Exercise haemodynamics : physiology and clinical consequences

High blood pressure (BP) is a leading risk factor for premature death relating to cardiovascular (CV) disease. Some individuals with normal resting BP may experience an excessive rise in BP with exercise; a condition termed 'hypertensive response to exercise' (HRE). Despite having normal resting BP, an HRE has been implicated in contributing to CV risk, but little is known on the condition. The broad aims of this research program were to determine; the prognostic and clinical significance of an HRE; the efficacy of a lifestyle intervention program to 'treat' an HRE and; the haemodynamic mechanisms contributing to exercise BP. In study 1 (chapter 2), the prognostic value of an HRE for predicting CV events and mortality was examined via systematic review and meta-analysis on data from 12 studies (46,314 individuals). Elevated BP at moderate intensity exercise predicted CV events and mortality, independent of resting BP, age and multiple CV risk factors (HR=1.36, 95% CI: 1.02-1.83, P=0.039). Study 2 (chapter 3) sought to determine a possible explanation as to why an HRE was associated with increased CV risk. In a cohort of 77 individuals with an HRE, a high prevalence (56%) of masked hypertension was observed. Moreover, moderate exercise systolic BP >190 mmHg revealed the presence of masked hypertension with high positive predictive value (94% sensitivity, P<0.001). In study 3 (chapter 4), the effects of a one-year lifestyle (exercise and diet) intervention on exercise BP was examined in 185 individuals with type 2 diabetes mellitus. An HRE was not significantly reduced by the intervention. However, development of an HRE was preventable in those individuals without an HRE at baseline (P=0.020). In study 4 (chapter 5), the haemodynamic mechanisms of exercise central BP were examined in 10 individuals undergoing coronary angiography. Exercise BP was principally related to increases in forward wave propagation generated by left-ventricular ejection, whereas mathematically-derived aortic reservoir function was unchanged with exercise. This mechanistic work was extended in study 5 (chapter 6), where aortic reservoir pressure was directly measured for the first time in 10 individuals undergoing coronary bypass surgery. Directly-measured and mathematically-derived aortic reservoir pressures were highly related, thus providing evidence for an 'aortic reservoir function' in generation of central BP. In summary, this research shows that an HRE is related to increased CV risk, and this may be due to masked hypertension. Furthermore, it was possible to attenuate progression towards an HRE with lifestyle intervention. Finally, exercise BP was found to be predominantly due to forward wave transmission, and mathematically-derived aortic reservoir pressure is a valid construct relevant to understanding the physiology of central BP.