Adapting to the Cold
Now that we have a basic understanding of how our body can make changes in order to adapt to acute exposures to the cold, it is imperative that we take a closer look to longer term adaptations and how it can have an effect on performance. There are three main methods that individuals can acclimatize themselves to cold climate which are through habituation, metabolic or insulative acclimatization.
Habituation
Castellani et al., 2006, describes habituation as a decrease in response pronunciation, relative to unacclimatized individuals. Habituation can also be defined as “a reduction in behavioural perception of a repeated stimulus.” Thus, a decrease in shivering and cold induced vasoconstriction will take place as a result (Young, 1996). Habituation can occur from long term exposure to moderate levels of cold temperature over long periods of time to produce warmer average core temperature and less discomfort while in the cold and furthermore greater drop in core temperature after prolonged cold exposure (Savourey et al., 1992).
Metabolic Acclimatization
The next approach to adaptation is metabolic acclimatization. This allows for an amplified shiver response resulting in an increase in heat production (Young, 1996). This could also mean there is increased oxygen consumption at maximal shivering and it occurs at an earlier instance in time. This is important because it means that it further reduces the risk of cold related injuries to the periphery and ensures that core temperature is regulated.
Insulative Acclimatization
And the final approach is insulative acclimatization where, according to Castellani et al., 2006, the body adopts improved heat conservation methods. This includes an increased decline in initial body temperature, resulting in an earlier vasoconstriction response of the body, possibly attributed by a stimulated sympathetic nervous system response from exposure to the cold (Young, 1996).
Effects on Performance
After looking at these basic concepts of the body’s physiological responses and adaptations, the next step would be to analyze their direct impacts on aerobic fitness and physical performance.
Studies done comparing sedentary to aerobically fit individuals (Bittel, 1988), lead us to believe that fitness does not have a large effect on overall capability to perform, but that these differences arise from individual differences from person to person such as body composition, age, and sex (to a certain extent). A study conducted by Lounsbury et al., in 2005 looked at novice and expert swimmers and their ability to swim in severe cold water condition. Results had suggested that the expert swimmers could swim further distances, but not longer durations (Lounsbury et al., 2005). This leads us to the conclusion that limb fatigue could have played a role in temperature maintenance and had caused the expert swimmers to cool down at a faster rate that the novice swimmers because they had expended larger amounts of energy over the course of their swim, consequentially meaning muscle cooling had caused expert swimmers to retire early. What is known with certainty is that increased metabolic activity from exercise can help warm the periphery and protect from frostbite (freezing of tissue) and hypothermia, where core drops to a temperature of 35°C or lower (Figure 3) (Blatteis et al., 1976).
Cold-Related Injuries
Majority of cold-related injuries are inclined to affect individuals who are genetically predisposed to them, but can still influence anyone exercising in the cold for long periods of time. The more relevant and concerning injuries relating to performance will be looked at in the following section.
Asthma and Cold-Induced Bronchoconstriction
Asthma is a condition characterized by inflammation and obstruction of the bronchi and bronchioles. Weiler and Ryan (2000) found that asthma rates of 60.7% for participants in Nordic skiing and short track speed-skating events, and 24% for those engaged in alpine skiing, long-track speed skating, figure skating, and snow boarding events. Shephard (2004) suggests that the “freezing of the lungs” phenomenon, as claimed by mountaineers and residents of arctic areas seem to unclear, he states that it is certain that winter sport increases the risk of asthma to an extent that it is worth mentioning.
Exercise induced bronchoconstriction or EIB, is known for is constriction of the bronchioles similar to asthma and is directly caused from stressing the respiratory pathways during intense aerobic exercise (Evans et al., 2005). EIB is known to be present in most individuals with asthma when they exercise, as EIB results in a decrease in forced expiratory volume of 10% or more over a one second maximal expiration (Mellion and Kobayashi, 1992). The cold air that enters the lungs stiffens and dries out the airways, only compounding the issue if the individual has asthma, but still remains a large problem if the individual is performing at high intensities.
Heart and Vasculature Complications
Exercise-cold stress alters sympathetic nervous activity such that it causes an increase in vascular resistance, mean arterial pressure, and strain on the heart because of increases in stroke volume to compensate for lack of peripheral blood flow and increase in heart rate to meet the demands of oxygenated blood to working muscle, peripheral tissue and visceral organs (Doubt, 1991). Knowing this should prove to be obvious that athletes that are hypertensive or have heart conditions, such as angina, should be extremely carefully when exercising at high intensities (>70% of VO2 max).
Prospective in Future Research
Majority of this research has been tested on rats, but provides a great deal of insight on ways to describe certain physiological occurrences that we currently cannot explain in great depth in humans, or need more plausible data to support any claims that we have at this point in time.
