Effects of exercise training and stem cell therapy on the left ventricle of infarcted rats.

INTRODUCTION AND OBJECTIVES: Stem cell therapy and aerobic exercise are non-pharmacological therapies following myocardial infarction. The aim of this study was to test whether aerobic exercise training enhances the benefits of mesenchymal stem cell (MSC) therapy on remodeling of the extracellular matrix and fetal gene expression in the left ventricle of infarcted rats. METHODS: Myocardial infarction was surgically induced in six-week old male Wistar rats. Animals were divided into four groups: sedentary control (SC) and sedentary and stem cell treated (SCMSC); exercised (EX) and exercised and stem cell treated (EXMSC). Bone marrow-derived MSCs were immediately transplanted via the tail vein (concentration: 1×106 cells). Exercise training (five days/week, 60 min/day; 60% of maximal running speed) started 24 hours after myocardial infarction and lasted for 12 weeks. RESULTS: Exercise capacity was higher in exercised than in sedentary groups. Animals in the SCMSC, EX and EXMSC groups exhibited better cardiac function than those in SC. Collagen content was lower in the SCMSC, EX and EXMSC groups than in SC and skeletal α-actin expression was lower in EX and EXMSC than in SC. The α/ß-MHC ratio was higher in EX and EXMSC than in SC. The combination of therapies further reduced collagen content in the remote region of the infarct (∼24%) and skeletal α-actin expression (∼30%). CONCLUSION: Aerobic exercise training appears to enhance the beneficial effects of stem cell therapy on remodeling of the extracellular matrix and fetal gene expression in the left ventricle of rats with moderate infarction.

Attenuation of Ca2+ homeostasis, oxidative stress, and mitochondrial dysfunctions in diabetic rat heart: insulin therapy or aerobic exercise?

We tested the effects of swimming training and insulin therapy, either alone or in combination, on the intracellular calcium ([Ca(2+)]i) homeostasis, oxidative stress, and mitochondrial functions in diabetic rat hearts. Male Wistar rats were separated into control, diabetic, or diabetic plus insulin groups. Type 1 diabetes mellitus was induced by streptozotocin (STZ). Insulin-treated groups received 1 to 4 UI of insulin daily for 8 wk. Each group was divided into sedentary or exercised rats. Trained groups were submitted to swimming (90 min/day, 5 days/wk, 8 wk). [Ca(2+)]i transient in left ventricular myocytes (LVM), oxidative stress in LV tissue, and mitochondrial functions in the heart were assessed. Diabetes reduced the amplitude and prolonged the times to peak and to half decay of the [Ca(2+)]i transient in LVM, increased NADPH oxidase-4 (Nox-4) expression, decreased superoxide dismutase (SOD), and increased carbonyl protein contents in LV tissue. In isolated mitochondria, diabetes increased Ca(2+) uptake, susceptibility to permeability transition pore (MPTP) opening, uncoupling protein-2 (UCP-2) expression, and oxygen consumption but reduced H2O2 release. Swimming training corrected the time course of the [Ca(2+)]i transient, UCP-2 expression, and mitochondrial Ca(2+) uptake. Insulin replacement further normalized [Ca(2+)]i transient amplitude, Nox-4 expression, and carbonyl content. Alongside these benefits, the combination of both therapies restored the LV tissue SOD and mitochondrial O2 consumption, H2O2 release, and MPTP opening. In conclusion, the combination of swimming training with insulin replacement was more effective in attenuating intracellular Ca(2+) disruptions, oxidative stress, and mitochondrial dysfunctions in STZ-induced diabetic rat hearts.

Ventricular remodeling in growing rats with experimental diabetes: The impact of swimming training.

Diabetic cardiomyopathy is associated with cardiac muscle remodeling, resulting in myocardial dysfunction, whereas exercise training (ET) is a useful nonpharmacological strategy for the therapy of cardiac diseases. This study tested the effects of low-intensity swimming-training on the structural remodeling of the left ventricle (LV) in growing rats with unmanaged experimental diabetes. Thirty-day-old male Wistar rats were divided into four groups (n=5/group): sedentary-control (SC), exercised-control (EC), sedentary-diabetic (SD), and exercised-diabetic (ED). Swimming-training rats exercised 5 days/week, 90min/day, with a load of 5% BW during 8 weeks. Sections of LV were stained with Periodic acid-Schiff, Sirius Red, and Gomori's reticulin. Seven days and 8 weeks after streptozotocin (STZ) induction (60mgkg(-1) BW), blood glucose (BG) in the diabetic groups (SD=581.40±40.48; ED=558.00±48.89) was greater (p<0.05) than in their controls (SC=88.80±21.70; EC=85.60±11.55). Swimming-training reduced BG by 23mg/dL in the diabetics (p>0.05). The LV of diabetic rats had increased interstitial collagen and reticular fibers on the extracellular matrix and presented glycogen accumulation. More importantly, all these adverse tissue changes induced by STZ were attenuated by ET. Together, these findings support the idea of a beneficial role of exercise in the LV remodeling in rats with unmanaged type-1 diabetes mellitus.

Pre-game hydration status, sweat loss, and fluid intake in elite Brazilian young male soccer players during competition.

In this study, we assessed the pre-game hydration status and fluid balance of elite young soccer players competing in a match played in the heat (temperature 31.0 ± 2.0 ° C, relative humidity 48.0 ± 5.0%) for an official Brazilian soccer competition. Fluid intake was measured during the match, as were urine specific gravity and body mass before and after the game to estimate hydration status. Data were obtained from 15 male players (age 17.0 ± 0.6 years, height 1.78 ± 0.06 m, mass 65.3 ± 3.8 kg); however, data are only analysed for 10 players who completed the full game. The mean (± s) sweat loss of players amounted to 2.24 ± 0.63 L, and mean fluid intake was 1.12 ± 0.39 L. Pre-game urine specific gravity was 1.021 ± 0.004, ranging from 1.010 to 1.025. There was no significant correlation between sweat loss and fluid intake (r = 0.504, P = 0.137) or between urine specific gravity and fluid intake (r = -0.276, P = 0.440). We conclude that young, native tropical soccer players started the match hypohydrated and replaced about 50% of the sweat lost. Thus, effective strategies to improve fluid replacement are needed for players competing in the heat.

Fluid balance of elite Brazilian youth soccer players during consecutive days of training.

In this study we investigated pre-training hydration status, fluid intake, and sweat loss in 20 elite male Brazilian adolescent soccer players (mean ± s: age 17.2 ± 0.5 years; height 1.76 ± 0.05 m; body mass 69.9 ± 6.0 kg) on three consecutive days of typical training during the qualifying phase of the national soccer league. Urine specific gravity (USG) and body mass changes were evaluated before and after training sessions to estimate hydration status. Players began the days of training mildly hypohydrated (USG > 1.020) and fluid intake did not match fluid losses. It was warmer on Day 1 (33.1 ± 2.4°C and43.4 ± 3.2% relative humidity; P < 0.05) and total estimated sweat losses (2822 ± 530 mL) and fluid intake (1607 ± 460 mL) were significantly higher (P < 0.001) compared with Days 2 and 3. Data also indicate a significant correlation between the extent of sweat loss and the volume of fluid consumed (Day 1: r = 0.560, P = 0.010; Day 2: r = 0.445, P = 0.049; Day 3: r = 0.743, P = 0.0001). We conclude that young, native tropical soccer players arrive hypohydrated to training and that they exhibit voluntary dehydration; therefore, enhancing athletes' self-knowledge of sweat loss during training might help them to consume sufficient fluid to match the sweat losses.