Sports Medicine

, Volume 11, Issue 6, pp 367–381

Physiology of Exercise in the Cold

  • Thomas J. Doubt
Review Article


Recreational and job requirements have increased the incidence in which humans exercise in cold environments. Understanding the physiological responses while exposed to cold entails knowledge of how exercise and cold interact on metabolic, cardiopulmonary, muscle and thermal aspects of human performance. Where possible, distinctions are made between responses in cold air and cold water.

While there is no consensus for diets most appropriate for working cold exposures, the evidence is strong that adequate amounts of carbohydrate are necessary. Carbohydrate loading appears to be efficacious, as it is for other athletic endeavours.

Contrary to conventional wisdom, the combination of exercise and cold exposure does not act synergistically to enhance metabolism of fats. Free fatty acid (FFA) levels are not higher, and may be lower, with exercise in cold air or water when compared to corresponding warmer conditions. Glycerol, a good indicator of lipid mobilisation, is likewise reduced in the cold, suggesting impaired mobilisation from adipose tissue.

Catecholamines, which promote lipolysis, are higher during exercise in cold air and water, indicating that the reduced lipid metabolism is not due to a lack of adequate hormonal stimulation. It is proposed that cold-induced vasoconstriction of peripheral adipose tissue may account, in part, for the decrease in lipid mobilisation. The respiratory exchange ratio (RER) is often similar for exercise conducted in warm and cold climates, suggesting FFA utilisation is equivalent between warm and cold exposures. The fractional portion of oxygen consumption (V̇O2) used for FFA combustion may decrease slightly during exercise in the cold. This decrease may be related to a relative decrease in oxygen delivery (i.e. muscle blood flow) or to impaired lipid mobilisation.

Venous glucose is not substantially altered during exercise in the cold, but lactate levels are generally higher than with work in milder conditions. The time lag between production of lactate within the muscle and its release into the venous circulation may be increased by cold exposure.

Minute ventilation is substantially increased upon initial exposure to cold, and a relative hyperventilation may persist throughout exercise. With prolonged exercise, though, ventilation may return to values comparable to exercise in warmer conditions. Exercise V̇O2 is generally higher in the cold, but the difference between warm and cold environments becomes less as workload increases. Increases in oxygen uptake may be due to persistence of shivering during exercise, to an increase in muscle tonus in the absence of overshivering, or to nonshivering thermogenesis.

Heart rate is often, but not always, lower during exercise in the cold. The linear relationship between heart rate and oxygen consumption is displaced such that at a given rate oxygen uptake is higher. Cardiac arrhythmias are more frequent in the cold. Stroke volume tends to be higher than under warmer control conditions, but may decline sooner or at a rate equivalent to warm controls at heavy workloads. Cardiac output is similar to the same work done in temperature environments.

Cold-induced vasoconstriction occurs both in cutaneous and resting skeletal muscle beds, but inactive muscle provides most of the passive body insulation. With exercise insulation provided by muscle decreases as blood flow increases. Relative to warmer conditions, muscle blood flow at a given workload may be reduced if deep muscle temperature is below normal (i.e. 39°C optimum).

Respiratory heat loss is often assumed to represent 8% of the total metabolic heat production. However, during exercise this value will increase as minute ventilation increases. Loss of significant amounts of heat from the distal extremities can limit performance, even though the area is not directly involved with exercise.

Cooled muscle has a decreased capacity to generate force expressed on cross-sectional area. As a consequence, it may be necessary to recruit more fast twitch motor units. Glycolysis is higher in cooled muscle, which may account for higher lactate levels and greater rates of muscle glycogen depletion. Brief intense exercise will not raise cooled muscle temperature to normal limits, but mild exercise can maintain normal temperatures if exercise begins before the muscles become cooled.

Regional heat flux increases with exercise in the cold in direct proportion to the workload. Differing rates of heat loss can occur between active and inactive limbs, and individual rates are not constant throughout steady-state exercise. Peak rates of heat flux for inactive limbs occur during exercise, but peak flux for active limbs occurs in the postexercise period. At equal metabolic rates, more heat is lost with arm than with leg exercise.

Most of the heat generated by exercising muscle is transferred convectively to the core via the venous circulation. The amount of heat lost conductively to the environment through tissue depends upon factors such as subcutaneous fat. Thus, individuals with higher levels of fat (e.g. skinfold thickness) generally are better able to maintain their core temperature in cold environments.

Steady-state exercise V̇O2 values of approximately 2.0 L/min have been shown to prevent falls in core temperature in water as low as 15°C. Warmer temperatures are required in order to maintain core homeostasis during intermittent exercise.

Predicting an individual’s response to exercise in the cold is quite difficult because of the interplay of many factors. Using existing data, responses to some forms of exercise and environmental stress can be estimated with reasonable accuracy. However, the number of these type responses is small compared to the total number of possible permutations, showing that much is yet to be learned.


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Copyright information

© Adis International Limited 1991

Authors and Affiliations

  • Thomas J. Doubt
    • 1
  1. 1.Hyperbaric Environmental Adaptation ProgramNaval Medical Research InstituteBethesdaUSA

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