Acute Exercise Session Research Articles

Acute and chronic effects of combined exercise on ambulatory blood pressure and its variability in hypertensive postmenopausal women.

The aim of this study was to investigate the acute and chronic effects, and their correlation, after combined aerobic and resistance exercises in blood pressure (BP) and its variability (BPV) in hypertensive postmenopausal women. Fourteen hypertensive postmenopausal women monitored BP at rest and during 24 h by ambulatory BP monitoring in a control day without exercise performance a pretraining (baseline), after an acute exercise session (acute), and after a chronic exercise training for 10 weeks (chronic). After exercise training, systolic BP (SBP, Δ = -150 mmHg.24 h), diastolic BP (DBP, Δ = -96 mmHg.24 h), and mean BP (MBP, Δ = -95 mmHg.24 h) area under the curve were smaller than baseline measurements (P < 0.05) with no difference between acute and baseline measurements. The SBP (ΔSD24 = -2, ΔSDdn = -1.7, and ΔARV24 = -1.9 mmHg), DBP (ΔSD24 = -0.9, ΔSDdn = -0.8, and ΔARV24 = -0.9 mmHg), and MBP (ΔSD24 = -1.5, ΔSDdn = -1.3, and ΔARV24 = -1.2 mmHg) variability reduced in acute session in relation to baseline, with no chronic effects. There are moderate correlations between acute and chronic responses in wake SBP, sleep DBP, and SD24. In conclusion, combined exercise reduces ambulatory BP chronically but not acutely. In contrast, BPV decreases after an acute session but not chronically. Awake SBP, sleep DBP, and SD24indices are promising candidates to predict individual cardiovascular responses to exercise.

Exercise Induces Different Molecular Responses in Trained and Untrained Human Muscle.

Human skeletal muscle is thought to have heightened sensitivity to exercise stimulus when it has been previously trained (i.e., it possesses "muscle memory"). We investigated whether basal and acute resistance exercise-induced gene expression and cell signaling events are influenced by previous strength training history. Accordingly, 19 training naïve women and men completed 10 wk of unilateral leg strength training, followed by 20 wk of detraining. Subsequently, an acute resistance exercise session was performed for both legs, with vastus lateralis biopsies taken at rest and 1 h after exercise in both legs (memory and control). The phosphorylation of AMPK and eEF2 was higher in the memory leg than that in the control leg at both time points. The postexercise phosphorylation of 4E-BP1 was higher in the memory leg than that in the control leg. The memory leg had lower basal mRNA levels of total PGC1α and, unlike the control leg, exhibited increases in PGC1α-ex1a transcripts after exercise. In the genes related to myogenesis (SETD3, MYOD1, and MYOG), mRNA levels differed between the memory and the untrained leg; these effects were evident primarily in the male subjects. Expression of the novel gene SPRYD7 was lower in the memory leg at rest and decreased after exercise only in the control leg, but SPRYD7 protein levels were higher in the memory leg. In conclusion, several key regulatory genes and proteins involved in muscular adaptations to resistance exercise are influenced by previous training history. Although the relevance and mechanistic explanation for these findings need further investigation, they support the view of a molecular muscle memory in response to training.

Exercise Intensity and Recovery on Circulating Brain-derived Neurotrophic Factor.

