3.1 Exercise-dependent, dehydration-induced hyperthermia

Heat production during exercise is 15-20 times greater than at rest, and it is sufficient to raise core body temperature by 1°C every 5 minutes if there are no thermoregulatory adjustments [25]. The body's multiple mechanisms for heat dissipation to prevent significant hyperthermia include conduction, convection, evaporation and radiation. As ambient temperature rises above 20°C, the contributions of conduction, convection and particularly radiation, become increasingly insignificant with the bulk of the heat dissipation during exercise resulting from evaporation as sweat. In hot, dry conditions, evaporation may account for as much as 98% of dissipated heat. Sweat evaporation leads to dehydration, which increases body temperature [25].

Any factor that limits evaporation, such as high humidity or dehydration will have profound effects on physiological function, athletic performance, and risk for heat illness [27]. There are five common types of heat illness, the milder forms including heat edema, heat cramps, heat syncope, and heat exhaustion. The most severe form of heat illness is heat stroke [28].

The milder forms of heat illness are widely underreported and underdiagnosed [25]. The symptoms go from none to fatigue, mental confusion, nausea, and vomiting with the signs beginning with peripheral edema developing to muscular spasm, loss of consciousness, hypotension and elevated core temperature up to 40.5°C [25].

Heat stroke is defined as a condition in which body temperature is elevated to a level that causes damage to body tissues, giving rise to a characteristic clinical and pathological syndrome that affects multiple organs [29]. Distinguishing features of heat stroke are marked core body temperature elevations greater than 40.5°C, failing sweating mechanisms, often complete cessation of sweating, and moderate to severe mental status impairment. It is a medical emergency in which total thermoregulatory failure will not reverse without external cooling measures and the mortality rates may exceed 10% [25].

3.2 Exercise-dependent dehydration-induced ischemia

Blood flow to central tissues (gut and liver) is reduced during exercise by almost 80%, at 70% of VO_2max [7]. Such decreased splanchnic blood flow and oxygen supply may induce changes in nutrient absorption, motility and the mucosal integrity of the GI tract, resulting in GI complaints [30]. GI distress has been reported to be common among 30%-50% of endurance athletes, especially during marathons, triathlons and other endurance events. The symptoms seem to occur more often during competition in a warm environment [30] in the presence of systemic dehydration and lower plasma volume [8]. Long-lasting high-dose creatine supplementation (80 g/day during four months) is reported to lead to acute renal failure when associated with exhausting strength exercises and related lower plasma volume [31]. However, few or no adverse effects are observed when taking the recommended dose of creatine (10 g/day) [32, 33].

3.3 Exercise-dependent ischemia-induced GI distress

Serious gut underperfusion often leads to shock-induced mucosal damage and invasion of gram-negative intestinal bacteria and/or their toxic constituents (endotoxins) into the blood circulation [36]. Elevated plasma endotoxin concentrations were found in 81% of ultramarathoners (90 km), with 2% presenting extremely high values [37].

Reduced GI blood flow induced by strenuous exercise makes the gut mucosa susceptible to ischemic injury, increases mucosa permeability and enhances hidden blood loss, as well as the translocation of protective microbiota and endotoxin generation. It is known that mucosal ischemia depletes cellular ATP leading to cell death and mucosal inflammation [11, 38]. Hence, strenuous exercise and dehydration states would be the causes of GI symptoms reported by 70% of athletes, and gut ischemia would be the main cause of nausea, vomiting, abdominal pain and (blood) diarrhea [3].

In an extensive literature review using an evidence-based approach, the risk factors for exercise-induced GI tract symptoms were dehydration (body weight loss > 4% during or after exercise), being a female, younger age, high-intensity exercise, vertical impact sports and medicine use. Poor conditioning, dietary factors and previous abdominal surgery are risk factors with weak evidence that was not well supported [39].

