changing mole, particularly one that is asymmetric, irregularly bordered, multi-coloured, growing, or simply different from your others; a sore that does not heal in a month; and any lesion that bleeds repeatedly (Chapter 55).

The endocrine glands

In short: A few dozen grams of tissue producing messages at parts-per-billion concentrations that set your metabolic rate, stress response, growth, and fertility.

A hormone is a chemical message released into the blood by one tissue to act on another. The system is slow compared with nerves (seconds to hours rather than milliseconds) and it reaches everywhere at once. Because receptors are extraordinarily sensitive, hormones work at concentrations of nanograms per litre.

GlandMassMain hormonesWhat they set
Hypothalamus~4 gReleasing hormonesThe master controller, linking nervous and endocrine systems
Pituitary~0.5 gTSH, ACTH, LH, FSH, growth hormone, prolactin, ADH, oxytocinInstructs most other glands
Thyroid~25 gT4 and T3Metabolic rate of essentially every cell (Chapter 51)
Parathyroids~0.1 g totalPTHBlood calcium
Adrenals~8 g togetherCortisol, aldosterone, adrenalineStress response, salt and water, blood pressure
Pancreas (islets)~1 to 2 g of islet tissueInsulin, glucagonBlood glucose (Chapter 18)
Ovaries / testesVariableOestrogen, progesterone / testosteroneReproduction, bone, muscle, mood, cardiovascular risk
Fat tissueVariableLeptin, adiponectin, inflammatory cytokines, oestrogenAppetite, insulin sensitivity, inflammation (Chapter 19)
BoneOsteocalcin, FGF23Phosphate handling and metabolic signalling

Note the last two rows: fat and bone are endocrine organs, which was not recognised until relatively recently and which reframes both obesity and kidney bone disease.

Nearly all of it runs on negative feedback through three levels: hypothalamus instructs pituitary, pituitary instructs gland, gland's hormone switches off both levels above. That is why two blood tests can localise a problem, and it is developed properly in Chapter 51.

The immune organs

In short: A distributed organ with no single location, and one part of it deliberately shrinks away after childhood.

The immune system's tissues are scattered by design:

  • Bone marrow: makes all immune cells.
  • Thymus: where T cells learn not to attack you. It is largest in childhood and progressively replaced by fat from adolescence onward, which is one of the reasons immunity declines with age.
  • Spleen: filters blood, removes old red cells, and clears encapsulated bacteria. Losing it, whether surgically or functionally as in sickle cell disease, leaves lifelong vulnerability to specific infections (Chapter 48).
  • Lymph nodes: several hundred filtering stations where immune cells meet what has been collected from tissue. Swollen nodes mean the local station is working.
  • Mucosal tissue in gut, airways, and elsewhere, which is where most immune activity actually happens.

The lymphatic system doubles as drainage: fluid leaking out of capillaries into tissue is collected and returned to the bloodstream. When that drainage is blocked, typically after lymph node surgery or radiotherapy, the result is lymphoedema, permanent swelling of a limb, which is one of the reasons cancer surgery has moved toward removing fewer nodes (Chapter 26).

The reproductive organs

In short: Organs whose hormones affect bone, muscle, mood, and cardiovascular risk throughout life, not only fertility.

The reproductive systems matter in a general health book mostly for what their hormones do elsewhere.

Oestrogen maintains bone density (which is why loss at menopause causes rapid bone loss), affects blood vessel function, influences fat distribution, and contributes to the lower rate of cardiovascular disease in women before menopause.

Testosterone maintains muscle and bone mass, red cell production, libido, and mood. It declines gradually with age, roughly 1 percent a year after 30 to 40, which is a far more gradual change than menopause and is not equivalent to it.

Two things worth stating because they are commonly misunderstood. Women are born with all the eggs they will ever have, and their number and quality decline from birth, which is the basis of age-related fertility decline and of the rise in chromosomal abnormalities with maternal age. Men produce sperm continuously, roughly 1,500 per second, with a production cycle of about two to three months, which is why factors affecting sperm quality often reverse within a few months.

The unifying principle of this chapter

In short: Bone and muscle are maintained on demand, so the demand has to come from you.

Almost every organ in the preceding chapters maintains itself automatically. Bone and muscle do not. They are expensive tissues, and the body will happily dismantle them if they are not being used, because in evolutionary terms carrying unused muscle and bone is a waste of calories.

That is the biological reason behind advice that otherwise sounds like exhortation:

  • Bone is maintained by impact and by muscle pulling on it.
  • Muscle is maintained by being asked to produce near-maximal force.
  • Neither responds to intention, only to load.

And it is why disuse is not neutral. Two weeks of bed rest in an older adult can cost several percent of leg muscle mass, which may take months to rebuild, and some of which is never rebuilt. That is the physiological argument for getting people out of hospital beds, and for not treating "rest" as automatically therapeutic.

Sources and notes

Standard physiology and anatomy references (Guyton and Hall; Marieb and Hoehn). Skeletal turnover of roughly 10 percent a year: bone remodelling literature. Peak bone mass timing and adolescent accrual: Bailey et al. and NIH consensus statements. Astronaut bone loss of 1 to 2 percent a month: NASA and spaceflight physiology studies. Tennis player bone asymmetry: Jones et al., Journal of Bone and Joint Surgery, 1977, and later replications. Sarcopenia rates of 3 to 8 percent per decade: standard geriatrics literature (Volpi, Nazemi, and Fujita, Current Opinion in Clinical Nutrition, 2004). Resistance training in the very old: Fiatarone et al., JAMA, 1990, and NEJM, 1994. Grip strength and mortality: Leong et al., The Lancet, 2015 (PURE study). Running and knee osteoarthritis: Alentorn-Geli et al., JOSPT, 2017, meta-analysis. Skin surface area, epidermal turnover, and sweat rates are standard dermatology and physiology. Thymic involution: standard immunology. Testosterone decline with age: Harman et al., Journal of Clinical Endocrinology & Metabolism, 2001 (Baltimore Longitudinal Study).

Open questions. How much of age-related muscle loss is inevitable biology versus accumulated disuse is genuinely debated, with masters athlete data suggesting the disuse component is larger than once assumed. Whether cartilage can be regenerated therapeutically remains unsolved.

Next: what happens to all of this when you eat. 👉