This is an excerpt from Advanced Environmental Exercise Physiology by Stephen S. Cheung.
Cold Injuries to the Extremities
If local blood flow and thermal responses such as CIVD are inadequate in preserving tissue integrity, the extremities can incur risk of injury and damage. Local cold injuries can arise from cold–dry or cold–wet environments and can entail both freezing (e.g., frostbite) and nonfreezing (e.g., trenchfoot) conditions (Hamlet 1988). Therefore, temperature by itself is not the sole determining factor for likelihood of injury. Other environmental factors can potentiate the risk of cold injuries, including wind speed and precipitation. In addition, individual characteristics and circumstances, such as race and level of acclimatization, can affect the risk of injury. It remains difficult to predict individual susceptibility, making awareness of predisposing factors and planning for injury prevention critical—because, when they happen, cold injuries are debilitating to the individual and also can deplete mission resources needed to assist the injured party.
The dominant sites for cold–wet injuries are the feet and legs, as these injuries are typically caused by prolonged immersion of the extremities in cold water. Freezing of the extremity does not cause the damage; rather, likely causes are the edema or high rates of sweating when the feet are wet or are in very humid environments (Hamlet 1988). The most problematic condition is popularly known as trenchfoot (see figure 5.2), the term stemming from initial mass diagnoses during World War I, in which troops were forced to live and fight in muddy terrain and flooded trenches. Immersion foot, a similar condition, has also been reported in shipwreck survivors even in fairly warm waters. Therefore, the prime predictors for the onset of cold–wet injuries are the water temperature and duration of exposure; the following list of injuries represents a continuum from initial to most severe (Hamlet 1988).
1. Chilbain. The initial manifestation of cold–wet injury is the presence of lesions on the dorsal surfaces of the hands and feet. This superficial injury represents damage to superficial blood vessels, resulting in local edema and inflammation. Features of this condition include redness, swelling, itching, and soreness. In worsening cases, chilbains can progress to more severe blisters or ulcers, and it may be months to years before the symptoms subside.
2. Pernio. The continuation from chilbain emerges with further ulceration and the initiation of skin necrosis, again primarily based in the dorsal surface of the hands and feet.
3. Trenchfoot. The culminating cold–wet injury, trenchfoot or immersion foot occurs with severe damage to the local vasculature and likely the nerves. An initial prehyperemic phase leaves the extremity numb, swollen, and discolored. Afterward, a hyperemic phase can lead to severe ulceration, pain, and the risk of infection from gangrene. Even upon eventual recovery, edema, loss of sensation, and severe reactions to cold may remain for the rest of the victim’s life.
Unlike cold–wet injuries, cold–dry injuries involve the actual destruction of cells from freezing and crystallization. The rate of local heat loss and cellular damage from convective heat loss are the prime determinants of frostnip and frostbite, and the onset can be much more rapid than for cold–wet injuries (Hamlet 1988).
1. Frostnip. The initial freezing of the epidermis and superficial skin tissue is painful but typically does not produce long-term damage. However, depending on the depth of freezing, it is possible for the superficial capillaries and nerves to become damaged. If this is the case, subsequent risk of frostnip and frostbite in the same region may increase due to decreased sensation of cold and also decreased blood supply.
2. Frostbite. Continued cooling and freezing of cells can lead to their crystallization, with the damaged regions often becoming waxen and insensitive to touch. Major clinical problems arise with rewarming, with intense pain, inflammation, and the threat of gangrene. Due to the risk of infection, it is critical that rewarming and frostbite treatment occur in medical settings rather than being attempted in the field.
Physiological Responses to Exercise in the Cold
An important fundamental question in the modeling of thermal response is whether heavy or prolonged exercise negatively affects the body’s ability to maintain thermal balance. Consider the grueling effort involved in mountaineering or transpolar missions, and also during intensive military training programs. In such situations, a multitude of nonthermal factors, including exercise-induced fatigue, depleted carbohydrate or lipid stores, altered nutrition, and sleep deprivation can influence the body’s ability to sense cold, vasoconstrict, or elevate heat production. Mountaineers also face the additional factors of reduced ambient pressure and hypoxia, which may additively or synergistically impair thermoregulation. Furthermore, these individual factors may impair cognitive capacity and lead to faulty decision making or an increased risk of accidents. For these reasons, individuals performing prolonged exercise during winter or in situations in which cold conditions can suddenly arise need to be aware of these contributing factors and take steps to minimize their risks.
Field Studies of Expeditions in Cold Environments
As is true in much of environmental physiology, scientists can design studies that track participants in “live” field settings, or more closely isolate individual variables and minimize confounding factors in a laboratory setting. One advantage of the former approach, of course, is that it typically involves exotic travel opportunities for the scientists! However, a common limitation in studying expeditions such as polar treks is the typically small sample size of only one or two subjects, making statistical analysis or generalization difficult. Two studies that tracked larger expeditions highlight the intense effect of prolonged exertion on thermoregulatory control in the cold. Savourey and colleagues (1992) were fortunate to be able to systematically test eight (five male, three female) volunteers prior to and following a three-week ski expedition across Greenland, where ambient conditions ranged from –20 to –30 °C. In laboratory tests, metabolic rate increased in thermoneutral environments following the journey. However, with cold exposure, the absolute rectal temperature for shivering onset decreased by approximately 0.5 °C (e.g., shivering was initiated at 36.0 rather than 36.5 °C). Such a hypothermic insulative adaptation, whereby individuals appear able to tolerate lower core temperatures prior to initiating heat production, may serve to minimize metabolic heat production and hence overall caloric requirements. A similar adaptation has been observed in specific groups native to cold environments, such as Lapps in Scandinavia and Aborigines wearing minimal clothing in the cold night in the Australian desert (Scholander et al. 1958).
Another example of the impact of prolonged exercise on cold tolerance was seen in U.S. Army Ranger recruits (Young et al. 1998). Eight candidates were tracked prior to and following 61 days of strenuous field training, over which they had an average daily caloric deficit of 800 kcal and slept around 4 h per day. Upon testing the recruits’ cold tolerance with 4 h of passive rest in 10 °C air immediately following the field training, and also 2 and 109 days afterward, the researchers found that wild swings in body weight occurred over the first two days of recovery, with the entire 6.4 kg (14 lb) body mass deficit restored but body fatness remaining low until longer in recovery. Rectal temperature during cold exposure was lower immediately and two days after training, demonstrating that chronic exertion can impair cold tolerance. This appeared again to be due to a depression in the core temperature threshold for shivering onset. At the same time, metabolic rate was lower immediately following training and at 109 days compared with 2 days afterward. Overall, this suggests that a brief period of recovery and heavy feeding can restore heat production capacity, but that tissue insulation and thermoregulatory control may not be restored until much later in recovery.