Effects of physical training on hypothalamic neuronal activation and expressions of vasopressin and oxytocin in SHR after running until fatigue.

To assess the influence of physical training on neuronal activation and hypothalamic expression of vasopressin and oxytocin in spontaneously hypertensive rats (SHR), untrained and trained normotensive rats and SHR were submitted to running until fatigue while internal body and tail temperatures were recorded. Hypothalamic c-Fos expression was evaluated in thermoregulatory centers such as the median preoptic nucleus (MnPO), medial preoptic nucleus (mPOA), paraventricular nucleus of the hypothalamus (PVN), and supraoptic nucleus (SON). The PVN and the SON were also investigated for vasopressin and oxytocin expressions. Although exercise training improved the workload performed by the animals, it was reduced in SHR and followed by increased internal body temperature due to tail vasodilation deficit. Physical training enhanced c-Fos expression in the MnPO, mPOA, and PVN of both strains, and these responses were attenuated in SHR. Vasopressin immunoreactivity in the PVN was also increased by physical training to a lesser extent in SHR. The already-reduced oxytocin expression in the PVN of SHR was increased in response to physical training. Within the SON, neuronal activation and the expressions of vasopressin and oxytocin were reduced by hypertension and unaffected by physical training. The data indicate that physical training counterbalances in part the negative effect of hypertension on hypothalamic neuronal activation elicited by exercise, as well as on the expression of vasopressin and oxytocin. These hypertension features seem to negatively influence the workload performed by SHR due to the hyperthermia derived from the inability of physical training to improve heat dissipation through skin vasodilation.

Validity and reproducibility of the CALERA Research Sensor to estimate core temperature at different intensities of a cycling exercise in the heat.

Recent heatwaves have highlighted the importance of accurate and continuous core temperature (TCORE) monitoring in sports settings. For example, accentuated rises in TCORE caused by physical exercises under environmental heat stress increase the risk of heat illnesses. Thus, using valid and reproducible devices is essential to ensure safe sports practice. In this study, we assessed the validity and reproducibility of the Calera Research Sensor (CRS) in estimating the TCORE of male and female participants during cycling exercise in a hot environment. Seven male (age: 36.2 ± 10.1 years) and eight female cyclists (age: 30.1 ± 5.0 years) underwent two identical cycling trials in a dry-bulb temperature of 32 °C and relative humidity of 60%. The protocol consisted of an initial 10-min rest followed by a 60-min exercise comprising 10 min at 20%, 25 min at 55%, and 25 min at 75% of maximal aerobic power, and an additional 25 min of post-exercise recovery. TCORE was recorded simultaneously every minute using a gastrointestinal capsule (TGi) and the CRS (TSENSOR). Bland-Altman analysis was performed to calculate bias, upper (LCS) and lower (LCI) concordance limits, and the 95% confidence interval (95%CI). The maximum acceptable difference between the two devices was predetermined at ±0.4 °C. A mixed linear model was used to assess the paired differences between the two measurement systems, considering the participants, trials, and environmental conditions as random effects and the cycling stages as fixed effects. An intra-class correlation coefficient (ICC) of 0.98 was recorded when analyzing data from the entire experiment. A non-significant bias value of 0.01 °C, LCS of 0.38 °C, LCI of -0.35 °C, and CI95% of ±0.36 °C were found. When analyzing data according to the participants' sex, CRS reproducibility was high in both sexes: ICC values of 0.98 and 0.99 were reported for males and females, respectively. CI95% was 0.35 °C in experiments with males and 0.37 °C with females, thereby falling within the acceptable margin of difference. Therefore, CRS was considered valid (compared to TGi) and reproducible in estimating TCORE in both sexes at various intensities of cycling exercise in the heat.

Impaired thermoregulation in spontaneously hypertensive rats during physical exercise is related to reduced hypothalamic neuronal activation.

This study aimed to evaluate the physical exercise-induced neuronal activation in brain nuclei controlling thermoregulatory responses in hypertensive and normotensive rats. Sixteen-week-old male normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs) were implanted with an abdominal temperature sensor. After recovery, the animals were subjected to a constant-speed treadmill running (at 60% of the maximum aerobic speed) for 30 min at 25 °C. Core (Tcore) and tail-skin (Tskin) temperatures were measured every minute during exercise. Ninety minutes after the exercise, the rats were euthanized, and their brains were collected to determine the c-Fos protein expression in the following areas that modulate thermoregulatory responses: medial preoptic area (mPOA), paraventricular hypothalamic nucleus (PVN), and supraoptic nucleus (SON). During treadmill running, the SHR group exhibited a greater increase in Tcore and an augmented threshold for cutaneous heat loss relative to the NWR group. In addition, the SHRs showed reduced neuronal activation in the mPOA (< 49.7%) and PVN (< 44.2%), but not in the SON. The lower exercise-induced activation in the mPOA and PVN in hypertensive rats was strongly related to the delayed onset of cutaneous heat loss. We conclude that the enhanced exercise-induced hyperthermia in hypertensive rats can be partially explained by a delayed cutaneous heat loss, which is, in turn, associated with reduced activation of brain areas modulating thermoregulatory responses.