Brain-derived neurotrophic factor (BDNF) is an exercise-induced neurotropin mediating neuroprotection and synaptic plasticity. Although exercise intensity is implicated as a potentially important mediator of BNDF release after exercise, the optimal exercise stimulus (interval vs continuous) and intensity (submaximal vs supramaximal) for augmenting circulating BDNF levels remains unknown. Irisin, an exercise-driven myokine, may also contribute to neuroprotection by upregulating BDNF. To examine the response and recovery of plasma BDNF and irisin after acute exercise of differing intensities. Eight males (23.1 ± 3.0 yr of age; V˙O2max 51.2 ± 4.4 mL·kg·min) completed four acute exercise sessions: 1) moderate-intensity continuous training (MICT, 65% V˙O2max); 2) vigorous-intensity continuous training (VICT, 85% V˙O2max); 3) sprint interval training (SIT, "all out"); and 4) no exercise (CTRL). Blood was collected preexercise as well as immediately, 30 min, and 90 min postexercise. Plasma BDNF and irisin were assessed with commercially available enzyme-linked immunosorbent assay kits. Plasma BDNF levels increased immediately after exercise in the SIT group (P < 0.0001) with plasma concentrations recovering 30 and 90 min postexercise. The BDNF levels after MICT were reduced 30 min postexercise compared with immediately postexercise (P = 0.0189), with no other changes across time points in MICT and VICT groups. Plasma BDNF area under the curve in SIT was significantly higher compared with CTRL, MICT, and VICT (P = 0.0020). No changes in plasma irisin across exercise groups and time points were found (P > 0.9999). Plasma BDNF levels increased in an intensity-dependent manner with SIT eliciting the highest BDNF concentration immediately postexercise. These results identify SIT as a time-efficient exercise modality to promote brain health through BDNF release.

Acute physical exercise increases APPL1/PI3K signaling in the hypothalamus of lean mice.

Adiponectin is an adipokine that acts in the control of energy homeostasis. The adaptor protein containing the pleckstrin homology domain, phosphotyrosine-binding domain, and leucine zipper motif 1 (APPL1) is a key protein in the adiponectin signaling. The APPL1 mediates a positive effect on the insulin signaling through the interaction with the phosphoinositide 3-kinase (PI3K). Thus, the present study aimed to explore the effects of an acute physical exercise session on the hypothalamic adiponectin signaling. Firstly, using bioinformatics analysis, we found a negative correlation between hypothalamic APPL1 mRNA levels and food consumption in several strains of genetically diverse BXD mice. Also, the mice and the human database revealed a positive correlation between the levels of APPL1 mRNA and PI3K mRNA. At the molecular level, the exercised mice showed increased APPL1 and PI3K (p110) protein contents in the hypothalamus of Swiss mice. Furthermore, the exercise increases co-localization between APPL1 and PI3K p110 predominantly in neurons of the arcuate nucleus of hypothalamus (ARC). Finally, we found an acute exercise session reduced the food intake 5hr after the end of fasting. In conclusion, our results indicate that physical exercise reduces the food intake and increases some proteins related to adiponectin pathway in the hypothalamus of lean mice.

“No Pain, More Gain”? Affect and Adherence to Exercise in Migraine Patients: A Prospective Cohort Study

Objectives: To compare the affective and perceptual responses to a standardized exercise session between episodic migraine patients and nonheadache persons, and its influence on adherence to an 12-week exercise training program. Methods: In a secondary analyses of a prospective cohort enrolled in a clinical trial, we assessed the affective response at rest, at 15th minof exercise, and immediately after an acute 40-min exercise session previously the training program. All measurements were undertaken in headache-free days. Participants were subsequently randomly assigned to a 12-week aerobic exercise-training program, or to a waitlist. In a multiple linear regression model, variables tested as possible predictors of adherence were body massindex, cardiorespiratory fitness, and the perceived exertion and affect scores elicited in the previous exercise session. Results: Fifty-four participants were analyzed for acute exercise session data (mean±SD age: 37.37±11.5; mean±SD BMI: 26.7±4.5). Patients (N=28) and controls (N=26) showed no differences in anthropometric characteristics and cardiorespiratory fitness. Compared to controls, migraine patients showed reduced affective response during and after exercise, but showed no differences in perceived exertion. Twentyfive participants (patients: N=13; controls: N=13) concluded the 12-week exercise-training program. Adherence was lower in migraine group (p = 0.1, d = 0.641). Multiple linear regression analysis showed post-exercise affect score as the only predictor variable of adherence to the exercise-training program (β =0.405, p = 0.040). Conclusions: This study indicates that migraine patientshave lower affective response to exercise, which was associated with adherence to the training program.

