Body mass, cardiac chambers mass, kidney mass, lung mass and wet: dry lung mass ratio of control (WT), heart failure placebo (KOS), heart failure exercise trained (KOT), heart failure carvedilol-treated (KOC) and, heart failure carvedilol-treated and exercise-trained (KOCT).

*<p>P<i><</i>0.05 vs. WT;</p>#<p>P<i><</i>0.05 vs. KOS;</p>‡<p>P<0.05 vs. KOT. The number of animals studied is shown between parentheses.</p

Lipid peroxidation in control (WT), heart failure placebo (KOS), heart failure exercise trained (KOT), heart failure carvedilol-treated (KOC) and, heart failure carvedilol-treated and exercise trained (KOCT) mice.

<p>Data are presented as mean ± SE. The number of animals studied is indicated by numerals on the abscissa. *P<0.05 among groups indicated by lines.</p

SERCA2 (A), SERCA2A:PLN (B), Phospho-Ser¹⁶-PLN:PLN (C), Phosphatase 1 (D), Phospho- Thr¹⁷-PLN:PLN (E), Na⁺– Ca²⁺ exchanger (NCX, F), Ryanodine receptor (RyR, G), Phospholamban (PLN, H).

<p>Data are presented as mean ± SE. *P<0.05 among groups indicated by lines.</p

Intracellular Ca²⁺ transient in isolated ventricular myocytes in control (WT), heart failure placebo (KOS), heart failure exercise trained (KOT), heart failure carvedilol-treated (KOC) and, heart failure carvedilol-treated and exercise trained (KOCT) mice.

<p>A: Averaged data showing peak of Ca²⁺ transient B: Bar graph shows a comparison of Ca²⁺ transient kinetics (time from peak to 90% decay) between the different groups of cells. Data are presented as mean ± SE. The number of cells studied is indicated by numerals on the abscissa. *P<0.05 for WT vs. indicated groups; (WT vs. all groups in Panel A and WT vs. KOT, KOC and KOCT in Panel B); ^#P<0.05 for KOS vs. KOT; ⁺P<0.05 for KOS vs. KOT, KOC and KOCT;^‡P<0.05 for KOT vs. KOC and KOCT; **P<0.05 for KOC vs. KOCT.</p

Experimental design.

<p>WT, wild type mice (control group); KOS, heart failure placebo; KOT, heart failure exercise trained; KOC, heart failure carvedilol-treated; and, KOCT, heart failure carvedilol-treated and exercise trained mice.</p

Survival (A), Exercise tolerance (B) and fractional shortening (FS, C) in control (WT), heart failure placebo (KOS), heart failure exercise trained (KOT), heart failure carvedilol-treated (KOC) and, heart failure carvedilol-treated and exercise trained (KOCT) mice.

<p>FS was evaluated after 8 weeks of intervention. Note that all interventions reduced mortality rate. However, only trained groups (KOT and KOCT) increased exercise tolerance. Data are presented as mean ± SE. The number of animals studied is shown between parentheses (Panel A) or indicated by numerals on the abscissa (Panels B and C). Panel A: *P<0.05 between KOS and WT, and among KOS and other groups. Panel B and C: *P<0.05 among groups indicated by lines.</p

Cardiomyocytes cross-sectional area (A) and ventricular collagen volume fraction (B) in control (WT), heart failure placebo (KOS), heart failure exercise trained (KOT), heart failure carvedilol-treated (KOC) and, heart failure carvedilol-treated and exercise trained (KOCT) mice.

<p>Data are presented as mean ± SE. The number of animals studied is indicated by numerals on the abscissa. *P<0.05 among groups indicated by lines.</p

Heart rate (A) and blood pressure (B) during interventions in control (WT), heart failure placebo (KOS), heart failure exercise trained (KOT), heart failure carvedilol-treated (KOC) and, heart failure carvedilol-treated and exercise-trained (KOCT) mice.

<p>Note that all interventions decreased to the same extent the baseline HR of KO mice, which became similar to HR of WT group. Data are presented as mean ± SE. The number of animals studied is shown between parentheses (Panel A) or indicated by numerals on the abscissa (Panel B). *P<0.05 vs. other groups (groups indicated by lines).</p