Introduction: Respiratory symptoms are common among competitive swimmers. The most respiratory symptoms have been reported during very hard, race pace swimming. lt has been suggested that extreme strain with high pulmonary load would have an effect on development of sthmatic symptoms among athletes. The aim of the study was to examine pulmonary ventilation during very hard intensity, race pace swimming in elite competitive swimmers. Methods: Fourteen healthy elite swimmers, 7 females and 7 males, 18 years old, with training history of 9 years on the average were studied. Maximal ventilation (VEmax) was measured breath-by-breath during race-pace swimming. Maximal voluntary ventilation (MVV) was measured on land (L) and in water (W) in prone swimming body position. MVV was also estimated (cMVV) by calculating 35·FEV 1 on Land W. Measurements were performed by portable Cosmed K4b 2 analyzer. Snorkel build for swimming testing was attached to the breathing valve. Results: During the swim, VEmax was 106 (4) l·min-1in females and 136 (14) l·min-1in males. Breathing reserve (Br) was 27% in females and 25% in males when LcMVV. However with WcMVV, Br decreased to 24% in females and 20% in males in comparison to LcMVV. When pooled data on LMVV, WMVV, LcMVV and WcMVV were examined, WMVV correlated the most with VEmax. During the race pace swim VEmax reached 76% in females and 80% in males of the calculated maximal voluntary ventilation in water. Discussion: Results indicate that during the race pace intensity swimming, the extremely high load on the pulmonary function induces asthmatic respiratory symptoms in elite competitive swimmers. The observation that the VEmax was 76-80% of the WcMVV, was higher than the target ventilations used to detect respiratory symptoms in physical exercise at 60% of LcMVV. Therefore, we suggest that the special effects of swimming and water environment on pulmonary function should be taken into account when analyzing respiratory hazards in elite swimmers.
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