Exercise Intensity as a Predictor of Mood States During a Group Cycling Class

Increases in positive mood states after exercise has been well documented. Group cycling classes are a popular mode of exercise in the fitness industry. There is limited research on the effect of group fitness classes on mood states and whether intensity level will have an impact on the mood enhancing benefits. PURPOSE: The purpose of this study was to determine if exercise intensity predicts changes in mood states during a group cycling class. METHODS: A total of 99 subjects, ages 18 to 25 years old, volunteered for the study. No previous experience with group cycling classes was required. The subjects participated in one group cycling class instructed by a certified cycling instructor. Prior to the cycling session the subjects filled out an informed consent, medical history, and Subjective Exercise Experience Scale (SEES). Subjects were then given a heart rate monitor, instructed on proper bike set up and how to operate the bike during class. The cycling class consisted of a 5 min warm up, a 30 min conditioning phase with a mix of sprints, hills and jumps typically performed in a cycling class. The class ended with a 5 minute cool down and 5 minute stretch off the bike. Heart rate and percent heart rate reserve (%HRR) was continuously tracked during class. After the class, subjects filled out a second (post) SEES. A hierarchical regression analysis was used to examine whether intensity measured by %HRR predicted changes in each of the 3 mood state categories on the SEES (positive well-being, psychological distress, fatigue). Three related sample t-tests were run examining changes in mood following the cycling class. RESULTS: % HRR was negatively related to positive well-being (β = -.178, p = .046) and positively related to fatigue (β = .30, p = .003). There were no significant differences in fatigue after the cycling class (p > .05), however positive well-being increased (p = .001) and psychological distress decreased (p = .021) after the class. CONCLUSION: The intensity level of an acute exercise session may affect the mood enhancing benefits of exercise. The group cycling class did increase positive well-being and decrease psychological distress. However, individuals who exercised at higher intensity levels had increased levels of perceived fatigue and decreased feelings of positive well-being.

TGF-β1 downregulation in the hypothalamus of obese mice through acute exercise.

Obesity and aging lead to abnormal transforming growth factor-β1 (TGF-β1) signaling in the hypothalamus, triggering the imbalance on glucose metabolism and energy homeostasis. Here, we determine the effect of acute exercise on TGF-β1 expression in the hypothalamus of two models of obesity in mice. The bioinformatics analysis was performed to evaluate the correlation between hypothalamic Tgf-β1 messenger RNA (mRNA) and genes related to thermogenesis in the brown adipose tissue (BAT) by using a large panel of isogenic BXD mice. Thereafter, leptin-deficient (ob/ob) mice and obese C57BL/6 mice fed on a high-fat diet (HFD) were submitted to the acute exercise protocol. Transcriptomic analysis by using BXD mouse reference population database revealed that hypothalamic Tgf-β1 mRNA is negatively correlated with genes related to thermogenesis in brown adipose tissue of BXD mice, such as peroxisome proliferator-activated receptor gamma coactivator and is positively correlated with respiratory exchange ratio. In agreement with these results, leptin-deficient (ob/ob) and HFD-fed mice displayed high levels of Tgf-β1 mRNA in the hypothalamus and reduction of Pgc1α mRNA in BAT. Interestingly, an acute exercise session reduced TGF-β1 expression in the hypothalamus, increased Pgc1α mRNA in the BAT and reduced food consumption in obese mice. Our results demonstrated that acute physical exercise suppressed hypothalamic TGF-β1 expression, increasing Pgc1α mRNA in BAT in obese mice.

