Vasoconstriction and Vasodilation in Cold Exposure

Vasoconstriction — the narrowing of blood vessels — is the cardiovascular system’s first response to cold and the primary mechanism for preserving core temperature. The body sacrifices peripheral warmth to maintain the 36.5–37.5°C core temperature range that vital organs require.

Mechanism of Cold-Induced Vasoconstriction

Cold exposure triggers peripheral vasoconstriction through two complementary pathways:

Neural (sympathetic) pathway (primary):

1. Cold thermoreceptors signal hypothalamus
2. Sympathetic nervous system activates
3. Norepinephrine released from sympathetic nerve terminals at vessel walls
4. Alpha-1 adrenergic receptors on vascular smooth muscle → constriction

Local cold pathway (secondary): Cold directly increases the sensitivity of vascular smooth muscle to norepinephrine, amplifying the neural signal. This local augmentation explains why peripheral vasoconstriction is greater at colder temperatures independently of the sympathetic signal magnitude.

Cardiovascular Response During Cold Exposure

Parameter	Change During CWI	Mechanism
Peripheral blood flow	↓ 60–90%	Sympathetic vasoconstriction
Core blood flow	↑ 40–60%	Redistribution
Heart rate	↑ initially (cold shock), then ↓	Sympathetic then vagal
Blood pressure	↑ 15–20 mmHg systolic	Increased vascular resistance
Cardiac output	Maintained initially	↑ HR compensates for ↓ SV

The Lewis Hunting Reaction

Sir Thomas Lewis (1930) described a paradoxical phenomenon in extremities: after initial intense vasoconstriction, finger and toe blood vessels periodically dilate, allowing brief intervals of warm blood flow before reconstricting. This cycles every 5–10 minutes.

Proposed mechanism: Extreme local cold impairs sympathetic nerve conduction. Temporarily reduced sympathetic tone allows vessels to dilate (local vasodilation), warming the tissue and restoring nerve function — which then reestablishes vasoconstriction. The cycle repeats.

Protective function: The hunting reaction prevents frostbite by periodically delivering warm blood to the coldest extremities. Individuals with impaired hunting reactions (Raynaud’s phenomenon, peripheral arterial disease) have higher frostbite risk.

Sex Differences in Vasoconstriction

Women exhibit stronger peripheral vasoconstriction responses to cold than men of equivalent body size and composition. Mäkinen et al. (2010) documented greater finger and toe temperature drops in women at equivalent cold air exposure. Proposed mechanisms:

• Higher estrogen levels enhance alpha-adrenergic vascular reactivity
• Lower body surface area-to-mass ratio means less insulation per surface area
• Different skin blood flow baseline in women

This sex difference means women experience colder extremities at equivalent environmental cold stress — relevant for both cold exposure safety and protocol design.

Recovery — Vasodilation After Cold

Rewarming activates the reverse process:

1. Rising skin temperature signals hypothalamus
2. Sympathetic vasoconstriction tone reduces
3. Cutaneous vessels dilate (reactive hyperemia)
4. Skin flushes red as blood floods previously restricted vessels
5. Core temperature may briefly drop (“afterdrop”) as cold peripheral blood returns to core

The afterdrop phenomenon is clinically significant: individuals rescued from cold water should be rewarmed gradually to prevent sudden core cooling from rapid peripheral vasodilation.