Mesenchymal stem cell therapy associated with endurance exercise training: Effects on the structural and functional remodeling of infarcted rat hearts.

We tested the effects of early mesenchymal stem cell (MSC) therapy associated with endurance exercise on the structural and functional cardiac remodeling of rats with myocardial infarctation (MI). Male Wistar rats (40 days old) were divided into 6 groups: control and exercise sham; control and exercise MI; and control and exercise MI MSC. MI was surgically induced and bone marrow-derived MSCs were immediately injected via caudal vein (concentration: 1 × 10(6 )cells). Twenty-four hours later ET groups exercised on a treadmill (5 days/week; 60 min/day; 60% of maximal running velocity) for 12 weeks. Structural and functional changes were determined by echocardiography. Contractility and intracellular global calcium ([Ca(2 +)]i) transient were measured in myocytes from the left ventricular (LV) non-infarcted area. Calcium regulatory proteins were measured by Western blot. MI increased (p < 0.05) heart, ventricular and LV weights and its ratios to body weight; LV internal dimension in diastole (LVID-D) and in systole (LVID-S) and LV free wall in diastole (LVFW-D), but reduced the thickness of interventricular septum in systole (IVS-S), ejection fraction (EF) and fractional shortening (FS). MI augmented (p < 0.05) the times to peak and to half relaxation of cell shortening as well as the amplitude of the [Ca(2 +)]i transient and the times to peak and to half decay. Early MSCs therapy restored LVFW-D, IVS-S and the amplitude and time to half decay of the [Ca(2 +)]i transient. Early endurance exercise intervention increased (p < 0.05) LVFW-S, IVS-S, EF and FS, and reduced the times to peak and to half relaxation of cell shortening, and the amplitude of the [Ca(2 +)]i transient. Exercise training also increased the expression of left ventricular SERCA2a and PLBser16. Nevertheless, the combination of these therapies did not cause additive effects. In conclusion, combining early MSCs therapy and endurance exercise does not potentiate the benefits of such treatments to structural and functional cardiac remodeling in infarcted rats.

Power spectrum analysis of cardiovascular variability during passive heating in conscious rats.

The cardiovascular system plays a direct role in the maintenance of body temperature. Whether passive heating alters cardiovascular autonomic modulation in conscious rats is still unknown. This study investigated the effects of passive heating on systolic blood pressure variability (SBPV) and heart rate variability (HRV) in conscious rats and the involvement of the renin-angiotensin system in the passive heating effects on SBPV and HRV. Fourteen male Wistar rats were randomly assigned to the control group or the losartan treatment group. A catheter was implanted in the left carotid artery to record pulsatile arterial pressure (PAP), and a telemetry sensor was implanted in the abdominal cavity to measure body temperature (Tbody). After recovering from surgery, the animals were subjected to a passive heating protocol (35°C; 30min) in resting conditions, during which Tbody, tail skin temperature and PAP were measured. The mean arterial pressure, systolic and diastolic blood pressure, heart rate, double product (i.e., the product of systolic blood pressure by heart rate), SBPV and HRV were calculated from the PAP. SBPV and HRV were analyzed in terms of both time and frequency domains. Increases in the thermoregulatory and cardiovascular parameters were observed during passive heating in both groups, and those increases were reflected in the higher time and frequency domains of the SBPV. However, passive heating was not effective in altering HRV. Passive heating altered SBPV but not HRV in conscious rats when they were treated with losartan.

The benefits of endurance training in cardiomyocyte function in hypertensive rats are reversed within four weeks of detraining.

