Exercise in the Heat and Acclimatization

This is an assignment I wrote at university, five years ago. For those that don’t know I studied Exercise Science. I came across it today looking through some old documents, and thought it might be of interest to some of you. Exercise in the heat can cause a lot of issues, especially for athletes. It is very important to acclimatize and get used to the conditions. This discusses what happens to the body during exercise in the heat, and ways that you can acclimatize to the conditions. Beware that is reasonably scientific and cites all the references, so for those who prefer a shorter version…

you can download the 1 page summary here:

Exercise in the Heat Summary

or a power point I made of it here:

Exercise in the Heat and Acclimatisation Powerpoint

Exercise In The Heat And Acclimatization

http://www.flickr.com/photos/sashawolff/3461164440/

An aspect of performance that athletes, coaches and conditioning staff cannot control is the environment. A particular aspect of environment that concerns many athletes is heat. Many sports are exposed to performance in the heat. It poses a complicated challenge for the body to perform at maximal potential. Exercise in the heat triggers a disturbance of the body’s internal environment. It must balance between preventing hyperthermia and maintaining an adequate fuel supply to the muscles. These are two significant competitive demands.

Temperature is regulated by the hypothalamus. The posterior hypothalamus is concerned with heat loss, and the anterior with heat gain, controlling sweating and skin blood flow responses. Messages are sent from the body to the hypothalamus and it acts accordingly (Mc Ardle, 2001). Heat loss can occur via four means. Radiation, Convection, Conduction and Evaporation (Casa, 1999). During exercise in a hot dry environment, 98% of the cooling can be attributed to evaporation (Casa, 1999).

ACUTE CHANGES DURING EXERCISE IN THE HEAT

During exercise in the heat the body must supply several demands, and as a result, several acute changes occur. The body needs to decrease the thermal load and dissipate heat, while also supplying the demands of the muscle. Acute changes are similar to those during exercise in normal temperature, however they are exacerbated in the heat.

As exercise intensity in the heat increases, core body temperature increases and the rate of rise is increased considerably (Casa, 1999). This is largely due to being hypo hydrated (Buono and Wall, 2000). Jentjens, Wagenmakers, and Jeukendrup, (2002) show during exercise in the heat after 60 minutes of exercise the body went from 37.1 to 39.1 degrees Celsius. As opposed to 36.9- 38 degrees in normal exercise conditions (Jentjens et al., 2002). High core temperatures lead to performance implications that will be discussed later.

Acute circulatory responses to heat occur at the start of exercise. Vasodilatation to the skin occurs in proportion to the degree of heat load, and the amount of blood supplied to the muscles is dictated by the intensity and duration of the exercise (Casa, 1999). Vasoconstriction of the visceral vascular system occurs to allow an increased blood supply to the active tissues (Casa, 1999). However, as the increase in demand to dissipate heat gets increasingly urgent during exercise in the heat, and thus, the sweat rate increases considerably resulting from a redirection of blood flow to the skin (Casa, 1999). An increased sweating rate contributes considerably to a decrease in plasma volume of the blood, causing a progressive decline in stroke volume (Casa, 1999; Sawka, Mountain and Latzka, 2001).  At the same time the muscles are demanding fuel as the exercise intensity is increased considerably in the heat. This hypovolemic state during exercise in the heat places two significant demands on the body (Casa, 1999).

The progressive decrease in plasma volume also causes heart rate to increase (Casa, 1999; Nielson, Strainge, Christensen, Warberg, and Saltin, 1997; Sawka, 2001). Stroke volume declines due to sweat and plasma volume losses. Heart rate is increased even further in an attempt to compensate for the drop in cardiac output (Casa, 1999). Heart rate cannot compensate enough for the drop in stroke volume, and as a result there is a progressive decline in cardiac output (Casa, 1999).

