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The impact of endurance exercise training on the heart has received significant research and clinical attention for well over a century. Despite this, many issues remain controversial and clinical interpretation can be complex of biomarkers of cardiomyocyte insult. This review assesses the current state of knowledge related to two areas of research where problems with clinical decision making may arise: (1) the impact of chronic endurance exercise training on cardiac structure, function and electrical activity to the point where the athletic heart phenotype may be similar to the expression of some cardiac pathologies (a diagnostic dilemma referred to as the 'grey-zone') and (2) the impact of acute bouts of prolonged exercise on cardiac function and the presentation of biomarkers and cardiomyocyte insult in the circulatory system. The combination of acute endurance exercise stress on the heart and prolonged periods of training are considered together in the final section.

Background: Prolonged steady state exercise can lead to a decrease in left ventricular (LV) function as well as promote the release of cardiac troponin T (cTnT). There is limited information on the effect of intermittent high intensity exercise of moderate duration., Objectives: To determine the effect of intermittent high intensity exercise of moderate duration on LV function., Methods: Nineteen male rugby and football players (mean (SD) age 21 (2) years) volunteered. Assessments, before, immediately after, and 24 hours after competitive games, included body mass, heart rate (HR), and systolic blood pressure (sBP) as well as echocardiography to assess stroke volume (SV), ejection fraction (EF), systolic blood pressure/end systolic volume ratio (sBP/ESV), and global diastolic filling (E:A) as well as to indirectly quantify preload (LV internal dimension at end diastole (LVIDd)). Serum cTnT was analysed using a 3rd generation assay. Changes in LV function were analysed by repeated measures analysis of variance. cTnT data are presented descriptively., Results: SV (91 (26) v 91 (36) v 90 (35) ml before, after, and 24 hours after the game respectively), EF (71 (8) v 70 (9) v 71 (7)%), and sBP/ESV (4.2 (1.8) v 3.8 (1.9) v 4.1 (1.6) mm Hg/ml) were not significantly altered (p>0.05). Interestingly, whereas LVIDd was maintained after the game (50 (5) v 50 (6) mm), sBP was transiently but significantly reduced (131 (3) v 122 (3) mm Hg; p<0.05). E:A was moderately (p<0.05) reduced after the game (2.0 (0.4) v 1.5 (0.4)) but returned to baseline within 24 hours. No blood sample contained detectable levels of cTnT., Conclusions: In this cohort, LV systolic function was not significantly altered after intermittent activity. A transient depression in global diastolic filling was partially attributable to a raised HR and could not be explained by myocyte disruption as represented by cTnT release.

Background: Exercise induced cardiac fatigue has recently been observed after prolonged exercise. A moderate to high altitude has been suggested as a possible stimulus in the genesis of such cardiac fatigue., Objective: To investigate if exercise induced cardiac fatigue and or cardiac damage occurs after prolonged exercise in a hypoxic environment., Methods: Eight trained male triathletes volunteered for the study. Each completed two 50 mile cycle trials, randomly assigned from normobaric normoxia and normobaric hypoxia (15% FIO(2)). Echocardiographic assessment and whole blood collection was completed before, immediately after, and 24 hours after exercise. Left ventricular systolic and diastolic functional variables were calculated, and serum was analysed for cardiac troponin T. Results were analysed using a two way repeated measures analysis of variance, with alpha set at 0.05., Results: No significant differences were observed in either systolic or diastolic function across time or between trials. Cardiac troponin T was detected in one subject immediately after exercise in the normobaric hypoxic trial., Conclusions: A 50 mile cycle trial in either normobaric normoxia or normobaric hypoxia does not induce exercise induced cardiac fatigue. Some people, however, may exhibit minimal cardiac damage after exercise in normobaric hypoxia. The clinical significance of this is yet to be elucidated.