The first study of concern looks at the effects of the catecholamine epinephrine on cold tolerance and brown adipose tissue. Catecholamines have been described to have a major role in non-shivering thermogenesis through adrenergic receptors (Schonbaum et al., 1966). In humans, infusion of epinephrine is highly thermogenic (Jequier et al., 1992) and has the ability to aid in metabolic heat production during circumstances of thermal debt. Epinephrine, a “fight or flight” hormone is released into the blood stream during times of stress to provide sufficient energy for the body to get out of a potentially life threatening situation, such a cold stress, for example. Epinephrine therefore reduces the need for vasoconstriction and allows for heat generation to occur, while maintaining peripheral blood flow to tissue and potentially working skeletal muscle.
Brown adipose tissue (BAT) is fat that generates heat via non-shivering thermogenesis in newborns and mammals, but in some studies has proven to be present in small quantities on adults as well and related to skeletal muscle (Nedergaard, Bengtsson, and Cannon, 2007). These results have not been replicated in enough studies to produce any solid claims. But it is proven that BAT is present in mammals and that gene expression of BAT mitochondria requires the presence of epinephrine (Sharara-Chamia et al., 2010). Therefore, if it is possible to isolate for the process or mechanism responsible for the removal of BAT, and halt its occurrence, then another door for heat maintenance can be opened in adult humans.
The next study of interest was conducted by Bruton et al. (2010) addressing the similarities between adaptations made in skeletal muscle of mice during cold exposure and adaptation during endurance training. They believed that increased myoplasmic free calcium is necessary for these adaptations to take place. Experiments were performed on flexor digitorum brevis (FDB) muscles, which are not effecting by the involuntary contractions of a shivering response, of cold acclimated mice. They had noticed that muscle fibres showed considerable increases in calcium levels, compared to fibres from the room-temperature control group mice. The cold-acclimated mice had an increased expression of genes and enzymes that imitate an enhanced production of mitochondria. As a result, muscle fibres had shown an improved resistance to fatigue (Figure 4). Bruton and his colleagues attribute their results to the presence of calcium during these adaptations. This shows that perhaps through calcium supplementation in cold acclimation, we can also produce more mitochondria to make work during the cold more efficient.
Experiment
Experimental Hypothesis:
Acclimation induced by long term exposure to moderate cold conditions should illicit hypothermic habituation. This will result in a more stable, efficient, and effective adaptation to sport performance in a cold environment, than that of acclimation induced from chronic short term exposures of severe cold that produce metabolic and insulative inclined acclimation. But athletes with combined approach will show a greater overall performance due to more thorough adaptation to the environment, equipping them with better means of performing, while the unacclimated group will perform the worst in comparison to other group.
Proposed Methods to Test Hypothesis
Twenty endurance trained runners of ideally same or similar body composition, age, sex, and aerobic fitness will be split equally into four groups. One group will be exposed to a moderate cold climate, intended to alter the athlete’s core temperature to 36.7°C for 10 hours per day, 4 days per week for a total of 3 weeks. The second group will be exposed to a severe cold climate to alter their core temperature to 35.5°C in order to induce a state of near hypothermia (provoking sub-maximal shivering) for 10 minutes straight per day, 5 days per week for a total of 3 weeks. The third group will receive a combination of moderate cold and sever cold conditions. On every odd day (day 1,3,5,7) athletes will experience the moderate cold climate for 10 hours, while on even days (day 2,4,6) athletes will experience the severe cold climate for 10 minutes and this will go on for 3 weeks. The fourth group will be a control group, not undergoing any form of acclimation. Athletes will be warmed up appropriately after time spent in cold room with vitals being constantly monitored to ensure that nothing goes wrong. At the end of the 3 week period, all athletes will compete in 3 trials (on 3 separate days) of a 10 km run in -10°C weather (without any wind chill). Ideally control over any nutritional difference across individuals will be made to remove any controllable bias. At the end of the run, mean times from each trial and group will be calculated and compared to see which group performed better during the run.
Predicted Results
The group that is predicted to perform the best during the run will be the athletes that went under the combined method of acclimation. Coming in a close second place will be the hypothermic habituation group that was in the moderate cold climate. Next, in a close third place should be the group that was in severe cold climate. Finally, the unacclimated group will perform the worst coming in last place.
Applying Knowledge to Support Hypothesis
The logic behind the combined acclimated group coming in first is simply because as stated in the hypothesis will have an advantage and be more prepared than the other groups during multiple trials of runs. The group that would come in second place would be close, but would be the moderate cold group. This is because the habituated group would have a blunted shiver response and decreased vasoconstriction of the periphery meaning that they would have a greater efficiency of blood flow to skeletal muscle. Because of this however, they are at a greater risk of cold-related injury, but considering they are competing for better times, they will be going at high intensities ensuring that body temperature is maintained throughout the race. In third place is the metabolic and insulative acclimated group. The increase in metabolic heat production might help them to generate more energy early on during the race, but this could predispose them to fatigue earlier in the race. Also these athletes might not find a heightened shivering response to be very useful when they are constantly moving for the race, but they put up a good fight. Finally, the unacclimated group performed the worst simply because their bodies went into shock during the run and were be unable to adapt to the cold efficiently enough in time to catch up or to outperform any of their counterparts from other groups.