When intense exercise occurs these demands simply cannot be met. There is a progressively decreasing cardiac output, caused from loss of plasma volume and stroke volume and a decreased venous return (Casa, 1999). Thus resulting in reduced blood pressure. Ultimately, the importance of maintenance of blood pressure will take precedence over temperature regulation (Casa, 1999). Baroreceptors throughout the body are sensitive to this drop, messages are sent to the cardiovascular control centre in the medulla and skin and active muscle vasoconstriction occurs, preserving blood pressure (Casa, 1999; Mc Ardle, 2001). Less blood flow to the skin results in less evaporative cooling, leading to hyperthermia, and abnormally high core body temperature(Casa, 1999; Sawka et al., 2001).

It has also been reported that muscular changes associated with exercise in the heat are an increased rate of glycogen synthesis, compromised buffering capacity of the tissue, and a decreased substrate exchange (Casa, 1999). Jentjens, et al., (2002) reported a 25% increase in muscle glycogen usage during exercise in the heat a significant increase in CHO oxidation all round. Its been suggested that this is due to the increased secretion of epinephrine during exercise in the heat, and possibly related to the increased activity of key enzymes (Jentjens et al., 2002). Thus, core and muscle temperature influences substrate utilization heavily. (Jentjens et al, 2002; Parkin, Carey, Zhao, and Febbraio, 1999). This increase in CHO oxidation could be related to the increase in lactate production during exercise in the heat (Casa, 1999; Nielson et al., 1997). However it is also suggested that the rise is due to a decreased lactate up take by the liver because of reduced hepatic blood flow, and reduced muscle blood flow during intense exercise in the heat (Casa, 1999; Mc Ardle, 2001).

Hormonal responses are also elicited to regulate the body’s response to exercise in the heat. The fluid loss resulting from dehydration causes a hypovolemic, hyperosmolaric state, which stimulates the body to conserve water via secretion of hormones (Casa, 1999; Montain et al., 1997). Aldosterone is released from the adrenal cortical area of the kidney (Mc Ardle, 2001). This hormone acts on the renal tubules to reabsorb sodium, and thus decreasing the sodium concentration of sweat and conserving electrolytes (Mc Ardle, 2001). Vasopressin increases the ability of the collecting tubules in the kidney to retain fluid. Its main stimulus is increased plasma osmolarity (Maresh et al., 2003).

PERFORMANCE IMPLICATIONS OF EXERCISING IN THE HEAT

Exercising in the heat has been shown to place psychological and physiological strain on an athlete and has been widely documented that exercising in the heat can have performance implication on long endurance events (Casa, 1999; Maughn, 2004; Montain, 1997). There is debate whether or not detriments to performance during anaerobic events occur, however some literature suggests it may (Tucker, Rauch, Harley, and Noakes, 2004).

As exercise in the heat increases the demand on thermoregulatory mechanisms, large amounts of fluid are going to be lost. Up to 2-3 L/ Hour of fluid can be lost during exercise in the heat (Burke, 2001). This hypo hydration impairs thermoregulation and thus leads to hyperthermia. High core temperatures elicit several responses on the body that can implicate performances (Maughn, 2004).

It has been well documented that exercising in a hot environment increases the rate of glycogen utilization (Hargreaves and Hawley, 2003; Jentjens et al., 2002). This would suggest glycogen depletion and increase in lactate production as forms of fatigue. It has been well proved that the rate of lactate production increases during intense heat stress (Nielson et al., 1997; Parkin et al., 1999; Tucker, 2004). However, other theories of fatigue have become more favourable.  Parkin et al. (1999) noted that glycogen content within contracting muscle at fatigue during exercise in the heat is not reduced to the levels that are observed during exercise in a comfortable temperature. Suggesting another mechanism of fatigue could be encountered before lack of glycogen becomes an issue.

One of these is a suggested mechanisms is a critical core temperature(Buono and Wall, 2000; Nielson, Bidstrup, Gonzalez-Alonso, Christoffersen, 2001; Nielson and Nybo , 2003). Fatigue has been observed to occur at a temperature of around 40 degrees Celsius (Nielson et al., 1997). This suggests that exhaustive fatigue during exercise in the heat is associated with a critical core temperature, and even without exercising in the heat; if this temperature is reached fatigue will occur. As core temperature rises at a faster rate during exercise in the heat, this temperature would be reached earlier.