The aim of the present study was to verify the effects of low-intensity endurance training and detraining on the mechanical and molecular properties of cardiomyocytes from spontaneously hypertensive rats (SHRs). Male SHRs and normotensive control Wistar rats at 16-weeks of age were randomly divided into eight groups of eight animals: NC8 and HC8 (normotensive and hypertensive control for 8weeks); NT8 and HT8 (normotensive and hypertensive trained at 50-60% of maximal exercise capacity for 8weeks); NC12 and HC12 (normotensive and hypertensive control for 12weeks); NDT and HDT (normotensive and hypertensive trained for 8weeks and detrained for 4weeks). The total exercise time until fatigue (TTF) was determined by a maximal exercise capacity test. Resting heart rate (RHR) and systolic arterial pressure (SAP) were measured. After the treatments, animals were killed by cervical dislocation and left ventricular myocytes were isolated by enzymatic dispersion. Isolated cells were used to determine intracellular global Ca(2+) ([Ca(2+)]i) transient and cardiomyocyte contractility (1Hz; ~25°C). [Ca(2+)]i regulatory proteins were measured by Western blot, and the markers of pathologic cardiac hypertrophy by quantitative real-time polymerase chain reaction (q-RT-PCR). Exercise training augmented the TTF (NC8, 11.4±1.5min vs. NT8, 22.5±1.4min; HC8, 11.7±1.4min vs. HT8, 24.5±1.3min; P<0.05), reduced RHR (NT8initial, 340±8bpm vs. NT8final, 322±10bpm; HT8initial, 369±8bpm vs. HT8final, 344±10bpm; P<0.05), and SBP in SHR animals (HC8, 178±3mmHg vs. HT8, 161±4mmHg; P<0.05). HC8 rats showed a slower [Ca(2+)]i transient (Tpeak, 83.7±1.8ms vs. 71.7±2.4ms; T50%decay, 284.0±4.3ms vs. 264.0±4.1ms; P<0.05) and cell contractility (Vshortening, 86.1±6.7µm/s vs. 118.6±6.7µm/s; Vrelengthening, 57.5±7.4µm/s vs. 101.3±7.4µm/s; P<0.05), and higher expression of ANF (300%; P<0.05), skeletal α-actin (250%; P<0.05) and a decreased α/ß-MHC ratio (70%; P<0.05) compared to NC8. Exercise training increased [Ca(2+)]i transient (NC8, 2.39±0.06F/F0 vs. NT8, 2.72±0.06F/F0; HC8, 2.28±0.05F/F0 vs. HT8, 2.82±0.05F/F0; P<0.05), and cell contractility (NC8, 7.4±0.3% vs. NT8, 8.4±0.3%; HC8, 6.8±0.3% vs. HT8, 7.8±0.3%; P<0.05). Furthermore, exercise normalized the expression of ANF, skeletal α-actin, and the α/ß-MHC ratio in HT8 rats, augmented the expression of SERCA2a (NC8, 0.93±0.15 vs. NT8, 1.49±0.14; HC8, 0.83±0.13 vs. HT8, 1.32±0.14; P<0.05) and PLBser16 (NC8, 0.89±0.18 vs. NT8, 1.23±0.17; HC8, 0.77±0.17 vs. HT8, 1.32±0.16; P<0.05), and reduced PLBt/SERCA2a (NC8, 1.21±0.19 vs. NT8, 0.50±0.21; HC8, 1.38±0.17 vs. HT8, 0.66±0.21; P<0.05). However, all these adaptations returned to control values within 4weeks of detraining in both SHR and normotensive control animals. In conclusion, low-intensity endurance training induces positive benefits to left ventricular myocyte mechanical and molecular properties, which are reversed within 4weeks of detraining.

Normal gastrointestinal temperature values measured through ingestible capsules technology: a systematic review.

Climate change has amplified the importance of continuous and precise body core temperature (Tcore) monitoring in the everyday life. In this context, assessing Tcore through ingestible capsules technology, i.e., gastrointestinal temperature (Tgastrointestinal), emerges as a good alternative to prevent heat-related illness. Therefore, we conducted a systematic review to point out values of normal Tgastrointestinal measured through ingestible capsules in healthy humans. The study followed PRISMA guidelines and searched the PubMed and Scielo databases from 1971 to 2023. Our search strategy included the descriptors ("gastrointestinal temperature") AND ("measurement"), and eligible studies had to be written in English and measured Tgastrointestinal using ingestible capsules or sensors in healthy adults aged 18-59 at rest. Two pairs of researchers independently reviewed titles and abstracts and identified 35 relevant articles out of 1,088 in the initial search. An average value of 37.13 °C with a standard deviation of 0.24 °C was observed, independently of the gender. The values measured ranged from 36.70 °C to 37.69 °C. In conclusion, this systematic review pointed out the mean value of 37.13 ± 0.24 °C measured by ingestible capsules as reference for resting Tgastrointestinal in healthy adult individuals.

