# Ageing Physiology > Ageing physiology for MBBS Physiology — presbyopia, presbycusis, declining GFR and reserve, menopause, sarcopenia and biological ageing theories. - Canonical URL: https://prepelephant.com/topics/mbbs/physiology/ageing-physiology - Exam / course: MBBS · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Ageing Physiology", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/ageing-physiology ## Direct answer Ageing narrows physiological reserve rather than destroying resting function: an 80-year-old may have a normal resting creatinine, cardiac output and minute ventilation yet survive neither a pneumonia nor a major surgery, because every system's maximum capacity has contracted. The changes follow predictable tracks — presbyopia from lens stiffening, presbycusis losing high frequencies first, creatinine clearance falling roughly a tenth per decade after 40, sarcopenia, thymic involution and menopause — against a background of competing biological theories of ageing itself: damage accumulation (free radicals, glycation) versus programmed senescence (telomere shortening and the Hayflick limit). ## What you must remember - Presbyopia: the near point recedes from about 10 cm at age 10 to 80 cm by 60 from loss of lens and ciliary muscle elasticity — convex reading glasses are the fix. - Presbycusis: sensorineural loss of the highest frequencies first (6–8 kHz, basal cochlear turn), progressing downwards. - Respiratory mechanics: chest wall stiffens and muscles weaken — vital capacity and maximum breathing capacity fall steadily from the third decade. - Renal: glomerular filtration falls roughly 8–10 mL/min per decade after 40; because muscle mass also falls, serum creatinine stays deceptively normal — dose drugs on estimated GFR, not creatinine. - Cardiovascular: arterial stiffening raises systolic pressure; baroreflex sensitivity declines, producing postural drops and falls. - Menopause: ovarian follicle exhaustion with low oestrogen and high FSH; bone mineral crashes in the following decade — osteoporosis defined as DEXA T-score of −2.5 or less. - Sarcopenia: muscle mass declines about 1–2% per year after 50, with strength lost faster than mass; protein intake and resistance exercise are the countermeasures. - Immune senescence: thymus involutes after puberty, naive T-cell output falls, vaccination responses weaken and latent infections such as herpes zoster reactivate. - Theories: damage-based (reactive oxygen species, glycation, somatic mutation) versus programmed (telomere shortening — most somatic cells divide roughly 50 times, the Hayflick limit); caloric restriction extends lifespan in nearly every species tested. - India defines geriatric age as 60 years and above and runs the National Programme for Health Care of the Elderly. ## Why pneumonia kills at 85 and not at 30 Admit the same pneumococcus to two chests and watch the margins. The 30-year-old doubles her cardiac output, raises ventilation several-fold, mounts a neutrophil response and fever, and her kidneys fine-tune fluid and acid-base around the clock; she leaves in four days. The 85-year-old arrives with reserve already spent at the corners: a maximum heart rate near 135, a vital capacity half its youth, a GFR of 50 with a non-creatinine-flagged creatinine, blunted febrile response and thymus long since fat-replaced, and a baroreflex too sluggish to buffer the hypotension of sepsis. Each system functions at rest — the ward round pronounces him "stable" — but the stress of infection crosses the narrowed margin, and decompensation is sudden and multi-system. This contraction of homeostatic range is homeostenosis, and it explains why geriatric medicine is pre-emptive: vaccination, balance training, deprescribing and hydration are not kindnesses but reserve protection. The same logic governs surgery and drugs. A normal creatinine in the elderly is not normal renal function; metformin, digoxin and aminoglycosides accumulate on a silent GFR. Polypharmacy multiplies faster than diseases do, and each added drug taxes the hepatic clearance and autonomic reflexes that would once have absorbed it. ## Where students slip Two traps recur in exams. First, normal-versus-disease: presbyopia and slower processing speed are universal ageing, while dementia and parkinsonism are diseases — conflating them costs both marks and clinical respect. Second, endocrine numbers: postmenopausal FSH is high (loss of negative feedback), not low — candidates write the reverse under time pressure. Also keep the Hayflick limit precise: about 50 population doublings for fetal fibroblasts in culture, the experimental basis of the programmed-ageing argument; and remember that women outlive men by several years in almost every population, a fact no single theory fully explains. ## Frequently asked questions ### What causes presbyopia and when does it typically begin? Loss of lens elasticity and ciliary muscle power from the fourth decade onward, pushing the near point away until reading requires convex correction. ### Why can serum creatinine be misleading in the elderly? Creatinine production falls with muscle mass as GFR falls, so a normal-looking creatinine can coexist with substantially reduced filtration. ### What is homeostenosis? The age-related narrowing of each organ system's functional reserve, so resting function appears normal while stress tolerance is sharply reduced. ### Which changes define immunological ageing? Thymic involution with reduced naive T-cell production, weaker antibody responses to vaccines, and reactivation of latent infections such as shingles. ### What is the Hayflick limit? The observation that normal somatic cells divide about 50 times in culture before senescing — experimental support for programmed ageing through telomere shortening.