scholarly journals Acute Exercise Stress Reveals Cerebrovascular Benefits Associated with Moderate Gains in Cardiorespiratory Fitness

2014 ◽  
Vol 34 (12) ◽  
pp. 1873-1876 ◽  
Author(s):  
Julien V Brugniaux ◽  
Christopher J Marley ◽  
Danielle A Hodson ◽  
Karl J New ◽  
Damian M Bailey

Elevated cardiorespiratory fitness improves resting cerebral perfusion, although to what extent this is further amplified during acute exposure to exercise stress and the corresponding implications for cerebral oxygenation remain unknown. To examine this, we recruited 12 moderately active and 12 sedentary healthy males. Middle cerebral artery blood velocity (MCAv) and prefrontal cortical oxyhemoglobin (cO2Hb) concentration were monitored continuously at rest and throughout an incremental cycling test to exhaustion. Despite a subtle elevation in the maximal oxygen uptake (active: 52 ± 9 ml/kg per minute versus sedentary: 33 ± 5 ml/kg per minute, P < 0.05), resting MCAv was not different between groups. However, more marked increases in both MCAv (+28 ± 13% versus +18 ± 6%, P < 0.05) and cO2Hb (+5 ±4% versus −2 ± 3%, P < 0.05) were observed in the active group during the transition from low- to moderate-intensity exercise. Collectively, these findings indicate that the long-term benefits associated with moderate increase in physical activity are not observed in the resting state and only become apparent when the cerebrovasculature is challenged by acute exertional stress. This has important clinical implications when assessing the true extent of cerebrovascular adaptation.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Blanca Marin Bosch ◽  
Aurélien Bringard ◽  
Maria G. Logrieco ◽  
Estelle Lauer ◽  
Nathalie Imobersteg ◽  
...  

AbstractRegular physical exercise enhances memory functions, synaptic plasticity in the hippocampus, and brain derived neurotrophic factor (BDNF) levels. Likewise, short periods of exercise, or acute exercise, benefit hippocampal plasticity in rodents, via increased endocannabinoids (especially anandamide, AEA) and BDNF release. Yet, it remains unknown whether acute exercise has similar effects on BDNF and AEA levels in humans, with parallel influences on memory performance. Here we combined blood biomarkers, behavioral, and fMRI measurements to assess the impact of a single session of physical exercise on associative memory and underlying neurophysiological mechanisms in healthy male volunteers. For each participant, memory was tested after three conditions: rest, moderate or high intensity exercise. A long-term memory retest took place 3 months later. At both test and retest, memory performance after moderate intensity exercise was increased compared to rest. Memory after moderate intensity exercise correlated with exercise-induced increases in both AEA and BNDF levels: while AEA was associated with hippocampal activity during memory recall, BDNF enhanced hippocampal memory representations and long-term performance. These findings demonstrate that acute moderate intensity exercise benefits consolidation of hippocampal memory representations, and that endocannabinoids and BNDF signaling may contribute to the synergic modulation of underlying neural plasticity mechanisms.


2018 ◽  
Vol 3 (2) ◽  
pp. 484-487
Author(s):  
Santosh Kumar Deo ◽  
Kopila Agrawal ◽  
Prem Bhattrai ◽  
Raju Kumar Chaudhary

Introduction: Working memory is a kind of short term memory important for reasoning and guiding decision-making and behavioral process.Objective: The goal of the present research was to study the outcome of single bout of acute moderate-intensity exercise on working memory.Methodology: Twenty two male subjects were asked to perform working memory task by 2n back task in baseline resting, immediately after exercise and after five minute of exercise session. 3 minute step test procedure was used as a moderate intensity exercise intervention.Results: The percentage correctness of 2n back task of working memory was found to be 64.36% for baseline resting condition, 78.01 % for immediately after 3-minute step test and 80.70% for 5 minute after the exercise. In both exercise session (i.e. immediately after exercise and after 5 minute of exercise), significant improvement (p value <0.05) in working memory was seen as compared to the baseline resting session while no such significant beneficial improvement was seen when compared between immediately after exercise and after 5 minute of exercise.Conclusion: Improvement in working memory after moderate exercise intervention was seen, which is important for learning and memory and decision-making.  BJHS 2018;3(2)6:484-487.


