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The effects of acute exercise on cardiovascular function in humans

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Title: The effects of acute exercise on cardiovascular function in humans
Author: Scott, Jessica
Degree: Doctor of Philosophy - PhD
Program: Human Kinetics
Copyright Date: 2009
Issue Date: 2009-07-23
Publisher University of British Columbia
Abstract: In spite of numerous studies examining cardiac fatigue following acute exercise, there is a significant need for descriptive research that documents the nature and magnitude of this phenomenon in various populations. Accordingly, the aim of this series of studies was to comprehensively investigate the cardiovascular consequences of acute exercise in endurance trained (ET) individuals, normally active (NA) individuals, and heart transplant recipients (HTR). In the first investigation, 25 ET athletes were examined before a 160 km ultra-marathon and were re-assessed immediately following the race using traditional echocardiography, speckle tracking imaging, and cardiac biomarkers. Significant pre to post-race changes in systolic function (ejection fraction (EF): 66.8 ± 3.8 vs. 61.2 ± 4.0 %, p < 0.05), and diastolic function (E:A ratio: 1.62 ± 0.37 vs. 1.35 ± 0.33, p < 0.05) were observed. The second investigation used cardiac magnetic resonance imaging with tagging to study the impact of interval exercise on biventricular function in nine ET (VO₂max: 69 ± 7 mL/kg/min) and nine NA (VO₂max: 44 ± 9 mL/kg/min) males. There were no significant changes in RV and LV EF, torsion, rotation rate, strain, or strain rate post-exercise in the NA group. In the ET group, RV and LV EF, untwisting rate, apical rotation rate and circumferential strain were significantly decreased post-exercise. These results suggest that biventricular systolic and diastolic dysfunction occur following 14 min of high intensity exercise in ET athletes, a phenomenon which is not observed in NA individuals. The final investigation examined the cardiovascular responses during incremental and sustained (1 hr) sub-maximal aerobic exercise in 9 clinically stable HTR (age: 63 ± 10 yr; VO₂peak: 24.2 ± 10.9 mL/kg/min) and 11 healthy age-matched controls (6 recipient age-matched, RM; age: 60 ± 11 yr; VO₂peak: 36.3 ± 10.7 mL/kg/min, and 5 donor age-matched, DM; age: 35 ± 8 yr; VO₂peak: 51.1 ± 10.4 mL/kg/min) using traditional echocardiography. Despite maintained systolic function during incremental exercise, HTR had significantly reduced peak cardiac output, secondary to blunted heart rate and preload during exercise conditions. These findings provide the basis for future work examining the underlying mechanisms contributing to exercise-induced cardiac fatigue.
Affiliation: Education, Faculty of
URI: http://hdl.handle.net/2429/11172
Scholarly Level: Graduate

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