The Clinical Translation Gap in Child Health Exercise Research: A Call for Disruptive Innovation

In children, levels of play, physical activity, and fitness are key indicators of health and disease and closely tied to optimal growth and development. Cardiopulmonary exercise testing (CPET) provides clinicians with biomarkers of disease and effectiveness of therapy, and researchers with novel insights into fundamental biological mechanisms reflecting an integrated physiological response that is hidden when the child is at rest. Yet the growth of clinical trials utilizing CPET in pediatrics remains stunted despite the current emphasis on preventative medicine and the growing recognition that therapies used in children should be clinically tested in children. There exists a translational gap between basic discovery and clinical application in this essential component of child health. To address this gap, the NIH provided funding through the Clinical and Translational Science Award (CTSA) program to convene a panel of experts. This report summarizes our major findings and outlines next steps necessary to enhance child health exercise medicine translational research. We present specific plans to bolster data interoperability, improve child health CPET reference values, stimulate formal training in exercise medicine for child health care professionals, and outline innovative approaches through which exercise medicine can become more accessible and advance therapeutics across the child health spectrum

Medical encounters (including injury and illness) at mass community-based endurance sports events: an international consensus statement on definitions and methods of data recording and reporting

Mass participation endurance sports events are popular but a large number of participants are older and may be at risk of medical complications during events. Medical encounters (defined fully in the statement) include those traditionally considered 'musculoskeletal' (eg, strains) and those due to 'illness' (eg, cardiac, respiratory, endocrine). The rate of sudden death during mass endurance events (running, cycling and triathlon) is between 0.4 and 3.3 per 100 000 entrants. The rate of other serious medical encounters (eg, exertional heat stroke, hyponatraemia) is rarely reported; in runners it can be up to 100 times higher than that of sudden death, that is, between 16 and 155 per 100 000 race entrants. This consensus statement has two goals. It (1) defines terms for injury and illness-related medical encounters, severity and timing of medical encounters, and diagnostic categories of medical encounters, and (2) describes the methods for recording data at mass participation endurance sports events and reporting results to authorities and for publication. This unifying consensus statement will allow data from various events to be compared and aggregated. This will inform athlete/patient management, and thus make endurance events safer

ACCIRT/WRC Newsletter [26 September, 2012]

Marathon running commonly causes a transient elevation of creatine kinase and cardiac troponin I (cTnI). The use of statins before marathon running exacerbates the release of creatine kinase from skeletal muscle, but the effect of statin use on exercise-induced cTnI release is unknown. We therefore measured cTnI concentrations in statin-using (n = 30) and nonstatin-using (n = 41) runners who participated in the 2011 Boston Marathon. All runners provided venous blood samples the day before, within an hour of finishing, and 24 hours after the marathon. cTnI was assessed at each time point via both a contemporary cTnI and high-sensitivity cTnI (hsTnI) assay. Before the marathon, cTnI was detectable in 99% of runners with the use of the hsTnI assay. All participants completed the marathon (finish time: 4:04:09 +/- 0:41:10), and none had symptoms of an acute coronary syndrome. cTnI increased in all runners (p <0.001) immediately after the marathon, and half (hsTnI = 54% vs contemporary cTnI = 47%) exceeded the diagnostic cut-point for an acute myocardial infarction. Statin use did not affect the magnitude of cTnI release (group*time p = 0.47) or the incidence of runners with cTnI elevation greater than the diagnostic cut-point for myocardial infarction (57% vs 51%, p = 0.65). In addition, there was no significant association between statin potency and cTnI release (r = 0.09, p = 0.65). In conclusion, marathon-induced cTnI increases are not altered by statin use