Kjaer M, Howlett K, Langfort J, Zimmerman-Belsing T, Lorentsen J, Bulow J, Ihlemann J, Feldt-Rasmussen U, Galbo H
Sports Medicine Research Unit, Departments of Rheumatology and Clinical Physiology, Copenhagen Muscle Research Centre, Bispebjerg Hospital, DK 2400.
J Physiol. 2000 Oct 15;528 Pt 2(Pt 2):371-8. doi: 10.1111/j.1469-7793.2000.00371.x.
The role of adrenaline in regulating muscle glycogenolysis and hormone-sensitive lipase (HSL) activity during exercise was examined in six adrenaline-deficient bilaterally adrenalectomised, adrenocortico-hormonal-substituted humans (Adr) and in six healthy control individuals (Con). Subjects cycled for 45 min at approximately 70% maximal pulmonary O2 uptake (VO2,max) followed by 15 min at approximately 86% VO2,max either without (-Adr and Con) or with (+Adr) adrenaline infusion that elevated plasma adrenaline levels (45 min, 4.49+/-0.69 nmol l(-1); 60 min, 12.41+/-1.80 nmol l(-1)). Muscle samples were obtained at 0, 45 and 60 min of exercise. In -Adr and Con, muscle glycogen was similar at rest (-Adr, 409+/-19 mmol (kg dry wt)(-1); Con, 453+/-24 mmol (kg dry wt)(-1)) and following exercise (-Adr, 237+/-52 mmol (kg dry wt)(-1); Con, 227+/-50 mmol (kg dry wt)(-1)). Muscle lactate, glucose-6-phosphate and glucose were similar in -Adr and Con, whereas glycogen phosphorylase (a/a + b x 100 %) and HSL (% phosphorylated) activities increased during exercise in Con only. Adrenaline infusion increased activities of phosphorylase and HSL as well as blood lactate concentrations compared with those in -Adr, but did not enhance glycogen breakdown (+Adr, glycogen following exercise: 274+/-55 mmol (kg dry wt)(-1)) in contracting muscle. The present findings demonstrate that during exercise muscle glycogenolysis can occur in the absence of adrenaline, and that adrenaline does not enhance muscle glycogenolysis in exercising adrenalectomised subjects. Although adrenaline increases the glycogen phosphorylase activity it is not essential for glycogen breakdown in contracting muscle. Finally, a novel finding is that the activity of HSL in human muscle is increased in exercising man and this is due, at least partly, to stimulation by adrenaline.
在6名双侧肾上腺切除且肾上腺素缺乏、接受肾上腺皮质激素替代治疗的患者（Adr）和6名健康对照个体（Con）中，研究了肾上腺素在运动过程中调节肌肉糖原分解和激素敏感性脂肪酶（HSL）活性的作用。受试者以约70%最大肺氧摄取量（VO2,max）进行45分钟的骑行，随后以约86%VO2,max进行15分钟的骑行，期间一组不进行肾上腺素输注（-Adr和Con），另一组进行肾上腺素输注（+Adr），使血浆肾上腺素水平升高（45分钟时为4.49±0.69 nmol l(-1)；60分钟时为12.41±1.80 nmol l(-1)）。在运动0、45和60分钟时采集肌肉样本。在-Adr和Con组中，静息时肌肉糖原水平相似（-Adr组为409±19 mmol(kg干重)(-1)；Con组为453±24 mmol(kg干重)(-1)），运动后也相似（-Adr组为237±52 mmol(kg干重)(-1)；Con组为227±50 mmol(kg干重)(-1)）。-Adr组和Con组的肌肉乳酸、6-磷酸葡萄糖和葡萄糖水平相似，而糖原磷酸化酶（a/a + b×100%）和HSL（磷酸化百分比）活性仅在Con组运动期间增加。与-Adr组相比，肾上腺素输注增加了磷酸化酶和HSL的活性以及血乳酸浓度，但并未增强收缩肌肉中的糖原分解（+Adr组运动后糖原：274±55 mmol(kg干重)(-1)）。目前的研究结果表明，运动期间肌肉糖原分解可在无肾上腺素的情况下发生，且肾上腺素不会增强肾上腺切除受试者运动时的肌肉糖原分解。尽管肾上腺素增加了糖原磷酸化酶的活性，但它对于收缩肌肉中的糖原分解并非必不可少。最后，一个新发现是，运动时人体肌肉中HSL的活性增加，这至少部分归因于肾上腺素的刺激。
