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Human Physiology · Endocrine and reproduction

Calcium, Phosphate and Bone

Bone is a living tissue that stores calcium, protects organs and responds to load. This page explains how parathyroid hormone and vitamin D defend blood calcium, how bone is remodelled, and how exercise builds and protects it.

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Part 8 · Endocrine and Reproduction · Chapter 38 of 47

Learning objectives

By the end of this page you should be able to:

  • State why blood calcium is tightly controlled and list the effects of low and high calcium.
  • Explain the actions of parathyroid hormone, vitamin D and calcitonin.
  • Describe the bone remodelling cycle and the cells involved.
  • Explain how mechanical loading and age change bone mass.
  • Summarise the evidence for exercise in low bone mass.
  • Prescribe bone-loading exercise safely.

Why it matters

Osteoporosis and fragility fractures are major causes of disability in older adults. Physiotherapists see the consequences after hip, wrist and vertebral fractures.

Bone is also one of the clearest examples of a tissue that adapts to load. Prescribing the right loading is a core physiotherapy skill.

Calcium and phosphate in the body

About 99% of body calcium and 85% of phosphate sit in bone as hydroxyapatite crystals. Only a small amount circulates, and roughly half of plasma calcium is ionised and active.

Ionised calcium stabilises nerve and muscle membranes, triggers transmitter release and contraction, and is needed for clotting.

StateTypical effects
Low ionised calciumTingling, muscle cramps and tetany, positive Chvostek and Trousseau signs, seizures
High calciumFatigue, weakness, constipation, kidney stones, confusion
Low phosphateMuscle weakness, including breathing muscles

Hormonal control

Figure 1 · Three organs defend blood calcium

Parathyroid hormone and vitamin D control of blood calcium through bone, kidney and gut When blood calcium falls, the parathyroid glands release parathyroid hormone. It releases calcium from bone, makes the kidney keep calcium, lose phosphate and activate vitamin D, and active vitamin D raises calcium absorption from the gut. Together these restore blood calcium. Calcitonin opposes parathyroid hormone but matters little in adults. Blood calcium fallssensed by parathyroid glandsParathyroid hormone (PTH)Boneosteoclasts releasecalcium and phosphateKidneykeeps calcium, loses phosphate,activates vitamin DGutactive vitamin D raisescalcium absorptionvit DBlood calcium restoredCalcitonin (thyroid C cells)opposes PTH; minor rolein adults
Blood comes before bone. Blood calcium is defended tightly because nerves and muscle depend on it; if intake is poor, the skeleton pays.
HormoneSourceMain actions
Parathyroid hormoneParathyroid glandsRaises calcium: bone resorption, renal calcium retention, phosphate loss, vitamin D activation
Calcitriol (active vitamin D)Skin, then liver, then kidneyRaises gut calcium and phosphate absorption; needed for mineralisation
CalcitoninThyroid C cellsLowers calcium by inhibiting osteoclasts; minor in adults

Vitamin D is made in skin exposed to sunlight, then activated in liver and kidney. Deficiency causes rickets in children and osteomalacia in adults, with bone pain and proximal muscle weakness.

Bone cells and remodelling

CellRole
OsteoclastLarge multinucleated cell that resorbs bone
OsteoblastForms osteoid and controls its mineralisation
OsteocyteOsteoblast buried in bone; senses strain and signals remodelling
Lining cellCovers resting bone surfaces

Figure 2 · The bone remodelling cycle

Stages of bone remodelling from activation to mineralisation Five stages: activation recruits osteoclasts; resorption digests a pit over two to four weeks; reversal prepares the surface; osteoblasts form new osteoid over three to four months; and the osteoid mineralises with osteocytes embedded inside. 1. Activationlining cells retract;osteoclasts recruited2. Resorptionosteoclasts dig a pit(about 2–4 weeks)3. Reversalpit is cleaned andprepared4. Formationosteoblasts lay osteoid(about 3–4 months)5. Mineralisationosteoid hardens;osteocytes embeddedOCosteoclast digs a pitosteoblasts refillLoading, hormones and calcium supply decide whether formation keeps up with resorption
Bone is replaced, not just stored. About a tenth of the adult skeleton is remodelled each year; loss occurs when resorption outpaces formation.

Osteocytes form a network that senses fluid flow caused by loading. Strain reduces their release of sclerostin, which otherwise restrains osteoblasts. This is how load becomes bone.

For anatomy of bone structure, see the Human Anatomy pages. This page focuses on function.

Bone across life

Figure 3 · Bone mass across life

Bone mass rising to a peak in early adulthood and falling later, faster after menopause Bone mass rises through childhood and adolescence to a peak in the late twenties. It then declines slowly, with a faster fall in women after menopause that can cross the fracture threshold in later life. fracture thresholdpeak bone mass, late 20smenopause: rapid loss0153045607590Age (years)Bone massSteady ageingAfter menopauseTwo levers:build a high peakslow later loss
Childhood loading pays off for life. Higher peak bone mass delays the age at which loss reaches the fracture threshold. Schematic.