2018 ◽  
Vol 7 (12) ◽  
pp. 486 ◽  
Author(s):  
Breanna Wade ◽  
Paul Loprinzi

Emerging work suggests that acute, moderate-intensity aerobic exercise may help to subserve episodic memory of neutral stimuli. Less investigated, however, is whether acute exercise is associated with enhanced memory recognition of emotional stimuli, which was the purpose of this experiment. A parallel-group randomized controlled experiment was employed. Participants (mean age = 20 yr) were randomized into an exercise (n = 17) or control group (n = 17). The exercise group engaged in a 15-min bout of moderate-intensity treadmill walking. Emotional memory recognition was assessed via images from the International Affective Picture System, including assessments of varying degrees of valence and arousal. Memory recognition was assessed at 1 day, 7 days, and 14 days post-memory encoding. We observed a significant main effect for time (F(2) = 104.2, p < 0.001, η2p = 0.77) and a significant main effect for valence–arousal classification (F(4) = 21.39, p < 0.001, η2p = 0.40), but there was no significant time by group interaction (F(2) = 1.09, p = 0.34, η2p = 0.03), classification by group interaction (F(4) = 0.12, p = 0.97, η2p = 0.01), time by classification interaction (F(8) = 1.78, p = 0.08, η2p = 0.05), or time by classification by group interaction (F(8) = 0.78, p = 0.62, η2p = 0.02). In conclusion, emotional memory recognition decreased over the 14-day follow-up period and this rate of memory decay was not altered by acute moderate-intensity exercise engagement. We discuss these findings in the context of exercise intensity and the temporal effects of exercise.


2020 ◽  
Vol 9 (2) ◽  
pp. 310-315
Author(s):  
Cornelius Coli ◽  
Gadis Meinar Sari ◽  
Purwo Sri Rejeki

This study aims to analyze acute moderate intensity exercise decreases oxygen saturation in obese women. True experiment with a randomized control group design posttest-only design using 14 obese women aged 19-24 years, body mass index 27-33 kg/m2, percentage body fat (PBF) above 30 % and fasting blood glucose (FBG) below 100 mg/dL, normal hemoglobin, normal systolic and diastolic blood pressure, normal resting heart rate and randomly divided into two groups, namely CON (n=7, control without intervention) and MIE (n=7, moderate intensity exercise). Moderate intensity exercise interventions carried out for 40 minutes using a treadmill. Blood sampling is done 10 minutes after the intervention. Measurement of oxygen saturation using a Pulse Oximeter. The results obtained mean oxygen saturation at CON (98.428±0.534) % and MIE (96.571±0.975) % (p=0.001). Based on the results of the study concluded that moderate moderate intensity acute exercise reduces oxygen saturation in obese women.


2019 ◽  
Vol 126 (1) ◽  
pp. 102-110 ◽  
Author(s):  
Corinna Serviente ◽  
Amy Burnside ◽  
Sarah Witkowski

Endothelial microparticles (EMPs) are related to cardiovascular disease (CVD) risk. Risk factors for CVD increase with menopause, and greater cardiorespiratory fitness is generally expected to reduce CVD risk. The effects of habitual physical activity on endothelial health may be due in part to the effect of acute exercise on circulating EMPs. This study was performed to evaluate the effect of an acute bout of exercise on CD62E+ and CD31+/42b− EMPs in healthy fit midlife women at different menopausal stages. Healthy, active premenopausal (PRE), perimenopausal (PERI), and postmenopausal (POST) women completed a single bout of moderate-intensity treadmill exercise. Activated (CD62E+) and apoptotic (CD31+/42b−) EMPs were evaluated before and 30 min after exercise by using fluorescent activated cell sorting. In an exploratory analysis, these results were compared with data from low-fit peri- and postmenopausal women. Differences by group and time point were evaluated with repeated-measure ANOVAs. There was a reduction in the number of total microparticles ( P < 0.001), CD62E+ ( P = 0.003), and CD31+/42b− ( P < 0.001) EMPs/μl plasma following acute exercise. The percentage of CD62E+ EMPs increased with acute exercise ( P < 0.001), whereas the percentage of CD31+/42b− EMPs did not change ( P = 0.40). There was no effect of menopausal status on CD62E+or CD31+/42b− EMPs, or on total microparticles (all P > 0.05). The exploratory analysis revealed that low-fit women had similar changes in EMPs with acute exercise. We concluded that acute moderate-intensity exercise reduces CD62E+and CD31+/42b− EMPs, as well as total microparticles, in healthy midlife women. These effects occurred despite differences in menopausal status and fitness. NEW & NOTEWORTHY This study demonstrates that acute moderate-intensity exercise reduces activated and apoptotic endothelial microparticles in healthy midlife women.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Katrin A Dias ◽  
James P Macnamara ◽  
Christopher M Hearon ◽  
Mitchel Samels ◽  
Aslan Turer ◽  
...  

