Swimming training attenuates the decrease of calcium responsiveness in female infarcted rats.

Aim: To evaluate the influence of swimming training on calcium responsiveness of the myocardium of rats with different infarction sizes (MI). Method: female Wistar rats, sedentary sham (SS = 14), sedentary moderate MI (SMI = 8) and sedentary large MI (SLI = 10) were compared to trained sham (TS = 16), trained moderate MI (TMI = 9) and trained large MI (TLI = 10). After 4 weeks of MI, the animals swam for 60 min/day, 5 days/week, for additional 8 weeks. Papillary muscles of the left ventricle were subjected to different concentrations of extracellular calcium. Inotropism was evaluated through the developed tension (DT), the maximum positive value of the first temporal derivation (+Td/td) and the time to peak tension (TPT). Lusitropism was evaluated by the maximum negative value of the first temporal derivation (-Td/td) and time to 50% relaxation (50%TR). Statistical significance was determined using multivariate analysis of variance and a Hotelling T2 test for the absolute power values of all four extracellular calcium concentrations (p < 0.05). Results: MI depressed inotropism (from 17% to 51%) and lusitropism (from 22% to 54%) of the sedentary rats, but exercise attenuated the losses, especially regarding + dT/dt, TPT, -dT/dt and 50%TR. Exercise attenuated the decrease in myocardial responsiveness, proportionally to the size of the MI. Conclusion: Myocardial calcium responsiveness is favorably affected in animals with moderate and large MI after swimming exercise.

Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training.

BACKGROUND: Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation. METHODS: Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated. RESULTS: Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway. CONCLUSIONS: Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.

Are there gender differences in left ventricular remodeling after myocardial infarction in rats?

OBJECTIVE: An unclear issue is whether gender may influence at cardiac remodeling after myocardial infarction (MI). We evaluated left ventricle remodeling in female and male rats post-MI. METHODS: Rats were submitted to anterior descending coronary occlusion. Echocardiographic evaluations were performed on the first and sixth week post-occlusion to determine myocardial infarction size and left ventricle systolic function (FAC, fractional area change). Pulsed Doppler was applied to analyze left ventricle diastolic function using the following parameters: E wave, A wave, E/A ratio. Two-way ANOVA was applied for comparisons, complemented by the Bonferroni test. A P≤=0.05 was considered significant. RESULTS: There were no significant differences between genders for morphometric parameters on first (MI [Female (FE): 44.0 ± 5.0 vs. Male (MA): 42.0 ± 3.0%]; diastolic [FE: 0.04 ± 0.003 vs. MA: 0.037 ± 0.005, mm/g] and systolic [FE: 0.03 ± 0.0004 vs. MA: 0.028 ± 0.005, mm/g] diameters of left ventricle) and sixth (MI [FE: 44.0 ± 5.0 vs. MA: 42.0 ± 3.0, %]; diastolic [FE: 0.043 ± 0.01 vs. MA: 0.034 ± 0.005, mm/g] and systolic [FE: 0.035 ± 0.01 vs. MA: 0.027 ± 0.005, mm/g] of LV) week. Similar findings were reported for left ventricle functional parameters on first (FAC [FE: 34.0 ± 6.0 vs. MA: 32.0 ± 4.0, %]; wave E [FE: 70.0 ± 18.0 vs. MA: 73.0 ± 14.0, cm/s]; wave A [FE: 20.0 ± 12.0 vs. MA: 28.0 ± 13.0, cm/s]; E/A [FE: 4.9 ± 3.4 vs. MA: 3.3 ± 1.8]) and sixth (FAC [FE: 29.0 ± 7.0 vs. MA: 31.0 ± 7.0, %]; wave E [FE: 85.0 ± 18.0 vs. MA: 87.0 ± 20.0, cm/s]; wave A [FE: 20.0 ± 11.0 vs. MA: 28.0 ± 17.0, cm/s]; E/A [FE: 6.2 ± 4.0 vs. MA: 4.6 ± 3.4]) week. CONCLUSION: Gender does not influence left ventricle remodeling post-MI in rats.