Acute BDNF and cortisol response to low intensity exercise and following ramp incremental exercise to exhaustion in humans

Vega, Sandra Rojas; Strüder, Heiko K.; Wahrmann, Bertha Vera; Schmidt, Annette; Bloch, Wilhelm; Hollmann, W

doi:10.1016/j.brainres.2006.08.105

Cited by 282 publications

(142 citation statements)

References 44 publications

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“…Similar to previous evidence in humans (Ferris et al, 2007; Knaepen et al, 2010; Rojas Vega et al, 2006; Winter et al, 2007), we found that a short bout of high intensity upper extremity cycling elicited a significant increase in serum BDNF relative to quiet rest. Surprisingly however, the magnitude of this increase did not differ between subjects with and without the Val66Met polymorphism.…”

Section: Discussionsupporting

confidence: 90%

“…In humans, aerobic and anaerobic exercise are thought to promote increases in systemic BDNF (Ferris, Williams, & Shen, 2007; Knaepen, Goekint, Heyman, & Meeusen, 2010; Rojas Vega et al, 2006; Skriver et al, 2014; Winter et al, 2007). However, direct causal evidence of BDNF’s moderating role in the relationship between exercise and learning, demonstrated in the animal literature, has not been demonstrated in humans.…”

Section: Introductionmentioning

confidence: 99%

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The influence of high intensity exercise and the Val66Met polymorphism on circulating BDNF and locomotor learning

Helm

Matt

Kirschner

et al. 2017

Neurobiology of Learning and Memory

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Brain-derived neurotrophic factor (BDNF) has been directly related to exercise-enhanced motor performance in the neurologically injured animal model; however literature concerning the role of BDNF in the enhancement of motor learning in the human population is limited. Previous studies in healthy subjects have examined the relationship between intensity of an acute bout of exercise, increases in peripheral BDNF and motor learning of a simple isometric upper extremity task. The current study examined the role of high intensity exercise on upregulation of peripheral BDNF levels as well as the role of high intensity exercise in mediation of motor skill performance and retention of a novel locomotor task in neurologically intact adults. In addition, the impact of a single nucleotide polymorphism in the BDNF gene (Val66Met) in moderating the relationship between exercise and motor learning was explored. It was hypothesized that participation in high intensity exercise prior to practicing a novel walking task (split-belt treadmill walking) would elicit increases in peripheral BDNF as well as promote an increased rate and magnitude of within session learning and retention on a second day of exposure to the walking task. Within session learning and retention would be moderated by the presence or absence of Val66Met polymorphism. Fifty-four neurologically intact participants participated in two sessions of split-belt treadmill walking. Step length and limb phase were measured to assess learning of spatial and temporal parameters of walking. Serum BDNF was collected prior to and immediately following either high intensity exercise or 5 minutes of quiet rest. The results demonstrated that high intensity exercise provides limited additional benefit to learning of a novel locomotor pattern in neurologically intact adults, despite increases in circulating BDNF. In addition, presence of a single nucleotide polymorphism on the BDNF gene did not moderate the magnitude of serum BDNF increases with high intensity exercise, nor did it moderate the relationship between high intensity exercise and locomotor learning.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

The influence of high intensity exercise and the Val66Met polymorphism on circulating BDNF and locomotor learning

Helm

Matt

Kirschner

et al. 2017

Neurobiology of Learning and Memory

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“…Peripheral sources of BDNF include platelets (Fujimura et al 2002), peripheral blood mononuclear cells (Lee and Kim 2010), and vascular cells (Scarisbrick et al 1993), although the mechanism of BDNF release during stress has not been identified. Our present findings, coupled with those observed following exercise (Gold et al 2003; Rojas Vega et al 2006), suggest that BDNF increases in response to both physical and psychological stressors and can occur with in 20-min post-stress. Although the time required to release BDNF during a stressor is unknown, our findings suggest that 20 min post-stress initiation is sufficient for BDNF to be released into the vasculature and taken up into the platelets.…”

