Clinical guidelines advocate for customization of exercise testing to address patient-specific diagnostic goals, including reproduction of presenting exertional symptoms. However, the diagnostic yield of adding customized exercise testing to graded exercise in patients presenting with exertional complaints has not been rigorously examined and is the focus of this study. Using prospectively collected data, we analyzed the diagnostic yield of customized additional exercise provocation following inconclusive graded exercise test with measurement of gas exchange. Additional testing was defined as "positive" if it revealed a clinically-actionable diagnosis related to the chief complaint or reproduced symptoms in the absence of an explanatory diagnosis or pathology. Of 1,110 patients who completed a graded test, 122 (11%) symptomatic patients underwent additional customized exercise testing (e.g., sprint intervals and race simulations). Compared with those who did not undergo additional testing, this group was younger (29 [interquartile range 19 to 45] vs 46 [25 to 58] year old) and disproportionately female (43% vs 27%). Presenting symptoms included palpitations (46%), lightheadedness/syncope (25%), chest pain (14%), dyspnea (11%), and exertional intolerance (3%). Additional testing was "positive" in 48 of 122 (39%) of patients by revealing a clinically actionable diagnosis in 26 of 48 (54%) or reproducing symptoms without an explanatory diagnosis in 22 of 48 (46%). In conclusion, while patient-centered customization of exercise testing is suggested by clinical guidelines, these data are the first to demonstrate that the selective addition of customized exercise provocation following inconclusive graded exercise testing improves the diagnostic yield of exercise assessment.

PURPOSE:Swim training is performed in the prone or supine position and obligates water immersion, factors that may augment cardiac volume loading more than other endurance sports. At present, prospective data defining the cardiac responses to swim training are lacking. We therefore studied myocardial adaptations among competitive swimmers to establish a causal relationship between swim training and left ventricular (LV) remodeling. METHODS:Collegiate swimmers were studied before and after a 90-d period of training intensification. Transthoracic echocardiography was used to examine LV structural and functional adaptations under resting conditions and during an acute LV afterload challenge generated by isometric handgrip testing (IHGT). A sedentary control population was identically studied with IHGT. RESULTS:In response to a discrete period of swim training intensification, athletes (n = 17, 47% female, 19 ± 0.4 yr old) experienced eccentric LV remodeling, characterized by proportionally more chamber dilation than wall thickening, with attendant enhancements of resting LV systolic (LV twist) and diastolic (early and late phase tissue velocities) function. Compared with baseline and controls, athletes posttraining demonstrated greater systolic twist impairment during IHGT. However, training-induced LV dilation coupled with gains in diastolic function offsets this acquired systolic susceptibility to acute afterload, resulting in the relative preservation of stroke volume during IHGT. CONCLUSION:Swim training, a sport characterized by unique cardiac loading conditions, stimulates eccentric LV remodeling with the concomitant augmentation of systolic twist and diastolic relaxation. This volume-mediated cardiac remodeling appears to result in greater systolic susceptibility to acute afterload challenge. Further work is required to establish how training-induced changes in function translate to human performance and whether these are accompanied by physiologic trade-offs with relevance to common forms of heart disease.

Exercise-induced cardiac remodeling (EICR) and the attendant myocardial adaptations characteristic of the athlete's heart may regress during periods of exercise reduction or abstinence. The time course and mechanisms underlying this reverse remodeling, specifically the impact of concomitant plasma volume (PV) contraction on cardiac chamber size, remain incompletely understood. We therefore studied recreational runners ( n = 21, age 34 ± 7 yr; 48% male) who completed an 18-wk training program (~7 h/wk) culminating in the 2016 Boston Marathon after which total exercise exposure was confined to <2 h/wk (no single session >1 h) for 8 wk. Cardiac structure and function, exercise capacity, and PV were assessed at peak fitness (10-14 days before) and at 4 wk and 8 wk postmarathon. Mixed linear modeling adjusting for age, sex, V̇o2peak, and marathon finish time was used to compare data across time points. Physiological detraining was evidenced by serial reductions in treadmill performance. Two distinct phases of myocardial remodeling and hematological adaptation were observed. After 4 wk of detraining, there were significant reductions in PV (Δ -6.0%, P < 0.01), left ventricular (LV) wall thickness (Δ -8.1%, <0.05), LV mass (Δ -10.3%, P < 0.001), and right atrial area (Δ -8.2%, P < 0.001). After 8 wk of detraining, there was a significant reduction in right ventricle chamber size (end-diastolic area Δ = -8.0%, P < 0.05) without further concomitant reductions in PV or LV wall thickness. Abrupt reductions in exercise training stimulus result in a structure-specific time course of reverse cardiac remodeling that occurs largely independently of PV contraction. NEW & NOTEWORTHY Significant reverse cardiac remodeling, previously documented among competitive athletes, extends to recreational runners and occurs with a distinct time course. Initial reductions in plasma volume and left ventricular (LV) mass, driven by reductions in wall thickness, are followed by contraction of the right ventricle. Consistent with data from competitive athletes, LV chamber volumes appear less responsive to detraining and may be a more permanent adaptation to sport.

