Mora-Rodriguez R, Hodgkinson B J, Byerley L O, Coyle E F
The Human Performance Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas 78712, USA.
Am J Physiol Endocrinol Metab. 2001 May;280(5):E752-60. doi: 10.1152/ajpendo.2001.280.5.E752.
We used beta-adrenergic receptor stimulation and blockade as a tool to study substrate metabolism during exercise. Eight moderately trained subjects cycled for 60 min at 45% of VO(2 peak) 1) during a control trial (CON); 2) while epinephrine was intravenously infused at 0.015 microg. kg(-1) x min(-1) (beta-STIM); 3) after ingesting 80 mg of propranolol (beta-BLOCK); and 4) combining beta-BLOCK with intravenous infusion of Intralipid-heparin to restore plasma fatty acid (FFA) levels (beta-BLOCK+LIPID). beta-BLOCK suppressed lipolysis (i.e., glycerol rate of appearance) and fat oxidation while elevating carbohydrate oxidation above CON (135 +/- 11 vs. 113 +/- 10 micromol x kg(-1) x min(-1); P < 0.05) primarily by increasing rate of disappearance (R(d)) of glucose (36 +/- 2 vs. 22 +/- 2 micromol x kg(-1) x min(-1); P < 0.05). Plasma FFA restoration (beta-BLOCK+LIPID) attenuated the increase in R(d) glucose by more than one-half (28 +/- 3 micromol x kg(-1) x min(-1); P < 0.05), suggesting that part of the compensatory increase in muscle glucose uptake is due to reduced energy from fatty acids. On the other hand, beta-STIM markedly increased glycogen oxidation and reduced glucose clearance and fat oxidation despite elevating plasma FFA. Therefore, reduced plasma FFA availability with beta-BLOCK increased R(d) glucose, whereas beta-STIM increased glycogen oxidation, which reduced fat oxidation and glucose clearance. In summary, compared with control exercise at 45% VO(2 peak) (CON), both beta-BLOCK and beta-STIM reduced fat and increased carbohydrate oxidation, albeit through different mechanisms.
我们使用β-肾上腺素能受体刺激和阻断作为工具来研究运动期间的底物代谢。八名中度训练的受试者在以下情况下以VO₂峰值的45%进行60分钟的骑行：1）在对照试验（CON）期间；2）静脉注射肾上腺素，剂量为0.015微克·千克⁻¹·分钟⁻¹（β-刺激）；3）摄入80毫克普萘洛尔后（β-阻断）；4）将β-阻断与静脉输注脂质乳剂-肝素相结合以恢复血浆脂肪酸（FFA）水平（β-阻断+脂质）。β-阻断抑制了脂肪分解（即甘油出现率）和脂肪氧化，同时使碳水化合物氧化高于CON（135±11对113±10微摩尔·千克⁻¹·分钟⁻¹；P<0.05），主要是通过增加葡萄糖的消失率（R(d)）（36±2对22±2微摩尔·千克⁻¹·分钟⁻¹；P<0.05）。血浆FFA恢复（β-阻断+脂质）使R(d)葡萄糖的增加减少了一半以上（28±3微摩尔·千克⁻¹·分钟⁻¹；P<0.05），这表明肌肉葡萄糖摄取的部分代偿性增加是由于脂肪酸能量减少。另一方面，β-刺激显著增加了糖原氧化，降低了葡萄糖清除率和脂肪氧化，尽管血浆FFA升高。因此，β-阻断导致血浆FFA可用性降低增加了R(d)葡萄糖，而β-刺激增加了糖原氧化，这降低了脂肪氧化和葡萄糖清除率。总之，与在45%VO₂峰值（CON）下的对照运动相比，β-阻断和β-刺激都减少了脂肪并增加了碳水化合物氧化，尽管机制不同。
