Differential contribution of elbow flexion and knee extension on vascular and hemodynamic parameters and arterial stiffness indices after acute strength exercise in young adults.

BACKGROUND: Different types of exercise, performed acutely or chronically, have different repercussions on central hemodynamics, arterial stiffness, and cardiac function. In this study, we aim to compare the effects of acute elbow flexion (EFlex) and knee extension (KExt) exercises on vascular and hemodynamic parameters and arterial stiffness indices in healthy young adults. METHODS: Young adults (20 to 39 years) underwent randomized muscle strength tests to obtain 1 repetition maximum (1RM) for elbow flexion (EFlex) and knee extension (KExt). After a minimum interval of 48 h, cardiovascular parameters were assessed using Mobil-O-Graph® (Mobil-O-Graph, IEM, Germany) at three-time points: at baseline (before exercise), immediately after elbow flexion or knee extension exercises with a load corresponding to 50% of 1RM (T0) and after 15 min of rest (T15). RESULTS: Immediately after exercise (T0), peripheral systolic blood pressure, peripheral pulse pressure, central systolic blood pressure, and central pulse pressure were significantly higher in KExt than EFlex (Δ 3.13; Δ 3.06; Δ 5.65; Δ 5.61 mmHg, respectively). Systolic volume, cardiac output, and cardiac index were significantly higher immediately after KExt when compared with EFlex (Δ 4.2 ml; Δ 0.27 ml/min and 0.14 l/min*1/m2, respectively). The reflection coefficient and the pulse wave velocity were also significantly higher at T0 in KExt compared to EFlex ( Δ 8.59 and Δ 0.12 m/sec, respectively). CONCLUSION: Our results show differential contribution of muscle mass in vascular and hemodynamic parameters evaluated immediately after EFlex and KExt. In addition, our study showed for the first time that the reflection coefficient, an index that evaluates the magnitude of the reflected waves from the periphery, was only affected by KExt.

Long-term heat acclimation training in mice: Similar metabolic and running performance adaptations despite a lower absolute intensity than training at temperate conditions.

This study investigated the impact of long-term heat acclimation (HA) training on mouse thermoregulation, metabolism, and running performance in temperate (T) and hot (H) environments. Male Swiss mice were divided into 1) Sedentary (SED) mice kept in T (22 °C; SED/T), 2) Endurance Trained mice (ET, 1 h/day, 5 days/week, 8 weeks, 60 % of maximum speed) in T (ET/T), 3) SED kept in H (32 °C; SED/H), and 4) ET in H (ET/H). All groups performed incremental load tests (ILT) in both environments before (pre-ET) and after four and eight weeks of ET. In the pre-ET period, H impaired (∼30 %) performance variables (maximum speed and external work) and increased (1.3 °C) maximum abdominal body temperature compared with T. In T, after four weeks, although ET/H exercised at a lower (∼30 %) absolute intensity than ET/T, performance variables and aerobic power (peak oxygen uptake, VO2peak) were similarly increased in both ET groups compared with SED/T. After eight weeks, the external work was higher in both ET groups compared with SED/T. Only ET/T significantly increased VO2peak (∼11 %) relative to its pre-ET period. In H, only after eight weeks, both ET groups improved (∼19 %) maximum speed and reduced (∼46 %) post-ILT blood lactate concentrations compared with their respective pre-ET values. Liver glycogen content increased (34 %) in both ET groups and SED/H compared with SED/T. Thus, ET/H was performed at a lower absolute intensity but promoted similar effects to ET/T on metabolism, aerobic power, and running performance. Our findings open perspectives for applying HA training as part of a training program or orthopedic and metabolic rehabilitation programs in injured or even obese animals, reducing mechanical load with equivalent or higher physiological demand.

Chronic supplementation of noni in diabetic type 1-STZ rats: effects on glycemic levels, kidney toxicity and exercise performance.