Routine moderate-intensity physical activity confers numerous cardiovascular benefits and reduces all-cause mortality. However, the health impact of exercise doses that exceed contemporary physical activity guidelines remains incompletely understood, and an emerging body of literature suggests that high levels of exercise may have the capacity to damage the cardiovascular system. This review focuses on the contemporary controversies regarding high-dose exercise and cardiovascular morbidity and mortality. We discuss the limitations of available studies, explore potential mechanisms that may mediate exercise-related cardiac injury, and highlight the gaps in knowledge for future research.

Enduranee exercise training (ET) stimulates eccentric left ventricular hypertrophy (LVH) with left atrial dilation. To date, the biochemical correlates of exercise-induced cardiac remodeling (EICR) remain incompletely understood. Collegiate male rowers (n = 9) were studied with echocardiography and maximal-effort cardiopulmonary exercise testing (MECPET) before and after 90 days of ET intensification. Midregional proatrial natriuretic peptide (MR-proANP), NH2-terminal pro B-type natriuretic peptide (NT-proBNP). and high-sensitivity troponin T were measured at rest peak MECPET, and 60 min post-MECPET at both study time points. Endurance exercise training resulted in eccentric LVH (LV mass = 102 +/- 8 vs. 110 +/- 11 g/m(2), P = 0.001; relative wall thickness = 0.36 +/- 0.04 vs. 0.37 +/- 0.04, P = 0.103), left atrial dilation (74 +/- 18 vs. 84 +/- 15 ml, P < 0.001), and increased exercise capacity (peak <(V) over dot>O-2 = 53.0 +/- 5.9 vs. 67.3 +/- 8.2 ml.kg (-1).min(-1) P < 0.001). Left ventricular remodeling was characterized by an similar to 7% increase in LV wall thickness but only a 3% increase in LV chamber radius. The magnitude of natriuretic peptide release, examined as percent change from rest to peak exercise, was significantly lower for both MRproANP (115 [95,127]% vs. 78 [59,87]%, P = 0.04) and NT-proBNP (46 [31.70]% vs. 27 [25,37]%, P = 0.02) after ET. Rowing-based ET and corollary EICR appear to result in an attenuated natriuretic peptide response to maximal effort exercise. This may occur as a function of decreased cardiac wall stress after ET as seen by disproportionally higher ventricular wall thickening compared with chamber dilation. NEW & NOTEWORTHY Using longitudinal pre- and postendurance training natriuretic peptide measurements, we demonstrate that the development of exercise-induced cardiac remodeling results in an attenuated natriuretic peptide response to acute bouts of maximal intensity exercise. Exercise-induced cardiac remodeling was associated with a disproportionally higher ventricular wall thickening compared with chamber dilation, a pattern that reduces cardiac wall stress. These observations advance our understanding of both the structural and biochemical adaptations that underlie the cardiovascular response to endurance training.

Introduction: Guidelines advocate for individualized exercise testing (IET) to address patient-specific diagnostic goals, including reproduction of presenting exertional symptoms, as standardized g...