Introduction: Patients with hypertrophic cardiomyopathy (HCM) are excluded from high intensity activities due to perceived fear of sudden cardiac death. Observational data from athletes with HCM suggest that engaging in high intensity exercise (HIE) may be safe and is associated with higher cardiorespiratory fitness. Whether HIE can safely elicit a superior increase in fitness compared to moderate intensity exercise in patients with HCM is unclear. Methods: Nine HCM patients (49 ± 7 years, 3 female) were assessed for maximal oxygen uptake (VO 2 max, Douglas Bag method), cardiac output (Q c , acetylene rebreathing), and peripheral oxygen extraction (av-O 2 diff, Fick equation) before randomization and after 5 months of MIE or HIE training. Patients completed 3-4 sessions of MIE each week, while the HIE group also incorporated 1-2 supervised high intensity interval training sessions/week from month 3 onwards. Arrhythmias were monitored via pre-existing implantable cardiac defibrillators or implantable loop recorders placed prior to training. Results: Five months of MIE increased absolute VO 2 max by 3% and relative VO 2 max by 4%, while HIE consistently increased absolute VO 2 max by 6% and relative VO 2 max by 5% (Figure). Maximal Q c did not change after MIE but increased in all HIE patients (+1.2L/min, 95% CI -1.4 to 3.9), while maximal av-O 2 diff remained stable in both groups. Training compliance was 84 ± 15% in HIE and 93 ± 11% in MIE. There were no serious exercise-related adverse events in either group though two HIE subjects had arrhythmias at rest: 1) 14-beat run of wide complex tachycardia of uncertain mechanism given underlying conduction disease prior to a training session, and 2) 11 beats of non-sustained ventricular tachycardia prior to post exercise testing. Conclusions: Preliminary findings show that five months of HIE safely and consistently increased cardiorespiratory fitness in patients with HCM, though overall the improvements were comparable to MIE.


2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.


Animals ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 486
Author(s):  
Wendy Pearson ◽  
Julia Guazzelli Pezzali ◽  
Renan Antunes Donadelli ◽  
Ashley Wagner ◽  
Preston Buff

There is little information available to describe the inflammatory consequences of and recovery from moderate-intensity exercise bouts in hunting dogs. The purpose of the current study is to generate pilot data on the appearance and disappearance of biomarkers of inflammation and inflammation resolution following a typical one-hour exercise bout in basset hounds. Four hounds were set out to find a scent and freely adopted running or walking over wooded terrain for approximately one hour. Venous blood samples were obtained before the exercise and at 1, 2, 4, 6, and 10 h following cessation of exercise and were analyzed for biomarkers of inflammation (prostaglandin E2 (PGE2), nitric oxide (NO), interleukin 1β (IL-1β)) tumour necrosis factor-α (TNF-α)), and inflammation resolution (resolvin D1 (RvD1)). There was an increase in inflammation one hour after the exercise, shown by a significant increase in PGE2. Following this peak, PGE2 steadily declined at the same time as RvD1 increased, with RvD1 peaking at six hours. This pilot study provides evidence that dogs that undergo an hour of hunt exercise experience transient inflammation that peaks one hour after the end of exercise; inflammation resolution peaks six hours after the end of exercise. Future studies should seek to further understand the distinct and combined roles of PGE2 and RvD1 in dog adaptation to exercise stress.