Swimming Training Does Not Affect the Recovery of Femoral Midshaft Structural and Mechanical Properties in Growing Diabetic Rats Treated with Insulin.

BACKGROUND: The effects of swimming training associated with insulin treatment on the cortical bone health in young rats with severe type 1 diabetes remain unclear, although there is evidence of such effects on the cancellous bone. This study examined the effects of swimming training combined with insulin therapy on the femoral midshaft structural and mechanical properties in growing rats with type 1 diabetes. METHODS: Male Wistar rats were divided into six groups (n = 10): control sedentary, control exercise, diabetic sedentary, diabetic exercise, diabetic sedentary plus insulin and diabetic exercise plus insulin. Diabetic rats received an injection (60 mg/kg body weight) of streptozotocin (STZ). Exercised animals underwent a swimming program for eight weeks. RESULTS: Diabetes induced by STZ decreased the bone mineral content (BMC) and density (BMD), and cortical thickness and maximum load and tenacity in the femoral midshaft. Insulin treatment partially counteracted the damages induced by diabetes on BMC, BMD and cortical thickness and tenacity. Swimming training did not affect the femoral structural and mechanical properties in diabetic rats. The combination of treatments did not potentiate the insulin effects. In conclusion, swimming training does not affect the benefits of insulin treatment on the femoral midshaft structural and mechanical properties in growing rats with severe type 1 diabetes.

Cardiac oxidative stress is involved in heart failure induced by thiamine deprivation in rats.

Thiamine is an important cofactor of metabolic enzymes, and its deficiency leads to cardiovascular dysfunction. First, we characterized the metabolic status measuring resting oxygen consumption rate and lactate blood concentration after 35 days of thiamine deficiency (TD). The results pointed to a decrease in resting oxygen consumption and a twofold increase in blood lactate. Confocal microscopy showed that intracellular superoxide (approximately 40%) and H(2)O(2) (2.5 times) contents had been increased. In addition, biochemical activities and protein expression of SOD, glutathione peroxidase, and catalase were evaluated in hearts isolated from rats submitted to thiamine deprivation. No difference in SOD activity was detected, but protein levels were found to be increased. Catalase activity increased 2.1 times in TD hearts. The observed gain in activity was attended by an increased catalase protein level. However, a marked decrease in glutathione peroxidase activity (control 435.3 + or - 28.6 vs. TD 199.4 + or - 30.2 nmol NADPH x min(-1) x ml(-1)) was paralleled by a diminution in the protein levels. Compared with control hearts, we did observe a greater proportion of apoptotic myocytes by TdT-mediated dUTP nick end labeling (TUNEL) and caspase-3 reactivity techniques. These results indicate that during TD, reactive oxygen species (ROS) production may be enhanced as a consequence of the installed acidosis. The perturbation in the cardiac myocytes redox balance was responsible for the increase in apoptosis.

Thermoregulation in Hypertensive Rats during Exercise: Effects of Physical Training.

BACKGROUND: Spontaneously hypertensive rats (SHR) show deficit in thermal balance during physical exercise. OBJECTIVE: To assess the effects of low-intensity physical exercise training on thermal balance of hypertensive rats undergoing an acute exercise protocol. METHODS: Sixteen-week-old male Wistar rats and SHR were allocated into four groups: control Wistar rats (C-WIS), trained Wistar (T-WIS), control SHR (C-SHR) and trained SHR (T-SHR). Treadmill exercise training was performed for 12 weeks. Blood pressure, resting heart rate and total exercise time was measured before and after the physical exercise program. After the exercise program, a temperature sensor was implanted in the abdominal cavity, and the animals subjected to an acute exercise protocol, during which internal body temperature, tail skin temperature and oxygen consumption until fatigue were continuously recorded. Mechanical efficiency (ME), work, heat dissipation threshold and sensitivity were calculated. Statistical significance was set at 5%. RESULTS: Physical training and hypertension had no effect on thermal balance during physical exercise. Compared with C-WIS, the T-WIS group showed higher heat production, which was counterbalanced by higher heat dissipation. Hypertensive rats showed lower ME than normotensive rats, which was not reversed by the physical training. CONCLUSION: Low-intensity physical training did not affect thermal balance in SHR subjected to acute exercise.

Effects of aerobic exercise on the inflammatory cytokine profile and expression of lipolytic and thermogenic genes in ß1-AR-/- mice adipose tissue.

