Department of Psychology and Neuroscience, University of Colorado at Boulder, Boulder, Colorado.
Alcohol Clin Exp Res. 2013 Sep;37(9):1508-15. doi: 10.1111/acer.12135. Epub 2013 Apr 2.
Chronic alcohol abuse is related to numerous deleterious neurobiological consequences, including loss of gray matter, damage to white matter (WM), and impairment of cognitive and motor functions. Aerobic exercise has been demonstrated to slow cognitive decline and decrease the negative neural changes resulting from normal aging and from several diseases. It is possible that exercise may also prevent or repair alcohol-related neurological damage. This study tested the hypothesis that aerobic exercise protects WM in anterior and dorsal areas of the brain from damage related to heavy alcohol use.
Sixty individuals underwent a diffusion tensor imaging session and completed measures of alcohol consumption, loss of control over drinking, and aerobic exercise participation. Analyses examined the relationship of exercise, alcohol, and their interaction to fractional anisotropy (FA) in the superior longitudinal fasciculus (SLF), external capsule (EC), superior and anterior corona radiata, and fornix. The relationship of aerobic exercise and alcohol consumption to self-reported loss of control over drinking were also examined.
A significant interaction was observed between alcohol consumption and aerobic exercise participation on FA in the SLF and EC. In the models examining loss of control over drinking, a significant interaction between aerobic exercise and alcohol consumption was observed, such that alcohol consumption was associated with loss of control more strongly for low exercisers than high exercisers.
These results indicate that the association between heavy alcohol consumption and WM damage in the EC and SLF and the association between alcohol consumption and loss of control over drinking are greater among individuals who do not exercise regularly. These results are consistent with the notion that exercise may protect WM integrity from alcohol-related damage.
慢性酒精滥用与许多有害的神经生物学后果有关,包括灰质损失、白质(WM)损伤以及认知和运动功能障碍。有氧运动已被证明可以减缓认知能力下降,并减少正常衰老和多种疾病引起的负面神经变化。运动可能也可以预防或修复与酒精有关的神经损伤。本研究检验了这样一个假设,即有氧运动可保护大脑前、背侧区域的 WM 免受与大量饮酒相关的损伤。
60 名个体接受了弥散张量成像检查,并完成了酒精摄入量、失控饮酒以及有氧运动参与度的测量。分析考察了运动、酒精及其相互作用与上纵束(SLF)、外囊(EC)、上额和前辐射冠以及穹窿的各向异性分数(FA)之间的关系。还检验了有氧运动和酒精摄入量与自我报告的失控饮酒之间的关系。
在 SLF 和 EC 中,观察到酒精摄入量和有氧运动参与度之间的 FA 存在显著交互作用。在检验失控饮酒的模型中,观察到有氧运动和酒精摄入量之间存在显著的交互作用,即对于低锻炼者而言,酒精摄入量与失控饮酒的相关性比高锻炼者更强。
这些结果表明,EC 和 SLF 中大量饮酒与 WM 损伤之间的关联,以及酒精摄入量与失控饮酒之间的关联,在不经常运动的个体中更为明显。这些结果与运动可能保护 WM 免受酒精相关损伤的观点一致。