Characterization of the dynamic changes in left ventricular morphology and function induced by exercise training and detraining

Abstract

Background: Although exercise-induced cardiac hypertrophy has been intensively investigated, its development and regression dynamics have not been comprehensively described. In the current study, we aimed to characterize the effects of regular exercise training and detraining on left ventricular (LV) morphology and function. Methods: Rats were divided into exercised (n = 12) and control (n = 12) groups. Exercised rats swam 200 min/day for 12 weeks. After completion of the training protocol, rats remained sedentary for 8 weeks (detraining period). Echocardiographic follow-up was performed regularly to obtain LV long-and short-axis recordings for speckle-tracking echocardiography analysis. Global longitudinal and circumferential strain and systolic strain rate were measured. LV pressure-volume analysis was performed using additional groups of rats to obtain haemodynamic data. Results: Echocardiographic examinations showed the development of LV hypertrophy in the exercised group. These differences disappeared during the detraining period. Strain and strain rate values were all increased after the training period, whereas supernormal values rapidly reversed to the control level after training cessation. Load-independent haemodynamic indices, e.g., preload recruitable stroke work, confirmed the exerciseinduced systolic improvement and complete regression after detraining. Conclusions and translational aspect: Our results provide the first comprehensive data to describe the development and regression dynamics of morphological and functional aspects of physiological hypertrophy in detail. Speckle-tracking echocardiography has been proven to be feasible to follow-up changes induced by exercise training and detraining and might provide an early possibility to differentiate between physiological and pathological conditions.

Long-term exercise results in morphological and biomechanical changes in coronary resistance arterioles in male and female rats

“…In agreement with previous results of the rodent model of exercise-induced cardiac hypertrophy, an increased heart weight/body weight was observed in response to the swimming-training program in both male and female rats [7,24]. Our 12-week swim training program can be considered intensive, as shown by the degree of ventricular hypertrophy developed in both males and females.…”

“…This complex adaptive cardiac remodeling is called athlete's heart. Exercise-induced cardiac hypertrophy is reversible, and cessation of training results in progressive morphological and functional regression [7,8]. The elevated myocardial mass requires increased perfusion, which can be provided by remodeling of only the coronary circulation [5].…”

Right ventricular mechanical pattern in health and disease: beyond longitudinal shortening

“…Regular exercise training is associated with significant changes in cardiac dimensions and function, which are also referred to as athlete’s heart [ 51 ]. Traditionally, it was believed that the RV is only exposed to volume overload due to increased cardiac output; however, recent data also suggest the presence of significant pressure overload [ 52 ].…”

Training/detraining-induced gender specific functional adaptations of isolated rat heart

“…Those adaptations are associated with the promotion of physiological cardiac hypertrophy (PCH) which is linked to the less cardiac fibrosis and better systolic and diastolic function when compared to pathological hypertrophy. Ventricular dilatation represents short-term adaptive response, while hypertrophy of the cardiac muscle fibers appears after longer time of regular physical activity 8,9,12,23,24 .…”

“…Improved oxygen supply and myocardial contractility both in health and disease, represent exercise-related cardiac adaptations 6 . In addition, the amelioration of cardiovascular capacity due to aerobic exercise training is associated with increased left ventricular (LV) mass and volume, myocyte hypertrophy, increased LV stroke volume and lower resting and submaximal heart rate (HR) 1,[6][7][8][9][10] .…”