Peak bone mass is reached in early adulthood. After menopause, falling oestrogen speeds resorption for several years. Immobility, glucocorticoids, low body weight, smoking and alcohol also accelerate loss.

Disuse is fast

Bed rest, paralysis and spaceflight cause rapid bone loss and raised urinary calcium. Early mobilisation and weight-bearing protect the skeleton as well as muscle.

Loading builds bone

Bone responds best to strains that are high in magnitude and applied quickly. The LIFTMOR trial tested this in 101 postmenopausal women with low bone mass [1].

Women did 8 months of supervised twice-weekly training: heavy lifts above 85% of one repetition maximum, 5 sets of 5 repetitions, combined with impact loading [1].

Figure 4 · Heavy, supervised loading built bone

Change in bone mineral density with high-intensity resistance and impact training versus low-intensity home exercise Lumbar spine bone density rose 2.9 per cent with high-intensity training and fell 1.2 per cent with low-intensity home exercise. Femoral neck density rose 0.3 per cent versus a fall of 1.9 per cent. +2.9%High-intensity−1.2%Low-intensity homeLumbar spine BMD+0.3%High-intensity−1.9%Low-intensity homeFemoral neck BMD08 months, twice weekly, 30 min, supervised; 101 women with low bone mass [1]
Heavy loading was safe under supervision. Only one minor adverse event was reported, and physical function improved too [1].

Spine and femoral neck density improved, height loss was prevented, and function improved, with only one minor adverse event [1].

A Cochrane review of 43 trials in 4,320 postmenopausal women found modest gains in bone density with exercise [2]. Combined programmes worked best for the spine and lower-limb resistance training for the hip [2].

Figure 5 · What exercise does to bone density

Pooled effects of exercise on bone density and fractures in postmenopausal women Combined exercise raised spine bone density by 3.22 per cent relative to control and lower-limb resistance training raised femoral neck density by 1.03 per cent. The odds ratio for fractures was 0.61 with a wide interval crossing one. Spine BMD, combined exercise+3.22%Femoral neck BMD, resistance training+1.03%024Mean difference in % change versus controlFractures (odds ratio)0.61 (0.23–1.64)0.250.51243 trials, 4,320 postmenopausal women; fracture data sparse [2]
Small but real. Effects on density are modest yet possibly important; trials were too small to show fewer fractures [2].

The trials were too small and short to show a clear fall in fractures [2]. Exercise also reduces falls, which matter as much as density for fracture risk.

Clinical relevance for the physiotherapist

  • Load heavily, progress carefully. High-intensity supervised training was effective and safe in screened women [1].
  • Combine. Resistance, impact and balance work cover bone and falls [2].
  • Spine care. Teach hip-hinge lifting; avoid loaded spinal flexion in vertebral fragility.
  • Disuse. Mobilise early to limit bone loss.
  • Calcium symptoms. Recognise tetany and weakness from abnormal calcium or phosphate.

Assessment and application

SituationInterpretationAction
Postmenopausal woman with osteopenia, otherwise wellCandidate for loading [1]Supervised progressive heavy resistance with impact
Older adult with osteoporosis and fallsFracture risk from bone and falls [2]Resistance plus balance training
Patient on long-term steroidsAccelerated bone lossLoading programme; check medical bone protection
Tingling and carpal spasm after thyroid surgeryPossible low calciumUrgent medical review

Common mistakes

  • Prescribing only gentle, low-load exercise for bone [1].
  • Expecting walking alone to build hip density [2].
  • Ignoring falls prevention.
  • Encouraging loaded spinal flexion in vertebral osteoporosis.
  • Forgetting that bed rest rapidly weakens bone.

Exam preparation

Long answer

Describe the regulation of plasma calcium. Add a note on bone remodelling.

  • Distribution and functions of calcium.
  • Parathyroid hormone, vitamin D, calcitonin (Figure 1).
  • Bone cells and remodelling cycle (Figure 2).
  • Bone mass across life (Figure 3).
  • Effect of exercise [1, 2].

Short notes

  • Vitamin D metabolism.
  • Tetany.
  • Osteocyte as mechanosensor.
  • Exercise and osteoporosis [2].

Viva and practical

  • “Which hormone raises calcium fastest?” — parathyroid hormone.
  • “Where is vitamin D activated?” — liver then kidney.
  • “Is heavy lifting safe in osteopenia?” — under supervision, yes in LIFTMOR [1].
  • OSCE: teach a safe hip-hinge lift to a patient with low bone mass.

Current evidence

Exam and traditional teaching

People with osteoporosis should avoid heavy loads and do gentle exercise.

