NaCl Supplementation appeared to Prevent EAMC in an NFL Player with High Sweat Sodium Losses and a History of Cramping Peduzzi C*, Fowkes Godek S†, Burkholder R*, Bartolozzi AR‡, Dorshimer G§: Philadelphia Eagles, Phila. PA, †The HEAT Institute at West Chester University, West Chester PA, ‡Pennsylvania Hospital, Phila. PA, §Delancy Medical Associates, Phila. Pa.

Background: A 25-year-old defensive lineman in the national football league (NFL) with a history of exercise associated muscle cramps (EAMC) during pre-season training camp was the subject of this case study. He was one of many players on this NFL team who had volunteered to participate in a series of on-going prospective research studies designed to evaluate thermoregulation and fluid/electrolyte balance in professional football players. This player had the following physical characteristics: height =191 cm, mass = 120 kg and body fat = 12% which was analyzed by air displacement plethysmography (BodPod). This athlete had a history of EAMC requiring intravenous saline treatment during pre-season training camp his rookie year in the NFL (2005) and then sustained 6 episodes of multi-site EAMC between 2nd and 10th day the following preseason (2006). The mean wet bulb globe temperature (WBGT) during the first week of 2005 was 79 ± 5 ⁰F and in 2006 was 80 ± 3 ⁰F. He was one of many players on this team who ingested a sensor that allowed core (intestinal) temperature (Tc) to be monitored (HQI) during the first 3 days of pre-season 2006. His mean maximal Tc in full-padded morning (AM) practices was 40 ºC (104 ºF) and in afternoon (PM) practices in shorts and shells was 39 ºC (102.2 ºF). His maximal Tc ranged over those 3 days from 38.5 ºC (101.3 ºF) to 41.1ºC (106 ºC). He was also a subject in a study designed to evaluate sweat sodium losses and therefore had an extensive sweat analysis performed. His daily sweat loss (liters) during practices was calculated by change in mass adjusted for urine produced and fluids consumed, and sweat rate was calculated by dividing by practice time in h. Additionally, a sweat sample was obtained, using standard research methodology from a sweat patch applied to the forearm, and subsequently analyzed for sodium concentration by flame photometry.

This player’s sweat rate was 2.48 l ∙ h-1 (daily sweat loss exceeded 11 liters), and his sweat sodium concentration was 85 mmol ∙ l-1 which is considered relatively high compared to the mean sweat sodium concentration (48 – 53 mm ∙ l-1 ) in college and professional football players. Consequently, the athlete lost over 21g of sodium (53 g NaCl or 10.7 tsp of table salt) in one day of two-a-day practices.

In response to his history of high daily sodium losses and EAMC the athlete was sodium supplemented during the first week of the 2007 training camp. At meals for the first 5 days he consumed low potassium fruit drinks with added table salt = 25 g of NaCl per day, which was estimated to replace about 50% of his daily sodium losses with the hope that the additional sodium requirements would be met by normal dietary intake. On day 6 his sodium supplementation regimen was decreased to 12.5 g of NaCl and then was discontinued on day 7.

This player practiced twice per day on days 2, 3, 4 and 6 and once in the AM of days 5 and 7 without incidence of EAMC. His average percent change in body mass (%Δmass) the first 7 days was 2.7% and 1.8% in AM and PM practices, respectively. After the AM practice on day 8, approximately 36 hr after the NaCl enhanced drinks were discontinued, the athlete sustained EAMC in multiple muscles (quadriceps, hamstrings, triceps, biceps and back). AM mean WBGT was 26.1 ± 2ºC days 2 through 7 and 26.4ºC on day 8.

Differential Diagnosis:

EAMC, heat cramps, metabolic alkalosis, hyperkalemia, hypochloridemia.

Treatment: An 18 gauge catheter was inserted into an anti-cubital vein and 10 cc of blood was drawn while the athlete in a state of active cramping. The blood was immediately analyzed in the on-site laboratory and revealed Na+ = 138 mmol ∙ l-1, K+ = 7.6 mmol ∙ l-1, Cl- = 98 mmol ∙ l-1, Hct = 52%, Hb = 17 mg ∙ dl-1 and lactate = 4.6 mmol ∙ l-1. The athlete was treated with 2 liters of IV fluids (saline and 5% dextrose) and ice application to the muscles that were cramping. EAMC resolved during fluid administration after which blood was again drawn and analyzed with the following results: Na+ = 138 mmol ∙ l-1, K+ = 4.5 mmol ∙ l-1, Cl- = 101 mmol ∙ l-1, Hct = 48%, Hb = 16.2 mg ∙ dl-1 and lactate = 2.4 mmol ∙ l-1. This player resumed the salt supplementation (~ 25 g NaCl per day) at his request and fully participated in all of the subsequent 6 practices over the next 4 days with no incidence of EAMC.

Uniqueness: We are unaware of any case study with extensive data related to history of EAMC (core temperature, sweat rate, sweat sodium losses and weight losses) including an intervention (NaCl replacement) which appeared to successfully prevent EAMC during the supplementation period. During EAMC, hyperkalemia, likely due to rhabdomyolysis and hypochloridemia are also of interest and require further study of the anion gap.

Conclusions: This case study suggests that sufficient NaCl replacement may be helpful in preventing EAMC although the exact reasons are still unknown. While many researchers and clinicians believe electrolyte imbalance is a causative factor in an athlete developing EAMC, sodium is the ion most frequently implicated. However Cl-, a passive ion not often thought to be important and therefore not typically studied, is highly correlated (r = .998) with sodium in sweat. Importantly, we reported significantly lower blood chloride in a group of football players while experiencing EAMC compared to after similar practices with no EAMC. Clinically low blood Cl- may play a role in reducing hyperpolarization of the alpha motor neuron thus allowing easier excitation. It is also possible that Cl- is being displaced by bicarbonate as a consequence of metabolic alkalosis. Regardless, replacement with simple table salt in amounts equal to at least 50% of sweat NaCl losses with minimal potassium intake may thwart EAMC in professional football players without contributing to the hyperkalemia we have often reported. Experimental data in professional football players who are supplemented with this amount of NaCl maintained normal blood electrolytes (sodium, potassium and chloride) throughout the first week of pre-season and experienced a significant increase in plasma volume. References

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