title: Complete Reversion of Cardiac Functional Adaptation Induced by Exercise Training.
abstract: Long-term exercise training is associated with characteristic cardiac adaptation, termed athlete's heart. Our research group previously characterized in vivo left ventricular (LV) function of exercise-induced cardiac hypertrophy in detail in a rat model; however, the effect of detraining on LV function is still unclear. We aimed at evaluating the reversibility of functional alterations of athlete's heart after detraining.
  
  
  
  Rats (n = 16) were divided into detrained exercised (DEx) and detrained control (DCo) groups. Trained rats swam 200 min·d for 12 wk, and control rats were taken into water for 5 min·d. After the training period, both groups remained sedentary for 8 wk. We performed echocardiography at weeks 12 and 20 to investigate the development and regression of exercise-induced structural changes. LV pressure-volume analysis was performed to calculate cardiac functional parameters. LV samples were harvested for histological examination.
  
  
  
  Echocardiography showed robust LV hypertrophy after completing the training protocol (LV mass index = 2.61 ± 0.08 DEx vs 2.04 ± 0.04 g·kg DCo, P < 0.05). This adaptation regressed after detraining (LV mass index = 2.01 ± 0.03 vs 1.97 ± 0.05 g·kg, n.s.), which was confirmed by postmortem measured heart weight and histological morphometry. After the 8-wk-long detraining period, a regression of the previously described exercise-induced cardiac functional alterations was observed (DEx vs DCo): stroke volume (SV; 144.8 ± 9.0 vs 143.9 ± 9.6 μL, P = 0.949), active relaxation (τ = 11.5 ± 0.3 vs 11.3 ± 0.4 ms, P = 0.760), contractility (preload recruitable stroke work = 69.5 ± 2.7 vs 70.9 ± 2.4 mm Hg, P = 0.709), and mechanoenergetic (mechanical efficiency = 68.7 ± 1.2 vs 69.4 ± 1.8, P = 0.742) enhancement reverted completely to control values. Myocardial stiffness remained unchanged; moreover, no fibrosis was observed after the detraining period.
  
  
  
  Functional consequences of exercise-induced physiological LV hypertrophy completely regressed after 8 wk of deconditioning.
authors.affiliation: Heart and Vascular Center, Semmelweis University, Budapest, HUNGARY.
authors.forename: Attila
authors.initials: A
authors.lastname: Oláh
authors.forename: Dalma
authors.initials: D
authors.lastname: Kellermayer
authors.forename: Csaba
authors.initials: C
authors.lastname: Mátyás
authors.forename: Balázs Tamás
authors.initials: BT
authors.lastname: Németh
authors.forename: Árpád
authors.initials: Á
authors.lastname: Lux
authors.forename: Lilla
authors.initials: L
authors.lastname: Szabó
authors.forename: Marianna
authors.initials: M
authors.lastname: Török
authors.forename: Mihály
authors.initials: M
authors.lastname: Ruppert
authors.forename: Anna
authors.initials: A
authors.lastname: Meltzer
authors.forename: Alex Ali
authors.initials: AA
authors.lastname: Sayour
authors.forename: Kálmán
authors.initials: K
authors.lastname: Benke
authors.forename: István
authors.initials: I
authors.lastname: Hartyánszky
authors.forename: Béla
authors.initials: B
authors.lastname: Merkely
authors.forename: Tamás
authors.initials: T
authors.lastname: Radovits
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D004452:Echocardiography; D006321:Heart / Q000033:anatomy & histology / Q000000981:diagnostic imaging / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D008297:Male; D023421:Models, Animal; D009200:Myocardial Contraction / Q000502:physiology; D010805:Physical Conditioning, Animal; D017208:Rats, Wistar; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*