Rat model of exercise-induced cardiac hypertrophy

• Verfasst von: Radovits, Tamás [VerfasserIn]
• Verfasst von: Oláh, Attila [VerfasserIn]
• Verfasst von: Lux, Árpád [VerfasserIn]
• Verfasst von: Németh, Balázs Tamás [VerfasserIn]
• Verfasst von: Hidi, László [VerfasserIn]
• Verfasst von: Birtalan, Ede [VerfasserIn]
• Verfasst von: Kellermayer, Dalma [VerfasserIn]
• Verfasst von: Mátyás, Csaba [VerfasserIn]
• Verfasst von: Szabó, Gábor [VerfasserIn]
• Verfasst von: Merkely, Béla [VerfasserIn]
• Titel: Rat model of exercise-induced cardiac hypertrophy
• Titelzusatz: hemodynamic characterization using left ventricular pressure-volume analysis
• Verf.angabe: Tamás Radovits, Attila Oláh, Árpád Lux, Balázs Tamás Németh, László Hidi, Ede Birtalan, Dalma Kellermayer, Csaba Mátyás, Gábor Szabó, and Béla Merkely
• E-Jahr: 2013
• Jahr: 1 July 2013
• Umfang: 11 S.
• Fussnoten: Gesehen am 13.12.2021
• Titel Quelle: Enthalten in: American journal of physiology / Heart and circulatory physiology
• Ort Quelle: Bethesda, Md. : American Physiological Society, 1977
• Jahr Quelle: 2013
• Band/Heft Quelle: 305(2013), 1 vom: Juli, Seite H124-H134
• ISSN Quelle: 1522-1539
• DOI: doi:10.1152/ajpheart.00108.2013
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: cardiac mechanoenergetics
• Sach-SW: diastolic function
• Sach-SW: exercise-induced cardiac hypertrophy
• Sach-SW: pressure-volume analysis
• Sach-SW: systolic function
• K10plus-PPN: 1782007121

Abstract

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressure-conductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 ± 0.09 vs. 2.03 ± 0.08 g/kg, P < 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV end-diastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 ± 0.8 vs. 64.1 ± 1.5%, P < 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 ± 6.8 vs. 54.3 ± 4.8 mmHg, P = 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 ± 0.02 vs. 0.65 ± 0.08, P < 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 ± 0.007 vs. 0.040 ± 0.006 mmHg/μl) and improved LV active relaxation (τ: 10.1 ± 0.6 vs. 11.9 ± 0.2 ms, P < 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.