scholarly journals Gender based EEG before and after acute bout of aerobic exercise

2014 ◽  
Vol 6 (2) ◽  
pp. 29-34
Author(s):  
Nirmala Limbu ◽  
Ramanjan Sinha ◽  
Meenakshi Sinha ◽  
Bishnu Hari Paudel

Objective: We aimed to investigate how EEG frequency bands change in females in response to acute exercise compared to males.Methods: Consenting healthy adult females (n=15) & males (n=15) bicycled an ergometer at 50% HRmax for 20 min. EEG was recorded using 10-20 system from mid-frontal (F4 & F3), central (C4 & C3), parietal (P4 & P3), temporal (T4 & T3) & occipital (O2 & O1) regions. Exercise-induced EEG changes were compared between two sexes by Mann Whitney test. EEG power (μV2) is presented as median & interquartile range.Results: In females, as compared to males, resting right side delta, alpha, and beta activities were more in almost all recorded sites [delta: F4= 49.82 (44.23-63.56) vs. 35.5 (32.70-44.44), p < 0.001; etc], [alpha F4: 127.62 (112.89-149.03) vs. 49.36 (46.37-52.98), p < 0.001; etc], [beta F4= 18.96 (15.83-25.38)  vs. 14.77 (10.34-17.55), p < 0.05; C4= 21.16 (18.4-25.9) vs. 15.48 (9.66-19.40), p < 0.01; etc]. Similarly, females resting right theta activity was more in parietal [P4= 33.04 (25.1-42.41) vs. 22.3 (18.36-34.33), p < 0.05] & occipital [O2= 50.81 (30.64-66.8) vs. 26.85 (22.18-34.42), p < 0.001] regions than in males. They had similar picture on the left side also. The delta values of right alpha power was less in female in frontal [F4= -11.61 (-45.24 -3.64) vs. 9.48 (1.05-16.58), p < 0.01] and central [C4= -72 (-32.98-9.48) vs. 22.69 (13.03-33.05), p < 0.01] regions compared to males. Also, they had less delta values of left central alpha [C3= -8.32 (-32.65-6.1) vs. 16.5 (0.36-36.36), p < 0.01] and temporal beta [T3= -6.29 (-10.09- -1.49) vs. 1.24 (-0.84- 2.8), p < 0.001] power compared to males.Conclusion: At rest females may have high EEG powers in different bands. In response to acute exercise, they respond in reverse way as compared to males.DOI: http://dx.doi.org/10.3126/ajms.v6i2.11116Asian Journal of Medical Sciences Vol.6(2) 2015 30-35

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Travis J. Saunders ◽  
Andrew Palombella ◽  
K. Ashlee McGuire ◽  
Peter M. Janiszewski ◽  
Jean-Pierre Després ◽  
...  

Objective. To examine the effect of acute and short-term (~1 week) aerobic exercise training on plasma adiponectin levels in inactive, abdominally obese men.Materials and Methods. Inactive and abdominally obese men (n=38, waist circumference ≥102 cm) recruited from Kingston, Canada were randomly allocated to perform three bouts of aerobic treadmill exercise at either low (50% VO2peak) or high (75% VO2peak) intensity during a 1-week period. Blood samples were taken before and after the first exercise session and 24–72 hours following the completion of the final exercise session.Results. Adiponectin levels were elevated immediately following an acute bout of exercise at both high and low intensities (High:5.79±0.42versus5.05±0.41 ug/mL; Low:5.24±0.44versus4.37±0.44 ug/mL,P<0.05) and remained elevated following 30 minutes of rest. In comparison to baseline, adiponectin levels were also elevated 24–72 hours following the final exercise session (High:5.47±0.48versus4.88±0.48 ug/mL; Low:5.18±0.49versus4.47±0.49 ug/mL,P<0.05).Conclusion. Both acute and short-term aerobic exercise result in a significant increase in plasma adiponectin levels in inactive, abdominally obese men independent of intensity.


1987 ◽  
Vol 63 (4) ◽  
pp. 1319-1323 ◽  
Author(s):  
V. A. Koivisto ◽  
H. Yki-Jarvinen

Acute exercise increases insulin binding to its receptors on blood cells. Whether the enhanced insulin binding explains the exercise-induced increase in glucose uptake is unclear, since insulin binding and glucose uptake have not been measured simultaneously in a target tissue of insulin. In this study, we determined insulin binding and the rate of glucose transport in adipocytes obtained by needle biopsy from 10 healthy men before and after 3 h of cycle-ergometric exercise. During the exercise, plasma glucose (P less than 0.01) and insulin (P less than 0.001) fell and serum free fatty acid level rose 4.3-fold (P less than 0.001). 125I-insulin binding to adipocytes remained unchanged during exercise. The rate of basal glucose transport clearance fell from 28.1 +/- 5.7 fl.cell-1.s-1 to 22.9 +/- 5.6 fl.cell-1.s-1 (P less than 0.005), and the insulin-stimulated increase in glucose transport rate rose from 196 +/- 26 to 279 +/- 33% (P less than 0.025) during the exercise. Thus, in the adipocytes during exercise, the basal glucose transport rate and the responsiveness of glucose transport to insulin changed in the absence of alterations in insulin binding. These data indicate that the exercise-induced changes in insulin binding show tissue specificity and do not always parallel alterations in glucose transport.


2012 ◽  
Vol 1 (6) ◽  
pp. 298-304
Author(s):  
Eizadi Mojtaba ◽  
Kohandel Mahdi ◽  
Kasbparast JR Mehdi ◽  
Sarshin Amir

 Leptin and adiponectin, adipose tissue secreted cytokines, play key role inobesity and cardiovascular disease. Although the physiopathological mechanisms underlying these associations are largely unknown. Venous blood samples were obtained before and after an acute bout of moderate cycling test in eighty non‐trained adult obese men (BMI: 33.54 ± 3.43 kg/m2) that participated in this study by accidentally. Blood samples were used for measuring serum leptin and adiponectin. No significant differences were found in serum leptin by cycling exercise with compared to baseline (P ≥ 0.05). But, serum adiponectin levels were significantly increased in response to acute exercise when compared with baseline levels (P < 0.05). Based on these data, we can say, although inflammation cytokines such as leptin does not affect by acute exercise for short time, but it seems that this exercise can increase anti‐inflamatory cytokines as adiponectin in obese subjects. The findings of this study indicate the fact that in response to short‐term exercise, changes in serum adiponectin levels are independent of the leptin response.


2011 ◽  
Vol 300 (6) ◽  
pp. R1326-R1332 ◽  
Author(s):  
D. E. Scofield ◽  
H. L. McClung ◽  
J. P. McClung ◽  
W. J. Kraemer ◽  
K. R. Rarick ◽  
...  

This study tested the hypothesis that transdermal fluid (TDF) provides a more sensitive and accurate measure of exercise-induced increases in insulin-like growth factor-I (IGF-I) than serum, and that these increases are detectable proximal, but not distal, to the exercising muscle. A novel, noninvasive methodology was used to collect TDF, followed by sampling of total IGF-I (tIGF-I) and free IGF-I (fIGF-I) in TDF and serum following an acute bout of exercise. Experiment 1: eight men (23 ± 3 yrs, 79 ± 7 kg) underwent two conditions (resting and 60 min of cycling exercise at 60% V̇o2peak) in which serum and forearm TDF were collected for comparison. There were no significant changes in tIGF-I or fIGF-I in TDF obtained from the forearm or from serum following exercise ( P > 0.05); however, the proportion of fIGF-I to tIGF-I in TDF was approximately fourfold greater than that of serum ( P ≤ 0.05). These data suggest that changes in TDF IGF-I are not evident when TDF is sampled distal from the working tissue. To determine whether exercise-induced increases in local IGF-I could be detected when TDF was sampled directly over the active muscle group, we performed a second experiment. Experiment 2: fourteen subjects (22 ± 4 yr, 68 ± 11 kg) underwent an acute plyometric exercise condition consisting of 10 sets of 10 plyometric jumps with 2-min rest between sets. We observed a significant increase in TDF tIGF-I following exercise ( P ≤ 0.05) but no change in serum tIGF-I ( P > 0.05). Overall, these data suggest that TDF may provide a noninvasive means of monitoring acute exercise-induced changes in local IGF-I when sampled in proximity to exercising muscles. Moreover, our finding that the proportion of free to tIGF-I was greater in TDF than in serum suggests that changes in local IGF-I may be captured more readily using this system.


1994 ◽  
Vol 16 (3) ◽  
pp. 326-333 ◽  
Author(s):  
Shannon Bezoian ◽  
W. Jack Rejeski ◽  
Edward McAuley

The present study examined the role that preexisting efficacy cognitions played in the generation of exercise-induced feeling states during and following an acute bout of exercise. In so doing, the construct validity of a newly developed measure of psychological responses to exercise, the Exercise-Induced Feeling Inventory (EFI; Gauvin & Rejeski, 1993), was investigated. Female undergraduates, classified as having either high or low physical efficacy, engaged in an acute exercise bout and feeling states were recorded prior to, during, and following the activity. More efficacious females maintained a sense of energy during exercise and felt more revitalized and experienced increased positive engagement postexercise than did their less efficacious counterparts. Such findings provide further support for a social-cognitive interpretation of how psychological responses to physical activity might be generated. Results are further discussed in terms of the measurement of exercise-induced feeling states and future applications of the EFI.


2013 ◽  
Vol 304 (12) ◽  
pp. E1379-E1390 ◽  
Author(s):  
Brynjulf Mortensen ◽  
Janne R. Hingst ◽  
Nicklas Frederiksen ◽  
Rikke W. W. Hansen ◽  
Caroline S. Christiansen ◽  
...  

Subjects with a low birth weight (LBW) display increased risk of developing type 2 diabetes (T2D). We hypothesized that this is associated with defects in muscle adaptations following acute and regular physical activity, evident by impairments in the exercise-induced activation of AMPK signaling. We investigated 21 LBW and 21 normal birth weight (NBW) subjects during 1 h of acute exercise performed at the same relative workload before and after 12 wk of exercise training. Multiple skeletal muscle biopsies were obtained before and after exercise. Protein levels and phosphorylation status were determined by Western blotting. AMPK activities were measured using activity assays. Protein levels of AMPKα1 and -γ1 were significantly increased, whereas AMPKγ3 levels decreased with training independently of group. The LBW group had higher exercise-induced AMPK Thr172 phosphorylation before training and higher exercise-induced ACC2 Ser221 phosphorylation both before and after training compared with NBW. Despite exercise being performed at the same relative intensity (65% of V̇o2peak), the acute exercise response on AMPK Thr172, ACC2 Ser221, AMPKα2β2γ1, and AMPKα2β2γ3 activities, GS activity, and adenine nucleotides as well as hexokinase II mRNA levels were all reduced after exercise training. Increased exercise-induced muscle AMPK activation and ACC2 Ser221 phosphorylation in LBW subjects may indicate a more sensitive AMPK system in this population. Long-term exercise training may reduce the need for AMPK to control energy turnover during exercise. Thus, the remaining γ3-associated AMPK activation by acute exercise after exercise training might be sufficient to maintain cellular energy balance.


2018 ◽  
Vol 315 (4) ◽  
pp. E723-E733 ◽  
Author(s):  
Randall F. D’Souza ◽  
Jonathan S. T. Woodhead ◽  
Nina Zeng ◽  
Cherie Blenkiron ◽  
Troy L. Merry ◽  
...  

MicroRNAs (miRNAs) regulate gene expression via transcript degradation and translational inhibition, and they may also function as long distance signaling molecules. Circulatory miRNAs are either protein-bound or packaged within vesicles (exosomes). Ten young men (24.6 ± 4.0 yr) underwent a single bout of high-intensity interval cycling exercise. Vastus lateralis biopsies and plasma were collected immediately before and after exercise, as well as 4 h following the exercise bout. Twenty-nine miRNAs previously reported to be regulated by acute exercise were assessed within muscle, venous plasma, and enriched circulatory exosomes via qRT-PCR. Of the 29 targeted miRNAs, 11 were altered in muscle, 8 in plasma, and 9 in the exosome fraction. Although changes in muscle and plasma expression were bidirectional, all regulated exosomal miRNAs increased following exercise. Three miRNAs were altered in all three sample pools (miR-1-3p, -16-5p, and -222-3p), three in both muscle and plasma (miR-21-5p, -134-3p, and -107), three in both muscle and exosomes (miR-23a-3p, -208a-3p, and -150-5p), and three in both plasma and exosomes (miR-486-5p, -126-3p, and -378a-5p). There was a marked discrepancy between the observed alterations between sample pools. A subset of exosomal miRNAs increased in abundance following exercise, suggesting an exercise-induced release of exosomes enriched in specific miRNAs. The uniqueness of the exosomal miRNA response suggests its relevance as a sample pool that needs to be further explored in better understanding biological functions.


2009 ◽  
Vol 34 (6) ◽  
pp. 1098-1107 ◽  
Author(s):  
Louise Croft ◽  
Jonathan D. Bartlett ◽  
Don P.M. MacLaren ◽  
Thomas Reilly ◽  
Louise Evans ◽  
...  

This aims of this study were to investigate the effects of carbohydrate availability during endurance training on the plasma interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α response to a subsequent acute bout of high-intensity interval exercise. Three groups of recreationally active males performed 6 weeks of high-intensity interval running. Groups 1 (LOW+GLU) and 2 (LOW+PLA) trained twice per day, 2 days per week, and consumed a 6.4% glucose or placebo solution, respectively, before every second training session and at regular intervals throughout exercise. Group 3 (NORM) trained once per day, 4 days per week, and consumed no beverage during training. Each group performed 50 min of high-intensity interval running at the same absolute workloads before and after training. Muscle glycogen utilization in the gastrocnemius muscle during acute exercise was reduced (p < 0.05) in all groups following training, although this was not affected by training condition. Plasma IL-6 concentration increased (p < 0.05) after acute exercise in all groups before and after training. Furthermore, the magnitude of increase was reduced (p < 0.05) following training. This training-induced attenuation in plasma IL-6 increase was similar among groups. Plasma IL-8 concentration increased (p < 0.05) after acute exercise in all groups, although the magnitude of increase was not affected (p > 0.05) by training. Acute exercise did not increase (p > 0.05) plasma TNF-α when undertaken before or after training. Data demonstrate that the exercise-induced increase in plasma IL-6 concentration in response to customary exercise is attenuated by previous exercise training, and that this attenuation appears to occur independent of carbohydrate availability during training.


2015 ◽  
Vol 119 (2) ◽  
pp. 124-134 ◽  
Author(s):  
David de Gonzalo-Calvo ◽  
Alberto Dávalos ◽  
Ana Montero ◽  
Ángela García-González ◽  
Iryna Tyshkovska ◽  
...  

While moderate acute exercise has been associated with strong anti-inflammatory mechanisms, strenuous exercise has been linked to deleterious inflammatory perturbations. It is therefore fundamental to elucidate the mechanisms that regulate the exercise-induced inflammatory cascade. Information on novel regulators such as circulating inflammatory microRNAs (c-inflammamiRs) is incomplete. In this study, we evaluated the response of a panel of c-inflammamiRs to different doses of acute aerobic exercise. We first studied the exercise-induced inflammatory cascade in serum samples of nine active middle-aged males immediately before and after (0 h, 24 h, 72 h) 10-km, half-marathon, and marathon races. Next, we analyzed the circulating profile of 106 specific c-inflammamiRs immediately before) and after (0 h, 24 h) 10-km (low inflammatory response) and marathon (high inflammatory response) races. Analysis of classical inflammatory parameters revealed a dose-dependent effect of aerobic exercise on systemic inflammation, with higher levels detected after marathon. We observed an increase in miR-150-5p immediately after the 10-km race. Levels of 12 c-inflammamiRs were increased immediately after the marathon (let-7d-3p, let-7f-2-3p, miR-125b-5p, miR-132-3p, miR-143-3p, miR-148a-3p, miR-223-3p, miR-223-5p, miR-29a-3p, miR-34a-5p, miR-424-3p, and miR-424-5p). c-inflammamiRs returned to basal levels after 24 h. Correlation and in silico analyses supported a close association between the observed c-inflammamiR pattern and regulation of the inflammatory process. In conclusion, we found that different doses of acute aerobic exercise induced a distinct and specific c-inflammamiR response, which may be associated with control of the exercise-induced inflammatory cascade. Our findings point to c-inflammamiRs as potential biomarkers of exercise-induced inflammation, and hence, exercise dose.


2014 ◽  
Vol 306 (3) ◽  
pp. C241-C249 ◽  
Author(s):  
Ayesha Saleem ◽  
Heather N. Carter ◽  
David A. Hood

An acute bout of exercise activates downstream signaling cascades that ultimately result in mitochondrial biogenesis. In addition to inducing mitochondrial synthesis, exercise triggers the removal of damaged cellular material via autophagy and of dysfunctional mitochondria through mitophagy. Here, we investigated the necessity of p53 to the changes that transpire within the muscle upon an imposed metabolic and physiological challenge, such as a bout of endurance exercise. We randomly assigned wild-type (WT) and p53 knockout (KO) mice to control, acute exercise (AE; 90 min at 15 m/min), and AE + 3 h recovery (AER) groups and measured downstream alterations in markers of mitochondrial biogenesis, autophagy, and mitophagy. In the absence of p53, activation of p38 MAPK upon exercise was abolished, whereas CaMKII and AMP-activated protein kinase only displayed an attenuated enhancement in the AER group compared with WT mice. The translocation of peroxisome proliferator-activated receptor-γ coactivator-1 α to the nucleus was diminished and only observed in the AER group, and the subsequent increase in messenger RNA transcripts related to mitochondrial biogenesis with exercise and recovery was absent in the p53 KO animals. Whole-muscle autophagic and lysosomal markers did not respond to exercise, irrespective of the genotype of the exercised mice, with the exception of increased ubiquitination observed in KO mice with exercise. Markers of mitophagy were elevated in response to AE and AER conditions in both WT and p53 KO runners. The data suggest that p53 is important for the exercise-induced activation of mitochondrial synthesis and is integral in regulating autophagy during control conditions but not in response to exercise.


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