Noni is a fruit with potential medicinal use preventing elevated blood glucose levels in diabetes mellitus. Its effects have been attributed to an antioxidant property in several other diseases. However, the effects of noni-chronic supplementation on exercise performance in the presence of diabetes conditions are not known. Thirty-two male Wistar rats were used to verify the effects of chronic noni (Morinda citrifolia L) juice administration on glycemia, triglyceride levels, and its relation to physical performance. In addition, it was verified if chronic noni supplementation is safe for clinical use through kidney morphology analysis. In half of the rats, diabetes mellitus (DM) was induced with STZ. All rats were submitted to an incremental workload running test (IWT) until fatigued so that oxygen consumption and performance indexes (exercise time to fatigue and workload) could be analyzed before noni administration. Then, the control and DM groups received a placebo (saline solution) or noni juice (dilution 2:1) at a dose of 2 mL/kg once a day for 60 days. The result was four groups: control + placebo (CP), control + noni (CN), DM + placebo (DMP), and DM + noni (DMN). Our dose was based on in previous study by Nayak et al. (2011) that observed a significant reduction in glycemia with 2 ml/kg of the noni juice without any toxicity effect cited. Groups were then given a third IWT to verify the effect of the noni juice on exercise performance (exercise time to fatigue, workload, maximal oxygen consumption) and glycemia. Twenty-four hours after the third test, all animals were euthanized and blood and kidneys were removed for posterior analysis. The DM induction with STZ impaired the performance by 39%. Noni administration improved the time to fatigue and workload in DM rats beyond reducing hyperglycemia. These results could be associated with an improved energy efficiency promoted by noni ingestion, since the oxygen consumption was not different between the groups, although the exercise was longer in animals with noni ingestion. Our results provided evidence that chronic noni administration causes kidney damage since increased Bowman's space area in the control rats, suggesting glomerular hyperfiltration at the same magnitude as the non-treated DM group.In conclusion, chronic noni ingestion promoted glycemic control and improved the performance in DM rats but caused kidney toxicity.

Sleep impairment and altered pattern of circadian biomarkers during a long-term Antarctic summer camp.

Antarctic expeditions include isolation and exposure to cold and extreme photoperiods (with continuous natural light during summer) that may influence psychophysiological responses modulated by luminosity and sleep. We assessed changes in night sleep patterns by actigraphy, salivary biomarkers, and perceptual variables in seven participants in the following time points along a 50-day camping expedition in Antarctica (Nelson Island): Pre-Field (i.e., on the ship before camp), Field-1, Field-2, Field-3, Field-4 (from 1st to 10th, 11th to 20th, 21st to 35th and 36th to 50th days in camp, respectively), and Post-Field (on the ship after camp). We also characterized mood states, daytime sleepiness, and sleep quality by questionnaires. Staying in an Antarctic camp reduced sleep efficiency (5.2%) and increased the number of awakenings and wakefulness after sleep onset (51.8% and 67.1%, respectively). Furthermore, transient increases in time in bed (16.5%) and sleep onset latency (4.8 ± 4.0 min, from Pre- to Field-3) was observed. These changes were accompanied by an altered pattern of the emerging circadian marker ß-Arrestin-1 and a trend to reduce nocturnal melatonin [57.1%; P = 0.066, with large effect size (ES) from Pre-Field to Field-2 (ES = 1.2) and Field-3 (ES = 1.2)]. All changes returned to Pre-Field values during the Post-Field. The volunteers reported sleep-related physical complaints (feeling of cold and pain, discomfort to breathe, and cough or loud snoring), excessive daytime sleepiness, and reduced vigor during the camp. Thus, a 50-day camp alters neuroendocrine regulation and induces physical discomfort, which may explain the impaired sleep pattern and the consequent daytime sleepiness and mood changes.

Acute exercise modulates the inflammatory response in adipose tissue in both lean and obese mice.

OBJECTIVES: Acute physical exercise acts as a metabolic stressor, promoting activation of the immune system, and this response could be relevant in the adipose tissue remodeling process. In addition, some cytokines have important functions in lipolysis. Because chronic exercise improves obesity-related metabolic and inflammatory dysfunction, herein we investigated the effect of acute exercise on the inflammatory responses in the adipose tissues of lean and obese mice. METHODS: Lean mice were fed a standard chow diet, whereas obese mice were fed a high-refined carbohydrate diet for 8 wk. Both groups were subjected to 60 min of moderate-intensity exercise. RESULTS: In the epididymal adipose tissue of lean mice, exercise enhanced interleukin (IL)-6 and tumor necrosis factor-α levels, which correlated positively with increased serum free fatty acid concentrations. In vivo confocal imaging of epididymal adipose tissue vessels revealed higher recruitment of neutrophils after exercise. Also, the number of leukocytes expressing CD11b+F480- was elevated 6 h after exercise. Similarly, the chemokine (C-X-C motif) ligand 1 level increased at 6 h and remained high until 24 h after exercise. Myeloperoxidase activity was increased at 6, 12, and 24 h after exercise. Surprisingly, however, no changes were observed in epididymal adipose tissue from obese mice, considering proinflammatory cytokines (IL-6 and tumor necrosis factor-α). On the other hand, IL-13, IL-4, and IL-10 levels were higher in obese mice after exercise. CONCLUSIONS: These data suggest that acute exercise promotes an inflammatory response in the adipose tissue of lean mice that is observed as part of its role in adipose tissue remodeling. In contrast, acute exercise promotes an antiinflammatory response in adipose tissue from obese mice, likely as an important tool for restoring homeostasis.

