Open water swimming (OWS), either ‘wild’ such as river swimming or competitive, is a fast growing pastime as well as a part of events such as triathlons. Little evidence is available on which to base high and low water temperature limits. Also, due to factors such as acclimatisation, which disassociates thermal sensation and comfort from thermal state, individuals cannot be left to monitor their own physical condition during swims. Deaths have occurred during OWS; these have been due to not only thermal responses but also cardiac problems. This paper, which is part of a series on ‘Moving in Extreme Environments’, briefly reviews current understanding in pertinent topics associated with OWS. Guidelines are presented for the organisation of open water events to minimise risk, and it is concluded that more information on the responses to immersion in cold and warm water, the causes of the individual variation in these responses and the precursors to the cardiac events that appear to be the primary cause of death in OWS events will help make this enjoyable sport even safer.

Exercise increases mean body temperature ( Tbody) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE2 can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T body in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), V O2 max: 53 ml⅐ kg Ϫ1 ⅐ min Ϫ1 (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running (ϳ75% V O2 max) followed by 45-min cycling and 60-min seated recovery (28°C, 50% relative humidity). Plasma cytokine (TNF-␣, IL-10) concentrations were measured at rest and 30-min recovery. T body was similar at rest in PLAC (35.59°C) and NSAID (35.53°C) and increased similarly during running, but became 0.33°C (SD 0.26) lower in NSAID during cycling (37.39°C vs. 37.07°C; P ϭ 0.03), and remained lower throughout recovery. Sweating was initiated at T body of ϳ35.6°C in both conditions but ceased at higher T body in PLAC than NSAID during recovery [36.66°C (SD 0.36) vs. 36.39°C (SD 0.27); P ϭ 0.03]. Cardiac frequency averaged 6 ⅐ min Ϫ1 higher in PLAC (P Ͻ 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W ⅐ m Ϫ2 ; P ϭ 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.

Heat acclimation (HA) in air confers adaptations that improve exercise capabilities in hot and possibly temperate air. Swimmers may benefit from HA, yet immersion may constrain adaptation. Therefore, we examined whether warm-water swimming constitutes effective HA. In a randomized-crossover study, eight male swimmers swam 60 min/day on 7 days in 33°C (

No abstract

No abstract