AIM: Investigate the effects of moderate continuous aerobic exercise (MCAE) on the inflammatory cytokine profile and expression of lipolytic and thermogenic genes in ß1-AR-/- mice adipose tissue. MAIN METHODS: Four- to five-month-old male wild type (WT) and ß1-AR-/- mice were divided into groups: WT control (WTc) and trained (WTt); and ß1-AR-/- control (ß1-AR-/-c) and trained (ß1-AR-/-t). Animals from trained groups were submitted to a MCAE regimen (60 min/day; 60% of maximal speed, 5 days/week) on a treadmill, for 8 weeks. After euthanasia, white epididymal (eWAT) and inguinal (iWAT) and brown (BAT) adipose tissues were dissected and used to determine: adiposity index; adipocyte histomorphometry; cytokine concentration; and gene expression. The content of fat, protein and water of the empty carcass was determined. KEY FINDINGS: MCAE reduced body weight, fat mass as well as iWAT and BAT adipocyte area in ß1-AR-/- animals. Aerobic exercise also diminished the concentrations of pro-inflammatory (IL-12p70, TNF-α, IL-6) and anti-inflammatory (IL-10) cytokines in adipose tissue (iWAT, eWAT or BAT) of ß1-AR-/- mice. However, MCAE had no effect on the expression lipolytic and thermogenic genes in ß1-AR-/- mice adipose tissue. SIGNIFICANCE: Alongside reductions in body weight, fat mass and adipocyte area eight weeks of MCAE improves the profile of inflammatory cytokines in ß1-AR-/- mice adipose tissue, despite no change in Lipolytic and thermogenic gene expression.

Swimming training potentiates the recovery of femoral neck strength in young diabetic rats under insulin therapy.

OBJECTIVE: To test whether swimming training benefits femoral neck strength in young diabetic rats under insulin therapy. METHODS: A total of 60 male Wistar rats (age: 40 days) were divided equally into the following six groups: control sedentary, control exercise, diabetic sedentary, diabetic exercise, diabetic sedentary plus insulin and diabetic exercise plus insulin. Diabetes was induced with a unique intraperitoneal injection (60 mg/kg body weight) of streptozotocin. Seven days after the injection and after 12 hours of fasting, the animals with blood glucose levels ≥300 mg/dL were considered diabetic. Seven days after the induction of diabetes, the animals in the exercise groups were subjected to progressive swimming training (final week: 90 min/day; 5 days/week; 5% load) for eight weeks. The animals in the insulin groups received a daily dose of insulin (2-4 U/day) for the same period. RESULTS: Severe streptozotocin-induced diabetes reduced the structural properties of the femoral neck (trabecular bone volume, trabecular thickness and collagen fiber content). The femoral neck mechanical properties (maximum load and tenacity) were also impaired in the diabetic rats. Insulin therapy partially reversed the damage induced by diabetes on the structural properties of the bone and mitigated the reductions in the mechanical properties of the bone. The combination of therapies further increased the femoral neck trabecular bone volume (∼30%), trabecular thickness (∼24%), collagen type I (∼19%) and type III (∼13%) fiber contents, maximum load (∼25%) and tenacity (∼14%). CONCLUSIONS: Eight weeks of swimming training potentiates the recovery of femoral neck strength in young rats with severe streptozotocin-induced diabetes under insulin therapy.

Voluntary running counteracts right ventricular adverse remodeling and myocyte contraction impairment in pulmonary arterial hypertension model.

AIM: Analyze the effects of voluntary running during the development of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) on the right ventricle (RV) structure, RV myocyte contractility and intracellular Ca2+ transient in rats with MCT-induced PAH. MAIN METHODS: Male Wistar rats were housed sedentary or with free access to a running wheel after MCT or saline injection for until HF or median end-point day of HF in sedentary animals (24 days). Echocardiographic examination and exercise tolerance test were carried out at specific time points of the experimental period. After euthanasia, the heart was dissected, weighed and processed for either histological or single myocyte contractility and intracellular Ca2+ transient analyzes. KEY FINDINGS: Voluntary running delayed the onset of HF (29 days) and the increase in pulmonary artery resistance, and improved exercise tolerance. In the median end-point day of HF, exercise retarded RV adverse remodeling (i.e. increase in extracellular matrix and collagen content). At this stage, exercise also delayed impairments in cell contractile function (i.e. amplitude and times to peak and to half relaxation) and intracellular calcium cycling (i.e. amplitude and times to peak and to half decay) in RV single myocytes. SIGNIFICANCE: Along with HF onset delay and physical effort tolerance enhancement, voluntary running during the development of PAH postpones pulmonary artery resistance increases, RV adverse remodeling and myocyte contractility and intracellular calcium cycling deterioration in rats. Therefore, self-paced intermittent exercise of high intensity may contribute positively to the health and survival of individuals with PAH.

