What mediates exercise effects on dietary choice? Clues from the brain stimulation literature

Abstract

To the Editor: A recent study by Joo and colleagues [1] found that a 15week exercise training program increased healthy dietary choice among adults. The effects were not large in magnitude but did emerge across a number of different indicators of dietary choice, which collectively suggested a decrease in calorie density and increase in nutritive value of dietary choices among those in the exercise intervention arm. In the context of discussing these findings, Joo and colleagues offer the hypothesis that exercise, specifically aerobic exercise, may result in healthier dietary choices via a general increase in motivation to live a healthy lifestyle. In short, the mediational mechanism thought to explain the causal effect of exercise on dietary choice was motivation. Motivation of course can be understood as both a social–cognitive variable and also with reference to enhanced activity in the brain’s reward pathways, both of which are plausible consequences of aerobic exercise. However, there is a third mediational mechanism that may involve the brain in a different way. Brain stimulation studies targeting the dorsolateral prefrontal cortex (dlPFC) show that attenuation increases and excitation decreases calorie-dense food consumption in humans [2–4]. The dlPFC is important in dietary restraint because it is centrally implicated in the behavioral inhibition facet of executive function, a set of cognitive operations that facilitate selfcontrol and goal-directed action more broadly [5]. Many studies have attested to the value of exercise for improving the functional and structural parameters of the dlPFC [6–8]. In our own studies, we have found that even single bouts of aerobic exercise can facilitate self-regulation in a subsequent taste test paradigm [9]. In two recent studies, we have found that the effects of dlPFC attenuation do not operate through any change in the evaluation of calorie-dense food items, nor do they affect sensory processing of such food items. Only changes in cognitive control per se accounted for changes in food consumption induced by the experimental manipulation [10]. In a second study, we examined the mediational mechanisms by which dlPFC attenuation resulted in increases in calorie-dense food consumption; again, we found that changes in motivational dynamics did not account for increases in consumption [11], but performance on a task of inhibitory control did. Kim and colleagues, on the other hand, found that excitatory stimulation of the dlPFC increases food choice quality and facilitates weight loss in obese adults [12]. Together, these above findings suggest that the impact of exercise on cognitive control networks may be an important mechanism, by which exercise—particularly aerobic exercise—may improve dietary choice. We encourage measurement of such candidate mediational pathways in future exercise intervention studies that measure dietary outcomes. Over long periods of time, bidirectional relationships between cognitive control nodes in the brain and obesity are an intriguing possibility [13, 14].