Effect of experimental pulmonary arterial hypertension on renal and bone parameters of rats submitted to resistance exercise training.

Pulmonary arterial hypertension (PAH) is characterized by right ventricular failure and diminished cardiac output, potentially leading to renal and bone impairments. In contrast, resistance exercise training (RT) offers cardiovascular and bone health benefits. This study aimed to assess the impacts of stable PAH induced by monocrotaline (MCT) and RT on renal morphometry, as well as bone morphometry and biomechanical properties in male Wistar rats. Four experimental groups, untrained control (UC, n=7), trained control (TC, n=7), untrained hypertensive (UH, n=7), trained hypertensive (TH, n=7), were defined. After the first MCT or saline injection (20 mg/kg), trained rats were submitted to a RT program (i.e., Ladder climbing), 5 times/week. Seven days later the rats received the second MCT or saline dose. After euthanasia, renal and femoral histomorphometry and femoral biomechanical properties were assessed. PAH reduced renal glomerular area and volume, which was prevented by the RT. While PAH did not harm the femoral morphometry, structural and mechanical properties, RT improved the femoral parameters (e.g., length, percentage of trabeculae and bone marrow, ultimte and yield loads). Experimental stable PAH promotes renal but not bone damages, whereas RT prevents renal deteriorations and improves the femoral morphological and biomechanical properties.

Differences between 48 and 72-hour intervals on match load and subsequent recovery: a report from the Brazilian under-20 national football team.

Purpose: To compare the external and internal load and subsequent recovery of football players after international tournament matches separated by 48 h vs. 72 h. Methods: A total of 14 male football players from the Brazilian National Team, competing in the 2019 South American Under-20 Championship, participated in the study. Match load was quantified using GPS variables and perceived exertion ratings (1). Additionally, before and 13-15 h after each match, players answered questions about the number of hours and quality of sleep, recovery status, and muscle soreness (0-10) and provided a blood sample for creatine kinase and reactive C-protein analysis. Values of all variables were compared between matches played with 48-h intervals (matches 1-4) and 72-h intervals (matches 5-8). Results: No significant differences in performance or perceptual parameters were observed between matches (p = 0.136-0.953). However, CK was higher in matches 1-4 compared to matches 5 and 6; and ΔPCR was higher in matches 2 and 3 compared to matches 5 and 6, and in match 4 compared to matches 5 and 8. Conclusions: After matches with a 48-h rest interval, players showed increased markers of inflammation and muscle damage compared to matches with a 72-h rest interval.

Effects of moderate-continuous and high-intensity interval aerobic training on cardiac function of spontaneously hypertensive rats.

The aim of this study was to verify the effects of moderate-intensity continuous (MICT) and high-intensity interval (HIIT) aerobic training on cardiac morphology and function and the mechanical properties of single cardiomyocytes in spontaneously hypertensive rats (SHR) in the compensated phase of hypertension. Sixteen-week-old male SHR and normotensive Wistar (WIS) rats were allocated to six groups of six animals each: SHR CONT or WIS CONT (control); SHR MICT or WIS MICT (underwent MICT, 30 min/day, five days per week for eight weeks); and SHR HIIT or WIS HIIT (underwent HIIT, 30 min/day, five days per week for eight weeks). Total exercise time until fatigue and maximum running speed were determined using a maximal running test before and after the experimental period. Systolic (SAP), diastolic (DAP), and mean (MAP) blood pressures were measured using tail plethysmography before and after the experimental period. Echocardiographic evaluations were performed at the end of the experimental period. The rats were euthanized after in vivo assessments, and left ventricular myocytes were isolated to evaluate global intracellular Ca2+ transient ([Ca2+]i) and contractile function. Cellular measurements were performed at basal temperature (~37°C) at 3, 5, and 7 Hz. The results showed that both training programs increased total exercise time until fatigue and, consequently, maximum running speed. In hypertensive rats, MICT decreased SAP, DAP, MAP, interventricular septal thickness during systole and diastole, and the contraction amplitude at 5 Hz. HIIT increased heart weight and left ventricular wall thickness during systole and diastole and reduced SAP, MAP, and the time to peak [Ca2+]i at all pacing frequencies. In conclusion, both aerobic training protocols promoted beneficial adaptations to cardiac morphology, function, and mechanical properties of single cardiomyocytes in SHR.

Spontaneously hypertensive rats have greater impairments in regulating abdominal temperature than brain cortex temperature following physical exercise.

This study aimed to evaluate the changes in brain (Tbrain) and abdominal (Tabd) temperatures in spontaneously hypertensive rats (SHRs) following fatiguing exercise. Male normotensive Wistar rats (NWRs) and SHRs were used at 16 weeks of age. Their arterial pressure was measured by tail plethysmography prior to the experiments to confirm the hypertensive status of the SHRs. Then, the rats underwent implantation of an abdominal temperature sensor to measure Tabd and a guide cannula in the frontal cortex to enable the insertion of a thermistor to measure Tbrain. After a familiarization period, each animal was subjected to incremental speed exercises until fatigue in either a temperate (25 °C) or warm (32 °C) environment, followed by a 60-min post-exercise period at the same temperature at which they exercised. Tbrain, Tabd and tail-skin temperature (Tskin) were measured every min throughout the experiments. SHRs exhibited higher Tabd values than NWRs, and these higher values were transiently and persistently observed at 25 °C and 32 °C, respectively. For example, at 32 °C, Tabd was 0.84 °C higher in SHRs at the 25th min (large effect size). In contrast, regardless of the ambient temperature, SHRs exhibited similar Tbrain values as NWRs, indicating preserved Tbrain regulation following exercise in hypertensive rats. SHRs presented higher Tskin during the last half of the post-exercise period at 25 °C, whereas no inter-group differences were observed at 32 °C. In conclusion, the present results highlight that SHRs, an animal model that mimics uncontrolled essential hypertension in humans, exhibited greater impairments in regulating Tabd than Tbrain during the post-exercise period.

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.