Prevention of Cold Injuries during Exercise

John W. Castellani, Ph.D., FACSM; Andrew J. Young, Ph.D., FACSM; Michel B. Ducharme, Ph.D.; Gordon G. Giesbrecht, Ph.D.; Ellen Glickman, Ph.D., FACSM; Robert E. Sallis, M.D., FACSM


March 01, 2010

In This Article

Physiological Responses to Cold

Acute Cold Exposure

Humans exhibit peripheral vasoconstriction upon cold exposure. The resulting decrease in peripheral blood flow reduces convective heat transfer between the body's core and shell (skin, subcutaneous fat and skeletal muscle), effectively increasing insulation by the body's shell.[39,168,178] Heat will then be lost from the exposed body surface faster than it is replaced, so skin and underlying tissue temperatures decline.[168] During whole-body cold exposure, the vasoconstrictor response occurs throughout the entire body's peripheral shell and the limbs effectively become part of the shell. Vasoconstriction begins when mean weighted skin temperature falls below 34-35°C,[159] and becomes maximal when mean skin temperature is about 31°C or less during whole-body water immersion[185] or 26-28°C during localized cooling.[22] Thus, the vasoconstrictor response to cold exposure helps retard heat loss and defend core temperature, but at the expense of a decline in skin and muscle temperatures.

The vasoconstriction-induced blood flow reduction and fall in skin temperature probably contribute to the etiology of peripheral cold injuries. Cold-induced vasoconstriction has pronounced effects in the hands and fingers making them particularly susceptible to cold injury and a loss of manual dexterity.[13] In these areas, another vasomotor response, cold-induced vasodilation (CIVD), modulates the effects of vasoconstriction.[114,133] Periodic oscillations of skin temperature follow the initial decline during cold exposure, resulting from transient increases in blood flow to the cooled finger. A similar CIVD also occurs in the forearm, likely reflecting the CIVD of the extremities.[40] It is believed that CIVD plays a substantial role in reducing the risk of local cold injuries[86] and may be beneficial for improving dexterity and tactile sensitivity during exposure to cold.[25] CIVD responses are more pronounced when the body core and skin temperatures are warm (hyperthermic state) and suppressed when they are cold (hypothermic state), when compared to normothermia.[26,27,135]

Cold exposure also elicits an increased metabolic heat production in humans, which can help offset heat loss. In humans, cold-induced thermogenesis is attributable to skeletal muscle contractile activity.[168] Humans initiate this thermogenesis through involuntary shivering or by voluntarily modifying behavior, i.e., increasing physical activity (exercise, increased "fidgeting," etc). While certain animals exhibit an increased metabolic heat production by noncontracting tissue (brown adipose tissue) in response to cold exposure, i.e., nonshivering thermogenesis, experimental evidence does not support a large role for brown-fat mediated thermogenesis in adult humans.[4,18]

Shivering, which consists of involuntary, repeated, rhythmic muscle contractions, may start immediately, or after several minutes of cold exposure, usually beginning in torso muscles, then spreading to the limbs.[8] The intensity and extent of shivering varies according to the severity of cold stress. As shivering intensity increases and more muscles are recruited to shiver, whole body oxygen uptake increases, typically reaching about 600-700 mL·min−1 during resting exposure to cold air, but often exceeding 1000 mL·min−1 during resting immersion in cold water.[178] Maximal shivering is difficult to quantify, but the highest oxygen uptake reported in the literature to date appears to be 2.2 L·min−1, recorded during cold-water immersion, and this was ~ 6 times the resting metabolic rate (50% V·O2max) for that subject.[47]

Patterns of Human Cold Acclimatization

Athletes exposed to cold weather may acclimatize but the physiologic adjustments are very modest and depend on the severity of the exposures. Cold acclimatization in persons repeatedly or chronically exposed to cold manifests in three different patterns of thermoregulatory adjustments: habituation, metabolic acclimatization, and insulative acclimatization.[193]

The most commonly observed acclimatization pattern exhibited is habituation, in which physiological responses to cold become less pronounced than in the unacclimatized state. Blunting of both shivering and cold-induced vasoconstriction are the hallmarks of habituation.[193] Cold-habituated persons with blunted shivering and vasoconstrictor responses to cold, sometimes, but not always, also exhibit a more pronounced decline in core temperature during cold exposure than nonacclimatized persons. Thus, this pattern of cold acclimatization is sometimes referred to as hypothermic habituation, or hypothermic acclimatization. Findings from different cold acclimation studies, when viewed collectively (see [193] for a detailed review), suggest that short intense cold exposures (e.g., less than 1 h), a few times per week will produce habituation, but that longer exposures (e.g., more than 8 h) to more moderate cold conditions, on consecutive days over a fairly long period (e.g., more than 2 wk) are required to induce the hypothermic form of habituation. Habituation also occurs locally (i.e., hands), leading to warmer skin temperatures and decreased discomfort.[1,108,161]

Chronic cold exposure can induce two other distinct patterns of acclimatization. A more pronounced thermogenic response to cold characterizes the metabolic acclimatization pattern.[193] An exaggerated shivering response has been reported to develop because of chronic cold exposure, and the possibility that humans develop a nonshivering thermogenesis continues to be argued. However, the evidence purporting to document the existence of this pattern does not definitively demonstrate whether this enhanced thermogenic response to cold represents an adjustment to chronic cold, or confounding effects of differences in diet or body composition among experimental and control subjects.

The third major pattern of cold acclimatization, referred to as insulative cold acclimatization, is characterized by enhanced heat conservation mechanisms.[193] With insulative acclimatization, cold-exposure elicits a more rapid and more pronounced decline in skin temperature and lower thermal conductance at the skin than in the unacclimatized state, mediated by a more pronounced vasoconstrictor response to cold, possibly due to enhanced sympathetic nervous response to cold. In addition, some data suggest that insulative cold acclimatization may also involve development of enhanced circulatory counter-current heat exchange mechanisms to limit convective heat loss, as evidenced by the observation that before wet-suits came into common usage, Korean diving women immersed in cool water exhibited lower forearm heat loss than control subjects, despite the fact that forearm blood flow remained higher in the diving women.[83] After wet-suit use became widespread, Korean diving women no longer exhibited any thermoregulatory adjustments compared to control subjects, suggesting that the previous differences truly reflected adjustments to frequent exposure to cold while diving (for review see [193]). Compared to the effects of heat acclimatization, physiological adjustments to chronic cold exposure are less pronounced, slower to develop, less reproducible, and less practical in terms of relieving thermal strain, defending normal body temperature, and preventing thermal injury.