ABSTRACT
Introduction
The structural and mechanical adaptations of the right ventricular (RV) myocytes in response to hypertension associated with low-intensity endurance training (LIET) have not been studied in experimental models.
Objective
To determine the effects of LIET on the structural and mechanical properties of RV myocytes in spontaneously hypertensive rats (SHRs).
Methods
Male SHRs and normotensive Wistar rats (age: 16 weeks) were allocated to groups (n=7): WIS (Wistar Controls); SHR-C (SHR Controls) and SHR-T (SHR Trained; 60 min/day, 50-60% of maximal exercise capacity, 5 days/week for 8 weeks). Systolic arterial pressure (SAP), isolated RV myocyte dimensions, contractility, intracellular Ca2+ transient ([Ca2+]i), and ventricular Ca2+ regulatory proteins were measured. The statistical analysis was performed by one-way ANOVA followed by the Tukey post hoc test (α=5%).
Results
LIET reduced the SAP in SHR animals (SHR-C, 164 ± 2 mmHg vs. SHR-T, 152 ± 4 mmHg; P<0.05). Hypertension increased cell length (WIS, 156.8 ± 2.7 µm; SHR-C, 166.6 ± 3.1 µm; P<0.05) but did not affect cell width or volume (P>0.05). LIET did not change the cell dimensions in the SHR-T. Neither hypertension nor LIET affected myocyte contractility or the expression of Ca2+ regulatory proteins in the RV of the SHR-C and SHR-T groups. Hypertension did not affect the amplitude of the [Ca2+]i transient or the time to half resting level (P>0.05), but increased the time to peak (WIS, 58 ± 1 ms vs. SHR-C, 79 ± 2 ms; P<0.05). LIET increased the amplitude of the [Ca2+]i transient (WIS, 2.28 ± 0.07 F/F0 and SHR-C, 2.48 ± 0.08 F/F0 vs. SHR-T, 2.87 ± 0.08 F/F0 P<0.05), but did not alter the times to peak or to half resting level.
Conclusion
LIET had no effect on the structural and mechanical properties of RV myocytes in the SHRs, although it increased the amplitude of the [Ca2+]i transient and reduced the SAP. Level of evidence I, Therapeutic Studies - Investigating the Results of Treatment.
Exercise; Rats; Hypertension; Heart
