The benefits of endurance training in cardiomyocyte function in hypertensive rats are reversed within four weeks of detraining

The aim of the present study was to verify the effects of low-intensity endurance training and detraining on the mechanical and molecular properties of cardiomyocytes from spontaneously hypertensive rats (SHRs). Male SHRs and normotensive control Wistar rats at 16-weeks of age were randomly divided into eight groups of eight animals: NC8 and HC8 (normotensive and hypertensive control for 8 weeks); NT8 and HT8 (normotensive and hypertensive trained at 50-60% of maximal exercise capacity for 8 weeks); NC12 and HC12 (normotensive and hypertensive control for 12 weeks); NDT and HDT (normotensive and hypertensive trained for 8 weeks and detrained for 4 weeks). The total exercise time until fatigue (TTF) was determined by a maximal exercise capacity test. Resting heart rate (RHR) and systolic arterial pressure (SAP) were measured. After the treatments, animals were killed by cervical dislocation and left ventricular myocytes were isolated by enzymatic dispersion. Isolated cells were used to determine intracellular global Ca2+ ([Ca2+](i)) transient and cardiomyocyte contractility (1 Hz; similar to 25 degrees C). [Ca2+](i) regulatory proteins were measured by Western blot, and the markers of pathologic cardiac ac hypertrophy by quantitative real-time polymerase chain reaction (q-RT-PCR). Exercise training augmented the TTF (NC8, 11.4 +/- 1.5 min vs. NT8, 22.5 +/- 1.4 min; HC8, 11.7 +/- 1.4 min vs. HC8, 24.5 +/- 13 min; P<0.05), reduced RHR 340 +/- 8 bpm vs. NT8final, 322 +/- 10 bpm; HT8initial, 369 +/- 8 bpm vs. HT8final, 344 +/- 10 bpm; P<0.05), and SBP in SHR animals (HC8, 178 3 mm Hg vs. HT8, 161 4 mm Hg; P<0.05). HC8 rats showed a slower [Ca2+]; transient (Tpeak, 83.7 +/- 1.8 ms vs. 71.7 +/- 2.4 ms; T50%decay, 284.0 +/- 4.3 ms vs. 264.0 +/- 4.1 ms; P<0.05) and cell contractility (Vshortening, 86.1 +/- 6.7 mu m/s vs. 118.6 6.7 pm/s; Vrelengthening, 57.5 7.4 mu m/s vs. 101.3 7.4 mu m/s; P<0.05), and higher expression of ANF (300%; P<0.05), skeletal a-actin (250%; P<0.05) and a decreased alpha/beta-MHC ratio (70%; P<0.05) compared to NC8. Exercise training increased [Ca2+]; transient (NC8, 2.39 +/- 0.06 F/Fo vs. NT8, 2.72 +/- 0.06 F/Fo; HC8, 228 +/- 0.05 F/Fo vs. HT8, 2.82 +/- 0.05 F/Fo; P<0.05), and cell contractility (NC8, 7.4 +/- 0.3% vs. NT8, 8.4 +/- 0.3%; HC8, 6.8 +/- 03% vs. HT8, 7.8 +/- 03%; P<0.05). Furthermore, exercise normalized the expression of ANF, skeletal a-actin, and the a/p-MHC ratio in HT8 rats, augmented the expression of SERCA2a (NC8, 0.93 +/- 0.15 vs. NT8, 1.49 +/- 0.14; HC8, 0.83 +/- 0.13 vs. HT8, 1.32 +/- 0.14; P<0.05) and PLBserio (NC8, 0.89 +/- 0.18 vs. NT8, 123 +/- 0.17; HC8, 0.77 +/- 0.17 vs. HT8, 132 +/- 0.16; P<0.05), and reduced PLBt/SERCA2a (NC8, 121 +/- 0.19 vs. NT8, 0.50 +/-.21; HC8, 138 +/- 0.17 vs. HT8, 0.66 +/- 0.21; P<0.05). However, all these adaptations returned to control values within 4 weeks of detraining in both SHR and normotensive control animals. In conclusion, low-intensity endurance training induces positive benefits to left ventricular myocyte mechanical and molecular properties, which are reversed within 4 weeks of detraining. (C) 2013 Elsevier Ltd. All rights reserved.