Introduction

Exercise addiction is part of behavioral addictions with symptoms including craving, loss of control, withdrawal, and tolerance. It has been suggested that common neurobiological mechanism underlying substance and behavioral addiction may involve the reward circuit, including the ventral striatum and the orbitofrontal cortex [1]. The neural mechanism of exercise addiction in the perspective of reward circuit is still poorly understood. Therefore, the aim of this study was to investigate the change of activation in reward circuit of the ventral striatum and the posterior orbitofrontal cortex in exercise addiction.

Methods

Seventy-seven right-handed healthy controls (22.8±2.3years, M:64, F:19) were included in this study. Participants were classified into three groups including exercise addiction, over-exercising, and moderate exercise group according to the Korean Exercise Addiction Scale. Each participant was presented physical exercise or neutral pictures during the fMRI acquisition (Figure 1). All fMRI data were acquired with a 3.0T MRI scanner (Discovery 750w; GE Healthcare). BOLD functional images were obtained using a single shot T2*-weighted gradignt EPI pulse sequence (TR=2000ms, TE=30ms, FOV=23cm, Matrix=64x64, Slice thickness=4.0mm, no gap, 32 contiguous axial slices, total scan time=6m8s). Image processing and statistical analysis for fMRI data were performed using SPM8 on MATLAB. The SPM{t} was thresholded at P<0.05, FWE-corrected for multiple comparisons across the whole brain for Monte Carlo simulation. Pearson correlation analysis were performed using SPSS software. Statistical significance was defined at P < 0.05.

Results

Exercise addiction group showed lower activation in ventral striatum than moderate exercise group (Figure 2). Furthermore, exercise addiction group showed less activation in posterior orbitofrontal cortex than the others group (Figure 3). In particular, exercise addicts showed higher scores than other groups in withdrawal, tolerance, and conflict of the Korean Exercise Addiction Scale. In addition, the activity of ventral striatum in exercise addicts has negative correlation with scores of withdrawal, tolerance, and conflict (Figure 4).

Discussion

We found that exercise addiction group showed less activation in ventral striatum and posterior orbitofrontal cortex than over-exercising group or moderate exercise group. The activation of ventral striatum in exercise addicts showed less than moderate exercise group. Specifically, the activity of ventral striatum has negative correlation with scores of withdrawal, tolerance, and conflict with Korean Exercise Addiction Scale. These findings may suggest two possible interpretation such as withdrawal symptoms and reward prediction. First, less activation of ventral striatum in exercise addiction group is related to withdrawal symptoms of addiction. Withdrawal of substance abuse in humans includes with fatigue, decreased motivation, and psychomotor retardation, which may be associated with the decrease in dopaminergic function [2]. Second, when exercise addicts watch a lower exerciser in pictures of physical exercise, the exercise addiction group felt less reward prediction. We also found that both over-exercising and moderate exercise group showed increased activation in the posterior orbitofrontal cortex than exercise addiction group. This finding suggests that exercise group with no addiction may consider various stimuli including body shape of exerciser and fitness equipment as reward value.

Conclusion

In the present study, we investigated the neural mechanism of exercise addiction, using fMRI. Our results may suggest that function of reward circuit in exercise addiction could be hypoactive. This study provides first evidence to elucidate neural mechanism in exercise addiction.

Acknowledgements

No acknowledgement found.