Cold Exposure

Cold exposure in humans causes specific acute and chronic physiological responses, with acute responses including cutaneous vasoconstriction and shivering thermogenesis that decrease heat loss and increase metabolic heat production. ^[1] Prolonged cold exposure produces cold acclimatization following three primary patterns: habituation, metabolic adjustment characterized by increased thermogenesis, and insulative adjustment that enhances heat-conserving mechanisms. ^[1]

Vasoconstriction is elicited through both reflex and local cooling and, in combination with shivering, operates to maintain thermal balance when the body is losing heat. ^[1] PGC-1alpha is strongly induced by cold exposure, linking this environmental stimulus to adaptive thermogenesis while stimulating mitochondrial biogenesis and a more oxidative muscle fiber-type composition. ^[2]

In a systematic review and meta-analysis of randomized trials with 3177 participants, cold-water immersion caused an acute increase in inflammation immediately after exposure and a significant reduction in stress 12 hours later, with narrative evidence of a 29% reduction in sickness absence among cold-shower users. ^[3] A meta-analysis of randomized trials found cold-water immersion improved recovery of muscular power 24 hours after both eccentric and high-intensity exercise and reduced serum creatine kinase after high-intensity exercise, with shorter durations and lower temperatures improving efficacy. ^[4] A narrative review noted that voluntary cold-water immersion appears to reduce or transform body adipose tissue and improve insulin sensitivity, but concluded the topic remains a subject of debate given small, heterogeneous studies. ^[5]

A systematic review and meta-analysis of 159 studies found that each 1 degree C decrease in temperature increased cardiovascular disease-related mortality by 1.6% and morbidity by 1.2%, so cold exposure carries cardiovascular risk that varies by disease type and climate zone. ^[6] Exercise performed in the cold often augments cardiac workload in persons with coronary artery disease more than in thermoneutral conditions and can reduce myocardial oxygen supply, leading to earlier ischemia and impaired performance. ^[7]