Section: Discussionsupporting

confidence: 81%

“…Serial cerebrospinal fluid concentrations of NPYare decreased in participants with post-traumatic stress disorder (Sah et al 2009) and cortisol and NPY positively correlate with stress in participants immediately and 24 h following a physical and psychological stressor (Morgan et al 2002). Intense (Rojas Vega et al 2006) and moderate (Gold et al 2003) exercise also increase serum BDNF in healthy humans. These studies support the relationship between NPY/BDNF and stress, although the data are limited.…”

Section: Introductionmentioning

confidence: 99%

Serum NPY and BNDF response to a behavioral stressor in alcohol-dependent and healthy control participants

Meng

Rao

et al. 2011

Psychopharmacology

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Rationale Neuropeptide Y (NPY) and brain-derived neurotrophic factor (BDNF) have been implicated in both the stress response and alcohol addiction. However, few studies have assessed the NPY and BDNF response to stress in alcohol-dependent participants and the concurrent measure of NPY and BDNF has not been reported in human participants. Objective The purpose of this study was to concurrently assess serum NPYand BDNF, as well as adrenocorticotropin (ACTH) and cortisol, in control and race- and aged-matched abstinent alcohol-dependent participants in response to a stress-inducing public-speaking task. Methods Basal and post-stress serum values of NPY and BDNF, as well as ACTH and cortisol, were assessed in 14 abstinent alcohol-dependent and ten healthy control male participants. Results Basal measures were stable over short periods of time and stress induced a significant increase in both NPY (p= 0.002) and BDNF (p=0.006) as well as ACTH (p<0.001) and cortisol (p<0.007). Alcohol-dependent and control groups did not significantly differ on any basal or stress-induced measure. Basal and delta responses of NPY and BDNF were not significantly correlated, and delta peak responses of NPY and BDNF did not correlate with one another or with their respective ACTH and cortisol responses. Conclusions These findings reveal that both serum NPY and BDNF are responsive to behavioral stressors, although their regulatory mechanisms appear to differ from one another and those of the hypothalamic–pituitary–adrenal axis. Differences in basal and stress-induced responses of NPY and BDNF were not supported between control and abstinent alcohol-dependent subjects.

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“…Recent studies have found that exercise increases the gene expression of brain-derived neurotrophic factor (BDNF) [16,17,18,19,20], although the exact mechanism is unknown. BDNF promotes proliferation and differentiation of neural stem cells in the hippocampus and enhances the survival of these new neurons, a process known as neurogenesis.…”

Section: Introductionmentioning

confidence: 99%

Exercise Treatment for Bipolar Disorder: Potential Mechanisms of Action Mediated through Increased Neurogenesis and Decreased Allostatic Load

Sylvia¹,

Ametrano²,

Nierenberg³

2009

Psychother Psychosom

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Outcomes are frequently suboptimal for patients with bipolar disorder who are treated with pharmacotherapy alone. Adjunct exercise has the potential to substantially improve acute and long-term outcomes, although how exercise would improve the course of bipolar disorder needs to be elucidated. We propose that exercise may improve mood and functioning by increasing neurogenesis and reducing allostatic load. We review data suggesting that exercise increases levels of brain-derived neurotrophic factor, which in turn increases neurogenesis and decreases allostatic load. Exercise as a psychosocial adjunct for bipolar disorder should be assessed with rigorous randomized clinical trials.

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Acute BDNF and cortisol response to low intensity exercise and following ramp incremental exercise to exhaustion in humans

Cited by 282 publications

References 44 publications

The influence of high intensity exercise and the Val66Met polymorphism on circulating BDNF and locomotor learning

The influence of high intensity exercise and the Val66Met polymorphism on circulating BDNF and locomotor learning

Serum NPY and BNDF response to a behavioral stressor in alcohol-dependent and healthy control participants

Exercise Treatment for Bipolar Disorder: Potential Mechanisms of Action Mediated through Increased Neurogenesis and Decreased Allostatic Load

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