Physical Exercise and Regulation of Intracellular Calcium in Cardiomyocytes of Hypertensive Rats.

BACKGROUND: Regulation of intracellular calcium (Ca2+) in cardiomyocytes is altered by hypertension; and aerobic exercise brings benefits to hypertensive individuals. OBJECTIVE: To verify the effects of aerobic exercise training on contractility and intracellular calcium (Ca2+) transients of cardiomyocytes and on the expression of microRNA 214 (miR-214) in the left ventricle of spontaneously hypertensive rats (SHR). METHODS: SHR and normotensive Wistar rats of 16 weeks were divided into 4 groups -sedentary hypertensive (SH); trained hypertensive (TH); sedentary normotensive (SN); and trained normotensive (TN). Animals of the TH and TN groups were subjected to treadmill running program, 5 days/week, 1 hour/day at 60-70% of maximum running velocity for 8 weeks. We adopted a p ≤ 0.05 as significance level for all comparisons. RESULTS: Exercise training reduced systolic arterial pressure in hypertensive rats. In normotensive rats, exercise training reduced the time to 50% cell relaxation and the time to peak contraction and increased the time to 50% decay of the intracellular Ca2+ transients. In SHR, exercise increased the amplitude and reduced the time to 50% decay of Ca2+ transients. Exercise training increased the expression of miR-214 in hypertensive rats only. CONCLUSION: The aerobic training applied in this study increased the availability of intracellular Ca2+ and accelerated the sequestration of these ions in left ventricular myocytes of hypertensive rats, despite increased expression of miR-214 and maintenance of cell contractility.

Moderate Continuous Aerobic Exercise Training Improves Cardiomyocyte Contractility in Β1 Adrenergic Receptor Knockout Mice.

BACKGROUND: The lack of cardiac ß1-adrenergic receptors (ß1-AR) negatively affects the regulation of both cardiac inotropy and lusitropy, leading, in the long term, to heart failure (HF). Moderate-intensity aerobic exercise (MCAE) is recommended as an adjunctive therapy for patients with HF. OBJECTIVE: We tested the effects of MCAE on the contractile properties of left ventricular (LV) myocytes from ß1 adrenergic receptor knockout (ß1ARKO) mice. METHODS: Four- to five-month-old male wild type (WT) and ß1ARKO mice were divided into groups: WT control (WTc) and trained (WTt); and ß1ARKO control (ß1ARKOc) and trained (ß1ARKOt). Animals from trained groups were submitted to a MCAE regimen (60 min/day; 60% of maximal speed, 5 days/week) on a treadmill, for 8 weeks. P ≤ 0.05 was considered significant in all comparisons. RESULTS: The ß1ARKO and exercised mice exhibited a higher (p < 0.05) running capacity than WT and sedentary ones, respectively. The ß1ARKO mice showed higher body (BW), heart (HW) and left ventricle (LVW) weights, as well as the HW/BW and LVW/BW than WT mice. However, the MCAE did not affect these parameters. Left ventricular myocytes from ß1ARKO mice showed increased (p < 0.05) amplitude and velocities of contraction and relaxation than those from WT. In addition, MCAE increased (p < 0.05) amplitude and velocities of contraction and relaxation in ß1ARKO mice. CONCLUSION: MCAE improves myocyte contractility in the left ventricle of ß1ARKO mice. This is evidence to support the therapeutic value of this type of exercise training in the treatment of heart diseases involving ß1-AR desensitization or reduction.

Brain Temperature in Spontaneously Hypertensive Rats during Physical Exercise in Temperate and Warm Environments.

This study aimed to evaluate brain temperature (Tbrain) changes in spontaneously hypertensive rats (SHRs) subjected to two different physical exercise protocols in temperate or warm environments. We also investigated whether hypertension affects the kinetics of exercise-induced increases in Tbrain relative to the kinetics of abdominal temperature (Tabd) increases. Male 16-week-old normotensive Wistar rats (NWRs) and SHRs were implanted with an abdominal temperature sensor and a guide cannula in the frontal cortex to enable the insertion of a thermistor to measure Tbrain. Next, the animals were subjected to incremental-speed (initial speed of 10 m/min; speed was increased by 1 m/min every 3 min) or constant-speed (60% of the maximum speed) treadmill running until they were fatigued in a temperate (25°C) or warm (32°C) environment. Tbrain, Tabd and tail skin temperature were measured every min throughout the exercise trials. During incremental and constant exercise at 25°C and 32°C, the SHR group exhibited greater increases in Tbrain and Tabd relative to the NWR group. Irrespective of the environment, the heat loss threshold was attained at higher temperatures (either Tbrain or Tabd) in the SHRs. Moreover, the brain-abdominal temperature differential was lower at 32°C in the SHRs than in the NWRs during treadmill running. Overall, we conclude that SHRs exhibit enhanced brain hyperthermia during exercise and that hypertension influences the kinetics of the Tbrain relative to the Tabd increases, particularly during exercise in a warm environment.

