The ultimate revelation of Obesity and Cognitive Function

1High intensity interval exercise is commonly recognized as the most time effective and efficient way to exercise. It could likewise be an effective strategy to prevent and combat cognitive dysfunction in obese individuals.

Obesity reduces the expression of brain-derived neurotrophic factor, a protein in the brain that promotes the survival of neurons. Lower levels of this protein are associated with Parkinson’s disease, Alzheimer’s disease, and obesity. Although research has shown that obesity is a risk factor for cognitive dysfunction, the mechanisms of this relationship are not fully understood.

To-date, studies on exercise and brain-derived neurotrophic factor response in obese individuals have only used continuous moderate intensity exercise without rest intervals. The researchers examine the modulatory role of obesity on exercise-induced BDNF release and to use an acute high-intensity interval exercise protocol as a practical model to measure the phenomena of brain-derived neurotrophic factor response release in both obese and normal-weight subjects. They also examined the potential relationship of exercise-induced brain-derived neurotrophic factor with blood lactate and cortisol.

Results of study, show that the brain-derived neurotrophic factor response to acute high intensity interval exercise was greater than continuous moderate-intensity exercise in obese subjects when compared to normal weight subjects. These findings recommend that acute high intensity interval exercise may be a more effective protocol to upregulate brain derived neurotrophic factor expression in an obese population, cortisol levels and independent of increased lactate.

Other findings from the study show statistically significant differences between the obese and normal weight groups for body weight, body mass index, systolic and diastolic blood pressures, and waist circumferences and ratio. Also, both the normal and obese weight groups had comparable heart rate responses during both exercise protocols, producing a similar relative exercise intensity and effort between groups. Therefore, the brain-derived neurotrophic factor response was likely not influenced by disparities between aerobic fitness, with a greater level in obese subjects than normal weight subjects following acute high intensity interval exercise vs. continuous moderate intensity exercise.

Also, both the fat and typical weight bunches had equivalent pulse reactions amid both exercise conventions, delivering a comparable relative exercise power and exertion between gatherings.

Increased levels of cortisol have been shown to down regulate brain-derived neurotrophic factor expression; however, this relationship in response to exercise still remains equivocal. Specifically, our study and others did not observe any correlation between cortisol and brain-derived neurotrophic factor following either acute high-intensity exercise or continuous moderate-intensity exercise protocol, yet, the report of such is opposite.

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