Gibala Martin J, Peirce Nick, Constantin-Teodosiu Dimitru, Greenhaff Paul L
Copenhagen Muscle Research Centre, Rigshospitalet Section 7652, DK-2200 Copenhagen, Denmark.
J Physiol. 2002 May 1;540(Pt 3):1079-86. doi: 10.1113/jphysiol.2001.012983.
We tested the hypotheses that: (i) exercise with low muscle glycogen would reduce pyruvate flux through the alanine aminotransferase (AAT) reaction and attenuate the increase in tricarboxylic acid (TCA) cycle intermediates, and (ii) attenuation of tricarboxylic acid cycle intermediate (TCAI) pool expansion would limit TCA cycle flux, thereby accelerating phosphocreatine (PCr) degradation. Eight men cycled for 10 min at 70 % of their (VO(2,max) on two occasions: (i) following their normal diet (CON) and (ii) after cycling to exhaustion and consuming a low carbohydrate diet for approximately 2 days (LG). Biopsies (m. vastus lateralis) confirmed that [glycogen] was lower in LG vs. CON at rest (257 +/- 18 vs. 611 +/- 54 mmol (kg dry mass)(-1); P 0.05); however, net glycogenolysis was not different after 1 or 10 min of exercise. PCr degradation from rest to 1 min was approximately 26 % higher in LG vs. CON (38 +/- 4 vs. 28 +/- 4 mmol (kg dry mass)(-1); P< or =0.05). The sum of five measured TCAIs (approximately 90 % of total pool) was not different between trials at rest and after 1 min, but was higher after 10 min in LG vs. CON (5.51 +/- 0.43 vs. 4.45 +/- 0.49 mmol (kg dry mass)(-1); P 0.05). Pyruvate dehydrogenase complex (PDC) activity was lower during exercise in LG vs. CON (2.2 +/- 0.2 vs. 1.4 +/- 0.2 mmol min(-1) (kg wet weight)(-1) after 10 min; P< or =0.05), and acetylcarnitine was approximately threefold less, implying increased pyruvate availability for flux through AAT. Resting muscle [glutamate] was higher in LG vs. CON (16.1 +/- 0.8 vs. 11.8 +/- 0.4 mmol (kg dry mass)(-1); P< or =0.05) and the net decrease in [glutamate] during exercise was approximately 30 % greater in LG vs. CON. These findings suggest that: (i) contrary to our hypotheses, LG increased anaplerosis by decreasing PDC flux and/or increasing the conversion of glutamate carbon to TCAIs, and (ii) accelerating the rate of muscle TCAI expansion did not affect oxidative energy provision during the initial phase of contraction, since changes in [TCAI] were not temporally related to PCr degradation.
（i）低肌肉糖原状态下的运动将减少丙酮酸通过丙氨酸转氨酶（AAT）反应的通量，并减弱三羧酸（TCA）循环中间产物的增加；（ii）三羧酸循环中间产物（TCAI）池扩张的减弱将限制TCA循环通量，从而加速磷酸肌酸（PCr）降解。八名男性在两种情况下以其最大摄氧量（VO₂max）的70%进行了10分钟的骑行：（i）按照正常饮食（CON）；（ii）骑行至力竭并食用约两天低碳水化合物饮食后（LG）。活检（股外侧肌）证实，静息时LG组的[糖原]低于CON组（257±18对611±54 mmol·(kg干质量)⁻¹；P<0.05）；然而，运动1分钟或10分钟后的净糖原分解并无差异。从静息到1分钟，LG组的PCr降解比CON组高约26%（38±4对28±4 mmol·(kg干质量)⁻¹；P≤0.05）。五次测量的TCAI之和（约占总池的90%）在静息时和运动1分钟后两组间无差异，但运动10分钟后LG组高于CON组（5.51±0.43对4.45±0.49 mmol·(kg干质量)⁻¹；P<0.05）。与CON组相比，LG组运动期间丙酮酸脱氢酶复合体（PDC）活性较低（10分钟后为2.2±0.2对1.4±0.2 mmol·min⁻¹·(kg湿重)⁻¹；P≤0.05），且乙酰肉碱减少约三倍，这意味着通过AAT通量的丙酮酸可用性增加。静息时LG组肌肉[谷氨酸]高于CON组（16.1±0.8对11.8±0.4 mmol·(kg干质量)⁻¹；P≤0.05），运动期间LG组[谷氨酸]的净减少比CON组大约30%。这些发现表明：（i）与我们的假设相反，LG组通过降低PDC通量和/或增加谷氨酸碳向TCAI的转化来增加回补反应；（ii）加速肌肉TCAI扩张速率在收缩初始阶段不影响氧化能量供应，因为[ TCAI ]的变化与PCr降解在时间上无关。
