A novel strategy to reduce exercise-induced hyperthermia in different age groups
- LEOZ ABAURREA, Iker
- Roberto Aguado Jiménez Director/a
Universidad de defensa: Universidad Pública de Navarra
Fecha de defensa: 06 de octubre de 2016
- Juan del Coso Garrigós Presidente/a
- Miguel Angel Barajas Vélez Secretario/a
- Cristina Granados Domínguez Vocal
Tipo: Tesis
Resumen
Exercise and heat stress The limitations to exercise performances have been a matter of interest that have fascinated humans throughout history. There are a number of factors that may influence the capacity of an individual to perform prolonged exercise, one of which is ambient temperature.1 In 1916, Lee and Scott 2 were the first scientists who observed an early fatigue in cats during exercise in a hot environment. Although their results were inconclusive, they were the first authors to report that exercising in the heat leads to a premature fatigue. Following research done in humans, demonstrated that endurance could be impaired in hot environments when compared to temperate climates.1, 3, 4 As an example, Parkin at al.4 investigated the effects of three different ambient temperatures (3, 20 and 40ºC) on exercise performance during fatiguing submaximal exercise (70% peak pulmonary oxygen uptake). Authors observed a progressive decline in exercise as ambient temperature increases. However, the reasons for a diminished exercise performance in hot environment compared to the rest of ambient temperatures is still debated and it is considered to be multifactorial, as it will depend on the type of exercise, training status, motivation of the participants, acclimatization and/or hydration status.8 During the last century there has been a great effort from the scientific community in order to understand the complexity of hyperthermia-induced fatigue. It is considered that different physiological factors might limit maximal intensity exercise than submaximal intensity aerobic performance when exercising in the heat.5 For maximal intensity exercise, cardiovascular mechanisms related to oxygen delivery are likely to limit aerobic performance in the heat.6 High skin temperatures and the resulting elevation in skin blood flow are associated with impaired cardiac filling, reductions in end-diastolic volume and heart rate increases as an attempt to compensate a decreased stroke volume.5 Whereas for submaximal exercise, it seems to be more complex and interaction between several physiological factors may be responsible for inducing premature fatigue during prolonged exercise in the heat.7, 8 One of these physiological factors, a critically high level of body temperature ~40ºC, was proposed by Nielsen et al.3 to be the main factor limiting endurance performance in hot environments. Thirteen trained participants, exercised at 60% peak oxygen uptake at an ambient temperature of 40ºC and 10% relative humidity for 9-12 consecutive days and observed that fatigue occurred when participants reached a core temperature of 39.7ºC despite large improvements in exercise performance (from 48 to 80 minutes). Six years later, Gonzalez-Alonso and colleagues,9 observed similar results in seven trained cyclists who exercised at 60% maximal oxygen uptake in the heat (40ºC) until volitional exhaustion. Again, all participants fatigued at an identical level of hyperthermia (esophageal temperatures of 40.1-40.2ºC), regardless different initial temperatures. Authors from both studies concluded that a high body temperature, per se, was the main factor for exhaustion during exercise in heat stress. These studies formed the basis of the belief that high core temperature might be important for impairing exercise performance. Temperature regulation mechanisms Maintaining thermal balance in a hot environment is not only critical to preserving life and reducing heat illnesses; it is also essential in order to prevent decrements in athletic performance.11 It is well known that more than 75% of the energy that is generated by skeletal muscle substrate oxidation is released as heat.10 In order to promote heat loss, excess heat is transported from the core to the skin and then to the environment. Once the metabolic heat is transferred to the skin, there are various ways in which it can be lost to the environment, including radiation, conduction, convection and evaporation.10 During rest in a thermoneutral environment, radiation accounts for approximate 60% of total heat loss, conduction and convection for 15% and evaporation for 25%. These percentages will change during exercise, where evaporation will be the main mechanism of heat loss. According to the heat balance equation, when heat gain exceeds heat loss, body heat storage increases, elevating body temperature. During fixed-intensity (constant power) exercise, metabolic heat production is constant, and therefore, heat loss is limited only to autonomic responses.12 Consequently, core body temperature rises until heat balance is achieved as indicated by a ‘plateau’ in core temperature.13, 14 However, during fixed-intensity exercise in a hot environment, the heat balance is impossible to achieve; therefore, core temperature will