Chesley A, Howlett R A, Heigenhauser G J, Hultman E, Spriet L L
Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph N1G 2W1, Canada.
Am J Physiol. 1998 Aug;275(2):R596-603. doi: 10.1152/ajpregu.1998.275.2.R596.
This study examined the effects of caffeine (Caf) ingestion on muscle glycogen use and the regulation of muscle glycogen phosphorylase (Phos) activity during intense aerobic exercise. In two separate trials, 12 untrained males ingested either placebo (Pl) or Caf (9 mg/kg body wt) 1 h before cycling at 80% maximum O2 consumption (VO2 max) for 15 min. Muscle biopsies were obtained from the vastus lateralis at 0, 3, and 15 min of exercise. In this study, glycogen "sparing" was defined as a 10% or greater reduction in muscle glycogen use during exercise after Caf ingestion compared with Pl. Muscle glycogen use decreased by 28% (Pl 255 +/- 38 vs. Caf 184 +/- 24 mmol/kg dry muscle) after Caf in six subjects [glycogen sparers (Sp)] but was unaffected by Caf in six other subjects [nonsparers (NSp), Pl 210 +/- 35 vs. Caf 214 +/- 37 mmol/kg dry muscle]. In both groups, Caf significantly increased resting free fatty acid concentration, significantly increased epinephrine concentration by twofold during exercise, and increased the Phos a mole fraction at 3 min of exercise compared with Pl, although not significantly. Caf improved the energy status of the muscle during exercise in the Sp group: muscle phosphocreatine (PCr) degradation was significantly reduced (Pl 47.9 +/- 3.6 vs. Caf 40.4 +/- 6.7 mmol/kg dry muscle at 3 min) and the accumulations of free ADP and free AMP (Pl 6.8 +/- 1.3 vs. Caf 3.1 +/- 1.4 micromol/kg dry muscle at 3 min; Pl 8.7 +/- 0.8 vs. Caf 4.7 +/- 1.1 micromol/kg dry muscle at 15 min) were significantly reduced. Caf had no effect on these measurements in the NSp group. It is concluded that the Caf-induced decrease in flux through Phos (glycogen-sparing effect) is mediated via an improved energy status of the muscle in the early stages of intense aerobic exercise. This may be related to an increased availability of fat and/or ability of mitochondria to oxidize fat during exercise preceded by Caf ingestion. It is presently unknown why the glycogen-sparing effect of Caf does not occur in all untrained individuals during intense aerobic exercise.
本研究探讨了摄入咖啡因（Caf）对高强度有氧运动期间肌肉糖原利用及肌肉糖原磷酸化酶（Phos）活性调节的影响。在两项独立试验中，12名未经训练的男性在以80%最大耗氧量（VO2 max）进行15分钟骑行前1小时，分别摄入安慰剂（Pl）或咖啡因（9毫克/千克体重）。在运动0、3和15分钟时，从股外侧肌获取肌肉活检样本。在本研究中，糖原“节省”定义为与摄入安慰剂相比，摄入咖啡因后运动期间肌肉糖原利用减少10%或更多。六名受试者摄入咖啡因后肌肉糖原利用减少了28%（安慰剂组为255±38，咖啡因组为184±24毫摩尔/千克干肌肉）[糖原节省者（Sp）]，但另外六名受试者[非节省者（NSp）]的肌肉糖原利用不受咖啡因影响（安慰剂组为210±35，咖啡因组为214±37毫摩尔/千克干肌肉）。在两组中，咖啡因均显著提高静息游离脂肪酸浓度，在运动期间显著使肾上腺素浓度增加两倍，与安慰剂相比，在运动3分钟时增加Phos a摩尔分数，尽管未达到显著水平。咖啡因改善了Sp组运动期间肌肉的能量状态：肌肉磷酸肌酸（PCr）降解显著减少（3分钟时，安慰剂组为47.9±3.6，咖啡因组为40.4±6.7毫摩尔/千克干肌肉），游离ADP和游离AMP的积累显著减少（3分钟时，安慰剂组为6.8±1.3，咖啡因组为3.1±1.4微摩尔/千克干肌肉；15分钟时，安慰剂组为8.7±0.8，咖啡因组为4.7±1.1微摩尔/千克干肌肉）。咖啡因对NSp组的这些测量指标没有影响。得出的结论是，咖啡因诱导的通过Phos的通量降低（糖原节省效应）是通过在高强度有氧运动早期改善肌肉能量状态介导的。这可能与摄入咖啡因后运动期间脂肪可用性增加和/或线粒体氧化脂肪的能力增强有关。目前尚不清楚为什么在高强度有氧运动期间，并非所有未经训练的个体都会出现咖啡因的糖原节省效应。