However, recently a study by Tucker et al. (2004) showed power output began to fall within the first 30% of maximal self-paced time trial in the heat. This suggested the decrease in performance was not associated with an altered temperature, heart rate or exercise perception. It suggests that fatigue occurs as part of the central regulation of skeletal muscle recruitment (Tucker et al., 2004). The body predetermines a level of recruitment and maintains this level to allow completion of exercise whilst thermal homeostasis is maintained (Tucker et al., 2004).

There are several ways an athlete can combat these adverse outcomes of exercising in the heat. A common method is the use of nutritional strategies. Burke (2001) and Sawka et al. (2004) suggest that hyper hydration may be able to prolong the onset of dehydration. A strategy discussed is the use of combined glycerol and water. Glycerol is used in conjunction with water to aid in fluid retention (Burke, 2001).  Burke (2001) suggests consistency in this strategy is unclear, however suggests that some studies have shown an increase in endurance performance. This method can cause nausea and gastrointestinal distress (Burke, 2001).

Hydration during exercise should be undertaken by all athletes, however it becomes of significant importance to an athlete exercising in high temperatures as hypo hydration can lead to hyperthermia (Casa, 1999). Burke (2001) suggests that only 30-70% of the bodies’ fluid losses can be countered by taking in fluids during exercise. It is shown that hypo hydration can negate the effects of a high aerobic fitness and heat acclimatization (Sawka et al., 2001). However it should be noted that when hydrating and re hydrating choice of drinks is very important. Drinks high in sodium should be consumed as taking in only water, can dilute the plasma osmolarity, which will reduce thirst (Sawka et al., 2001). This can lead the athlete to further dehydration (Burke, 2001). Sodium drinks also stimulate the retention of water, preventing dehydration (Burke, 2001).

Another strategy that is being used currently for athletes exercising in the heat is pre-cooling. The basis of pre-cooling is to reduce body temperature before exercise, thereby increasing the margin for heat production and increasing time to reach the suggested critical core temperature (Marino, 2002). It has generally been shown to increase time to exhaustion or increase the distance able to be traveled. In a review article Marino (2002) suggests the methods of pre-cooling are, ice vests / whole body cooling, cold air fans, or water immersion. However as is evident water immersion may not be practical for use in most sports. Marino (2002) showed that pre-cooling was able to improve performance ranging from 3-12%.

The wet bulb globe temperature is an estimation of heat stress. It has proved useful when determining cooling methods and necessities of them in modern sporting situations. It accounts for the levels of humidity, radiation, wind movement and ambient temperature (Sparling and Millard- Stafford, 1999).

This table adapted from Sparling and Millard- Stafford (1999) shows the Wet Bulb Globe temperatures and the risk each imposes to athletes.

ACCLIMATISATION

Acclimatisation is just one of many methods athletes use to reduce the effects of exercising in the heat. Repeated exposures to the heat results in adaptations within the body that make the athlete less susceptible to the demands imposed (Cheung and Mc Lellan, 1998; Mac Donald, 2002; Maughn, 2004; Yates, 2004).

There are conflicting views on the duration and strategies regarding heat acclimatisation, but it is generally thought that 7-14 days with one exercise session synonymous to the activity being performed later will produce adequate adaptations (Armstrong, 1998; Cheung and Mc Lellan, 1998; Mac Donald, 2002).The early adaptations which involve an improved control of cardiovascular function, will occur within 1-5 days (Armstrong, 1998; Hue, Voltaire, Galy, and Costes, 2004). Neilson (1997) suggests that acclimatisation must be synonymous with the activity being performed otherwise the adaptations will be inappropriate.

One of the most important adaptations that can occur is the increased maintenance of core temperature. As was suggested earlier core temperature is behind almost every theory of fatigue during exercise in the heat. By maintaining and decreasing core temperature at given intensities, it will enable an athlete to work at a higher intensity for longer (Maughn, 2004). Core temperature adaptation occurs as a result of thermoregulatory and cardiovascular adaptations, a lower core temperature means that less blood flow needs to be distributed to the skin, freeing more cardiac output for the working muscles. (Armstrong, 1998; Mac Donald, 2002; Yates, 2004).

