Neurobiological changes as an explanation of benefits of exercise

It has been hypothesized that depression and anxiety are caused by dysfunction of neurochemical systems controlling catecholamines and 5-hydroxytryptamine (5-HT) synthesis and release in the brain, the monoamine hypothesis. Normally the problem is insufficient synthesis and release, although excess of these monoamines can also induce depression and anxiety. Some theorists have argued that problems are morphological but may require the synthesis and release of the proteins brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1) and vascular endothelial growth factor (VEGF) to aid neurogenesis and neuroplasticity. We review the human and animal studies which show that acute and/or chronic exercise induces increased synthesis and release of catecholamines, 5-HT, BDNF, IGF-1, and VEGF in the brain. Moreover, we present evidence from humans and animals of chronic exercise-induced increases in hippocampal, basal ganglia, and prefrontal cortex volumes, as well as improved functional connectivity in the brain, all of which would relieve the morphological problems that are thought to result in depression and anxiety. However, the empirical literature reviewed shows very little support for exercise-induced, neurochemical and morphological changes being responsible for the observed improvements in psychological well-being following exercise. We argue that this is due to a lack of research and that literature examining the positive effects of exercise on brain concentrations of the neurochemicals involved in feelings of psychological well-being provides strong circumstantial evidence that it is the exercise-induced effects on these neurochemicals and brain structures that induce relief and protection from depression and anxiety.