Gibala Martin J, González-Alonso José, Saltin Bengt
Copenhagen Muscle Research Centre, Rigshospitalet Section 7652, DK-2200 Copenhagen, Denmark.
J Physiol. 2002 Dec 1;545(2):705-13. doi: 10.1113/jphysiol.2002.028084.
It has been suggested that a decrease in the total concentration of tricarboxylic acid cycle intermediates (TCAIs)--secondary to a reduction in glycogen availability--compromises oxidative energy provision in skeletal muscle during prolonged exercise. However, no study has directly tested this hypothesis. We therefore studied six men (28 +/- 2 years) during 90 min of leg kicking exercise at an intensity equivalent to 70 % of maximum. Biopsies (vastus lateralis) were obtained at rest and after 5, 10, 15, 30, 60 and 90 min of exercise, and thigh oxygen uptake (V(O(2),thigh)) was calculated according to the Fick principle. The sum of six measured TCAIs (approximately 95 % of total pool size) was 1.30 +/- 0.15 mmol (kg dry wt)(-1) at rest and increased (P < or = 0.05) rapidly during exercise to a peak value of 3.15 +/- 0.23 mmol (kg dry wt)(-1) after 10 min. Thereafter, the [TCAI] declined to 2.14 +/- 0.23, 1.73 +/- 0.32 and 1.62 +/- 0.10 mmol (kg dry wt)(-1) after 30, 60 and 90 min, respectively (P < or = 0.05 vs.10 min). Despite the 50 % decrease in [TCAI], aerobic energy provision was not compromised, as evidenced by stable V(O(2),thigh) values throughout the entire exercise bout and little change in muscle [phosphocreatine] after 10 min. The largest decrease in [TCAI] (delta = 1.00 +/- 0.24 mmol (kg dry wt)(-1)) occurred from 10 to 30 min of exercise despite the fact that muscle [glycogen] remained relatively high at this point in exercise (approximately 274 +/- 24 mmol (kg dry wt)(-1) after 30 min; approximately 65 % of rest value). Conversely, there was little change in [TCAI] during the final 30 min of exercise (delta = 0.11 +/- 0.29 mmol (kg dry wt)(-1)) despite a decrease in [glycogen] to approximately 72 +/- 3 mmol (kg dry wt)(-1) after 90 min (approximately 13 % of rest value). We conclude that there is a progressive decrease in muscle [TCAI] during prolonged exercise in humans; however this decrease does not compromise aerobic energy provision and is not attributable to the depletion of muscle [glycogen].
有人提出,三羧酸循环中间体(TCAIs)的总浓度降低——继发于糖原可用性的降低——会在长时间运动期间损害骨骼肌中的氧化能量供应。然而,尚无研究直接验证这一假设。因此,我们对6名男性(28±2岁)进行了研究,让他们以相当于最大强度70%的强度进行90分钟的腿部踢腿运动。在休息时以及运动5、10、15、30、60和90分钟后获取活检样本(股外侧肌),并根据Fick原理计算大腿摄氧量(V(O₂,大腿))。6种测得的TCAIs的总和(约占总池大小的95%)在休息时为1.30±0.15 mmol(kg干重)⁻¹,并在运动期间迅速增加(P≤0.05),在10分钟后达到峰值3.15±0.23 mmol(kg干重)⁻¹。此后,[TCAI]在30、60和90分钟后分别降至2.14±0.23、1.73±0.32和1.62±0.10 mmol(kg干重)⁻¹(与10分钟时相比,P≤0.05)。尽管[TCAI]降低了50%,但有氧能量供应并未受到损害,这在整个运动过程中稳定的V(O₂,大腿)值以及10分钟后肌肉中[磷酸肌酸]几乎没有变化中得到了证明。[TCAI]的最大降幅(δ=1.00±0.24 mmol(kg干重)⁻¹)发生在运动10至30分钟之间,尽管此时运动过程中肌肉中的[糖原]仍然相对较高(30分钟后约为274±24 mmol(kg干重)⁻¹;约为休息值的65%)。相反,在运动的最后30分钟内,[TCAI]几乎没有变化(δ=0.11±0.29 mmol(kg干重)⁻¹),尽管90分钟后[糖原]降至约72±3 mmol(kg干重)⁻¹(约为休息值的13%)。我们得出结论,在人类长时间运动期间,肌肉中的[TCAI]会逐渐降低;然而,这种降低不会损害有氧能量供应,也不归因于肌肉中[糖原]的耗尽。