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|Title:||Potential causes and mechanisms of postexercise hypotension|
|Authors:||MacDonald, Jay R.|
|Advisor:||MacDougall, Duncan J.|
|Abstract:||<p>This thesis consists of five studies, conducted with the objective of advancing our understanding of post exercise hypotension (PEH) and its mechanisms. Studies 1, 2 and 3 examined the effects of exercise intensity (30 min of cycle ergometry at 50 and 75% V O2 Peak ), exercise duration (10, 15, 30 and 45 min of cycle ergometry at 70% V O2 Peak ) and the effects of exercising muscle mass (arms vs. legs) on PEH. In all cases, blood pressure was lower after exercise and the magnitude of this decrease was unaffected by the variations in protocol. Heart rate and V O 2 were elevated through much of the hypotensive period in these studies, suggesting that a decrease in total peripheral resistance mediated the blood pressure effect as opposed to a decrease in cardiac output. Study 4 was conducted to determine whether or not the hypotension following exercise is maintained during normal simulated activities of daily living (ADL). This study demonstrated a relative PEH, which persisted for at least 70 min of ADL. Systolic (SBP), diastolic (DBP) and mean (MAP) blood pressure were significantly decreased following exercise as compared to the non-exercise trial as well as from baseline measures. From this study, it can be concluded that acute exercise has the potential to serve as a non-pharmacological aid to hypertension. Study 5 was conducted to determine the possible role of the central serotonergic system as a cause of PEH. While taking a placebo or selective serotonin reuptake inhibitor (SSRI) (randomised order) participants completed 30 min of cycling at 70% of V O2 Peak . Peripheral measures of serotonin (5-HT) were decreased during SSRI treatment, whereas 5-hydroxyindoleacetic acid, was not statistically increased, suggesting elevated central 5-HT levels. However, the significant decrements in blood pressure were similar between trials indicating that the central serotonergic system was not responsible for PEH in a borderline hypertensive population. This thesis was supported by the Natural Sciences and Engineering Research Council of CANADA.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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