What the evidence adds

Supervised heavy resistance and impact training improved bone density and function in women with low bone mass [1].

Across trials, exercise produces small but possibly important density gains [2].

What the student should understand

Bone adapts to the loads it receives. Too little load is the bigger risk for most patients.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. In the LIFTMOR trial, high-intensity resistance and impact training changed lumbar spine BMD by about:
  1. (A) −1.2%
  2. (B) +0.3%
  3. (C) +2.9%
  4. (D) +10%

Answer: (C) Lumbar spine BMD rose 2.9% versus a 1.2% fall in the control group [1].

Q2. The LIFTMOR training load was:
  1. (A) Under 30% of one repetition maximum
  2. (B) Over 85% of one repetition maximum, 5 sets of 5
  3. (C) Walking only
  4. (D) Swimming

Answer: (B) Participants lifted more than 85% of one repetition maximum, 5 sets of 5 repetitions [1].

Q3. How many adverse events were reported with supervised high-intensity training in LIFTMOR?
  1. (A) None at all
  2. (B) One minor back spasm
  3. (C) Ten fractures
  4. (D) Not recorded

Answer: (B) Only one minor lower back spasm was reported [1].

Q4. LIFTMOR participants had:
  1. (A) Normal bone mass
  2. (B) Low bone mass (osteopenia or osteoporosis)
  3. (C) Recent hip fracture
  4. (D) Paget disease

Answer: (B) Women had T-scores below −1.0 [1].

Q5. Besides bone density, high-intensity training in LIFTMOR also:
  1. (A) Worsened function
  2. (B) Improved all functional performance measures
  3. (C) Reduced height
  4. (D) Had no other effect

Answer: (B) All functional measures improved [1].

Q6. In the Cochrane review, which exercise type had the largest effect on spine BMD?
  1. (A) Walking alone
  2. (B) Combination exercise programmes
  3. (C) Stretching
  4. (D) Whole-body vibration

Answer: (B) Combination programmes raised spine BMD by 3.22% versus control [2].

Q7. The most effective exercise for femoral neck BMD in the Cochrane review was:
  1. (A) Non-weight-bearing high-force exercise such as lower-limb resistance training
  2. (B) Swimming
  3. (C) Balance only
  4. (D) Yoga

Answer: (A) Progressive resistance training for the lower limbs raised femoral neck BMD by 1.03% [2].

Q8. The Cochrane review found that exercise reduced fractures:
  1. (A) By 90%
  2. (B) With no significant effect; odds ratio 0.61 with a wide interval
  3. (C) Not at all, it increased them
  4. (D) By exactly half

Answer: (B) The odds ratio was 0.61 (0.23 to 1.64), not significant [2].

Q9. How many trials and participants were in the Cochrane review?
  1. (A) 5 trials, 300 women
  2. (B) 43 trials, 4,320 women
  3. (C) 200 trials, 1 million women
  4. (D) 1 trial

Answer: (B) Forty-three trials with 4,320 participants [2].

Q10. Bone responds best to loads that are:
  1. (A) Low, slow and repetitive
  2. (B) High in magnitude and applied quickly
  3. (C) Absent
  4. (D) Only in water

Answer: (B) LIFTMOR was designed on the principle that high strains at high rates are most osteogenic [1].

Quick review

Key takeaways

  • 99% of calcium is in bone; ionised calcium controls excitability.
  • PTH raises calcium via bone, kidney and vitamin D.
  • Osteoclasts resorb; osteoblasts form; osteocytes sense strain.
  • Peak bone mass in the late twenties; faster loss after menopause.
  • Heavy supervised loading raised spine BMD 2.9% [1].
  • Exercise gives modest density gains; fracture effect uncertain [2].

Further reading

SourceWhy it earns its place
Watson SL et al. — J Bone Miner Res, 2018The LIFTMOR trial [1]
Howe TE et al. — Cochrane, 2011Exercise and bone density [2]
Guyton and Hall, Textbook of Medical PhysiologyCalcium and bone chapters

References

  1. Watson SL, Weeks BK, Weis LJ, et al. High-intensity resistance and impact training improves bone mineral density and physical function in postmenopausal women with osteopenia and osteoporosis: the LIFTMOR randomized controlled trial. Journal of Bone and Mineral Research. 2018;33(2):211–220. doi:10.1002/jbmr.3284 PMID 28975661 Randomised controlled trial
  2. Howe TE, Shea B, Dawson LJ, et al. Exercise for preventing and treating osteoporosis in postmenopausal women. Cochrane Database of Systematic Reviews. 2011;(7):CD000333. doi:10.1002/14651858.CD000333.pub2 PMID 21735380 Systematic review and meta-analysis

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Reviewed by the Physiotherapist India Team. · Human Physiology contents