■咖啡因是最广泛消费的精神兴奋剂。尽管如此,急性咖啡因摄入对大脑代谢产物水平的影响在很大程度上仍是未知的。我们旨在研究不同咖啡因消费习惯组中急性咖啡因摄入对大脑代谢物浓度的影响,并探讨代谢物变化与嗜睡之间的关系。
■根据每天的咖啡因摄入量将45名健康成年人分为几组:≥1杯/天,<1杯/天,没有消费。排除标准是存在神经系统疾病,习惯性消费改变精神的物质,以及无法进行磁共振成像的个体。Mescher-Garwood点分辨光谱学和常规光谱学数据在3特斯拉下从丘脑和后扣带回皮质(PCC)的体素获得。使用卡罗林斯卡嗜睡量表测量主观嗜睡。
■双向重复测量方差分析的结果表明,时间与谷氨酸组之间存在显着的交互作用,甘油磷酸胆碱和磷酸胆碱(GPC+PCH),肌醇,谷氨酸+谷氨酰胺(Glx),丘脑的肌酸和磷酸肌酸(CrPCr)(均P<0.01),和谷氨酸(P<0.0001),GPC+PCH(P=0.016),PCC的Glx(P<0.0001)。咖啡因摄入前后的变化导致γ-氨基丁酸阳性大分子(GABA)(丘脑,P=0.011),Glx(丘脑,P=0.002),谷氨酸(PCC,P<0.0001),GPC+PCH(丘脑,P=0.012和PCC,P<0.0001),肌醇(丘脑,P=0.009),和Glx(PCC,P<0.0001)。群体之间的变化,≥1杯/天显着高于<1杯/天或不食用谷氨酸(PCC,P=0.028),GPC(丘脑,P=0.001;PCC,P=0.026),和Cr+PCr(PCC,P=0.035);≥1杯/天显着低于<1杯/天且不食用谷氨酸(丘脑,P<0.0001),Cr+PCr(丘脑,P=0.003),Glx(丘脑,P=0.014),和肌醇(PCC,P=0.009)。双变量相关分析显示丘脑体素中GABA+(r=-0.7676;P<0.0001)与主观嗜睡呈负相关。
■较高的咖啡因摄入量对大脑代谢产物有重大影响。磁共振波谱在测量咖啡因摄入后的脑代谢物波动方面很敏感,特别是丘脑中GABA+的水平,与嗜睡显著相关。
UNASSIGNED: Caffeine is the most widely consumed psychostimulant. Despite this, the effects of acute caffeine intake on brain metabolite levels remain largely unknown. We aimed to investigate the effect of acute caffeine intake on brain metabolite concentrations in different caffeine consumption habit groups and to explore the association between metabolite changes and sleepiness.
UNASSIGNED: Forty-five healthy adults were divided into groups based on their daily caffeine consumption: ≥1 cup/day, <1 cup/day, and no consumption. The exclusion criteria were the presence of neurological disorder, habitual consumption of mind-altering substances, and individuals who were unable to undergo magnetic resonance imaging. Mescher-Garwood point resolved spectroscopy and conventional spectroscopy data were acquired at 3 Tesla from voxels in the thalamus and posterior cingulate cortex (PCC). Subjective sleepiness was measured with the Karolinska Sleepiness Scale.
UNASSIGNED: The results of two-way repeated measures analysis of variance indicated a significant interaction effect between time and group for glutamate, glycerylphosphocholine and phosphocholine (GPC + PCH), myo-inositol, glutamate + glutamine (Glx), and creatine and phosphocreatine (Cr + PCr) of the thalamus (all P<0.01), and glutamate (P<0.0001), GPC + PCH (P=0.016), and Glx (P<0.0001) of the PCC. The change between pre- and post-caffeine intake results with significant reductions in γ-aminobutyric acid-positive macromolecule (GABA+) (thalamus, P=0.011), Glx (thalamus, P=0.002), glutamate (PCC, P<0.0001), and significant increments in GPC + PCH (thalamus, P=0.012 and PCC, P<0.0001), myo-inositol (thalamus, P=0.009), and Glx (PCC, P<0.0001). The change among the groups, with the ≥1 cup/day was significantly higher than the <1 cup/day or no consumption for glutamate (PCC, P=0.028), GPC (thalamus, P=0.001; PCC, P=0.026), and Cr + PCr (PCC, P=0.035); ≥1 cup/day was significantly lower than <1 cup/day and no consumption for glutamate (thalamus, P<0.0001), Cr + PCr (thalamus, P=0.003), Glx (thalamus, P=0.014), and myo-inositol (PCC, P=0.009). Bivariate correlation analysis revealed that GABA+ in the thalamus voxel (r=-0.7676; P<0.0001) was negatively correlated with subjective sleepiness.
UNASSIGNED: Higher caffeine consumption had a significant impact on brain metabolites. Magnetic resonance spectroscopy was sensitive in measuring brain metabolite fluctuations after caffeine intake, particularly the levels of GABA+ in the thalamus, which was significantly correlated with sleepiness.