The human body constantly works to maintain a stable internal environment, a process known as homeostasis, despite external temperature extremes. Environmental temperatures fundamentally challenge this stability. To endure thermal stressors, the body uses a sophisticated system of physiological responses designed to shed excess heat or generate and conserve warmth. Understanding these biological mechanisms provides insight into the limits of human endurance and the failure points that lead to heat- or cold-related illness.
Defining the Danger Zones: Thermoregulation Basics
Thermoregulation governs the body’s steady state, balancing heat production and loss to maintain a core temperature of approximately $37.0 \pm 0.5^\circ\text{C}$. This narrow range is required because the body’s enzymes, which drive metabolic functions, are temperature-sensitive and fail if the internal temperature deviates too far. The hypothalamus, located in the brain, acts as the central thermostat and control center.
It receives constant feedback from thermoreceptors in the skin (peripheral) and deep tissues (central). When sensors detect a deviation, the hypothalamus initiates autonomic responses to restore equilibrium. Regulatory mechanisms are overwhelmed in the danger zones, leading to systemic failure. Hypothermia begins when the core temperature drops below $35^\circ\text{C}$, while a sustained temperature exceeding $40^\circ\text{C}$ is associated with severe heat illness, or heat stroke.
Physiological Breakdown: Surviving Extreme Heat
The primary challenge in extreme heat is dissipating the thermal load from the environment and the body’s metabolic processes. The first major response is active cutaneous vasodilation, where blood vessels near the skin surface widen. This increases blood flow to the periphery, transferring heat from the warmer core to the skin surface for exchange via radiation and convection.
Simultaneously, the body activates eccrine sweat glands to initiate evaporative cooling, the most effective heat loss mechanism. As sweat evaporates, it draws heat away from the skin, cooling the underlying blood. This process strains the cardiovascular system, which must increase output and redistribute blood flow to the skin without causing a drastic drop in blood pressure.
The system fails when environmental conditions overwhelm the body’s capacity, leading to heat-related illness. Heat exhaustion involves profuse sweating and inadequate blood pressure due to fluid loss, but core thermoregulation remains intact. Heat stroke represents the failure of the core system, defined by a core temperature above $40^\circ\text{C}$ and central nervous system dysfunction like delirium or coma. This failure is linked to the circulatory system collapsing and a systemic inflammatory response.
Physiological Breakdown: Surviving Extreme Cold
When exposed to cold, the body prioritizes conserving heat and generating warmth to protect the core temperature. The immediate response is peripheral vasoconstriction, the narrowing of blood vessels in the extremities (fingers, toes, and skin). This reduces the volume of blood exposed to the cold, minimizing heat transfer away from the core.
If conservation is insufficient, the body initiates shivering, an involuntary mechanism of rapid muscle contractions. Shivering can increase the body’s heat production rate by two to five times its normal resting metabolic rate, converting mechanical energy into thermal energy. This response is energetically costly and relies on adequate glycogen stores.
The failure of cold defense manifests as hypothermia, beginning when the core temperature drops below $35^\circ\text{C}$. In mild hypothermia ($32^\circ\text{C}$ to $35^\circ\text{C}$), vasoconstriction and shivering are maximized, accompanied by confusion and increased urine production. As the core temperature falls further, shivering often ceases below $32^\circ\text{C}$, and all physiological functions, including heart and respiratory rates, slow significantly.
Localized tissue damage, known as frostbite, occurs when skin and underlying tissues freeze due to prolonged exposure below $0^\circ\text{C}$. Severe vasoconstriction compounds this freezing by starving the extremities of warm blood and oxygen. The injury progresses from superficial frostnip, which causes reversible numbness, to deep frostbite, where ice crystals form, leading to cellular damage, microvascular stasis, and tissue death.
Why Vulnerability Varies: Acclimation and Risk Factors
The efficiency of the thermoregulatory system varies widely, meaning not all individuals respond identically to extreme temperatures. Biological acclimation is a significant factor, involving physiological adjustment over days or weeks of repeated exposure to a new thermal environment. Heat acclimation, for instance, increases plasma volume, sustains blood flow to the skin for cooling, and results in an earlier onset of sweating at a higher rate with less salt loss.
Repeated cold exposure can lead to metabolic acclimation, though it is less pronounced in humans than heat acclimation. This adaptation may involve a more rapid vasoconstriction response or a sustained, non-shivering increase in metabolic heat production.
The effectiveness of these responses is compromised by several intrinsic risk factors. Age is a major determinant of vulnerability, as both the very young and the elderly have less efficient systems. Older adults often have reduced circulation and fewer functional sweat glands. Infants have a greater surface area-to-body mass ratio, leading to faster heat gain or loss. Pre-existing medical conditions, particularly cardiovascular issues, limit the heart’s ability to cope with circulatory demands in both heat and cold. Furthermore, certain medications, such as those with anticholinergic effects, can interfere with sweat gland signaling, compromising the body’s ability to cool itself.