Dehydration reduces blood flow to the human brain and increases oxygen extraction during prolonged exercise in humans

Steven Trangmar; Scott T Chiesa; Kameljit Kalsi; Niels H. Secher; Jose Gonzalez-Alonso

Dehydration reduces blood flow to the human brain and increases oxygen extraction during prolonged exercise in humans

Steven Trangmar, Scott T Chiesa, Kameljit Kalsi, Niels H. Secher, Jose Gonzalez-Alonso

Research output: Contribution to conference › Poster › peer-review

Abstract

Background: Dehydration accrued during prolonged exercise in the heat induces significant cardiovascular strain on the human body characterised by reductions in cardiac output, active muscle and skin blood flow, arterial blood pressure, vascular conductance and an overall impaired exercise capacity (1). However, it is presently unknown whether progressive dehydration during exercise in the heat reduces blood flow to the brain, thereby impairing aerobic metabolism. A hyperthermic-hyperventilation induced lowering of the PaCO2 may reduce blood flow to the brain, assuming that reductions in middle cerebral artery velocity (MCA V mean) reflect reductions in cerebral blood flow (CBF) (2,3,4,5). This study tested the hypothesis that progressive dehydration reduces CBF during prolonged exercise in the heat, in part through mechanisms associated with PaCO2, but without impairing brain VO2. Methods: We assessed blood flow in the internal carotid artery (CBF) using Doppler ultrasonography and middle cerebral artery velocity (MCA V mean) in ten cyclists (VO2PEAK: 59 ± 2 ml/kg/min), who performed two hours of prolonged cycling exercise in a warm environment (182 ± 6 W; 35°C), without fluids to induce moderate dehydration (DEH; 3.1 ± 0.3 % body mass loss). Subjects returned one week later to repeat the protocol, but with regular fluid ingestion to maintain hydration status (Control). Blood samples were obtained from the brachial artery and left internal jugular vein (DEH only) to measure a-vO2 differences and for the calculation of brain VO2. All data are mean ± SEM and were compared with ANOVA and Pearson correlation (SPSS). Results: During dehydration CBF and MCA V mean increased by 13 ± 3 % from rest to 30 min (p<0.05). Thereafter CBF declined to resting values with flow at 120 min significantly lower than at 30, 60 and 90 min (p<0.001). During control, CBF and MCA V mean increased from rest to 30 min and were subsequently maintained throughout exercise (Increase ≥ 25%, p<0.05). Reductions in CBF and MCA V mean during DEH were accompanied with significant increases (p<0.05) in a-vO2 diff resulting in an unchanged brain VO2. PaCO2 declined in accordance with flow and velocity (p<0.05) with changes in flow correlated to changes in PaCO2 (R2 = 0.75, p<0.001), supporting a role for PaCO2 in cerebral vasoconstriction. Discussion: The present findings show that progressive dehydration during prolonged exercise results in a marked reduction in CBF, whereas in control CBF did not decline. Compensatory increases in cerebral oxygen extraction allow for the maintenance of brain VO2 throughout exhaustive exercise. These findings suggest that a reduction in brain VO2 is an unlikely mechanism underpinning exercise capacity during prolonged, exhaustive exercise with dehydration.

Original language	English
Publication status	Published - Jul 2013

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http://www.physoc.org/proceedings/abstract/Proc%2037th%20IUPSPCC254

Cite this

@conference{8994cc1c6f244be794a4c1ef8e73e2c8,

title = "Dehydration reduces blood flow to the human brain and increases oxygen extraction during prolonged exercise in humans",