Figures
Figure 1: Eyolfson et al., 2001.
Figure 2: Eyolfson et al., 2001.
Figure 3: Castellani et al., 2006.
Figure 4: Bruton et al. (2010)
References
Bell, D. G., P. Tikuisis, and I. Jacobs. Relative intensity of muscular contraction during shivering. J. Appl. Physiol. 72:2336-2342, 1992.
Blatteis, C. M., and L. O. Lutherer. Effect of altitude exposure on thermoregulatory response of man to cold. J. Appl. Physiol. 41:848-858, 1976.
Bittel, J. H. M., C. Nonott-Varly, G. H. Livecchi-Gonnot, G. Savourey, and A. M. Hanniquet. Physical fitness and thermoregulatory reactions in a cold environment in men. J. Appl. Physiol. 65:1984-1989, 1988.
Brajkovic, D., and M. B. Ducharme. Finger dexterity, skin temperature, and blood flow during auxiliary heating in the cold. J. Appl. Physiol. 95:758-770, 2003.
Bruton J.D., Aydin J., Yamada T., Shabalina I. G., Ivarsson N., Zhang S., Wada M., Tavi P., Nedergaard J., Katz A., and Westerblad H. Increased fatigue resistance linked to Ca2+-stimulated mitochondrial biogenesis in muscle fibres of cold-acclimated mice. J Physiol 588.21 (2010) pp 4275–4288
, , , , , ; . Prevention of Cold Injuries during Exercise. 38(11):2012-29, 2006.
Doubt, T. J. Physiology of exercise in the cold. Sports Med. 11:367-381, 1991.
Dougherty, S. M., L. M. Sheldahl, N. A. Wilke, S. G. Levandoski, M. D. Hoffman, and F. E. Tristani. Physiologic responses to shoveling and thermal stress in men with cardiac disease. Med. Sci. Sports Exerc. 25:790-795, 1993.
Evans, T. M., K. W. Rundell, K. C. Beck, A. M. Levine, and J. M. Baumann. Cold air inhalation does not affect the severity of EIB after exercise or eucapnic voluntary hyperventilation. Med. Sci. Sports Exerc. 37:544-549, 2005.
Eyolfson, D. A., P. Tikuisis, X. Xu, G. Weseen, and G. G. Giesbrecht. Measurement and prediction of peak shivering intensity in humans. Eur. J. Appl. Physiol. 84:100-106, 2001.
Iida, T. Studies concerning vascular reaction to cold (Part I), Physiological significance of vascular reactions to cold [In Japanese]. J. Physiol. Soc. Japan 11:73-78, 1949.
Jequier, E., Munger, R., et al., 1992. Thermogenic effects of various beta-adrenoceptor agonists in humans: their potential usefulness in the treatment of obesity. Am. J. Clin. Nutr. 55 (1 Suppl.), 249S–251S.
Lounsbury, D. S. and M. B. Ducharme. Self-rescue strategies during accidental cold water immersion: performance and thermal considerations. In Proceedings of the 11th International Conference on Environmental Ergonomics. Ystad, Sweden: Lund University, pp. 553-556, 2005.
Mellion, M. B., and R. H. Kobayashi. Exercise-induced asthma. Am. Fam. Physician 45:2671-2677, 1992.
Nedergaard J, Bengtsson T, Cannon B. . Am. J. Physiol. Endocrinol. Metab. 293 (2): E444–52, 2007.
Savourey, G., L. Clerc, A. L. Vallerand, G. Leftheriotis, H. Mehier, and J. H. M. Bittel. Blood flow and muscle bio-energetics by 31p-NMR after local cold acclimation. Eur. J. Appl. Physiol. 64:127-133, 1992.
Schonbaum, E., Johnson, G.E., et al., 1966. Adrenergic beta-receptors and nonshivering thermogenesis. Nature 210 (5034), 426.
Sharara-Chamia R. I., Joachimb M., Mulcaheyb M., Ebertc S., Majzoubb J. A. Effect of epinephrine deficiency on cold tolerance and on brown adipose tissue. Molecular and Cellular Endocrinology 328 (2010) 34–39
. Does cold air damage the lungs of winter athletes? 2004 Dec;3(6):289-91.
Toner, M. M., and W. D. McArdle. Human thermoregulatory responses to acute cold stress with special reference to water immersion. In: Handbook of Physiology: Environmental Physiology, M. J. Fregley and C. M. Blatteis (Eds.). Bethesda, MD: American Physiological Society, pp. 379-418, 1996.
Weiler JM, Ryan EJ: Asthma in United States Olympic athletes who participated in the 1988 Olympic Winter Games. J Allergy Clin Immunol 2000, 106:267–271.
Young, A. J. Homeostatic responses to prolonged cold exposure: human cold acclimatization. In: Handbook of Physiology: Environmental Physiology, M. J. Fregly and C. M. Blatteis (Eds.). Bethesda, MD: American Physiological Society, pp. 419-438, 1996.
by
xxkeziaxx (student)