Background: Deliberate exercise abstinence, “prescribed detraining”, has been proposed as means to differentiate the athlete's heart from occult cardiomyopathy. At present, data defining the myocardial response to detraining among healthy athletes are sparse. Methods: Marathon runners

PURPOSE: Dietary nitrate supplementation in the form of beetroot extract (BRE) has recently emerged as a potential modulator of exercise capacity. To date, the impact of BRE ingestion on lactate kinetics, a key determinant of endurance exercise performance, has not been rigorously assessed. METHODS: We performed a single-blinded, randomized crossover study in which competitive masters rowers underwent graded stepwise (3 mins, 20W increment) rowing ergometer testing to define lactate handling profiles. Each participant was tested 2.5 hours after ingestion of a commercially available BRE product (Beet-It Sport Shot, Ipswich, UK) and blackcurrant juice placebo (R.W. Knudsen Just Black Currant, Chico, CA). Capillary lactate concentrations were measured at the completion of each testing stage to develop lactate handing curves. RESULTS: Participants (n = 12, 50% men, age = 54 ± 5 years, peak VO2 = 47 ± 7 ml/kg) with 24 ± 12 years of rowing experience completed all aspects of this protocol. Heart rate, oxygen consumption, respiratory exchange ratio, and perceived effort were similar at all exercise intensities during testing following ingestion of BRE and placebo. Similarly, parameters of lactate handling including absolute lactate concentrations at each exercise intensity, workload at onset of blood lactate accumulation, and workload at 4 mmol lactate concentration were similar following ingestion of the active BRE compound and placebo (Figure). CONCLUSION: Ingestion of a single dose of commercially available BRE does not appear to have a significant impact on lactate handling. Performance during activities that depend on lactate handling may be unresponsive to BRE ingestion. Figure. Capillary lactate concentrations during stepwise rowing ergometer exercise testing following ingestion of beetroot extract (BRE) and placebo.

Masters athletes (MAs), people over the age of 35 that participate in competitive sports, are a rapidly growing population that may be uniquely at risk for cardiovascular (CV) disease. The objective of this study was to develop a comprehensive clinical CV profile of MA.

OBJECTIVES:This study sought to determine the relationships among American-style football (ASF) participation, acquired left ventricular (LV) hypertrophy, and LV systolic function as assessed using contemporary echocardiographic parameters. BACKGROUND:Participation in ASF has been associated with development of hypertension and LV hypertrophy. To what degree these processes impact LV function is unknown. METHODS:This was a prospective, longitudinal cohort study evaluating National Collegiate Athletic Association Division I football athletes stratified by field position (linemen: n = 30; vs. nonlinemen, n = 57) before and after a single competitive season, using transthoracic echocardiography. LV systolic function was measured using complementary parameters of global longitudinal strain (GLS) (using 2-dimensional speckle-tracking) and ejection fraction (EF) (2-dimensional biplane). RESULTS:ASF participation was associated with field position-specific increases in systolic blood pressure (SBP) (a Δ SBP of 10 ± 8 mm Hg in linemen vs. a Δ SBP of 3 ± 7 mm Hg in nonlinemen; p < 0.001) and an overall increase in incident LV hypertrophy (pre-season = 8% vs. post-season = 25%, p < 0.05). Linemen who developed LV hypertrophy had concentric geometry (9 of 11 [82%]) with decreased GLS (Δ = -1.1%; p < 0.001), whereas nonlinemen demonstrated eccentric LV hypertrophy (8 of 10 [80%]) with increased GLS (Δ = +1.4%; p < 0.001). In contrast, LV ejection fraction in the total cohort, stratified by field position, was not significantly affected by ASF participation. Among the total cohort, lineman field position, post-season weight, SBP, average LV wall thickness, and relative wall thickness were all independent predictors of post-season GLS. CONCLUSIONS:ASF participation at a lineman field position may lead to a form of sport-related myocardial remodeling that is pathologic rather than adaptive. Future study will be required to determine if targeted efforts to control blood pressure, minimize weight gain, and to include an element of aerobic conditioning in this subset of athletes may attenuate this process and translate into tangible downstream health benefits.

wall thickness of 14 mm as stated in the caption of Figure 2. The incidence of intraventicular septal thickness of more than 13 mm (14 to 16 mm) was 11% (17 of 156 subjects) as stated in the Results section. The incidence of either the intraventricular septal wall or left ventricular free wall being more than 13 mm was actually higher (13%; 20 of 156 subjects). The findings presented in our study demonstrate the chamber size, wall thickness, and ejection fraction of elite professional American football players in the NFL. Because both the size and the types of physical effort of these players are different from those of bodybuilders, rowers, canoists, or cyclists, we believe these observations will be useful in separating physiologic adaptations from pathologic findings when evaluating such players.

