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Age, aerobic fitness and cerebral perfusion during exercise: Role of carbon dioxide


Flück, Daniela; Braz, Igor D; Keiser, Stefanie; Hüppin, Fabienne; Haider, Thomas; Hilty, Matthias; Fisher, James P; Lundby, Carsten (2014). Age, aerobic fitness and cerebral perfusion during exercise: Role of carbon dioxide. American Journal of Physiology - Heart and Circulatory Physiology, 307(4):H515-H523.

Abstract

Middle cerebral artery mean velocity (MCAvmean) is attenuated with increasing age both at rest and during exercise. The aim of this study was to determine the influence of the age dependent reduction in arterial PCO2 (PaCO2) and physical fitness hereon. We administered supplemental CO2 (CO2 trial) or no additional gas (Control trial) to the inspired air in a blinded and randomized manner, and assessed middle cerebral artery mean flow velocity during graded exercise in 1) twenty one young (Y; age 24±3 yrs (±SD)) volunteers of whom eleven where trained (YT) and ten considered untrained (YUT) and, 2) seventeen old (O; 66±4 yrs) volunteers of which eight and nine were considered trained (OT) and untrained (OUT), respectively. A resting hypercapnic reactivity test was also performed. MCAvmean and PaCO2 were lower in O (44.9±3.1 cm∙s(-1) and 30±1 mmHg (±SEM)) compared to Y (59.3±2.3 cm∙s(-1) and 34±1 mmHg,p<0.01) at rest, independent of aerobic fitness level. The age related decreases in MCAvmean and PaCO2 persisted during exercise. Supplemental CO2 reduced the age-associated decline in MCAvmean by 50 %, suggesting that PaCO2 is a major component in the decline. On the other hand, relative hypercapnic reactivity was neither influenced by age (p=0.46) nor aerobic fitness (p=0.36). Although supplemental CO2 attenuated exercise-induced reduction in cerebral oxygenation (near infrared spectroscopy) this did not influence exercise performance. In conclusion, PaCO2 contributes to the age-associated decline in MCAvmean at rest and during exercise, however exercise capacity did not diminish this age effect.

Abstract

Middle cerebral artery mean velocity (MCAvmean) is attenuated with increasing age both at rest and during exercise. The aim of this study was to determine the influence of the age dependent reduction in arterial PCO2 (PaCO2) and physical fitness hereon. We administered supplemental CO2 (CO2 trial) or no additional gas (Control trial) to the inspired air in a blinded and randomized manner, and assessed middle cerebral artery mean flow velocity during graded exercise in 1) twenty one young (Y; age 24±3 yrs (±SD)) volunteers of whom eleven where trained (YT) and ten considered untrained (YUT) and, 2) seventeen old (O; 66±4 yrs) volunteers of which eight and nine were considered trained (OT) and untrained (OUT), respectively. A resting hypercapnic reactivity test was also performed. MCAvmean and PaCO2 were lower in O (44.9±3.1 cm∙s(-1) and 30±1 mmHg (±SEM)) compared to Y (59.3±2.3 cm∙s(-1) and 34±1 mmHg,p<0.01) at rest, independent of aerobic fitness level. The age related decreases in MCAvmean and PaCO2 persisted during exercise. Supplemental CO2 reduced the age-associated decline in MCAvmean by 50 %, suggesting that PaCO2 is a major component in the decline. On the other hand, relative hypercapnic reactivity was neither influenced by age (p=0.46) nor aerobic fitness (p=0.36). Although supplemental CO2 attenuated exercise-induced reduction in cerebral oxygenation (near infrared spectroscopy) this did not influence exercise performance. In conclusion, PaCO2 contributes to the age-associated decline in MCAvmean at rest and during exercise, however exercise capacity did not diminish this age effect.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Division of Surgical Intensive Care Medicine
04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > Center for Integrative Human Physiology
05 Vetsuisse Faculty > Institute of Veterinary Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:20 June 2014
Deposited On:23 Oct 2014 07:38
Last Modified:05 Apr 2016 18:25
Publisher:American Physiological Society
ISSN:0363-6135
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1152/ajpheart.00177.2014
PubMed ID:24951752

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