Experimental Manipulation of Psychological Control Scenarios: Implications for Exercise and Memory Research

The purpose of this experiment was to evaluate the extent to which variations in control activities influence memory function, as well as to investigate the participants’ memory expectations for the various conditions. A within-subject, counterbalanced experimental design was employed. Across four visits, participants engaged in four tasks, including an acute exercise session, and three cognitive-engagement control tasks of varying degrees of cognitive engagement and valence, namely reading neutral text, looking at a video, and puzzle completion. Participants’ perceived expectations for how each condition would improve their memory performance was also assessed. We observed no differences in objective cognitive performance or outcome expectations across the three evaluated control tasks, and thus, future studies may wish to employ either of these control tasks, which should not compromise making comparisons across studies.

Muscle damage responses to resistance exercise performed with high-load versus low-load associated with partial blood flow restriction in young women

The aim of this study was to compare if an acute exercise session of high-load resistance training (HL-RT, e.g. 70% of 1 repetition-maximum, 1 RM) induces a higher magnitude of muscle damage compared with a RT protocol with low-loads (e.g. 20% 1 RM) associated with partial blood flow restriction (LL-BFR), and investigate the recovery in the days after the protocols. We used an unilateral crossover research design in which 10 young women (22(2) y; 162(5) cm; 66(11) kg) performed HL-RT and LL-BFR in a randomized, counterbalanced manner with a minimum interval of 2 weeks between protocols. Indirect muscle damage markers were evaluated before and once a day for 4 days into recovery. Main results showed decreases of 8–12% at 24–48 h in maximal voluntary isometric and concentric contraction torques (P < 0.03), and changes in muscle architecture markers (P < 0.03) for HL-RT and LL-BFR, with no differences between protocols (P > 0.05). Moreover, delayed onset muscle soreness increased only after LL-BFR (P < 0.001). We conclude that an acute bout of low volume HL-RT or LL-BFR to failure resulted in edema-induced muscle swelling, but do not induce major or long-lasting decrements in muscle function and the level of soreness promoted from LL-BFR was mild.

Short-time high-intensity exercise increases peripheral BDNF in a physical fitness-dependent way in healthy men

BDNF is associated with brain health and positively modulated by exercise; however, the influence of physical fitness status on BDNF is incipient. This study investigated the BDNF response after acute-exercise sessions performed at low, moderate, and high intensities and the relationship between physical fitness status and BDNF response. Twenty-eight men, divided according to physical fitness status (<50th or >50th percentile for VO2max), performed three randomised acute exercise sessions at low (90% of VT1), moderate (midpoint between VT1-VT2), and high (midpoint between VT2-Wmax) intensities until exhaustion or for up to 60 min. Lactate and BDNF were determined pre and post-exercises. For BDNF, there were main effects of time (p = 0.003) and interaction (p < 0.001), showing an increase post high-intensity exercise (p < 0.001). Changes in BDNF presented differences between conditions (p < 0.001) with greater increase in high-intensity compared with the others (p = 0.003). For lactate, there were main effects of time (p < 0.001), condition (p < 0.001), and interaction (p < 0.001) with greater concentration in high-intensity. High-intensity exercise exhibited inverse correlation between the changes in BDNF and lactate (r=−0.38, p = 0.044). There was significant correlation between BDNF and VO2max for moderate (r = −0.57, p = 0.002) and a trend for high-intensity condition (r = −0.37, p = 0.050) and when evaluating BDNF according to physical fitness level, it was observed that subjects with lower physical fitness levels had greater increases in BDNF in short-time high-intensity exercise (p = 0.041). In conclusion, short-time high-intensity exercise seems to be more efficient in increasing BDNF concentration, and physical fitness level influences this response, as healthy individuals with lower physical fitness levels were more responsive.