abstract = "Background: Dehydration accrued during prolonged exercise in the heat induces significant cardiovascular strain on the human body characterised by reductions in cardiac output, active muscle and skin blood flow, arterial blood pressure, vascular conductance and an overall impaired exercise capacity (1). However, it is presently unknown whether progressive dehydration during exercise in the heat reduces blood flow to the brain, thereby impairing aerobic metabolism. A hyperthermic-hyperventilation induced lowering of the PaCO2 may reduce blood flow to the brain, assuming that reductions in middle cerebral artery velocity (MCA V mean) reflect reductions in cerebral blood flow (CBF) (2,3,4,5). This study tested the hypothesis that progressive dehydration reduces CBF during prolonged exercise in the heat, in part through mechanisms associated with PaCO2, but without impairing brain VO2. Methods: We assessed blood flow in the internal carotid artery (CBF) using Doppler ultrasonography and middle cerebral artery velocity (MCA V mean) in ten cyclists (VO2PEAK: 59 ± 2 ml/kg/min), who performed two hours of prolonged cycling exercise in a warm environment (182 ± 6 W; 35°C), without fluids to induce moderate dehydration (DEH; 3.1 ± 0.3 % body mass loss). Subjects returned one week later to repeat the protocol, but with regular fluid ingestion to maintain hydration status (Control). Blood samples were obtained from the brachial artery and left internal jugular vein (DEH only) to measure a-vO2 differences and for the calculation of brain VO2. All data are mean ± SEM and were compared with ANOVA and Pearson correlation (SPSS). Results: During dehydration CBF and MCA V mean increased by 13 ± 3 % from rest to 30 min (p<0.05). Thereafter CBF declined to resting values with flow at 120 min significantly lower than at 30, 60 and 90 min (p<0.001). During control, CBF and MCA V mean increased from rest to 30 min and were subsequently maintained throughout exercise (Increase ≥ 25%, p<0.05). Reductions in CBF and MCA V mean during DEH were accompanied with significant increases (p<0.05) in a-vO2 diff resulting in an unchanged brain VO2. PaCO2 declined in accordance with flow and velocity (p<0.05) with changes in flow correlated to changes in PaCO2 (R2 = 0.75, p<0.001), supporting a role for PaCO2 in cerebral vasoconstriction. Discussion: The present findings show that progressive dehydration during prolonged exercise results in a marked reduction in CBF, whereas in control CBF did not decline. Compensatory increases in cerebral oxygen extraction allow for the maintenance of brain VO2 throughout exhaustive exercise. These findings suggest that a reduction in brain VO2 is an unlikely mechanism underpinning exercise capacity during prolonged, exhaustive exercise with dehydration.",

author = "Steven Trangmar and Chiesa, {Scott T} and Kameljit Kalsi and Secher, {Niels H.} and Jose Gonzalez-Alonso",

year = "2013",

month = jul,

language = "English",

}

TY - CONF

T1 - Dehydration reduces blood flow to the human brain and increases oxygen extraction during prolonged exercise in humans

AU - Trangmar, Steven

AU - Chiesa, Scott T

AU - Kalsi, Kameljit

AU - Secher, Niels H.

