Heat-related illnesses vary from relatively minor conditions such as heat rash and cramps to more serious and life threatening conditions such as heat stroke (Davis, 1997). The majority of heat-related mortalities in adults occur during heat waves where affected individuals such as the chronically ill or elderly lack the physiological capacity to adequately respond to acute heat exposure (McGeehin and Mirabelli, 2001). Pre-pubertal children may also be susceptible to developing heat-related illness due to the physiological restrictions discussed below. Individuals undertaking strenuous physical activities are also at an increased risk due to heat generated by muscular contraction (Shapiro and Seidman, 1990). Therefore, physically active pre-pubertal children are at the most risk of being affected by the development of heat-related illnesses such as heat exhaustion and exertional heat stroke (Davis, 1997; Shapiro and Seidman, 1990).

In functional terms, heat exhaustion represents an inability to continue exercising in hot environments due to hypohydration and cardiovascular responses being unable to cope with the exercise workload (Armstrong et al., 1996). Typically, heat exhaustion results in T_C > 39 ^oC but < 40.5 ^oC associated with heat stroke ( Barrow and Clark, 1998; Davis, 1997; Khosla and Guntupalli, 1999). Additional symptoms of heat exhaustion are displayed in Table 1. Failure to discontinue the progression of these symptoms can lead to the onset of heat stroke, the most serious heat-related syndrome with loss of consciousness occurring in the majority of cases (Barrow and Clark, 1998; Shapiro and Seidman, 1990; Wexler, 2002). Heat stroke may be fatal if untreated and can be divided into two categories: exertional or classical. Classical heat stroke is a condition primarily affecting the elderly, chronically ill and very young (infants to preschool aged children) during heat waves and results from an inability to dissipate passive thermal loads (Davis, 1997). Exertional heat stroke develops as a result of excessive heat production from muscular contractions during strenuous exercise in hot environments (Davis, 1997). Unlike classical heat stroke, the onset of exertional heat stroke is predominantly sporadic and sudden (Shapiro and Seidman, 1990).Symptoms of classical and exertional heat stroke are displayed in Table 1.

Heat exhaustion can develop as a consequence of severe water loss (> 3% body mass) resulting from prolific sweating in response to heat stress (Armstrong et al., 1996; Bross et al., 1994). The relative magnitude of water loss and potential for hypohydration are similar between pre- pubertal children (10 - 12 yr) and adults as both often fail to ingest sufficient fluids ad libitum during exercise (Bar-Or et al., 1980; Meyer and Bar-Or, 1994). Major consequences of hypohydration include accentuated reduction in blood volume (haemoconcentration) (Harrison, 1986), increased cardiovascular strain due to diminished cardiac filling resulting in reduced stroke volume (SV) and an elevated T_C (Sawka et al., 1992). One study found, elevated rectal temperatures (T_RE) correlated well (r = 0.65) with the hydration status of 10 - 12 yr boys during an intermittent cycle protocol (45% VO_2max) in 39 ^oC and 45% relative humidity (%RH). In this study, the rate T_RE increased in the hypohydrated boys (0. 28^oC) was similar to obese adults (~0.2^oC) but twice that of lean adults (~0.1^oC) per 1% initial body mass loss (Bar-Or et al., 1980). However, under greater thermal stress (41 - 43^oC and 18 - 20%RH), pre-pubertal children (9.1 - 12.2 yr) cycling at 50% VO_2max experienced greater increases in T_RE (0.7 - 0.8^oC) with smaller changes in body mass (0.09 - 0.29%) (Falk et al., 1992a; 1992b; Meyer et al., 1992).

Hypohydrated 10 - 12 yr boys (1 - 2% initial body mass) and girls (1.1 - 1.8% initial body mass) experienced reduced exercise tolerance when working between 30 - 45% VO_2max under hot, humid (35°C and 50 - 65%RH) (Drinkwater et al., 1977; Wilk et al., 2002) and hot, dry conditions (48°C and 10%RH) (Drinkwater et al., 1977). In adults, body mass loss of 1.9% can compromise athletic performance by up to 22% (Craig and Cummings, 1966) via reduced circulating blood volume, blood pressure, sweat production and peripheral blood flow (Armstrong et al., 1996; 1998). Further body mass losses may induce signs of heat exhaustion (5%), hallucinations (7%) and may result in heat stroke or death (10%) (Bar-Or et al., 1988). As pre-pubertal children experience a small absolute blood volume (Bar-Or et al., 1971) and greater reliance on peripheral blood flow for thermal load dissipation (Drinkwater et al., 1977; Falk et al., 1992b), they appear to be more prone to severe consequences of hypohydration compared to adults.

Homeostatic control over elevated body temperatures requires the human body to dissipate all additional heat produced or accumulated. Dry heat exchange resulting from radiation, conduction and convection throughout the body, and subsequently with the environment, account for ~75% of heat loss at rest under thermoneutral conditions (Fortney and Vroman, 1985). Dry heat exchange is dependent upon exposed surface area, passive flow along temperature gradients from hottest to coldest, and represents the dominant heat loss mechanism in pre-pubertal children (Bar-Or et al., 1971). The rate of heat exchanged is dictated by environmental characteristics including ambient dry-bulb temperature (T_DB), %RH, air movement and velocity as well as clothing, T_SK and skin wettedness (Pascoe et al., 1994).

Importantly, when ambient temperature equals or exceeds that of the skin, evaporation is the only mechanism for dissipating excessive heat loads (Berglund and Gonzalez, 1977). In contrast to dry heat exchanged via temperature gradients, the potential for evaporation is dictated by the water vapour pressure gradient between water amassed on the skin and that of the immediate ambient environment (Nadel, 1979). Wet bulb temperature (T_WB) and %RH represent the potential for evaporation to occur (Nadel, 1979). As T_WB approaches that of the skin or > 60%RH, the potential for efficient evaporation diminishes (Brotherhood, 1987; Binkley et al., 2002). Additionally, the velocity of surface air movement and geometry of the surface area also determine the effectiveness of evaporation (Saunders et al., 2005). However, the water vapour pressure of the air layer closest to the skin surface is the most influential factor determining evaporation rates (Gleeson, 1998). If sweat amassed on the skin is unable to evaporate it will accumulate and eventually roll off the body, resulting in minimal heat loss (Gleeson, 1998).

The ability of pre-pubertal children to regulate body tem-peratures in thermoneutral environments is similar to that of an adult albeit via differing routes (Bar-Or, 1989; Falk, 1998). However, this ability is deficient when exposed to extreme environments (Bar-Or et al. , 1988; Bar-Or, 1989; Haymes et al., 1974; 1975; Drinkwater et al., 1977; Falk, 1998). Thermoregulatory responses of pre-pubertal children differ from adults via several morphologic and physiological changes which occur during growth and maturation disadvantaging pre- pubertal children when exercising in hot and humid environments (Bar-Or, 1989; Falk, 1998). When compared to adults, pre-pubertal children have a greater surface-area-to-mass ratio (A_DM) (Bar-Or, 1989), differing body composition (Falk, 1998) and smaller absolute blood volume (Bar-Or et al., 1971; Drinkwater et al., 1977). Pre-pubertal children differ physiologically with a lower cardiac output (Q) (Bar-Or et al., 1971), greater metabolic heat production per kg body mass during work (Astrand, 1952) and a less efficient sweating mechanism (Bar-Or, 1989). These characteristics will be discussed in more detail below.