Thermoregulatory responses in exercising rats: methodological aspects and relevance to human physiology.

Rats are used worldwide in experiments that aim to investigate the physiological responses induced by a physical exercise session. Changes in body temperature regulation, which may affect both the performance and the health of exercising rats, are evident among these physiological responses. Despite the universal use of rats in biomedical research involving exercise, investigators often overlook important methodological issues that hamper the accurate measurement of clear thermoregulatory responses. Moreover, much debate exists regarding whether the outcome of rat experiments can be extrapolated to human physiology, including thermal physiology. Herein, we described the impact of different exercise intensities, durations and protocols and environmental conditions on running-induced thermoregulatory changes. We focused on treadmill running because this type of exercise allows for precise control of the exercise intensity and the measurement of autonomic thermoeffectors associated with heat production and loss. Some methodological issues regarding rat experiments, such as the sites for body temperature measurements and the time of day at which experiments are performed, were also discussed. In addition, we analyzed the influence of a high body surface area-to-mass ratio and limited evaporative cooling on the exercise-induced thermoregulatory responses of running rats and then compared these responses in rats to those observed in humans. Collectively, the data presented in this review represent a reference source for investigators interested in studying exercise thermoregulation in rats. In addition, the present data indicate that the thermoregulatory responses of exercising rats can be extrapolated, with some important limitations, to human thermal physiology.

Estresse térmico ambiental e termorregulação em jogadores de futebol: uma revisão sistemática / Environmental thermal stress and thermoregulation in soccer players: a systematic review / Estrés térmico ambiental y termorregulación en jugadores de fútbol: una revisión sistemática

Resumo O objetivo do estudo foi fazer uma revisão sistemática acerca dos efeitos do estresse térmico ambiental sobre a termorregulação em jogadores de futebol. Foram avaliados estudos em bases de dados pertencentes ao portal Periódicos Capes. Foi empregado o método Prisma para o desenvolvimento da revisão. Jogadores de futebol apresentam grande aumento da temperatura corporal associada à redução de desempenho físico durante o jogo em ambiente quente. Em relação às estratégias para amenizar esse prejuízo (ex. resfriamento, hidratação, aclimatação e aquecimento), o pequeno número de trabalhos encontrado (n = 18) apresenta resultados controversos, portanto são necessários mais estudos.

Abstract The objective of the study was to systematically review the effects of the environmental thermal stress on thermoregulation in soccer players. We analyzed studies from databases belonging to the Periódicos Capes portal. The PRISMA method was used to perform the review. Soccer players exhibit high increase in body temperature associated with reduction in physical performance during game in warm environment. Concerning strategies to mitigate such impairment (e.g. cooling, hydration, acclimatization, warm up and heating), the small number of studies analyzed (n = 18) showed controversial results, which warrants more studies.

Resumen El objetivo del estudio fue llevar a cabo una revisión sistemática sobre los efectos del estrés térmico ambiental en la termorregulación de jugadores de fútbol. Se evaluaron estudios en bases de datos pertenecientes al portal Periódicos Capes. Se empleó el método PRISMA para el desarrollo de la revisión. Los jugadores de fútbol presentan un gran aumento de la temperatura corporal asociada con la reducción de rendimiento físico durante el juego en un entorno caluroso. En cuanto a las estrategias para disminuir esta alteración (p. ej., enfriamiento, hidratación, aclimatación y calentamiento), el pequeño número de trabajos encontrados (n= 18) presentan resultados controvertidos, por lo que es necesaria la realización de más estudios.