4.1 Fluid volume

The maximum rate of intestinal absorption is 0.5 L/hour when cycling at 85% VO_2max [8]. It was estimated that ~ 0.9L remained in the stomach and intestine at the end of exercise, and subjects complained about abdominal fullness. The intake of large volumes may not be advantageous [8], because no enhance in performance is observed [41, 42].

Fluid delivery during exercise represents the integration of GE and intestinal absorption. GE of liquids is regulated by the interaction of gastric volume and feedback inhibition, including nutrient-induced duodenal feedback. This occurs in such a way that the GE rate at any given moment represents the balance between feedback inhibition from the small intestine and the stimulatory effect of gastric volume. It is this balance that is responsible for the inverse relationship between beverage CHO content and GE rate [43].

Fluids empty from the stomach in an exponential manner with an initial rapid emptying phase. In fact, one of the major stimulants of GE is the volume in the stomach with a positive relationship between stomach volume and rate of emptying from the stomach. The absorption of water in the intestine is primarily passive, where water passes across the intestinal membrane due to an osmotic gradient [8].

4.2 Fluid composition

In order to determine the effect of osmolality on intestinal (duodenum and/or jejunum) fluid absorption of an orally fluid-replacement beverage intake containing 6% carbohydrate, Gisolfi et al (1998) [44] formulated groups of fluid replacement as hypo, iso or hypertonic with water as placebo. Fluid absorption was given during 85 min of cycling exercise (63.3% VO_2max) in a mild environment (22°C). There were no differences between groups in GE, total fluid absorption, urine production or plasma volume variations. Water was absorbed faster from the duodenum than the jejunum. It was concluded that osmolality has only a modest effect on gastric emptying and that total fluid absorption of 6% CHO-beverage from the duodenum/jejunum during exercise, within 197-414 osmotic range, is not different from that of water.

The effectiveness of different carbohydrate solutions in restoring fluid balance in situations of voluntary fluid intake was examined in 1.99% body mass dehydrated (intermittent route) subjects [26]. Beginning 30 min after cessation of exercise, the subjects drank ad libitum for a period of 120 minutes. Drinks contained 31 mmol/L sodium as NaCl and either 0%, or 2% or 10% glucose, with osmolality of 74,188 and 654 mosm/kg respectively. No differences were observed in total fluid intake, urine output, net fluid balance or in the fraction of the drink intake retained. The authors concluded that in situations of voluntary fluid intake, hypertonic carbohydrate-electrolyte solutions are as effective as hypotonic carbohydrate-electrolyte solutions at restoring whole-body fluid balance [26].

Glucose is actively transported across the intestinal membrane, a process aided by the inclusion of sodium. Water co-transportation during this process is controversial; nevertheless, the addition of sodium and CHO to sports drinks is widely recommended to enhance water absorption [8]. The risks of exercise-induced fluid and electrolyte balance are considerably minimized if oral replacement products are used. If activity is prolonged beyond 60 minutes, then CHO sources and potassium should also be included in the ingested fluid [2].

During competition, optimal CHO concentration seems to be in the range of 5-8%, and athletes should aim to achieve a CHO intake of 60-70 g/hour. Athletes should attempt to limit body mass loss to 1% of body mass. In all cases, a drink should contain sodium (30-50 mmol/L) for optimal absorption and hyponatremia prevention. Post-exercise rehydration is best achieved by consuming beverages that have high sodium content (>60 mmol) in a volume equivalent to 150% of body mass loss [8].

There is convincing evidence that the limitation of 1.0-1.1 g/minute CHO oxidation is not at the muscular level, but most likely located in the intestine or the liver. Intestinal perfusion studies suggest that the capacity to absorb glucose is only slightly in excess of the observed entrance of glucose into the blood, and the absorption rate may thus be a factor that contributes to the limitations. The liver, however, may play an additional important role in that it provides glucose to the blood stream at a rate of only 1.0-1.3 g/min by balancing glucose from the gut and from glycogenolysis/gluconeogenesis. It is possible that when large amounts of glucose are ingested, absorption is a limiting factor, and the liver will retain some glucose and will thus act as a second limiting factor to exogenous CHO oxidation [8].

