High-intensity interval training in spontaneously hypertensive rats improved functional capacity (33.8 vs 20.6 min) and reduced heart failure features, but did not modulate cardiac remodeling.
Does high-intensity interval training reduce heart failure development and cardiac remodeling in spontaneously hypertensive rats?
Long-term high-intensity interval training improves functional capacity and reduces clinical heart failure features in spontaneously hypertensive rats, without modulating cardiac remodeling.
Abstract Introduction Systemic arterial hypertension (SAH) causes cardiac pressure overload characterized by myocyte hypertrophy, myocardial fibrosis and oxidative stress, and changes in intracellular proteins, such as IGF1/Akt and MAPK signaling pathways. Physical exercise plays an important role in the non-pharmacologic treatment of SAH. The aim of this study was to evaluate the effects of high-intensity interval training on heart failure development, cardiac remodeling and molecular hypertrophic signaling pathways in spontaneously hypertensive rats (SHR) at an advanced stage of SAH. Methods Three experimental groups were assigned: normotensive Wistar rats (W, n=24); SHR (n=27); and exercised SHR (SHR-EX, n=14). At 13 months SHR-EX was subjected to a high-intensity interval exercise protocol performed on a treadmill, three times a week, for four months. Cardiac structures and left ventricular function were evaluated by echocardiogram. Myocyte diameter was measured by histology. Myocardial and serum malondialdehyde (MDA) concentrations were assessed by spectrophotometry and protein expression quantified by Western blot. Metalloproteinase-2 (MMP-2) activity was analyzed by zymography. Statistical analysis: ANOVA complemented by Tukey's test or Kruskal-Wallis and Dunn's test, at a 5% significance level. Results SHR-EX presented higher functional capacity than W and SHR groups (test time: W 17.0±2.21; SHR 20.6±1.85; SHR-EX 33.8±3.00 min). Initial (W 109±15.6; SHR 175±24.7; SHR-EX 174±19.3 mmHg) and final W 119 (111-126); SHR 163 (154-193); SHR-EX 188 (174–204) mmHg systolic arterial pressure was higher in SHR-EX and SHR than W. SHR-EX had a lower frequency of clinical heart failure features than SHR. Myocyte diameter did not differ between groups. SHR-EX and SHR had concentric hypertrophy and larger left cardiac chamber diameters normalized to body weight than W. Structural and functional echocardiography parameters did not differ between SHR-EX and SHR. SHR-EX and SHR had higher inactive MMP-2 than W; SHR had higher active intermediate MMP-2 than W (W 1.02 ± 0.37; SHR 1.94 ± 0.86; SHR-EX 1.68 ± 0.52 arbitrary units). MDA levels and protein expression of Types I and III collagen, MAPKs, and IGF-1 did not differ between groups. Conclusion Long-term high-intensity interval training is safe, improves functional capacity, reduces the frequency of heart failure features, and attenuates metalloproteinase-2 activity in spontaneously hypertensive rats with uncontrolled hypertension. Cardiac remodeling is not modulated by high-intensity interval training.
Pagan et al. (2025) studied Systemic arterial hypertension (n=65). High-intensity interval training vs. Sedentary spontaneously hypertensive rats and normotensive Wistar rats was evaluated on Heart failure development, cardiac remodeling and molecular hypertrophic signaling pathways. High-intensity interval training in spontaneously hypertensive rats improved functional capacity (33.8 vs 20.6 min) and reduced heart failure features, but did not modulate cardiac remodeling.