Abstract

Rodent research indicates that acute physical exercise facilitates fear learning and inhibition. Expression of brain-derived neurotrophic factor (BDNF) may moderate the memory enhancing effects of acute exercise. We assessed the role of acute exercise in modulating extinction retention in humans, and investigated the extent to which the BDNF polymorphism influenced extinction retention. Seventy non-clinical participants engaged in a differential fear potentiated startle paradigm involving conditioning and extinction followed by random assignment to either intense exercise (n = 35) or no exercise (n = 35). Extinction retention was assessed 24 h later. Saliva samples were collected to index BDNF genotype. Exercised participants displayed significantly lower fear 24 h later relative to non-exercised participants. Moderation analyses indicated that after controlling for gender, the BDNF Val66Met polymorphism moderated the relationship between exercise and fear recovery 24 h later, such that exercise was associated with greater fear recovery in individuals with the Met allele. These findings provide initial evidence that acute exercise can impact fear extinction in humans and this effect is reduced in Met-allele carriers. This finding accords with the role of BDNF in extinction learning, and has implications for augmenting exposure-based therapies for anxiety disorders.

Highlights

  • Fear extinction is a form of inhibitory associative learning whereby a previously conditioned stimulus (CS) becomes associated with safety via repeated exposure to it in the absence of an aversive outcome[1]

  • We aimed to examine the effect of an acute bout of exercise in modulating extinction retention

  • Maximum heart rate data was missing for 14 exercised and 16 non-exercised participants due to technical difficulties, and as such were replaced with the mean for the respective group

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Summary

Introduction

Fear extinction is a form of inhibitory associative learning whereby a previously conditioned stimulus (CS) becomes associated with safety via repeated exposure to it in the absence of an aversive outcome[1]. This new safety memory competes with the original fear conditioned memory, such that under certain conditions it can function to actively inhibit fear expression[2]. Fear extinction forms the basis of exposure therapy for anxiety-related disorders. Despite strong empirical validation for exposure therapy[3,4], many individuals do not optimally benefit from this treatment and this has prompted an exploration of ways to enhance retention of fear extinction.

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