Combined Training Improves Executive Functions Without Changing Brain-Derived Neurotrophic Factor Levels of Middle-Aged and Older Adults with Type 2 Diabetes.

BACKGROUND: Type 2 diabetes mellitus (T2DM) provokes executive function and long-term memory decrements, and aerobic plus resistance training (combined training) may alleviate this T2DM-related cognitive impairment. Brain-derived neurotrophic factor (BDNF) levels have been found to be related to cognitive performance. AIM: To analyze the effects of 8-week combined training on executive functions and circulating BDNF levels of subjects with T2DM and verify the association between BDNF levels and combined training-induced changes in executive functions and long-term memory. METHODS: Thirty-five (63±8 years old) subjects of both sexes were allocated to combined training (n=17, thrice weekly for 8 weeks) or the control group (n=18). Executive functions (evaluated through Trail making test, Stroop color task, and Digit Span), long-term memory (evaluated through the Taylor Complex Figure Test simplified), and plasma samples were compared pre- and post-intervention. RESULTS: Combined training improved executive function z-score compared to control (d=1.31). Otherwise, BDNF levels were not statistically altered (combined training group: 179±88 pg/mL vs. 148±108 pg/mL; control group: 163±71 pg/mL vs. 141±84 pg/mL, p>0.05). However, pre-training BDNF levels explained 50.4% of the longitudinal improvements in composite executive function z-score (r=0.71, p<0.01), 33.6% of inhibitory control (r=0.58; p=0.02), and 31.4% of cognitive flexibility (r=0.56, p=0.04) in the combined training group. CONCLUSION: Combined training improved executive functions independently of alterations in resting BDNF levels after 8 weeks. Furthermore, pre-training BDNF levels explained one-half of the variance in combined training-induced improvements in executive functions.

Thirty days of combined consumption of a high-fat diet and fructose-rich beverages promotes insulin resistance and modulates inflammatory response and histomorphometry parameters of liver, pancreas, and adipose tissue in Wistar rats.

OBJECTIVE: The aim of this study was to verify the effects of consumption of a high-fat diet (HFD) combined with fructose-rich beverages (FRT) in promoting metabolic and physiologic changes associated with insulin resistance. METHODS: Thirty-two male Wistar rats (250 ± 10 g) were randomly allocated into four groups (n = 8) that received either a standard diet (CON), HFD, FRT, or HFD + FRT for 30 d. Insulin sensitivity and glucose tolerance were evaluated using the insulin tolerance test (ITT) and oral glucose tolerance test (OGTT). Serum samples were used to analyze the metabolic parameters and hormone levels. Interleukin (IL)-6, IL-10, IL-1ß, and tumor necrosis factor-α assays were performed in the liver, pancreas, gastrocnemius muscle, and epididymal adipose tissue by enzyme-linked immunosorbent assay. Histologic and morphometric analyses were performed on the liver, pancreas, and adipose tissues. RESULTS: Consumption of HFD + FRT promoted a significant increase (P < 0.05) in body weight, index adiposity, and in the area under the curve of ITT (P < 0.001) and OGTT (P < 0.001) when compared with the CON group. Consumption of FRT alone increased fasting glucose (P = 0.015), insulin (P = 0.035), and homeostasis model assessment index (P = 0.018), and these changes were of greater magnitude when FRT was combined with HFD. Moreover, the rats fed an HFD + FRT demonstrated a significant increase in lipid droplets in the liver (P < 0.001), an increase in adipocyte area, and an increase in inflammatory cytokines in the liver, pancreas, skeletal muscle, and adipose tissue. CONCLUSION: Consumption of an HFD + FRT promotes insulin resistance, increases inflammatory cytokines, and modulates histomorphometric parameters of the liver, pancreas, and adipose tissue, typical of insulin resistance in humans.

Physical exercise-induced thermoregulatory responses in trained rats: Effects of manipulating the duration and intensity of aerobic training sessions.