Pathologic forms of left ventricular hypertrophy (LVH) are associated with impaired myocardial metabolic efficiency (MME), the ratio of myocardial work to oxygen consumption (MVO2), which may serve as a key mechanistic link between LVH and the development of heart failure syndromes [(1,2)][1]. At

A 72 year-old woman with a distant history of a cryptogenic right middle cerebral artery stroke presented with three days of fatigue, confusion, and recrudescence of old stroke symptoms. . Head and neck imaging demonstrated a small subarachnoid hemorrhage, orbital pseudotumors, cerebellar lesions, and circumferential thickening of the aortic arch and great vessels. Additional imaging of the chest, abdomen, pelvis, and legs revealed a large pericardial effusion, pan-aortitis, and sclerotic intramedullary lesions in both femurs. An electrocardiogram showed sinus rhythm, RBBB, and low voltage. Pulsus paradoxus was 10 mmHg. Laboratory analysis was notable for elevated serum inflammatory markers. Echocardiogram showed brief right ventricular diastolic inversion and a right atrioventricular groove mass. Diagnostic and therapeutic pericardiocentesis yielded 350cc of serosanguinous fluid, and evaluation for rheumatologic, infectious, and neoplastic etiologies was unremarkable. Cardiac magnetic resonance imaging (MRI) confirmed the presence of a right atrioventricular groove pseudotumor with avid late gadolinium enhancement and non-obstructive fibrotic encasement of the right and left anterior descending coronary arteries. The combination of pan-aortitis, orbital pseudotumors, pericardial effusion, coronary encasement, and right heart pseudotumor raised suspicion for Erdheim-Chester disease. Femoral bone biopsy revealed infiltration by CD68 (+), CD1a (-) histiocytes, confirming this diagnosis. Genetic testing identified a mutation in the gene for B-type RAF Kinase (BRAF) protein. Treatment with vemurafenib, a BRAF inhibitor, was initiated, and the patient’s disease has not progressed in the eighteen months since starting this treatment. Erdheim-Chester disease is a rare systemic illness caused by proliferation of non-Langerhans cell histiocytes. Cardiovascular manifestations—such as those seen in this case—complicate a majority of cases, and are the predominant cause of death. At least 50% of cases have mutations in the BRAF gene. While Erdheim-Chester disease has no known cure, vemurafenib represents a promising new therapy for BRAF mutation (+) cases.

There are clear health benefits to exercise; even so, patients with cardiac conditions who engage in exercise and athletic competition may on rare occasion experience sudden cardiac death (SCD). This article reviews the epidemiology and common causes of SCD in specific athlete populations. There is ongoing debate about the optimal mechanism for SCD prevention, specifically regarding the inclusion of the ECG and/or cardiac imaging in routine preparticipation sports evaluation. This controversy and contemporary screening recommendations are also reviewed.

Background: The term endurance sport (ES) is broadly used to characterize any exercise that requires maintenance of high cardiac output over extended time. However, the relative amount of isotonic (volume) versus isometric (pressure) cardiac stress varies across ES disciplines. To what degree ES-mediated cardiac remodeling varies, as a function of superimposed isometric stress, is uncertain. The aim of this study was to compare the cardiac remodeling characteristics associated with two common yet physiologically distinct forms of ES.Methods: Healthy competitive male long-distance runners (high isotonic, low isometric stress; n = 40) and rowers (high isotonic, high isometric stress; n = 40) were comparatively studied after 3 months of sport-specific exercise training with conventional and speckle-tracking two-dimensional echocardiography.Results: Rowers demonstrated dilated left ventricular (LV) volumes and elevated LV mass (i.e., eccentric LV hypertrophy), whereas runners demonstrated normal LV mass (runners, 88 +/- 11 g/m(2); rowers, 108 +/- 13 g/ m(2); P <.001) despite comparatively larger LV volumes (runners, 101 +/- 10 mL/m(2); rowers, 89 +/- 13 mL/m(2); P <.001) consistent with eccentric LV remodeling. Increasing LV mass was associated with increased reliance on early diastolic filling (LV mass vs E'/A' ratio, R = 0.47, P <.001) indicating "mass-dependent'' diastolic function. Right ventricular dilation of similar magnitude and LV systolic function, as assessed by numerous complementary indices, were similar in both groups.Conclusions: Cardiac adaptations differ significantly as a function of ES discipline. Further work is required to determine the mechanisms for this differential adaptation, to develop definitive ES discipline-specific normative values, and to evaluate the optimal therapeutic use of specific ES disciplines among patients with common cardiovascular diseases. (J Am Soc Echocardiogr 2015; 28: 1434-40.)