Exercise-induced AMPK activation and IL-6 muscle production are disturbed in adiponectin knockout mice

BackgroundAdiponectin exhibits anti-inflammatory actions and is mainly expressed in adipose tissue. However, recent studies have shown that adiponectin can also be secreted by skeletal muscle fibers with autocrine and paracrine effects. ObjectivesTo analyze the role of adiponectin in the metabolic and inflammatory response of skeletal muscle after acute exhaustive aerobic exercise. MethodsC57BL/6 (WT) and adiponectin knockout (AdKO) mice underwent four days of treadmill running adaptation and at the fifth day, they performed an incremental maximum test to determine the maximum speed (Vmax). Acute exercise consisted of one hour at 60% Vmax. Mice were euthanatized 2 and 24 h after acute exercise session. ResultsSerum and gastrocnemius adiponectin increased after 2-hours of acute exercise. NEFA concentrations were lower in non-exercise AdKO, and decreased 2-hours after exercise only in WT. No differences were found in muscle triacylglycerol content; however, glycogen content was higher in AdKO in non-exercise (p-value = 0.005). WT showed an increase in AMP-activated protein kinase (AMPK) phosphorylation 2-hours after exercise and its level went back to normal after 24-hours. Otherwise, exercise was not able to modify AMPK in the same way as in AdKO. WT showed an increase in the phosphorylation of ACC (Ser79) 2-hours after exercise and return to normal after 24-hours of exercise (p-value < 0.05), kinects that was not observed in AdKO mice. IL-10 and IL-6 concentration was completely different among genotypes. In WT, these cytokines were increased at 2 (p-value < 0.01) and 24 h (p-value < 0.001) after exercise when compared with AdKO. NF-κBp65 protein and gene expression were not different between genotypes. ConclusionAdiponectin influences muscle metabolism, mainly by the decrease in exercise-induced AMPK phosphorylation, inflammatory profile and IL-6 in the muscle.

Late Neutrophil Priming Following a Single Session of High-intensity Interval Exercise.

This study evaluated the effect of an acute high-intensity interval exercise (HIIE) session on the function of human neutrophils. Twelve sedentary men performed a HIIE session (8 bouts of 60 s at 90% of peak power, intercalated with 75 s of active recovery at 30 W). Neutrophils were collected before, 30 min and 24 h after the exercise session for the evaluation of phagocytic capacity, expression of phagocytic receptors, reactive oxygen species generation, and redox status. 24 h after the HIIE session, an increase was observed in both neutrophil phagocytic capacity and yeast-induced generation of reactive oxygen species, which indicates neutrophil priming in response to an acute HIIE session. Neutrophils also presented an increase in superoxide dismutase activity 24 h after the exercise. Improvement in neutrophil function was accompanied by increased serum levels of IL-8 and increased concentration of plasma lactate dehydrogenase. Our findings show a late activating effect of one HIIE session on neutrophils. We propose that priming of neutrophils by HIIE may play a role in skeletal muscle inflammation after exercise.

“No Pain, More Gain”? Resposta Afetiva e Aderência ao Exercício em Pacientes com Migrânea: Um Estudo Prospectivo

Objectives: To compare the affective and perceptual responses to a standardized exercise session between episodic migraine patients and nonheadache persons, and its influence on adherence to an 12-week exercise training program. Methods: In a secondary analyses of a prospective cohort enrolled in a clinical trial, we assessed the affective response at rest, at 15th minof exercise, and immediately after an acute 40-min exercise session previously the training program. All measurements were undertaken in headache-free days. Participants were subsequently randomly assigned to a 12-week aerobic exercise-training program, or to a waitlist. In a multiple linear regression model, variables tested as possible predictors of adherence were body massindex, cardiorespiratory fitness, and the perceived exertion and affect scores elicited in the previous exercise session. Results: Fifty-four participants were analyzed for acute exercise session data (mean±SD age: 37.37±11.5; mean±SD BMI: 26.7±4.5). Patients (N=28) and controls (N=26) showed no differences in anthropometric characteristics and cardiorespiratory fitness. Compared to controls, migraine patients showed reduced affective response during and after exercise, but showed no differences in perceived exertion. Twentyfive participants (patients: N=13; controls: N=13) concluded the 12-week exercise-training program. Adherence was lower in migraine group (p = 0.1, d = 0.641). Multiple linear regression analysis showed post-exercise affect score as the only predictor variable of adherence to the exercise-training program (β =0.405, p = 0.040). Conclusions: This study indicates that migraine patientshave lower affective response to exercise, which was associated with adherence to the training program.