This study investigated the effects of increasing the intensity and/or duration of aerobic training sessions on thermoregulatory responses in rats subjected to exercises in temperate and warm environments. Thirty-two adult male Wistar rats were divided into four groups: a control (CON) group and three groups that were subjected to an 8-week aerobic training, during which the physical overload was achieved by predominantly increasing the exercise intensity (INT), duration (DUR) or by increasing both in an alternate manner (ID). During the last week of training, the rats received an abdominal sensor implant to measure their core body temperature (TCORE) by telemetry. After the training protocol, the 32 rats were subjected to incremental speed-exercises in temperate (23 °C) and warm (32 °C) environments. The rats had their TCORE recorded while running on a treadmill, and the ratio between the increase in TCORE and distance traveled was calculated to estimate thermoregulatory efficiency. All training protocols increased the rats' thermoregulatory efficiency during the incremental-speed exercise at 23 °C; i.e., trained rats attained faster running speeds but unchanged TCORE at fatigue compared to CON rats. However, none of the load components of training sessions - intensity or duration - was more effective than the other in improving this efficiency. At 32 °C, the aerobic training protocols did not influence the exercise-induced thermoregulatory responses. Our data indicate that different progressions in aerobic training performed at temperate conditions improved thermoregulatory efficiency during incremental exercise in the same environment; this training-induced adaptation was not clearly observed when running in warmer conditions.

Combined exercise training improves specific domains of cognitive functions and metabolic markers in middle-aged and older adults with type 2 diabetes mellitus.

AIM: To investigate the effects of 8-weeks of CT on specific domains of cognitive function, metabolic and cardiovascular parameters of subjects with Type 2 Diabetes Mellitus (T2DM). METHODS: 31 sedentary T2DM adults and older divided into CT (3x/week, during 8-week, n = 16) or Control group (CONT, n = 15). Before and after the intervention, a cognitive task battery, blood samples, and functional tests were assessed. RESULTS: CT improved inhibitory control (d = 0.89), working memory (d = 0.88), cognitive flexibility (d = 0.67) and attention/concentration (d = 0.64) in T2DM subjects. However, memory, verbal fluency, and processing speed (d < 0.1, p > 0.05 for all) were not changed. The CT-induced improvements on global cognitive z-score (r = -0.51; p < 0.001) were inversely correlated to cognitive screening scores. Moreover, CT improved functional performance (p < 0.05) and reduced insulin levels (p = 0.04). Although there was no statistical significance, there were a clinically relevant reduction of peripheral insulin sensitivity (d = 0.51, p = 0.09), resistin levels (d = 0.53, p = 0.08), diastolic (d = 0.63, p = 0.09) and mean blood pressure (d = 0.50, p = 0.09). Conversely, no changes were observed for glucose, fructosamine and blood lipids (d < 0.2 for all). CONCLUSION: CT partially reversed the negative effects of T2DM on specific cognitive domains possibly by amelioration of metabolic regulation. Moreover, lower cognitive scores may modulate the responsivity of cognitive function to CT.

The magnitude of physical exercise-induced hyperthermia is associated with changes in the intestinal permeability and expression of tight junction genes in rats.

We investigated whether the magnitude of exercise-induced hyperthermia influences intestinal permeability and tight junction gene expression. Twenty-nine male Wistar rats were divided into four groups: rest at 24 °C and exercise at 13 °C, 24 °C or 31 °C. The exercise consisted of a 90-min treadmill run at 15 m/min, and different ambient temperatures were used to produce distinct levels of exercise-induced hyperthermia. Before the experimental trials, the rats were treated by gavage with diethylenetriaminepentaacetic acid labeled with technetium-99 metastable as a radioactive probe. The rats' core body temperature (TCORE) was measured by telemetry. Immediately after the trials, the rats were euthanized, and the intestinal permeability was assessed by measuring the radioactivity of blood samples. The mRNA levels of occludin and zonula occludens-1 (ZO-1) genes were determined in duodenum samples. Exercise at 24 °C increased TCORE to values close to 39 °C, without changing permeability compared with the resting trial at the same environment. Meanwhile, rats' TCORE exceeded 40 °C during exercise at 31 °C, leading to greater permeability relative to those observed after exercise in the other ambient temperatures (e.g., 0.0037%/g at 31 °C vs. 0.0005%/g at 13 °C; data expressed as medians; p < 0.05). Likewise, the rats exercised at 31 °C exhibited higher mRNA levels of ZO-1 and occludin genes than the rats exercised at 24 °C or 13 °C. The changes in permeability and gene expression were positively and significantly associated with the magnitude of hyperthermia. We conclude that marked hyperthermia caused by exercise in the warmer environment increases intestinal permeability and mRNA levels of tight junction genes.