rise linearly until exhaustion occurs. The inability to continue exercising in a hot environment is directly associated with the failure to achieve heat balance as heat exhaustion is accompanied by high core temperatures and an increased challenge for the cardiovascular system to simultaneously meet the demands for both the working musculature and temperature regulation.12 Aging: A risk factor for heat stress The ability to physiologically maintain body core temperature during heat stress becomes compromised with age.15 Individuals over the age of 60 years are the most vulnerable population during heat waves.16 Adults in this age group experience greater thermal strain during passive heat exposures 17, 18 and this could be heightened when exercising in the heat.19 Furthermore, age-related reductions in whole-body heat loss capacity are evident when exercising in hot environments.20, 21 This progressive reduction in the thermoregulatory ability can be associated with reduced sweat gland outputs, decreased skin blood flow, smaller increase in cardiac output and/or less redistribution of blood flow from renal and splanchnic circulations.22 Moreover, the problem can be exacerbated by the decreases in overall physical fitness and increases in body adiposity that may accompany aging, and experts have suggested that, in combination, these age-related changes in thermoregulatory and cardiovascular function can decrease the body’s ability to maintain body core temperature at safe levels, especially during extended exposure to heat or to physical activity in the heat.19 However, older adults up to the seventh decade of life and who are well trained, can safely complete the same relative workloads, comparing to moderately trained young men, without an increased risk of heat stress or heat stroke.23 Conversely, older adults show a decreased ability to sense and adapt to dehydration. In physiology studies in which dehydration was induced through heat exposure alone, through physical activity in the heat or through hypertonic saline infusion, healthy older individuals displayed lower subjective levels of thirst, decreased plasma volume and reduced water intake while dehydrated relative to younger counterparts.19 Furthermore, recovery from dehydration is prolonged in older adults, which may exacerbate their risk of heat-related injuries during extended periods of heat exposure. Strategies to reduce hyperthermia Over the last decade, there has been an increasing interest in designing intervention strategies to reduce and/or delay increases in core temperature and therefore enhance exercise performance. This topic is, this year again, becoming relevant with such an important sport event as it is Rio 2016 Olympics, where it is expected to reach temperatures of up to 30ºC and 60% relative humidity. According to the review by Wendt and colleagues,10 there are two main strategies that have been proven to be particularly effective in reducing health problems and performance decrements associated with hot environments: heat acclimatization and rehydration. In recent years, many other different strategies have been put in practice in order to prevent and/or delay increases in core temperature. Examples include ice-water immersion, ice-pack application, continual dousing with water combined with fanning,24 ice slurry ingestion 25 or the use of compression garments 26 to name a few. Compression garments. Studies on compression garments have recently emerged although fundamental effects on thermoregulatory strain remain equivocal.27 Claims from manufacturers include enhanced comfort perception,28 increased muscle blood flow and/or enhanced lactate removal.29 Further, recent developments in these garments have led to claims of thermoregulatory benefits attributed to increased heat dissipation as a result of improved sweat efficiency. However, this remains a contentious issue, as there remains a lack of research supporting these statements. While the use of lower body compression garments seems to be widely studied,26, 28, 30-32 there is limited research regarding the effects of wearing upper body compression garments. It has been shown that when male athletes exercise at 55% and 75% of the maximal oxygen consumption in moderate warm conditions (25ºC and 50% relative humidity), the highest sweat rates occur on the central (upper and mid) and lower back.33 As the evaporation of the sweat from the skin surface is the main mechanism to reduce heat storage during exercise, clothing designs that facilitate the heat dissipation in the upper body through compression may lead to lower body temperature increments and therefore delay the appearance of hyperthermia during exercise. References 1. Galloway SD, Maughan RJ. Effects of ambient temperature on the capacity to perform prolonged cycle exercise in man. Med Sci Sports Exerc. 1997 Sep;29(9):1240-9. PubMed PMID: 9309637. 2. Lee FS, Scott EL. The action of temperature and humidity on the working power of muscles and on the sugar of the blood. American Journal of Physiology -- Legacy Content. 1916 1916-05-01 00:00:00;40(3):486-501. 3. 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