With the increase in the prevalence of anabolic steroid (AS) use for non-medical performance and image enhancement purposes, the impact of AS on cardiovascular health is an issue of growing public concern. AS use has long been associated with a number of negative CV outcomes such as acute myocardial infarction, stroke, thrombo-embolisms and sudden death. These associations, however, are largely assumed from case study findings where no cause and effect can be apportioned. Small cohort studies have suggested a negative effect of AS on a number of established CV disease risk factors including, blood pressure (BP), lipid profiles (e.g total cholesterol, LDL and HDL), C-reactive proteins and homocysteine, although data is limited both in number of studies and number of participants and is often contradictory. Another potential mechanism to link AS use to cardiac events has been to assess cardiac structure and function. Available data is contradictory but recent developments in imaging technologies suggest that new mechanistic insights could be developed and/or tested. In study one we investigated the impact of AS use on a broad profile of CV risk factors as well as an in-depth cardiac assessment utilising speckle tracking echocardiography which can assess regional and global cardiac deformation in multiple planes. In AS users we observed an increase in resting heart rate and low- density lipoprotein concomitant to a decrease in high-density lipoprotein levels. 2D and speckle-tracking echocardiography revealed a significant effect of AS use on cardiac function, most notably a decreased diastolic (relaxation) function that suggests a stiffer left ventricle in the AS users. This imposes a greater workload on the heart and increases the risk of CV events. In study two we developed the assessment of cardiac structural assessment in AS users by adopting state-of-the-art magnetic resonance imaging that provides a greater accuracy in morphology assessment as well as allowing us to determine the presence of perfusion defects and interstitial fibrosis. We observed that AS users had a hypertrophy of both the left and right ventricles that was concomitant with diastolic dysfunction in the left ventricle and a reduction in right ventricular contractility. Despite these findings no AS user presented with any perfusion defect or evidence of interstitial fibrosis, suggesting that these pathways to CV events were not apparent in the current group of AS users. The final study comprised two pilot or feasibility studies of the impact of resistance exercise on left ventricular function in AS users. Trial 1 assessed blood pressure and cardiac tissue velocities during an acute leg press with and without valsalva. Systolic blood pressure was significantly elevated even after one repetition and this was mediated by AS use. In trial 2 cardiac function and blood biomarkers of cardiac cell damage were assessed before and after a standard resistance exercise training session. Left ventricular systolic function was maintained in recovery in both AS and NAS participants. Diastolic function was reduced in both groups with some evidence that AS use exaggerated this effect. Multiple technical, design and participant lessons were gained to take these feasibility studies forward to full studies. Overall we add new data to the concept that AS use can place the participant at an increased CV risk. It is probably not obligatory that AS use leads to increased CV risk but in some the route from AS use to CV event may be mediated by changes in structure and function of both the L V and RV. Exercise stress may add an additional CV risk to the AS user.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:570728 |
| Date | January 2011 |
| Creators | Angell, Peter James |
| Publisher | Liverpool John Moores University |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://researchonline.ljmu.ac.uk/6126/ |
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