Interleukin-10 responses from acute exercise in healthy subjects: A systematic review.

Interleukin 10 (IL-10) is a cytokine that plays a critical role with potent anti-inflammatory properties when produced during exercise, limiting host immune response to pathogens and preventing tissue damage. The purpose of this systematic review was to assess the response of IL-10 after acute exercise session in healthy adults. Databases of Ovid Medline (1978-2016), CINAHL (1998-2016), EMBASE (2003-2016), SportDiscus (1990-2016), and Web of Science library (1990-2016) were carefully screened. Clinical trials comparing exercise types in healthy individuals were included for pooled analysis. The trials of exercise were methodologically appraised by PEDro Scale. Twelve randomized controlled and crossover trials containing 176 individuals were identified for inclusion. The Kruskal-Wallis test showed no significant differences between type of exercise and the corresponding values in IL-10 [X2(4) = 2.878; p = 0.449]. The duration of exercise was significantly correlated with increase in IL-10 changes (Pearson's r = 1.00, 95%CI: 0.015-0.042, p < 0.0001) indicating that 48% of the variation in IL-10 levels can be explained by the duration of the exercise performed. In addition, despite a linear increase, we did not find a significant correlation with the intensity of exercise and IL-10 changes (Pearson's r = 0.218, 95%CI: -0.554-0.042, p < 0.035). Overall, the duration of the exercise is the single most important factor determining the magnitude of the exercise-induced increase of plasma IL-10.

Effects of prenatal exercise on fetal heart rate, umbilical and uterine blood flow: a systematic review and meta-analysis.

To perform a systematic review and meta-analysis examining the influence of acute and chronic prenatal exercise on fetal heart rate (FHR) and umbilical and uterine blood flow metrics. Systematic review with random-effects meta-analysis and meta-regression. Online databases were searched up to 6 January 2017. Studies of all designs were included (except case studies) if published in English, Spanish or French, and contained information on the population (pregnant women without contraindication to exercise), intervention (subjective or objective measures of frequency, intensity, duration, volume or type of exercise, alone ["exercise-only"] or in combination with other intervention components [eg, dietary; "exercise + co-intervention"]), comparator (no exercise or different frequency, intensity, duration, volume and type of exercise) and outcomes (FHR, beats per minute (bpm); uterine and umbilical blood flow metrics (systolic:diastolic (S/D) ratio; Pulsatility Index (PI); Resistance Index (RI); blood flow, mL/min; and blood velocity, cm/s)). 'Very low' to 'moderate' quality evidence from 91 unique studies (n=4641 women) were included. Overall, FHR increased during (mean difference (MD)=6.35bpm; 95% CI 2.30 to 10.41, I2=95%, p=0.002) and following acute exercise (MD=4.05; 95% CI 2.98 to 5.12, I2=83%, p<0.00001). The incidence of fetal bradycardia was low at rest and unchanged with acute exercise. There were no significant changes in umbilical or uterine S/D, PI, RI, blood flow or blood velocity during or following acute exercise sessions. Chronic exercise decreased resting FHR and the umbilical artery S/D, PI and RI at rest. Acute and chronic prenatal exercise do not adversely impact FHR or uteroplacental blood flow metrics.

Anti-inflammatory response to acute exercise is related with intensity and physical fitness.