Background/aim The international governing body for competitive rowing recently mandated the inclusion of 12-lead ECG during preparticipation screening. We therefore sought to describe normative ECG characteristics and to examine the prevalence of abnormal ECG findings as defined by contemporary athlete ECG interpretation criteria among competitive rowers. Methods Competitive rowers (n=330, 56% male) underwent standard 12-lead ECG at the time of collegiate preparticipation screening. ECGs were analysed quantitatively to develop a sport-specific normative database and then for the presence of abnormalities in accordance with the 2010 European Society of Cardiology (ESC) recommendations and 2013 ‘Seattle Criteria.’ Results 94% of rowers had one or more training-related ECG patterns including sinus bradycardia (51%), sinus arrhythmia (55%), and incomplete right bundle branch block (42%). Males were more likely than females to have isolated voltage criteria for left ventricular hypertrophy (LVH) (51% vs 8%, p<0.001) and early repolarisation pattern (76% vs 23%, p<0.001). Application of the 2010 ESC criteria, compared to the Seattle criteria, resulted in the classification of a significantly greater number of abnormal ECGs (47% vs 4%; p<0.001). The detection of true pathology, accomplished by both interpretation criteria, was confined to a single case of ventricular pre-excitation. Conclusions Training-related ECG patterns with several gender-based differences are common among competitive rowers. The diagnostic accuracy and down-stream clinical implications of ECG-inclusive preparticipation screening among rowers will be dictated by the choice and future refinement of ECG interpretation criteria.

Background—Myocardial adaptations to exercise have been well documented among competitive athletes. To what degree cardiac remodeling occurs among recreational exercisers is unknown. We sought to evaluate the effect of recreational marathon training on myocardial structure and function comprehensively. Methods and Results—Male runners (n=45; age, 48±7 years; 64% with ≥1 cardiovascular risk factor) participated in a structured marathon-training program. Echocardiography, cardiopulmonary exercise testing, and laboratory evaluation were performed pre and post training to quantify changes in myocardial structure and function, cardiorespiratory fitness, and traditional cardiac risk parameters. Completion of an 18-week running program (25±9 miles/wk) led to increased cardiorespiratory fitness (peak oxygen consumption, 44.6±5.2 versus 46.3±5.4 mL/kg per minute; P<0.001). In this setting, there was a significant structural cardiac remodeling characterized by dilation of the left ventricle (end-diastolic volume, 156±26 versus 172±28 mL, P<0.001), right ventricle (end-diastolic area=27.0±4.8 versus 28.6±4.3 cm2; P=0.02), and left atrium (end-diastolic volume, 65±19 versus 72±19; P=0.02). Functional adaptations included increases in both early (E′=12.4±2.5 versus 13.2±2.0 cm/s; P=0.007) and late (A′=11.5±1.9 versus 12.2±2.1 cm/s; P=0.02) left ventricular diastolic velocities. Myocardial remodeling was accompanied by beneficial changes in cardiovascular risk factors, including body mass index (27.0±2.7 versus 26.7±2.6 kg/m2; P<0.001), total cholesterol (199±33 versus 192±29 mg/dL; P=0.01), low-density lipoprotein (120±29 versus 114±26 mg/dL; P=0.01), and triglycerides (100±52 versus 85±36 mg/dL; P=0.02). Conclusions—Among middle-aged men, recreational marathon training is associated with biventricular dilation, enhanced left ventricular diastolic function, and favorable changes in nonmyocardial determinants of cardiovascular risk. Recreational marathon training may, therefore, serve as an effective strategy for decreasing incident cardiovascular disease.