Many scientific studies have considered physiological aspects of swimming, but largely in the areas of endurance or strength and power. This thesis includes six studies that attempt to provide more information about the metabolic responses to single and repeated sprint swimming and the physiological mechanisms behind the limitation to sprint swimming performance. The first experimental chapter describes the metabolic responses to single and repeated sprinting in male and female swimmers. Peak blood lactate (male 18.7 and female 14.4 mmol 1-1;P <0.01) and ammonia (male 232.0 and female 154.3 ýtmol 1-1;P <0.05) values following repeated swimming (8 x 50 yards) were almost double those measured during a single 50 yards sprint and were significantly higher in males than females. It is likely that differences in body dimensions and composition between male and female swimmers account for the majority of the -12% performance differences and higher metabolic response in males than females. Energy contribution to single and repeated tethered swimming sprints was examined in chapter V. Determination of energy contribution by an accumulated oxygen deficit test found estimated anaerobic contribution of -67% in 30 s sprinting and -74%, -53%, -51% and -47% during four 30 s sprint bouts. These were much lower than values estimated previously and recommended to coaches and swimmers in popular swimming texts. Energy contribution to 55 s maximal tethered swimming in chapter VI found anaerobic contributions of -30-40%. Metabolic responses to Controlled frequency breathing (CFB) have been studied previously in endurance swimming, but not in splint swimming (chapter VI). There was increased hypercapnia, but no significant reduction in performance during 55 s maximal sprint tethered swimming between self-selected breathing and breathing every 10 strokes. Differences in metabolic responses (higher extraction of oxygen from inspired air and lower ventilation, oxygen consumption, carbon dioxide production and respiratory exchange ratio) suggest a greater efficiency during swimming with CFB. Swimmers who can train to overcome the urge to breath should not compromise performance, but benefit from avoiding an increase in drag resistance while turning the head to breath. Active recovery following intense swimming has been suggested to increase the speed of recovery and improve subsequent performance. Chapter VII illustrates that the timing and intensity of active recovery is crucial when prescribing repeated sets of repeated sprint training. Lower blood lactate was matched by a tendency for poorer performance in the trial using active recovery between repetitions. This demonstrates that the blood lactate concentration does not reflect the metabolic state of the muscle and therefore the ability to perform subsequent sprint swims. Chapters VIII and IX consider the effects of creatine supplementation on sprint swimming. No differences in single sprint swimming performance were found, but creatine supplementation improve times in a typical training set of 8x 50 yards by -4 s. Faster times recorded in the creatine group support the hypothesis that increasing resting levels of creatine and phosphocreatine will enhance recovery during repeated sprints. Supplementing with 3g creatine day-' for 22-27 weeks had no additional benefit to race performance than just 'loading' before the training period and immediately prior to the major swimming race of the year. It is likely that any enhanced training adaptation would have to be from creatine supplementation allowing swimmers to perform more training rather than just supplementation per se. The studies in this thesis describe the physiological and metabolic responses of elite male and female swimmers to single and repeated sprint swimming in detail for the first time. By manipulating breathing frequency during sprinting, metabolism altered but without compromising performance. Active recovery was successful in reducing blood lactate concentration, but performance was poorer. The blood metabolite and respiratory response to sprint training following interventions of this type allow us to determine the mechanisms behind the limitation to swimming performance. Creatine supplementation enhances repeated sprint swimming performance, but not training for success in competition. Results of this thesis suggest that phosphocreatine availability or energy supply are not limitations to sprint swimming training performance.