Thermoregulation in Hypertensive Rats during Exercise: Effects of Physical Training / Termorregulação durante o Exercício em Ratos Hipertensos: Efeitos do Treinamento Físico

Abstract Background: Spontaneously hypertensive rats (SHR) show deficit in thermal balance during physical exercise. Objective: To assess the effects of low-intensity physical exercise training on thermal balance of hypertensive rats undergoing an acute exercise protocol. Methods: Sixteen-week-old male Wistar rats and SHR were allocated into four groups: control Wistar rats (C-WIS), trained Wistar (T-WIS), control SHR (C-SHR) and trained SHR (T-SHR). Treadmill exercise training was performed for 12 weeks. Blood pressure, resting heart rate and total exercise time was measured before and after the physical exercise program. After the exercise program, a temperature sensor was implanted in the abdominal cavity, and the animals subjected to an acute exercise protocol, during which internal body temperature, tail skin temperature and oxygen consumption until fatigue were continuously recorded. Mechanical efficiency (ME), work, heat dissipation threshold and sensitivity were calculated. Statistical significance was set at 5%. Results: Physical training and hypertension had no effect on thermal balance during physical exercise. Compared with C-WIS, the T-WIS group showed higher heat production, which was counterbalanced by higher heat dissipation. Hypertensive rats showed lower ME than normotensive rats, which was not reversed by the physical training. Conclusion: Low-intensity physical training did not affect thermal balance in SHR subjected to acute exercise.

Resumo Fundamento: Ratos espontaneamente hipertensos (SHR) apresentam déficits no balanço térmico durante o exercício físico. Objetivo: Avaliar os efeitos do treinamento físico de baixa intensidade sobre o balanço térmico de ratos hipertensos submetidos a um protocolo de exercício físico agudo. Métodos: Ratos machos Wistar e SHR, com 16 semanas de idade, foram divididos em quatro grupos experimentais: Wistar controle (WIS-C), Wistar treinado (WIS-T), SHR controle (SHR-C) e SHR treinado (SHR-T). O treinamento físico em esteira rolante foi realizado durante 12 semanas. A pressão arterial, a frequência cardíaca de repouso e o tempo de exercício foram medidos previamente e após o programa de treinamento físico. Após o programa de treinamento físico, um sensor de temperatura foi implantado na região intraperitoneal e os ratos foram submetidos a um protocolo de exercício físico agudo com registros contínuos da temperatura corporal interna, temperatura da pele da cauda e do consumo de oxigênio até a fadiga. A eficiência mecânica (EM), o trabalho, o limiar e a sensibilidade para dissipação de calor foram calculados. Para as análises estatísticas o nível de significância adotado foi de 5%. Resultados: O treinamento físico e a hipertensão arterial não alteraram o balanço térmico durante o exercício físico. O grupo WIS-T quando comparado ao WIS-C, apresentou maior produção de calor, que foi contrabalanceado por uma maior dissipação de calor. Os animais hipertensos apresentaram menor EM em comparação aos animais normotensos, e o treinamento físico não foi capaz de reverter esta alteração. Conclusão: O treinamento físico de baixa intensidade não provocou alterações no balanço térmico de ratos hipertensos submetidos a um protocolo de exercício físico agudo.

Swimming training potentiates the recovery of femoral neck strength in young diabetic rats under insulin therapy

OBJECTIVE: To test whether swimming training benefits femoral neck strength in young diabetic rats under insulin therapy. METHODS: A total of 60 male Wistar rats (age: 40 days) were divided equally into the following six groups: control sedentary, control exercise, diabetic sedentary, diabetic exercise, diabetic sedentary plus insulin and diabetic exercise plus insulin. Diabetes was induced with a unique intraperitoneal injection (60 mg/kg body weight) of streptozotocin. Seven days after the injection and after 12 hours of fasting, the animals with blood glucose levels ≥300 mg/dL were considered diabetic. Seven days after the induction of diabetes, the animals in the exercise groups were subjected to progressive swimming training (final week: 90 min/day; 5 days/week; 5% load) for eight weeks. The animals in the insulin groups received a daily dose of insulin (2-4 U/day) for the same period. RESULTS: Severe streptozotocin-induced diabetes reduced the structural properties of the femoral neck (trabecular bone volume, trabecular thickness and collagen fiber content). The femoral neck mechanical properties (maximum load and tenacity) were also impaired in the diabetic rats. Insulin therapy partially reversed the damage induced by diabetes on the structural properties of the bone and mitigated the reductions in the mechanical properties of the bone. The combination of therapies further increased the femoral neck trabecular bone volume (∼30%), trabecular thickness (∼24%), collagen type I (∼19%) and type III (∼13%) fiber contents, maximum load (∼25%) and tenacity (∼14%). CONCLUSIONS: Eight weeks of swimming training potentiates the recovery of femoral neck strength in young rats with severe streptozotocin-induced diabetes under insulin therapy.