Hughson R L, Smyth G A
Eur J Appl Physiol Occup Physiol. 1983;52(1):107-10. doi: 10.1007/BF00429035.
The kinetics of oxygen uptake (VO2) were assessed in 17 normal subjects with beta-blockade and placebo. beta-blockade was achieved with either 50 mg oral metoprolol or 40 mg oral propranolol, each twice per day. Tests were conducted on the cycle ergometer at work rates approximating 80% of the work rate at ventilatory anaerobic threshold. Work rate was initiated as a square wave starting from prior rest. Data obtained 48 h, 1 week, and 4 weeks after starting drug or placebo were pooled to increase the number of points for regression analysis of kinetic parameters. While there were no differences in the plateau values for VO2 with and without beta-blockade, the rate of adaptation to steady state was significantly slower with beta-blockade than with placebo (P less than 0.05). This resulted in an increase of oxygen deficit by approximately 200 ml O2. Cardiac output measured by CO2 rebreathing was significantly reduced by beta-blockade (metoprolol by 4.1%, propranolol by 12.2%, both P less than 0.05). Blood lactate concentration was unaffected by beta-blockade. It was concluded that the influence of beta-blockade on the oxygen transport system was responsible for the significantly slower increase of VO2 to steady state in submaximal exercise.
在17名正常受试者中评估了使用β受体阻滞剂和安慰剂时的摄氧量(VO2)动力学。通过口服50毫克美托洛尔或40毫克普萘洛尔实现β受体阻滞,均每日两次。在功率自行车上以接近通气无氧阈时工作率80%的工作强度进行测试。工作强度以方波形式从先前的休息状态开始启动。将开始使用药物或安慰剂后48小时、1周和4周获得的数据汇总,以增加动力学参数回归分析的点数。虽然使用和未使用β受体阻滞剂时VO2的平台值没有差异,但与安慰剂相比,使用β受体阻滞剂时达到稳态的适应速率明显较慢(P<0.05)。这导致氧亏增加约200毫升O2。通过二氧化碳重呼吸测量的心输出量因β受体阻滞剂而显著降低(美托洛尔降低4.1%,普萘洛尔降低12.2%,两者P<0.05)。血乳酸浓度不受β受体阻滞剂影响。得出的结论是,β受体阻滞剂对氧运输系统的影响是导致次最大运动中VO2达到稳态的增加明显较慢的原因。