2015 ◽  
Vol 308 (11) ◽  
pp. H1443-H1450 ◽  
Author(s):  
B. Bond ◽  
P. E. Gates ◽  
S. R. Jackman ◽  
L. M. Corless ◽  
C. A. Williams ◽  
...  

Acute exercise transiently improves endothelial function and protects the vasculature from the deleterious effects of a high-fat meal (HFM). We sought to identify whether this response is dependent on exercise intensity in adolescents. Twenty adolescents (10 male, 14.3 ± 0.3 yr) completed three 1-day trials: 1) rest (CON); 2) 8 × 1 min cycling at 90% peak power with 75 s recovery [high-intensity interval exercise (HIIE)]; and 3) cycling at 90% of the gas exchange threshold [moderate-intensity exercise (MIE)] 1 h before consuming a HFM (1.50 g/kg fat). Macrovascular and microvascular endothelial function was assessed before and immediately after exercise and 3 h after the HFM by flow-mediated dilation (FMD) and laser Doppler imaging [peak reactive hyperemia (PRH)]. FMD and PRH increased 1 h after HIIE [ P < 0.001, effect size (ES) = 1.20 and P = 0.048, ES = 0.56] but were unchanged after MIE. FMD and PRH were attenuated 3 h after the HFM in CON ( P < 0.001, ES = 1.78 and P = 0.02, ES = 0.59). FMD remained greater 3 h after the HFM in HIIE compared with MIE ( P < 0.001, ES = 1.47) and CON ( P < 0.001, ES = 2.54), and in MIE compared with CON ( P < 0.001, ES = 1.40). Compared with CON, PRH was greater 3 h after the HFM in HIIE ( P = 0.02, ES = 0.71) and MIE ( P = 0.02, ES = 0.84), with no differences between HIIE and MIE ( P = 0.72, ES = 0.16). Plasma triacylglycerol concentration and total antioxidant status concentration were not different between trials. We conclude that exercise intensity plays an important role in protecting the vasculature from the deleterious effects of a HFM. Performing HIIE may provide superior vascular benefits than MIE in adolescent groups.


1998 ◽  
Vol 275 (4) ◽  
pp. E655-E664 ◽  
Author(s):  
Amy E. Halseth ◽  
Nathalie Rhéaume ◽  
Allison B. Messina ◽  
Erica K. Reed ◽  
Mahesh G. Krishna ◽  
...  

The goal of this study was to determine how liver glutamine (Gln) metabolism adapts to acute exercise in the 18-h-fasted dogs ( n = 7) and in dogs that were glycogen depleted by a 42-h fast ( n = 8). For this purpose, sampling (carotid artery, portal vein, and hepatic vein) and infusion (vena cava) catheters and Doppler flow probes (portal vein, hepatic artery) were implanted under general anesthesia. At least 16 days later an experiment, consisting of a 120-min equilibration period, a 30-min basal sampling period, and a 150-min exercise period was performed. At the start of the equilibration period, a constant-rate infusion of [5-15N]Gln was initiated. Arterial Gln flux was determined by isotope dilution. Gut and liver Gln release into and uptake from the blood were calculated by combining stable isotopic and arteriovenous difference methods. The results of this study show that 1) in the 18-h-fasted dog, ∼10% and ∼35% of the basal Gln appearance in arterial blood is due to Gln release from the gut and liver, respectively, whereas ∼30% and ∼25% of the basal Gln disappearance is due to removal by these tissues; 2) extending the fast to 42 h does not affect basal arterial Gln flux or the contribution of the gut to arterial Gln fluxes but decreases hepatic Gln release, causing a greater retention of gluconeogenic carbon by the liver; 3) moderate-intensity exercise increases hepatic Gln removal from the blood regardless of fast duration but does not affect the hepatic release of Gln; and 4) Gln plays an important role in channeling nitrogen into the ureagenic pathway in the basal state, and this role is increased by ∼80% in response to exercise. These studies illustrate the quantitative importance of the splanchnic bed contribution to arterial Gln flux during exercise and the ability of the liver to acutely adapt to changes in metabolic requirements induced by the combined effects of fasting and exercise.


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