AU - Gonzalez-Alonso, Jose

PY - 2013/7

Y1 - 2013/7

N2 - Background: Dehydration accrued during prolonged exercise in the heat induces significant cardiovascular strain on the human body characterised by reductions in cardiac output, active muscle and skin blood flow, arterial blood pressure, vascular conductance and an overall impaired exercise capacity (1). However, it is presently unknown whether progressive dehydration during exercise in the heat reduces blood flow to the brain, thereby impairing aerobic metabolism. A hyperthermic-hyperventilation induced lowering of the PaCO2 may reduce blood flow to the brain, assuming that reductions in middle cerebral artery velocity (MCA V mean) reflect reductions in cerebral blood flow (CBF) (2,3,4,5). This study tested the hypothesis that progressive dehydration reduces CBF during prolonged exercise in the heat, in part through mechanisms associated with PaCO2, but without impairing brain VO2. Methods: We assessed blood flow in the internal carotid artery (CBF) using Doppler ultrasonography and middle cerebral artery velocity (MCA V mean) in ten cyclists (VO2PEAK: 59 ± 2 ml/kg/min), who performed two hours of prolonged cycling exercise in a warm environment (182 ± 6 W; 35°C), without fluids to induce moderate dehydration (DEH; 3.1 ± 0.3 % body mass loss). Subjects returned one week later to repeat the protocol, but with regular fluid ingestion to maintain hydration status (Control). Blood samples were obtained from the brachial artery and left internal jugular vein (DEH only) to measure a-vO2 differences and for the calculation of brain VO2. All data are mean ± SEM and were compared with ANOVA and Pearson correlation (SPSS). Results: During dehydration CBF and MCA V mean increased by 13 ± 3 % from rest to 30 min (p<0.05). Thereafter CBF declined to resting values with flow at 120 min significantly lower than at 30, 60 and 90 min (p<0.001). During control, CBF and MCA V mean increased from rest to 30 min and were subsequently maintained throughout exercise (Increase ≥ 25%, p<0.05). Reductions in CBF and MCA V mean during DEH were accompanied with significant increases (p<0.05) in a-vO2 diff resulting in an unchanged brain VO2. PaCO2 declined in accordance with flow and velocity (p<0.05) with changes in flow correlated to changes in PaCO2 (R2 = 0.75, p<0.001), supporting a role for PaCO2 in cerebral vasoconstriction. Discussion: The present findings show that progressive dehydration during prolonged exercise results in a marked reduction in CBF, whereas in control CBF did not decline. Compensatory increases in cerebral oxygen extraction allow for the maintenance of brain VO2 throughout exhaustive exercise. These findings suggest that a reduction in brain VO2 is an unlikely mechanism underpinning exercise capacity during prolonged, exhaustive exercise with dehydration.

AB - Background: Dehydration accrued during prolonged exercise in the heat induces significant cardiovascular strain on the human body characterised by reductions in cardiac output, active muscle and skin blood flow, arterial blood pressure, vascular conductance and an overall impaired exercise capacity (1). However, it is presently unknown whether progressive dehydration during exercise in the heat reduces blood flow to the brain, thereby impairing aerobic metabolism. A hyperthermic-hyperventilation induced lowering of the PaCO2 may reduce blood flow to the brain, assuming that reductions in middle cerebral artery velocity (MCA V mean) reflect reductions in cerebral blood flow (CBF) (2,3,4,5). This study tested the hypothesis that progressive dehydration reduces CBF during prolonged exercise in the heat, in part through mechanisms associated with PaCO2, but without impairing brain VO2. Methods: We assessed blood flow in the internal carotid artery (CBF) using Doppler ultrasonography and middle cerebral artery velocity (MCA V mean) in ten cyclists (VO2PEAK: 59 ± 2 ml/kg/min), who performed two hours of prolonged cycling exercise in a warm environment (182 ± 6 W; 35°C), without fluids to induce moderate dehydration (DEH; 3.1 ± 0.3 % body mass loss). Subjects returned one week later to repeat the protocol, but with regular fluid ingestion to maintain hydration status (Control). Blood samples were obtained from the brachial artery and left internal jugular vein (DEH only) to measure a-vO2 differences and for the calculation of brain VO2. All data are mean ± SEM and were compared with ANOVA and Pearson correlation (SPSS). Results: During dehydration CBF and MCA V mean increased by 13 ± 3 % from rest to 30 min (p<0.05). Thereafter CBF declined to resting values with flow at 120 min significantly lower than at 30, 60 and 90 min (p<0.001). During control, CBF and MCA V mean increased from rest to 30 min and were subsequently maintained throughout exercise (Increase ≥ 25%, p<0.05). Reductions in CBF and MCA V mean during DEH were accompanied with significant increases (p<0.05) in a-vO2 diff resulting in an unchanged brain VO2. PaCO2 declined in accordance with flow and velocity (p<0.05) with changes in flow correlated to changes in PaCO2 (R2 = 0.75, p<0.001), supporting a role for PaCO2 in cerebral vasoconstriction. Discussion: The present findings show that progressive dehydration during prolonged exercise results in a marked reduction in CBF, whereas in control CBF did not decline. Compensatory increases in cerebral oxygen extraction allow for the maintenance of brain VO2 throughout exhaustive exercise. These findings suggest that a reduction in brain VO2 is an unlikely mechanism underpinning exercise capacity during prolonged, exhaustive exercise with dehydration.

M3 - Poster

ER -