Ironman and half-Ironman competition resulted in reversible abnormalities in resting left ventricular diastolic and systolic function. Results suggest that myocardial damage may be, in part, responsible for cardiac dysfunction, although the mechanisms responsible for this cardiac damage remain to be fully elucidated.

Regular physical exercise is recommended for the primary prevention of cardiovascular disease. Although the high prevalence of physical inactivity remains a formidable public health issue, participation in exercise programs and recreational sporting events, such as marathons and triathlons, is on the rise. Although regular exercise training reduces cardiovascular disease risk, recent studies have documented elevations in cardiac troponin (cTn) consistent with cardiac damage after bouts of exercise in apparently healthy individuals. At present, the prevalence, mechanism(s), and clinical significance of exercise-induced cTn release remains incompletely understood. This paper will review the biochemistry, prevalence, potential mechanisms, and management of patients with exercise-induced cTn elevations.

Human growth hormone (hGH) is secreted in a pulsatile fashion, generally following a circadian rhythm. A number of physiological stimuli can initiate hGH secretion, the most powerful, non-pharmacological of which are sleep and exercise. hGH has many varied roles throughout life, from growth itself, including the turnover of muscle, bone and collagen, to the regulation of selective aspects of metabolic function including increased fat metabolism and the maintenance of a healthier body composition in later life. The exercise-induced growth hormone response (EIGR) is well recognised and although the exact mechanisms remain elusive, a number of candidates have been implicated. These include neural input, direct stimulation by catecholamines, lactate and or nitric oxide, and changes in acid-base balance. Of these, the best candidates appear to be afferent stimulation, nitric oxide and lactate. Resistance training results in a significant EIGR. Evidence suggests that load and frequency are determining factors in the regulation of hGH secretion. Despite the significant EIGR induced by resistance training, much of the stimulus for protein synthesis has been attributed to insulin-like growth factor-1 with modest contributions from the hGH-GH receptor interaction on the cell membrane. The EIGR to endurance exercise is associated with the intensity, duration, frequency and mode of endurance exercise. A number of studies have suggested an intensity 'threshold' exists for EIGR. An exercise intensity above lactate threshold and for a minimum of 10 minutes appears to elicit the greatest stimulus to the secretion of hGH. Exercise training above the lactate threshold may amplify the pulsatile release of hGH at rest, increasing 24-hour hGH secretion. The impact of chronic exercise training on the EIGR remains equivocal. Recent evidence suggests that endurance training results in decreased resting hGH and a blunted EIGR, which may be linked to an increased tissue sensitivity to hGH. While the potential ergogenic effects of exogenous GH administration are attractive to some athletes, the abuse of GH has been associated with a number of pathologies. Identification of a training programme that will optimise the EIGR may present a viable alternative. Ageing is often associated with a progressive decrease in the volume and, especially, the intensity of exercise. A growing body of evidence suggests that higher intensity exercise is effective in eliciting beneficial health, well-being and training outcomes. In a great many cases, the impact of some of the deleterious effects of ageing could be reduced if exercise focused on promoting the EIGR. This review examines the current knowledge and proposed mechanisms for the EIGR, the physiological consequences of endurance, strength and power training on the EIGR and its potential effects in elderly populations, including the aged athlete.