During the first five days the improved control of cardiovascular function includes an expansion of plasma volume, a reduced heart rate at given exercise intensities, and a better distribution of cardiac output (Armstrong, 1998; Cheung and Mc Lellan, 1998). Plasma volume expansion results from an increase in plasma proteins and increased sodium retention. It will expand in the first few days and will sustain in the following days of acclimatisation if physiological strain is continually applied (Patterson, Stocks and Taylor, 2004). Aldosterone works to retain sodium at the renal tubules and is secreted in response in low sodium levels to mediate this response to heat acclimatisation (Mc Ardle, 2001). Plasma renin levels after acclimatisation are also elevated (Nielson et al., 1997). Both these hormones work to increase the plasma volume following heat acclimatisation. As cardiac output is equal to stroke volume, multiplied by heart rate, the heart rate of an individual will decrease relative to given exercise intensities. This occurs because plasma volume has a direct effect on stroke volume, and increasing the stroke volume will negate the need to increase heart rate as intensely to maintain cardiac output (Mc Ardle, 2001). The increase in cardiac output potential, means that the distribution is much more effective. Working muscles receive adequate supply, there is enough blood distributed to the skin for evaporative cooling and blood pressure will be maintained with more ease (Mac Donald, 2002).

There are several adaptations that occur via the sweating response to maximise evaporative cooling. Sweating begins at a lower core temperature, as there is a more effective distribution of cardiac output (Mac Donald, 2002). The rate of sweating also increases, and there is an increased distribution of active sweat glands (Cheung and Mc Lellan, 1998; Mac Donald, 2002). This adaptation could be slightly negative as dehydration could occur faster, however if hydration levels are adequate before and during activity it can be maintained (Hue et al., 2004). Despite contributing to dehydration, this adaptation boosts the dissipation of body heat via evaporative cooling. The process prevents body temperature rising critically and also allows for a reduction in skin blood flow as the body cools more effectively, increasing the blood available to supply active tissues (Mac Donald, 2002). Neilson (1997) suggests that these adaptations will be slightly different in humid environments, as the need for evaporative cooling changes.

An important adaptation regarding the sweating response is the decreased sodium concentration following heat acclimatisation (Sawka et al., 2001). Sodium lost through urine is also reduced. Heat acclimatisation improves the bodies ability to reabsorb sodium allowing athletes to have up to a 50% decrease in sweat sodium concentration (Sawka et al, 2001). Plasma aldosterone levels increase significantly during the early stages of acclimatisation, aldosterone helps to retain sodium in the renal tubules (Mc Ardle, 2001; Montain et al., 1997). Less sodium lost via the sweating response and urine production, means that the body is able to retain water better, improving the body’s thermoregulatory mechanisms.

Finally, in a slightly different adaptation, glycogen usage is decreased following acclimatisation (Casa, 1999). This response is synonymous with a reduction in plasma epinephrine levels (Jentjens et al., 2002; Mc Ardle, 2001). However, Neilson, (1997) showed no change in glycogen utilisation or lactate levels after acclimatisation suggesting that the intensity worked at to gain this adaptation must be high enough. This adaptation is important as it enables the athlete to spare glycogen and thus work longer.

Acclimatisation has the ability to increase performance by enabling an athlete to work at a higher intensity in the heat and delay the onset of fatigue, resulting in a lower rating of perceived exertion (Mac Donald, 2002; Yates, 2004). As better evaporative cooling occurs, the athlete is able to slow down the increase in core temperature and thus the onset of hyperthermia, and distribute cardiac output to working muscles more effectively(Mac Donald, 2002). It will also allow the athlete to delay dehydration, as there are better water retention capabilities and better thermoregulatory mechanisms. However, it should be noted that benefits of acclimatisation could be lost very quickly, which leads to a suggestion that heat acclimatisation programs should occur directly before the competition (Armstrong, 1998). Some adaptations can disappear within a few days, and most within a few weeks.

Exercise in the heat does pose a challenge to athletes, however it can be rectified following the use of strategies to prevent the onset of fatiguing factors. Acclimatisation is one of the most effective strategies however hydration is important as it can negate the adaptations that occur.

If you got through all that… congratulations!!

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