Table 1.
Exercise Protocols and Work for HS-ET and HS-HIIT rats at weeks 1–4 of training.
Table 2.
Morphometrics and hemodynamics of LS-SED, HS-SED, HS-ET and HS-HIIT rats before and after 4 weeks of training.
Fig 1.
Mitochondrial content and citrate synthase (CS) activity in the left ventricle (LV).
A. Representative western blot of LV OXPHOS proteins in low sodium sedentary (LS-SED), high sodium SED (HS-SED), HS endurance training (HS-ET) and HS high intensity interval training (HS-HIIT) B-E. Density quantifications of LV OXPHOS in LS-SED, HS-SED, HS-ET and HS-HIIT, demonstrating no change in mitochondrial content in both ET and HIIT. F. CS activity as expressed per gram wet weight. HS had no effect on CS activity. Data are means ± SEM.
Fig 2.
Left ventricular (LV) fibrosis in response to high sodium (HS) with endurance training (ET) and high intensity interval training (HIIT).
A. Composite wide field microscopy images of LV; with picrosirius red stain for fibrosis; low sodium-SED (LS-SED; top left), HS-SED (top right), HS-ET (bottom left) and HS-HIIT (bottom right). B. Quantification (% area) of fibrosis; HS-ET demonstrates significantly less % area of fibrosis vs. all other groups: * vs. LS-SED, HS-SED and HS-HIIT, P<0.05 C. Data are means ± SEM.
Fig 3.
Effect of high sodium (HS) with endurance training (ET) and high intensity interval training (HIIT) on heart weight and cardiac fibre cross-sectional area.
A. Heart weight normalized to tibia length (HW/TL) in low sodium (LS), HS-ET and HS-HIIT. HS-HIIT demonstrates a significant increase in HW/TL when compared to all other groups: * vs. LS-SED, P<0.05. B. Composite wide field microscopy images of left ventricle; LS-SED (top left), HS-SED (top right), HS-ET (bottom left) and HS-HIIT (bottom right). C. Left ventricle cardiac fibre cross-sectional area in LS-SED, HS-SED, HS-ET and HS-HIIT. HS-HIIT demonstrates a decrease in cross-sectional area when compared to HS-SED and HS-ET: * vs. HS-SED, vs. † HS-ET; P<0.05. Data are means ± SEM.
Fig 4.
Western blot analysis of brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MHC).
A. Representative blots; α-tubulin is presented as a loading control. B. Density quantifications of BNP of low sodium sedentary (LS-SED), high sodium SED (HS-SED), HS endurance training (HS-ET) and HS high intensity interval training (HS-HIIT), demonstrating an decrease in protein as a result of HS-HIIT; • vs. LS-SED, HS-SED and HS-ET; P<0.05. C. Density quantifications of ANP protein. D. Density quantifications of protein. Data are means ± SEM.
Fig 5.
Western blot analysis for FOXO3a (Ser253), MuRF1 and MAFbx.
A. Representative blots; α-tubulin is presented as a loading control. B. Density quantifications of FOXO3a (Ser253) protein in LV of low sodium sedentary (LS-SED), high sodium SED (HS-SED), HS endurance training (HS-ET) and HS high intensity interval training (HS-HIIT). C. Density quantifications of MAFbx. D. Density quantifications of MuRF1 protein. Data are means ± SEM.
Fig 6.
Left ventricular (LV) capillary to fibre ratio.
A. Composite wide field microscopy images of LV; of low sodium sedentary (LS-SED-top left), high sodium SED (HS-SED-top right), HS endurance training (HS-ET-bottom left) and HS high intensity interval training (HS-HIIT-bottom right) B. LV capillary to fibre ratio demonstrating a significant increase in response to HS-ET; * vs. LS-SED, HS-SED and HS-HIIT; P<0.05. Data are means ± SEM.
Fig 7.
Western blot analysis of eNOS, HIF1α, and VEGF.
A. Representative blots; α-tubulin is presented as a loading control. B. Density quantifications of eNOS protein in LV of low sodium sedentary (LS-SED), high sodium SED (HS-SED), HS endurance training (HS-ET) and HS high intensity interval training (HS-HIIT), demonstrating a significant increase as a result of ET, * vs. all other groups; P<0.05 C. Density quantifications of HIF1α, demonstrating a significant increase in response to both HS and HS-HIIT; * vs. LS-SED; ‡ vs. HS-ET. D. Density quantifications of VEGF protein. Data are means ± SEM.