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In contrast to muscle cramps that are brought on by muscle overload or fatigue, exertional heat cramps seem to be prompted by extensive sweating and a significant sweat-induced whole-body sodium deficit. As a result of a consequent contracted interstitial compartment, axon terminals of selected motor neurons can become hyper-excitable and spontaneously discharge. Barely detectable muscle fasciculations or “twitches” in the affected muscles can rapidly progress to debilitating muscle cramps in just 20 to 30 minutes. To aid recovery, salt (NaCl) and water lost from sweating should be sufficiently replaced so as to restore the extracellular volume and interstitial fluid spaces. Sweat sodium, chloride, and fluid losses incurred during training and competition need to be closely matched by daily salt and fluid intake, in order to prevent an excessive sodium deficit, maintain sufficient fluid balance, and avoid exertional heat cramps.

A 17-year-old, nationally ranked, male tennis player (AH) had been experiencing heat cramps during tennis match play. His medical history and previous physical exams were unremarkable, and his in-office blood chemistry profiles were normal. On-court evaluation and an analysis of a 3-day dietary record revealed that AH's sweat rate was extensive (2.5 L · hr⁻¹) and that his potential daily on-court sweat sodium losses (89.8 mmol · hr of play') could readily exceed his average daily intake of sodium (87.0-174.0 mmol · day⁻¹). The combined effects of excessive and repeated fluid and sodium losses likely predisposed AH to heat cramps during play. AH was ultimately able to eliminate heat cramps during competition and training by increasing his daily dietary intake of sodium.

In the present study, the effects of an increased daily dose of a dietary supplement (ATP-E, 0.2 g · ${\text{kg}}^{-1}$ · ${\text{day}}^{-1}$ ) on Wingate test performance were examined in 12 men (21 ± 1.6 years) prior to and following 14 days of supplement and placebo ingestion. A double-blind and counterbalanced design was used. Results revealed higher (p < .007) preexercise blood ATP (95.4 ± 10.5 μmol · ${\text{dl}}^{-1}$ ) for the entire group following 14 days of ATP-E ingestion compared to placebo measures (87.6 ± 10.9 μmol · ${\text{dl}}^{-1}$ ). Mean power (667 ± 73 W) was higher (p < .008) after 14 days of ATP-E ingestion versus placebo (619 ± 67 W). Peak plasma lactate was lower (p < .07) after 14 days of ATP-E ingestion (14.9 ± 2.8 mmol · ${\text{L}}^{-1}$ ) compared to placebo (16.3 ± 1.6 mmol · ${\text{L}}^{-1}$ ). These data suggested that the improvement in 30-s Wingate test performance in this group may be related to the increased dose of ATP-E.

Twenty (12 male and 8 female) tennis players from two Division I university tennis teams performed three days of round-robin tournament play (i.e., two singles tennis matches followed by one doubles match per day) in a hot environment (32.2 ± $1.5{}^{°}\text{C}$ and 53.9 ± 2.4% rh at 1200 hr), so that fluid-electrolyte balance could be evaluated. During singles play, body weight percentage changes were minimal and were similar for males and females (males -1.3 ± 0.8%, females -0.7 ± 0.8%). Estimated daily losses (mmol · ${\text{day}}^{-1}$ ) of sweat sodium (Na⁺) and potassium (K⁺) (males, ${\text{Na}}^{+}$ 158.7, ${\text{K}}^{+}$ 31.3; females, ${\text{Na}}^{+}$ 86.5, ${\text{K}}^{+}$ 18.9) were met by the players' daily dietary intakes (mmol · ${\text{day}}^{-1}$ ) of these electrolytes (males, ${\text{Na}}^{+}$ 279.1 ± 109.4, ${\text{K}}^{+}$ 173.5 ± 57.7; females, ${\text{Na}}^{+}$ 178.9 ± 68.9, ${\text{K}}^{+}$ 116.1 ± 37.5). Daily plasma volume and electrolyte (Na⁺, ${\text{K}}^{+}$ ) levels were generally conserved, although, plasma [Na⁺] was lower (p < .05) on the morning of Day 4. This study indicated that these athletes generally maintained overall fluid-electrolyte balance, in response to playing multiple tennis matches on 3 successive days in a hot environment, without the occurrence of heat illness.