The relationship between inflammatory markers and energetic metabolism has been explored. However, the relationship between exercise intensity and fitness status is unclear, and it is necessary to understand this relationship to apply specific exercise guidance. The purpose of the study was to analyze metabolic and inflammatory responses imposed by acute exercise sessions performed at moderate, heavy, and severe intensities and their relationship with the physical fitness status. Nineteen healthy male volunteers performed three acute exercise sessions until exhaustion or up to 60 minutes on a cycle ergometer at moderate (90% of first ventilatory threshold [VT1]), heavy (midpoint between VT1 and second ventilatory threshold [VT2]), and severe (midpoint between VT2 and maximal aerobic power) intensities. Blood lactate, glucose, NEFA, endotoxin, and cytokines were determined for each exercise session. Peripheral andlipopolysaccharide (LPS)-stimulated release of tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, and IL-10 was analyzed before, after, and 60 minutes after sessions. In peripheral blood, severe intensity increased lactate, endotoxin, and TNF-α immediately after exercise and glucose at 60 min after exercise. There was a trend for IL-10 increase at 60 minutes after exercise in peripheral blood. Immediately after exercise, LPS-stimulated TNF-α, IL-6, IL-6/IL-10 ratio, and lactate levels were higher in the severe intensity while nonester fatty acid levels decreased at this time. At 60 minute after exercise, higher concentrations of glucose and a trend for increased IL-10 were observed in severe intensity. A positive correlation was observed between maximal aerobic power and IL-10 ( r = 0.513; P = 0.042), and negative correlations between maximal aerobic power and endotoxin ( r = -0.531; P = 0.034) and lactate ( r = -0.538; P = 0.031) in heavy intensity. Our data show a novel finding that higher cytokine responses occur at higher intensities, mainly in severe intensity. However, the anti-inflammatory (IL-10) response was physical fitness-dependent.

Molecular hydrogen reduces acute exercise-induced inflammatory and oxidative stress status

Physical exercise induces inflammatory and oxidative markers production in the skeletal muscle and this process is under the control of both endogenous and exogenous modulators. Recently, molecular hydrogen (H2) has been described as a therapeutic gas able to reduced oxidative stress in a number of conditions. However, nothing is known about its putative role in the inflammatory and oxidative status during a session of acute physical exercise in sedentary rats. Therefore, we tested the hypothesis that H2 attenuates both inflammation and oxidative stress induced by acute physical exercise. Rats ran at 80% of their maximum running velocity on a closed treadmill inhaling either the H2 gas (2% H2, 21% O2, balanced with N2) or the control gas (0% H2, 21% O2, balanced with N2) and were euthanized immediately or 3 h after exercise. We assessed plasma levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)−1β and IL-6] and oxidative markers [superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. In addition, we evaluated the phosphorylation status of intracellular signaling proteins [glycogen synthase kinase type 3 (GSK3α/β) and the cAMP responsive element binding protein (CREB)] that modulate several processes in the skeletal muscle during exercise, including changes in exercise-induced reactive oxygen species (ROS) production. As expected, physical exercise increased virtually all the analyzed parameters. In the running rats, H2 blunted exercise-induced plasma inflammatory cytokines (TNF-α and IL-6) surges. Regarding the oxidative stress markers, H2 caused further increases in exercise-induced SOD activity and attenuated the exercise-induced increases in TBARS 3 h after exercise. Moreover, GSK3α/β phosphorylation was not affected by exercise or H2 inhalation. Otherwise, exercise caused an increased CREB phosphorylation which was attenuated by H2. These data are consistent with the notion that H2 plays a key role in decreasing exercise-induced inflammation, oxidative stress, and cellular stress.

The Effect of 1 Week of a Multi-ingredient Dietary Preworkout Supplement on Resting and Postacute Resistance Exercise Vascular Function.

