{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/16494"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/16494","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Effects of hypervolemia on arterial oxygenation in thoroughbred horses performing exercise simulating the second day of a 3-day equestrian event","abstract":"Exercising horses can lose in excess of 10-12 L/hour of fluid as sweat, and during prolonged exercise, effective circulating volume is diminished. During the second day of an equestrian 3-day event (3DE) there is only a limited opportunity for horses to consume fluids. Dehydration is, therefore, a critical issue for horses performing the second day of a 3DE, particularly if weather conditions are hot and/or humid. Pre-exercise hydration (hyperhydration or ‘fluid-loading’) schemes have been investigated to help maintain blood volume during exercise. However, it has been suggested that pre-exercise hyperhydration might adversely affect arterial oxygenation in horses exercising at ~55-60% of maximum oxygen consumption (Sosa Leon et al. 2002). Exercise induced arterial hypoxemia is not typically seen during moderate exercise in normal horses and hyperhydration (and hypervolemia) does not affect arterial oxygen tension or hemoglobin saturation during short term maximal exertion (Manohar et al. 2003). Studies were carried out on 7 Thoroughbred horses under control and hyperhydration conditions. Hyperhydration (and hypervolemia) was induced by administering NaCl (0.425 g/kg) via nasogastric tube 5 hours pre-exercise followed by free access to water. Two sets of experiments utilizing different treadmill exercise protocols were performed. The first (Protocol 1) simulated the second day of a mid-level 3DE and was identical to that of Sosa Leon et al. (2002). The second exercise test (Protocol 2) was shorter in duration but incorporated high intensity exercise known to induce arterial hypoxemia and hemoglobin de-saturation. Blood-gas tensions, hemoglobin saturation, and pH were measured pre-exercise and at various times throughout exercise. In addition, plasma protein concentration, hemoglobin concentration, blood lactate concentration, heart rate and core (pulmonary artery) body temperature were monitored during exercise. Sodium chloride administered as described induced plasma volume expansion estimated on the basis of change in plasma protein concentration of 11.3 ± 3.2% (SE) prior to exercise Protocol 1 and a 15.5 ± 1.1% (SE) increase prior to Protocol 2. Despite establishing significant hypervolemia, we were unable to demonstrate any effect of pre-exercise hyperhydration on arterial oxygen tension or hemoglobin saturation during either exercise test. Arterial CO2 tension, blood lactate concentrations, and pH were not affected by pre-exercise hyperhydration. In both exercise protocols, there was a reduction in the “arterial to mixed-venous blood O2 content difference” in the hyperhydrated treatment during much of the exercise protocol, that was likely offset by an increase in cardiac output.","abstract_html":"Exercising horses can lose in excess of 10-12 L/hour of fluid as sweat, and during prolonged exercise, effective circulating volume is diminished. During the second day of an equestrian 3-day event (3DE) there is only a limited opportunity for horses to consume fluids. Dehydration is, therefore, a critical issue for horses performing the second day of a 3DE, particularly if weather conditions are hot and/or humid. Pre-exercise hydration (hyperhydration or ‘fluid-loading’) schemes have been investigated to help maintain blood volume during exercise. However, it has been suggested that pre-exercise hyperhydration might adversely affect arterial oxygenation in horses exercising at ~55-60% of maximum oxygen consumption (Sosa Leon et al. 2002). Exercise induced arterial hypoxemia is not typically seen during moderate exercise in normal horses and hyperhydration (and hypervolemia) does not affect arterial oxygen tension or hemoglobin saturation during short term maximal exertion (Manohar et al. 2003). Studies were carried out on 7 Thoroughbred horses under control and hyperhydration conditions. Hyperhydration (and hypervolemia) was induced by administering NaCl (0.425 g/kg) via nasogastric tube 5 hours pre-exercise followed by free access to water. Two sets of experiments utilizing different treadmill exercise protocols were performed. The first (Protocol 1) simulated the second day of a mid-level 3DE and was identical to that of Sosa Leon et al. (2002). The second exercise test (Protocol 2) was shorter in duration but incorporated high intensity exercise known to induce arterial hypoxemia and hemoglobin de-saturation. Blood-gas tensions, hemoglobin saturation, and pH were measured pre-exercise and at various times throughout exercise. In addition, plasma protein concentration, hemoglobin concentration, blood lactate concentration, heart