More recently, advice has been given for athletes engaged in moderate- intensity prolonged exercise to increase CHO intake in the form of multiple transportable carbohydrates (glucose plus fructose) to a rate as high as 90 g/hour (or 1.5 g/min), and this has been shown to increase exogenous CHO oxidation above a single CHO [43]. Furthermore, the intake of a glucose-fructose combined solution increases GE and fluid delivery when compared with a glucose-only solution. Additionally, the combined sugar attenuates heart-rate increase and results in lower rates of perceived exertion and lower loss of body weight than glucose alone or water [43]. Moreover, a solution intake with 1.2 g/min of maltodextrin + 0.6 g/min of fructose show higher carbohydrate oxidation (approximately 1.5 g/min) than 1.8 g/min of maltodextrin (alone) [45].

The effects of increasing carbohydrate (0%, 3%, 6% and 9%) and sodium (0, 20, 40, 60 mmol/L) content upon fluid delivery (using deuterium oxide water) were studied in healthy male seated (twenty-four) subjects. It was concluded that increasing the amount of sodium in a 6% glucose beverage did not lead to increases in fluid delivery and that fluid delivery was compromised when the carbohydrate beverage was increased above 6% [40].

When glucose is used as the CHO source, its concentration is limited to < 2.5% since higher concentrations may delay GE and fluid absorption. In general, the combination of different CHO sources should be > 5% to provide sufficient fuel for the maintenance of muscle performance during activity. However, total CHO concentrations are limited to < 10% since higher CHO content is associated with increased risk for GI distress (abdominal cramps, diarrhea and nausea) owing to the high osmolar load [2]. Hypertonic solutions tend to delay water absorption in the intestine as water instead flows into the intestine to dilute the solution before water is absorbed [8].

Additionally, there is contention as to whether hypertonic solutions reduce the GE rate [46]. However, energy density is considered to be more important in determining GE when solutions with an osmolality close to those normally found in sports drinks are used [8].

The rate of fluid absorptions is closely related to the CHO content of drinks with high CHO concentrations, thus compromising fluid delivery. Hence, a balance must be met between the goal of maintaining hydration status and providing CHO to the working muscle [8]. Slowed gastric emptying associated with high-intensity exercise is further slowed by the consumption of hypertonic carbohydrate beverages, usually given after running [38].

5.1 Hyponatremia

Electrolyte imbalance which is commonly referred to as "water intoxication" and results from hyponatremia (low plasma sodium) due to excessive water intake has occasionally been reported in long-distance triathletes [47]. The symptoms of hyponatremia are similar to those associated with dehydration and include mental confusion, weakness and fainting. Such symptoms are usually seen at serum sodium concentrations of 126-130 mmol/L. Below 126 mmol/L, seizures, coma and death may occur [8].

Because the symptoms of hyponatremia are so similar to those of dehydration, that condition may be dangerously misdiagnosed in endurance races athletes. The usual treatment for dehydration is oral and intravenous administration of fluids. If such treatment were to be given to a hyponatremic individual, the consequences could be fatal [8].

Hyponatremia may occur in a state of euhydration or even dehydration, but it is generally associated with fluid overload [47] and the cause is the fluid intake higher than sweat rate, that causes dilutional hyponatraemia [48]. Triathletes may often develop hyponatremia without displaying symptoms [8].

In order to prevent hyponatremia, avoiding overhydration and informing athletes about the potential dangers of drinking too much water are recommended. When compared with water, a sodium-containing drink attenuated the drop in plasma sodium [49]. However, when salt tablets (700 mg/h) were given to ironmen-distance triathletes, there was no evidence that sodium intake significantly influenced changes in plasma sodium concentration or plasma volume more than did fluid replacement alone [50].

Nutritional Recommendations