Iron electrodes were used for electrocoagulation (EC) treatment of wastewater from a dairy plant. Electrolysis time, pH, current density and distance between electrodes were considered to assess the removal efficiency of chemical oxygen demand (COD), total solids (TS) and their fractions and turbidity. Samples were collected from the effluent of a dairy plant using a sampling methodology proportional to the flow. The treatments were applied according to design factorial of half fraction with two levels of treatments and three repetitions at the central point. The optimization of parameters for treating dairy industry effluent by electrocoagulation using iron electrodes showed that electric current application for 15 minutes, an initial sample pH close to neutral (pH 7.0) and a current density of 50 A ^{. m−2} resulted in a significant reduction in COD by 58 %; removal of turbidity, suspended solids and volatile suspended solids by 95 %; and a final treated effluent pH of approximately 9.5. Negative consequences of the type of electrode used were the emergence of an undesirable color and an increase in the proportion of dissolved solids in the treated effluent.

The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05). Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium. Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties.

We tested the effects of low-intensity endurance training (LIET) on the structural and mechanical properties of right (RV) and left ventricular (LV) myocytes. Male Wistar rats (4 mo old) were randomly divided into control (C, n = 7) and trained (T, n = 7, treadmill running at 50–60% of maximal running speed for 8 wk) groups. Isolated ventricular myocyte dimensions, contractility, Ca²⁺transients {intracellular Ca²⁺concentration ([Ca²⁺]_i)}, and ventricular [Ca²⁺]_iregulatory proteins were measured. LIET augmented cell length (C, 152.5 ± 2.0 μm vs. T, 162.2 ± 2.1 μm; P < 0.05) and volume (C, 5,162 ± 131 μm³vs. T, 5,506 ± 132 μm³; P < 0.05) in the LV but not in the RV. LIET increased cell shortening (C, 7.5 ± 0.3% vs. T, 8.6 ± 0.3%; P < 0.05), the [Ca²⁺]_itransient amplitude (C, 2.49 ± 0.06 F/F₀vs. T, 2.82 ± 0.06 F/F₀; P < 0.05), the expression of sarcoplasmic reticulum Ca²⁺-ATPase 2a (C, 1.07 ± 0.13 vs. T, 1.59 ± 0.12; P < 0.05), and the levels of phosphorylated phospholamban at serine 16 (C, 0.99 ± 0.11 vs. T, 1.34 ± 0.10; P < 0.05), and reduced the total phospholamban-to-sarcoplasmic reticulum Ca²⁺-ATPase 2a ratio (C, 1.19 ± 0.15 vs. T, 0.40 ± 0.16; P < 0.05) in the LV without changing such parameters in the RV. In conclusion, LIET affected the structure and improved the mechanical properties of LV but not of RV myocytes in rats, helping to characterize the functional and morphological changes that accompany the endurance training-induced cardiac remodeling.