Key result
Low-intensity endurance training reduced systolic arterial pressure (152 ± 4 vs 164 ± 2 mmHg, P<0.05) and increased the amplitude of the intracellular Ca2+ transient in hypertensive rats.
Why the study?
The structural and mechanical adaptations of right ventricular myocytes in response to hypertension combined with low-intensity endurance training had not been studied in experimental models.
Does low-intensity endurance training improve structural and mechanical properties of right ventricular myocytes in spontaneously hypertensive rats?
Does low-intensity endurance training improve structural and mechanical properties of right ventricular myocytes in spontaneously hypertensive rats?
Low-intensity endurance training reduces systolic arterial pressure and increases intracellular calcium transient amplitude in hypertensive rats, without altering right ventricular myocyte structure or contractility.
Answers are grounded in this paper and cite their sources.
LIET does not improve RV myocyte structure or contractility in SHR; leaves open translation of calcium transient effects to clinical hypertension.
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.
No takes yet. Share an insight, caveat, or question.
Carneiro‐Júnior et al. (2019) studied Hypertension (n=21). Low-intensity endurance training (LIET) vs. Sedentary controls (SHR-C and WIS) was evaluated on Systolic arterial pressure (SAP) (p=<0.05). Low-intensity endurance training reduced systolic arterial pressure (152 ± 4 vs 164 ± 2 mmHg, P<0.05) and increased the amplitude of the intracellular Ca2+ transient in hypertensive rats.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: