Aerobic Exercise Induced Neural Activation and its Modulation: A Review of Task Based fMRI Studies

Author(s):  
Joshua McGillivray ◽  
Hubert Debruin ◽  
Dinesh Kumbhare ◽  
Michael Noseworthy
2021 ◽  
Author(s):  
Sarah Ahmad ◽  
Rodney Hansen ◽  
Matthew Schmolesky

AbstractResearch suggests strong inter-relationships between physical exercise, levels of brain-derived neurotrophic factor (BDNF), levels of estrogen, and the menstrual cycle, and yet no single study has examined these factors collectively in humans. The current study assessed the effect of an acute bout of vigorous aerobic exercise (20 minutes of stationary cycling at 80% of heart rate reserve) on serum BDNF and estradiol in healthy, eumenorrheic women, ages 18-28. In addition, this study determined whether basal BDNF or the exercise-induced increase in BDNF varies throughout the menstrual cycle. Thirty-four subjects were assigned to an experimental (n = 27) or control condition (n = 7). Exercise transiently increased both estradiol (51.2%) and BDNF (23.6%), and basal levels of BDNF and estradiol predicted the magnitude of the exercise-induced increases. Basal BDNF did not vary significantly throughout the menstrual cycle. Exercise-induced changes in BDNF did not correlate with menstrual cycle day or basal estradiol. Basal estradiol and basal BDNF showed a marginally significant positive correlation. Taken together, these results indicate that brief, vigorous aerobic exercise is sufficient to elevate both BDNF and estradiol in healthy women and that the menstrual cycle dramatically influences the magnitude of exercise-induced changes in estradiol, but not BDNF


Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Megan M Wenner ◽  
Caitlin Dow ◽  
Jared Greiner ◽  
Brian Stauffer ◽  
Christopher Desouza

Endothelin-1 (ET-1)-mediated vasoconstrictor tone is elevated in postmenopausal women (PMW), contributing to their increased cardiovascular risk. Although aerobic exercise is beneficial in reducing ET-1 system activity in men, it is unknown whether this favorable vascular effect is conferred in women. In fact, contrary to men, it is uncertain whether aerobic exercise training improves endothelial dysfunction in PMW. We tested the hypothesis that aerobic exercise training reduces ET-1-mediated vasoconstriction in PMW. We further hypothesized reductions in ET-1 vasoconstrictor tone underly exercise-induced improvements in endothelium-dependent vasodilatation in PMW. Methods: Forearm blood flow (FBF) responses to intra-arterial infusion of selective ET A receptor blockade (BQ-123, 100 nmol/min for 60 min), acetylcholine (4.0, 8.0 and 16.0 μg/100 mL tissue/min) in the absence and presence of ET A receptor blockade and sodium nitroprusside (1.0, 2.0 and 4.0 μg/100 mL tissue/min) were determined before and after a 12-week aerobic exercise training intervention in 20 healthy, sedentary PMW (56 + 1 yr). Results: All 20 PMW completed the exercise intervention, walking an average of 4.9 + 0.1 d/wk for 50 + 2 min/d at 71 + 1% of maximal heart rate. After the exercise intervention, BQ-123 elicited no significant change in resting FBF in the previously sedentary PMW compared with significant vasodilation (~25%) before exercise. FBF responses to acetylcholine were markedly higher (~25%; P<0.05) after (from 4.3 + 0.3 to 13.8 + 0.8 mL/100 ml tissue/min) vs before (from 4.1 + 0.2 to 11.3 + 0.8 mL/100 ml tissue/min) exercise training. Moreover, before exercise training the co-infusion of BQ-123 with acetylcholine enhanced (~25%; P<0.05) the vasodilator response (from 4.3 + 0.3 to 13.7 + 0.7 mL/100 mL tissue/min) compared with acetylcholine alone; after exercise training, the presence of BQ-123 did not significantly affect the vasodilator response to acetylcholine. Conclusions: These data demonstrate that aerobic exercise training reduces ET-1-mediated vasoconstriction in PMW. Furthermore, decreased ET-1-mediated vasoconstriction is an important mechanism underlying aerobic exercise-induced improvement in endothelium-dependent vasodilation in PMW.


2014 ◽  
Vol 46 (4) ◽  
pp. 817-825 ◽  
Author(s):  
KELLY MARIE NAUGLE ◽  
KEITH E. NAUGLE ◽  
ROGER B. FILLINGIM ◽  
BRIAN SAMUELS ◽  
JOSEPH L. RILEY

2011 ◽  
Vol 97 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Taiki Miyazawa ◽  
Masahiro Horiuchi ◽  
Daisuke Ichikawa ◽  
Kohei Sato ◽  
Naoki Tanaka ◽  
...  

2018 ◽  
Vol 122 (1) ◽  
pp. 79-95
Author(s):  
Tad T. Brunyé ◽  
Caroline R. Mahoney

The present experiment examined whether physiological arousal induced by acute bouts of aerobic exercise would influence attention and memory for scenes depicting or not depicting weapons. In a repeated-measures design, participants exercised at either low or high exertion levels. During exercise, they were presented with images, some of which depicted weapons; immediately following exercise, they completed a recognition test for portions of central and peripheral scene regions. Two primary results emerged. First, in the low exertion condition, we replicated extant research showing inferior peripheral scene memory when images contained, versus did not contain, weapons. Second, the high exertion condition increased central scene memory relative to low exertion, and this effect was specific to images containing weapons. Thus, we provide evidence for accentuated weapon focus effects during states of exercise-induced physiological arousal. These results contribute new applied and theoretical understandings regarding the interactions between physiological state, breadth of attention, and memory.


2018 ◽  
Vol 25 (1) ◽  
pp. 65-85 ◽  
Author(s):  
Jenin El-Sayes ◽  
Diana Harasym ◽  
Claudia V. Turco ◽  
Mitchell B. Locke ◽  
Aimee J. Nelson

Aerobic exercise improves cognitive and motor function by inducing neural changes detected using molecular, cellular, and systems level neuroscience techniques. This review unifies the knowledge gained across various neuroscience techniques to provide a comprehensive profile of the neural mechanisms that mediate exercise-induced neuroplasticity. Using a model of exercise-induced neuroplasticity, this review emphasizes the sequence of neural events that accompany exercise, and ultimately promote changes in human performance. This is achieved by differentiating between neuroplasticity induced by acute versus chronic aerobic exercise. Furthermore, this review emphasizes experimental considerations that influence the opportunity to observe exercise-induced neuroplasticity in humans. These include modifiable factors associated with the exercise intervention and nonmodifiable factors such as biological sex, ovarian hormones, genetic variations, and fitness level. To maximize the beneficial effects of exercise in health, disease, and following injury, future research should continue to explore the mechanisms that mediate exercise-induced neuroplasticity. This review identifies some fundamental gaps in knowledge that may serve to guide future research in this area.


2012 ◽  
Vol 303 (6) ◽  
pp. R571-R579 ◽  
Author(s):  
Mads Rosenkilde ◽  
Pernille Auerbach ◽  
Michala Holm Reichkendler ◽  
Thorkil Ploug ◽  
Bente Merete Stallknecht ◽  
...  

The amount of weight loss induced by exercise is often disappointing. A diet-induced negative energy balance triggers compensatory mechanisms, e.g., lower metabolic rate and increased appetite. However, knowledge about potential compensatory mechanisms triggered by increased aerobic exercise is limited. A randomized controlled trial was performed in healthy, sedentary, moderately overweight young men to examine the effects of increasing doses of aerobic exercise on body composition, accumulated energy balance, and the degree of compensation. Eighteen participants were randomized to a continuous sedentary control group, 21 to a moderate-exercise (MOD; 300 kcal/day), and 22 to a high-exercise (HIGH; 600 kcal/day) group for 13 wk, corresponding to ∼30 and 60 min of daily aerobic exercise, respectively. Body weight (MOD: −3.6 kg, P < 0.001; HIGH: −2.7 kg, P = 0.01) and fat mass (MOD: −4.0 kg, P < 0.001 and HIGH: −3.8 kg, P < 0.001) decreased similarly in both exercise groups. Although the exercise-induced energy expenditure in HIGH was twice that of MOD, the resulting accumulated energy balance, calculated from changes in body composition, was not different (MOD: −39.6 Mcal, HIGH: −34.3 Mcal, not significant). Energy balance was 83% more negative than expected in MOD, while it was 20% less negative than expected in HIGH. No statistically significant changes were found in energy intake or nonexercise physical activity that could explain the different compensatory responses associated with 30 vs. 60 min of daily aerobic exercise. In conclusion, a similar body fat loss was obtained regardless of exercise dose. A moderate dose of exercise induced a markedly greater than expected negative energy balance, while a higher dose induced a small but quantifiable degree of compensation.


2014 ◽  
Vol 77 ◽  
pp. 313-324 ◽  
Author(s):  
Giovane Galdino ◽  
Thiago R.L. Romero ◽  
José Felipe P. Silva ◽  
Daniele C. Aguiar ◽  
Ana Maria de Paula ◽  
...  

2002 ◽  
pp. 65-70 ◽  
Author(s):  
R Dall ◽  
J Kanaley ◽  
TK Hansen ◽  
N Moller ◽  
JS Christiansen ◽  
...  

OBJECTIVE: To characterise plasma levels of the recently identified endogenous ligand for the GH secretagogue receptor (ghrelin) during submaximal aerobic exercise in healthy adults and in GH-deficient adults. DESIGN: Eight healthy males (mean+/-s.e. age, 40.8+/-2.9 years) and eight hypopituitary males with verified GH deficiency (mean+/-s.e. age, 40.8+/-4.7 years) underwent a baseline test of their peak aerobic capacity (VO(2) peak) and lactate threshold (LT) on a cycle ergometer, as well as an evaluation of body composition. The patients were then studied on two occasions in random order when they exercised for 45 min at their LT. On one occasion, GH replacement had been discontinued from the evening before, whereas on the other occasion they received their evening GH in addition to an intravenous infusion of GH (0.4 IU) during exercise the following day. The healthy subjects exercised at their LT on one occasion without GH. RESULTS: The patients were significantly more obese and had lower VO(2) max (corrected for body weight) and LT as compared with the control subjects. Exercise induced a peak in serum GH concentrations after 45 min in the control group (11.43+/-3.61 microg/l). Infusion of GH in the patients resulted in a peak level after 45 min, whereas no increase was detected when exercising without GH (9.77+/-2.40 (GH) vs 0.11+/-0.07 microg/l (no GH)). Plasma ghrelin levels did not change significantly with time in either study, and no correlations were detected between ghrelin levels and parameters such as GH and IGF-I levels, age or body composition. Plasma ghrelin levels were significantly lower during the study period with GH as compared with the study with no GH. CONCLUSIONS: Submaximal aerobic exercise of an intensity sufficient to stimulate GH release was not associated with significant alterations in plasma ghrelin concentrations, which indicated that systemic ghrelin is not involved in the exercise-induced stimulation of GH secretion. The observation that ghrelin levels were lower during GH replacement suggests that GH may feedback-inhibit systemic ghrelin release.


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