Dietary preworkout supplements are popular among recreational exercisers and athletes. However, the effects of these supplements on the vasculature, both at rest and during exercise, are not well studied. Therefore, the purpose of this study was to determine the effect of 1 week of supplementation with a multi-ingredient dietary preworkout supplement on measures of vascular function at rest and immediately following acute resistance exercise in young, recreationally active adults. Twelve participants (9 males and 3 females; mean ± SD: age = 24.5 ± 3.4 years and body mass index = 24.3 ± 4.7kg/m2) completed this double-blind, randomized, crossover design study. After familiarization, participants were randomized to either a taste-matched placebo or the preworkout supplement for 1 week preceding the testing visits. Participants underwent measures of vascular function, including brachial artery flow-mediated dilation, measures of central and peripheral blood pressure, and measures of arterial stiffness via pulse wave analysis and pulse wave velocity. All measures were taken at rest and immediately following an acute bilateral leg press exercise session. Resting and postacute exercise flow-mediated dilation, blood pressure, and arterial stiffness were similar between the placebo and the preworkout supplement visits. One week of multi-ingredient preworkout supplementation does not affect vascular function at rest or in response to an acute bout of resistance exercise in young, healthy, recreationally active individuals.

Exercise activates the hypothalamic S1PR1-STAT3 axis through the central action of interleukin 6 in mice.

Hypothalamic sphingosine-1-phosphate receptor 1 (S1PR1), the G protein-coupled receptor 1 of sphingosine-1-phosphate, has been described as a modulator in the control of energy homeostasis in rodents. However, this mechanism is still unclear. Here, we evaluate the role of interleukin 6 (IL-6) associated with acute physical exercise in the control of the hypothalamic S1PR1-signal transducer and activator of transcription 3 (STAT3) axis. Acute exercise session and an intracerebroventricular IL-6 injection increased S1PR1 protein content and STAT3 phosphorylation in the hypothalamus of lean and obese mice accompanied by a reduction in food consumption. Transcriptome analysis indicated a strong positive correlation between Il-6 and S1pr1 messenger RNA in several tissues of genetically diverse BXD mice strains and humans, including in the hypothalamus. Interestingly, exercise failed to stimulate the S1PR1-STAT3 axis in IL-6 knockout mice and the disruption of hypothalamic-specific IL-6 action blocked the anorexigenic effects of exercise. Taken together, our results indicate that physical exercise modulates the S1PR1 protein content in the hypothalamus, through the central action of IL-6.

Intense physical exercise potentiates glucose inhibitory effect over food intake of male Wistar rats.

What is the central question of this study? How does an acute session of exercise affect food intake of male Wistar rats? What is the main finding and its importance? Food intake in male Wistar rats is decreased in the first hour after physical exercise independent of the intensity. Moreover, high-intensity exercise potentiates the anorexic effect of peripheral glucose administration. This work raises new feeding-related targets that would explain how exercise drives body weight loss. Obesity has emerged as a critical metabolic disorder in modern society. An adequate lifestyle with a well-oriented programme of diet and physical exercise (PE) can prevent or potentially even cure obesity. Additionally, PE might lead to weight loss by increasing energy expenditure and decreasing hunger perception. In this article, we hypothesize that an acute exercise session would potentiate the glucose inhibitory effects on food intake in male Wistar rats. Our data show that moderate- or high-intensity PE significantly decreased food intake, although no changes in the expression of feeding-related neuropeptide in the arcuate nucleus of the hypothalamus were found. Exercised animals demonstrated a reduced glucose tolerance and increased blood insulin concentration. Intraperitoneal administration of glucose decreased food intake in control animals. In the animals submitted to moderate-intensity PE, the decrease in food intake promoted by glucose was similar to controls; however, an interaction was observed when glucose was injected in the high-intensity PE group, in which food intake was significantly lower than the effect produced by glucose alone. A different pattern of expression was observed for the monocarboxylate transporter isoforms (MCT1, 2 and 4) and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFBP3) in the hypothalamus, which was dependent on the exercise intensity. In conclusion, PE decreases food intake independently of the intensity. However, an interaction between PE and the anorexic effect of glucose is only observed when a high-intensity exercise is performed. These data show an essential role of exercise intensity in the modulation of the glucose inhibitory effect on food intake.