rate and core (pulmonary artery) body temperature were monitored during exercise. Sodium chloride administered as described induced plasma volume expansion estimated on the basis of change in plasma protein concentration of 11.3 ± 3.2% (SE) prior to exercise Protocol 1 and a 15.5 ± 1.1% (SE) increase prior to Protocol 2. Despite establishing significant hypervolemia, we were unable to demonstrate any effect of pre-exercise hyperhydration on arterial oxygen tension or hemoglobin saturation during either exercise test. Arterial CO2 tension, blood lactate concentrations, and pH were not affected by pre-exercise hyperhydration. In both exercise protocols, there was a reduction in the “arterial to mixed-venous blood O2 content difference” in the hyperhydrated treatment during much of the exercise protocol, that was likely offset by an increase in cardiac output.","abstract_has_math":false,"creators":["Tennent-Brown, Brett S."],"institution":"University of Illinois at Urbana-Champaign","degree_name":"M.S.","degree_level":"Thesis","degree_discipline":"VMS-Veterinary Clinical Medicine","degree_department":null,"school":null,"contributors":["Wilkins, Pamela A."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-06-22T19:46:37Z","date_published":"2010-06-22T19:46:37Z","updated_at":"2026-07-22T22:25:09Z","subjects":["Hypervolemia","exercise","horse","pulmonary functions"],"languages":["en"],"rights":["Copyright 2010 Brett S. 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However, it has been suggested that pre-exercise hyperhydration might adversely affect arterial oxygenation in horses exercising at ~55-60% of maximum oxygen consumption (Sosa Leon et al. 2002). Exercise induced arterial hypoxemia is not typically seen during moderate exercise in normal horses and hyperhydration (and hypervolemia) does not affect arterial oxygen tension or hemoglobin saturation during short term maximal exertion (Manohar et al. 2003). Studies were carried out on 7 Thoroughbred horses under control and hyperhydration conditions. Hyperhydration (and hypervolemia) was induced by administering NaCl (0.425 g/kg) via nasogastric tube 5 hours pre-exercise followed by free access to water. Two sets of experiments utilizing different treadmill exercise protocols were performed. The first (Protocol 1) simulated the second day of a mid-level 3DE and was identical to that of Sosa Leon et al. (2002). The second exercise test (Protocol 2) was shorter in duration but incorporated high intensity exercise known to induce arterial hypoxemia and hemoglobin de-saturation. Blood-gas tensions, hemoglobin saturation, and pH were measured pre-exercise and at various times throughout exercise. In addition, plasma protein concentration, hemoglobin concentration, blood lactate concentration, heart rate and core (pulmonary artery) body temperature were monitored during exercise. Sodium chloride administered as described induced plasma volume expansion estimated on the basis of change in plasma protein concentration of 11.3 ± 3.2% (SE) prior to exercise Protocol 1 and a 15.5 ± 1.1% (SE) increase prior to Protocol 2. Despite establishing significant hypervolemia, we were unable to demonstrate any effect of pre-exercise hyperhydration on arterial oxygen tension or hemoglobin saturation during either exercise test. Arterial CO2 tension, blood lactate concentrations, and pH were not affected by pre-exercise hyperhydration. 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Hyperhydration (and hypervolemia) was induced by administering NaCl (0.425 g/kg) via nasogastric tube 5 hours pre-exercise followed by free access to water. Two sets of experiments utilizing different treadmill exercise protocols were performed. The first (Protocol 1) simulated the second day of a mid-level 3DE and was identical to that of Sosa Leon et al. (2002). The second exercise test (Protocol 2) was shorter in duration but incorporated high intensity exercise known to induce arterial hypoxemia and hemoglobin de-saturation. Blood-gas tensions, hemoglobin saturation, and pH were measured pre-exercise and at various times throughout exercise. In addition, plasma protein concentration, hemoglobin concentration, blood lactate concentration, heart rate and core (pulmonary artery) body temperature were monitored during exercise. Sodium chloride administered as described induced plasma volume expansion estimated on the basis of change in plasma protein concentration of 11.3 ± 3.2% (SE) prior to exercise Protocol 1 and a 15.5 ± 1.1% (SE) increase prior to Protocol 2. Despite establishing significant hypervolemia, we were unable to demonstrate any effect of pre-exercise hyperhydration on arterial oxygen tension or hemoglobin saturation during either exercise test. Arterial CO2 tension, blood lactate concentrations, and pH were not affected by pre-exercise hyperhydration. 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