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Imaging spectrum of sudden athlete cardiac death.Sudden athlete death (SAD) is a widely publicized and increasingly reported phenomenon. For many, the athlete population epitomize human physical endeavour and achievement and their unexpected death comes with a significant emotional impact on the public. Sudden deaths within this group are often without prior warning. Preceding symptoms of exertional syncope and chest pain do, however, occur and warrant investigation. Similarly, a positive family history of sudden death in a young person or a known family history of a condition associated with SAD necessitates further tests. Screening programmes aimed at detecting those at risk individuals also exist with the aim of reducing fatalities. In this paper we review the topic of SAD and discuss the epidemiology, aetiology, and clinical presentations. We then proceed to discuss each underlying cause, in turn discussing the pathophysiology of each condition. This is followed by a discussion of useful imaging methods with an emphasis on cardiac magnetic resonance and cardiac computed tomography and how these address the various issues raised by the pathophysiology of each entity. We conclude by proposing imaging algorithms for the investigation of patients considered at risk for these conditions and discuss the various issues raised in screening.
The physiology of growth hormone and sport.The growth hormone (GH)/ insulin-like growth factor-I (IGF-I) axis exerts short-and long-term metabolic effects that are potentially important during exercise. Exercise is a potent stimulus to GH release and there is some evidence that the acute increase in GH is important in regulating substrate metabolism post-exercise. Regular exercise also increases 24-hour GH secretion rates, which potentially contributes to the physiologic changes induced by training. The effects of GH replacement in GH-deficient adults provide a useful model with which to study the effects of the more long-term effects of the GH/ IGF-I axis. There is convincing evidence that GH replacement increases exercise capacity. Measures of exercise performance including maximal oxygen uptake (VO2max) and ventilatory threshold (VeT) are impaired in GH deficiency and improved by GH replacement, probably through some combination of increased oxygen delivery to exercising muscle, increased fatty acid availability with glycogen sparing, increased muscle strength, improved body composition and improved thermoregulation. Administration of supraphysiologic doses of GH to athletes increases fatty acid availability and reduces oxidative protein loss particularly during exercise, and increases lean body mass. It is not known whether these effects translate to improved athletic performance, although recombinant human GH is known to be widely abused in sport. The model of acromegaly provides evidence that long-term GH excess does not result in improved performance but it is possible that a "window" exists in which the protein anabolic effects of supraphysiologic GH might be advantageous.