Cardiac effects of detraining in athletes: A narrative review.

BACKGROUND: Routine physical activity stimulates numerous morphologic and functional adaptations of the cardiac system, which are commonly referred to as exercise-induced cardiac remodeling (EICR). EICR has been well documented in elite and recreational athletes, but comparatively little is known about the "reverse" cardiac adaptations during detraining in an athletic population. OBJECTIVE: To assess the morphologic and functional cardiac effects of detraining in athletes. METHODS: Eligible studies were identified in PubMed from inception to May 2020. Studies were included if they assessed the cardiac effects of detraining periods in athletes. RESULTS: A total of 16 studies from the literature search were identified and included in this review. These studies included athletes from multiple different sporting disciplines and detraining periods ranged from 3 weeks to 13 years. Detraining periods led to significantly decreased right ventricular and left (LV) ventricular dimensions, LV mass, and LV wall thickness, but only limited changes in systolic and diastolic functional parameters were observed. CONCLUSIONS: From the limited data available in this population, cardiac atrophy has been observed with short periods of detraining (1-8 weeks) but often spares systolic and diastolic heart function. Supplemental exercise training during times of rehabilitation to combat cardiac regression has not been vigorously studied in athletes, so the ideal frequency, intensity, and modality of exercise needed to maintain EICR remains unclear.

Association of Ascending Aortic Dilatation and Long-term Endurance Exercise Among Older Masters-Level Athletes.

Importance: Aortic dilatation is frequently encountered in clinical practice among aging endurance athletes, but the distribution of aortic sizes in this population is unknown. It is additionally uncertain whether this may represent aortic adaptation to long-term exercise, similar to the well-established process of ventricular remodeling. Objective: To assess the prevalence of aortic dilatation among long-term masters-level male and female athletes with about 2 decades of exercise exposure. Design, Setting, and Participants: This cross-sectional study evaluated aortic size in veteran endurance athletes. Masters-level rowers and runners aged 50 to 75 years were enrolled from competitive athletic events across the United States from February to October 2018. Analysis began January 2019. Exposures: Long-term endurance exercise. Main Outcomes and Measures: The primary outcome was aortic size at the sinuses of Valsalva and the ascending aorta, measured using transthoracic echocardiography in accordance with contemporary guidelines. Aortic dimensions were compared with age, sex, and body size-adjusted predictions from published nomograms, and z scores were calculated where applicable. Results: Among 442 athletes (mean [SD] age, 61 [6] years; 267 men [60%]; 228 rowers [52%]; 214 runners [48%]), clinically relevant aortic dilatation, defined by a diameter at sinuses of Valsalva or ascending aorta of 40 mm or larger, was found in 21% (n = 94) of all participants (83 men [31%] and 11 women [6%]). When compared with published nomograms, the distribution of measured aortic size displayed a rightward shift with a rightward tail (all P < .001). Overall, 105 individuals (24%) had at least 1 z score of 2 or more, indicating an aortic measurement greater than 2 SDs above the population mean. In multivariate models adjusting for age, sex, body size, hypertension, and statin use, both elite competitor status (rowing participation in world championships or Olympics or marathon time under 2 hours and 45 minutes) and sport type (rowing) were independently associated with aortic size. Conclusions and Relevance: Clinically relevant aortic dilatation is common among aging endurance athletes, raising the possibility of vascular remodeling in response to long-term exercise. Longitudinal follow-up is warranted to establish corollary clinical outcomes in this population.

Diagnostic Yield of Customized Exercise Provocation Following Routine Testing.

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.

Catecholamine response to exercise in patients with non-obstructive hypertrophic cardiomyopathy.

KEY POINTS: Intense physical activity, a potent stimulus for sympathetic nervous system activation, is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM). As a result, the majority of patients with HCM deliberately reduce their habitual physical activity after diagnosis and this lifestyle change puts them at risk for sequelae of a sedentary lifestyle: weight gain, hypertension, hyperlipidaemia, insulin resistance, coronary artery disease, and increased morbidity and mortality. We show that plasma catecholamine levels remain stably low at exercise intensities below the ventilatory threshold, a parameter that can be defined during cardiopulmonary exercise testing, but rise rapidly at higher intensities of exercise. These findings suggest that cardiopulmonary exercise testing may be a useful tool to provide an individualized moderate-intensity exercise prescription for patients with HCM. ABSTRACT: Intense physical activity, a potent stimulus for sympathetic nervous system activation, is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic cardiomyopathy (HCM). However, the impact of exercise intensity on plasma catecholamine levels among HCM patients has not been rigorously defined. We conducted a prospective observational case-control study of men with non-obstructive HCM and age-matched controls. Laboratory-based cardiopulmonary exercise testing coupled with serial phlebotomy was used to define the relationship between exercise intensity and plasma catecholamine levels. Compared to controls (C, n = 5), HCM participants (H, n = 9) demonstrated higher left ventricular mass index (115 ± 20 vs. 90 ± 16 g/m2 , P = 0.03) and maximal left ventricular wall thickness (16 ± 1 vs. 8 ± 1 mm, P < 0.001) but similar body mass index, resting heart rate, peak oxygen consumption (H = 40 ± 13 vs. C = 42 ± 7 ml/kg/min, P = 0.81) and heart rate at the ventilatory threshold (H = 78 ± 6 vs. C = 78 ± 4% peak heart rate, P = 0.92). During incremental effort exercise in both groups, concentrations of adrenaline and noradrenaline were unchanged through low- and moderate-exercise intensity until reaching a catecholamine threshold (H = 82 ± 4 vs. C = 85 ± 3% peak heart rate, P = 0.86) after which levels of both molecules rose rapidly. In patients with mild non-obstructive HCM, plasma catecholamine levels remain stably low at exercise intensities below the ventilatory threshold but rise rapidly at higher intensities of exercise. Routine cardiopulmonary exercise testing may be a useful tool to provide an individualized moderate-intensity exercise prescription for patients with HCM.