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11. 7. 2012.

Physiological responses to exercise in the cold

Muscle function

Cooling a new muscle causes it to contract with less force. The nervous system responds to muscle cooling by altering the normal muscle fiber recruitment patterns. Some researchers have suggested that this change in fiber selection for force development decreases the efficiency of the muscle’s actions. Both muscle shortening velocity and power decrease significantly when temperature is lowered. Luckily, large deep muscles seldom experience such low temperatures because they are protected from heat loss by the mechanisms previously described.
If clothing insulation and exercise metabolism are sufficient to maintain the athlete’s body temperature in the cold, aerobic exercise performance may be unimpaired. However, as fatique sets in and muscle activity slows, body heat production gradually decreases. Long-distance running, swimming, and skiing in the cold can expose the participant to such conditions. At the beginning of these activities, the athlete can exercise at a rate that generates sufficient internal heat to maintain body temperature. However, late in the activity, when the energy reserves have diminished, exercise intensity declines, and this reduces metabolic heat production. Subsequent hypothermia causes the individual to become even more fatiqued and less capable of generating heat. In these conditions, the athlete is confronted with a potentially dangerous situation.
Cold conditions affect muscle function in another way. As small muscles in the periphery like the fingers become cold, muscle function can be severely affected. This results in a loss of manual dexterity and limits the ability to perform fine motor skills like writing and manual labor tasks.

Metabolic responses

Prolonged exercise increases the mobilization and oxidation of free fatty acids(FFAs). The primary stimulus for this increased lipid metabolism is the release of catecholamines(epinephrine and norepinephrine). Exposure to cold markedly increases epinephrine and norepinephrine secretion, but FFA levels increase substantially less than during prolonged exercise in warmer conditions. Cold exposure triggers vasoconstriction in the vessels supplying not only the skin but fatty subcutaneous tissues as well. The subcutaneous fat is a major storage site for lipids(as adipose tissue), so this vasoconstriction reduces the blood flow to the area from which the FFAs would be mobilized. Thus, FFA levels do not increase as much as the elevated levels of epinephrine and norepinephrine would predict.
Blood glucose plays an important role in both cold tolerance and exercise endurance. For example, hypoglycemia(low blood sugar) suppresses shivering and may therefore significantly reduce rectal temperature. The reasons for these changes are unknown. Fortunately, blood glucose levels are maintained reasonably well during cold exposure. Muscle glycogen, on the other hand, is used at a somewhat higher rate in cold water than in warmer conditions. However, studies on exercise metabolism in the cold are limited, and our knowledge regarding hormonal regulation of metabolism in the cold is too limited to support any definitive conclusions.

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