Exercise-associated hyponatremia in marathon runners: a two-year experience.

This study was conducted to better define the pathophysiology, risk factors, and therapeutic approach to exercise-associated hyponatremia. Medical records from all participants in the 1998 Suzuki Rock 'N' Roll Marathon who presented to 14 Emergency Departments (EDs) were retrospectively reviewed to identify risk factors for the development of hyponatremia. Hyponatremic patients were compared to other runners with regard to race time and to other marathon participants seen in the ED with regard to gender, clinical signs of dehydration, and use of nonsteroidal anti-inflammatory drugs (NSAIDs). An original treatment algorithm incorporating the early use of hypertonic saline (HTS) was evaluated prospectively in our own ED for participants in the 1999 marathon to evaluate improvements in sodium correction rate and incidence of complications. A total of 26 patients from the 1998 and 1999 marathons were hyponatremic [serum sodium (SNa) < or =135 mEq/L] including 15 with severe hyponatremia (SNa < or = 125 mEq/L). Three developed seizures and required intubation and admission to an intensive care unit. Hyponatremic patients were more likely to be female, use NSAIDS, and have slower finishing times. Hyponatremic runners reported drinking "as much as possible" during and after the race and were less likely to have clinical signs of dehydration. An inverse relationship between initial SNa and time of presentation was observed, with late presentation predicting lower SNa values. The use of HTS in selected 1999 patients resulted in faster SNa correction times and fewer complications than observed for 1998 patients. It is concluded that the development of exercise-associated hyponatremia is associated with excessive fluid consumption during and after extreme athletic events. Additional risk factors include female gender, slower race times, and NSAID use. The use of HTS in selected patients seems to be safe and efficacious.

Masters athletes: factors affecting performance.

In recent years there has been an increase in interest in issues related to the enhancement of the performance of the masters athlete. Many of the changes in health status that have been thought to be the normal result of aging have been found to be actually the result of a long-standing sedentary lifestyle. Thus, masters athletes may be able to increase their athletic performance to higher levels than what was once thought. Decreases in muscle strength thought to be the result of aging do not appear to be so. The masters athlete may be able to maintain and increase strength in situations where strength training has not been previously engaged in. However, the literature lacks longitudinal studies demonstrating improvements in strength with age in masters athletes who have maintained habitual strength training. Studies in the past have shown that aging results in changes in fibre type, with a shift towards a higher percentage of type I fibres. This again may be an adaptation to lack of use. Decreases in heart function and aerobic capacity appear to be immutable, but in the masters athlete the rate of this decrease can be slowed. The masters athlete has certain elevated nutritional needs over younger athletes. Degenerative joint disease, although effecting most persons as they age, is not a certain result of aging and disability as the condition is reduced in the active person. Some orthopaedic conditions are related to decreases in flexibility of soft tissues that appear to accompany the aging process. Performance improvement in the masters athlete requires the same commitment to hard training that it requires from younger athletes, with some modifications for changes that are associated with aging.

Mutagenicity of dieldrin in the Salmonella-microsome test.

Dieldrin was assayed in vitro for its mutagenic activity in several strains of S. typhimurium with and without Aroclor 1254 treated mouse liver homogenate (S-9M). The mutagenicity of the insecticide was expressed maximally in all strains in the presence of liver S-9M and less so in three strains without liver microsomes.