The body is modeled as two thermal compartments — a core (viscera, brain) and a shell (skin, subcutaneous fat) — each obeying a lumped heat-balance (bioheat) equation:
C_core · dT_c/dt = M − W − Q_c→s
C_shell· dT_s/dt = Q_c→s − Q_s→env
Q_c→s = BF · ρc_blood · (T_c − T_s) (convective transfer by blood)
Q_s→env = h·A·(T_s − T_amb) + E_sweat − M_shiver
The hypothalamus normally defends T꜀ near 37 °C by two effector arms: vasomotor tone (skin blood flow BF, which rises up to ~6× at rest normally to dump heat, or falls toward a minimum to conserve it) and eccrine sweating (evaporative cooling E, driven by the number of thermally-active sweat glands and their maximal secretion rate).
Why aging blunts this system — three independent, well-documented mechanisms are combined here:
- Reduced vasomotor gain — peripheral vasoconstrictor and vasodilator responses weaken with age (reduced α-adrenergic reactivity, stiffer vessels), so the BF swing available to fight cold or heat shrinks roughly linearly after ~50.
- Fewer active sweat glands — eccrine gland density and per-gland output decline with age, cutting maximal evaporative heat loss and delaying sweat onset (a higher T꜀ threshold before sweating starts).
- Weaker shivering thermogenesis — lower muscle mass (sarcopenia) and a blunted shiver reflex cut cold-defense heat production.
The age slider scales all three gains continuously between the young-adult and frail-elderly parameters below, which is why the same ambient temperature produces a much faster, larger core-temperature drift at age 90 than at age 20 — the mechanistic reason hypothermia and heat stroke both carry disproportionately higher mortality in older adults.
Color coding: the inner sphere is core temperature, the outer translucent shell is skin temperature (blue → cold, red → hot), particles show blood volume flux between core and shell, and droplets appear on the shell once sweating is triggered.