Shivering Thermogenesis: Physiology and Data

Category: physiology Updated: 2026-02-27

Shivering increases metabolic rate 2–5-fold above resting, generating heat primarily in skeletal muscle. Threshold: core temp below ~36°C or skin temp below 25°C. Cold-acclimatized individuals exhibit more non-shivering thermogenesis and less shivering.

Key Data Points
MeasureValueUnitNotes
Metabolic rate increase (maximal shivering)2–5×above restingCastellani & Young 2016; max ~400–500 W in cold-adapted adults
Shivering onset threshold (core)~35.5–36°CHypothalamic set-point; varies ±0.5°C between individuals
Shivering onset threshold (skin)~25°CMean skin temperature; integrated with core temperature signal
Primary fuel for shiveringMuscle glycogen + lipidsMuscle glycogen initially; blood glucose and fatty acids sustain prolonged shivering
Duration before glycogen depletion1–3hoursDepends on glycogen stores, shivering intensity, and fat availability
Shivering frequency4–8cycles/secRhythmic bursting pattern; coordinates across muscle groups
Heat generation efficiency~80% of metabolic rate → heatVs typical exercise where mechanical work consumes ~25% of energy

Shivering is the body’s primary rapid-response thermogenesis mechanism — involuntary, rhythmic muscle contractions that generate heat through mechanical energy dissipation. Unlike brown adipose tissue thermogenesis, which operates silently at the cellular level, shivering is a gross motor response visible from outside.

Neural Control

The hypothalamus integrates two temperature signals:

SignalLocationWeight in Shivering Control
Core temperaturePreoptic area (hypothalamus)~80% of shivering signal
Skin temperaturePeripheral thermoreceptors → spinal cord → hypothalamus~20% of shivering signal

The preoptic area of the hypothalamus contains warm-sensitive neurons that tonically inhibit shivering centers in the posterior hypothalamus and brainstem. When core temperature falls, this inhibition weakens and shivering circuits activate.

Skin temperature plays a modulatory role: cold skin can trigger shivering even before core temperature drops, serving as an early warning system.

Metabolic Data

Shivering IntensityMetabolic RateExample Context
Minimal (thermogenesis stage 1)1.2–1.5× RMRSitting in 15°C room
Moderate2–3× RMRCold water immersion, 10 min
Vigorous (maximal shivering)4–5× RMRExtended cold stress, core cooling

RMR = resting metabolic rate (~70 W for average adult). Maximal shivering can reach ~350–500 W of heat production.

Fuel Sources

Shivering depends on available substrates:

  1. Immediate (first 30 min): Muscle glycogen (fast, anaerobic pathway contributes early)
  2. Extended (30 min–2 hours): Blood glucose and circulating fatty acids
  3. Prolonged (>2 hours): Lipid mobilization from subcutaneous and intramuscular fat becomes dominant

Blondin et al. (2014) demonstrated that intramyocellular lipid contributes substantially to prolonged shivering — challenging the earlier view that shivering is primarily a glucose-dependent process.

Shivering vs Non-Shivering Thermogenesis

FeatureShiveringNon-Shivering Thermogenesis (NST)
Primary tissueSkeletal muscleBrown adipose tissue, beige fat
Speed of onsetFast (seconds to minutes)Slower (minutes to hours)
Maximum capacityHigher in cold-naiveEnhanced with cold acclimatization
EfficiencyHigh (heat per unit metabolic cost)Moderate
VisibilityObservableInvisible
Metabolic pathwayATP hydrolysis in myosin ATPaseUCP1 proton uncoupling

Cold-acclimatized individuals rely proportionally more on NST and less on shivering — their enhanced BAT and beige fat generate sufficient heat at lower temperature thresholds, reducing the need for gross muscle contraction.

Post-Shivering Thermogenesis

After shivering ceases, metabolic rate remains elevated for 30–60 minutes via increased mitochondrial activity and residual hormonal stimulation. This “afterdrop” period of elevated thermogenesis contributes to total cold-induced energy expenditure beyond the shivering episode itself.

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