High Intensity Exercise and Depression: Therapeutic Implications through BDNF Upregulation
Vivy Phan
Introduction. Major depressive disorder (MDD) is a world-wide health burden that severely affects a person’s mental health, specifically mood, consisting of persistent sadness or anhedonia leading to a constellation of cognitive and somatic symptoms that impacts a person’s daily life. The neurotropic hypothesis of depression proposes that changes in brain derived neurotrophic factor (BDNF) can affect the development and plasticity of neuronal connections. It has been shown that when exposed to stress, BDNF deficient mice have increased corticosterone levels, increased malodialdehyde (MDA) levels, and decreased catalase (CAT) antioxidant enzyme levels, alluding to a decreased ability to cope with stress1. Additionally, patients with MDD have low serum BDNF concentrations compared to healthy controls, therefore BDNF deficiency could be a target for depression therapy2. Exercise has been shown to increase serum BDNF in MDD patients3. When comparing various exercise regimens, HIIT training greatly increases BDNF in experimental rats over control rats without training and rats who underwent continuous training (CT)4. This suggests HIIT training could be an effective therapy for MDD through the upregulation of BDNF and could be more beneficial than other types of training. Methods. Studies submitted rats to varying levels of exercise intensities via motorized treadmills and used immunoassays to measure various levels of neurotrophic factors, oxidative stress factors, and inflammatory mediators4,5,6. Exercise intensity was assessed through relationship with VO2 max values4,5,6. Results. In experimental mice, HIIT increased levels of hydrogen peroxide (H2O2) and TNF-a more in comparison to CT5. Another study showed that following 6 weeks of HIIT, experimental HIIT rats had elevated BDNF, reduced TNF, IL-6, IL1b, and IL10, increased SOD, and decreased TBARS4. High intensity exercise was associated with elevated proliferative cell density from P31 to P40, higher levels of IL6 from P21 to P30, and higher levels of BDNF, TNF-a, and IL106. Conclusions. Studies have found high intensity exercise to be associated with increased BDNF levels, reduced inflammatory mediators, and increased response to oxidative damage, over both control rats and continuous exercise rats. This suggests high intensity exercise as a potential treatment for MDD patients through its effect on BDNF.
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