Cummin A R, Iyawe V I, Mehta N, Saunders K B
J Physiol. 1986 Jan;370:567-83. doi: 10.1113/jphysiol.1986.sp015951.
Three normal subjects performed rest--exercise transitions on a cycle ergometer, from rest to unloaded pedalling (0 W), 50, 100 and 150 W. Each experiment was performed in triplicate, with randomized work load order, in two sessions. Ventilation was obtained breath-to-breath by integration of a pneumotachygraph signal, and cardiac output beat-to-beat by a new development of the Doppler technique. Results were bin-averaged in 4 s bins over the first 20 s, and compared to resting values. Both ventilation and cardiac output increased significantly in the first 2 s. This initial rise in ventilation was due entirely to an increase in rate, the subsequent rise mainly to increase in tidal volume. Cardiac output increased predominantly through change in rate with smaller increases in stroke volume. A striking feature was a tendency for ventilation and cardiac output responses to be biphasic with an initial rise followed by a slight fall at the 14 s mark, and a subsequent rise, at all work loads. Overall correlation between ventilation and cardiac output was therefore high (r = 0.92). Six normal subjects hyperventilated for 45 s voluntarily, (a) at rate 24/min and normal tidal volume; (b) at normal rate and tidal volume of 1.5 l; (c) at rate 24/min and tidal volume of 1.5 l. Cardiac output, averaged over 10-45 s, rose by 0.4, 0.5, and 1.0 l min-1 respectively, with falls in end-tidal PCO2 of 4, 6, and 8 mmHg. Six normal subjects hyperventilated for 60 s with rate 24/min and tidal volume of 1.4 l, and end-tidal PCO2 maintained at 38 +/-2 mm Hg. Cardiac output, averaged from 10-60 s, rose by 1.0 l min-1. With increased rate and tidal volume, whether isocapnic or hypocapnic, cardiac output responses showed an overshoot with a peak value at about 30 s. The hypothesis of 'cardiodynamic hyperpnoea' considers a possible effect of increasing cardiac output on ventilation. The effects of ventilation on cardiac output must also be considered. We propose an extended hypothesis involving stable positive feed-back.
三名正常受试者在自行车测力计上进行了静息 - 运动转换,从静息状态到无负荷蹬车(0瓦)、50瓦、100瓦和150瓦。每个实验重复进行三次,工作负荷顺序随机,分两个阶段进行。通过整合呼吸流速仪信号逐次呼吸获取通气量,通过多普勒技术的新进展逐搏获取心输出量。在前20秒内以4秒为间隔对结果进行二分平均,并与静息值进行比较。通气量和心输出量在最初2秒内均显著增加。通气量的初始增加完全是由于频率增加,随后的增加主要是由于潮气量增加。心输出量的增加主要是通过心率变化,而每搏输出量增加较小。一个显著特征是,在所有工作负荷下,通气量和心输出量的反应都有双相趋势,最初上升,在14秒时略有下降,随后再次上升。因此,通气量和心输出量之间的总体相关性很高(r = 0.92)。六名正常受试者自愿进行了45秒的过度通气,(a)频率为24次/分钟,潮气量正常;(b)频率正常,潮气量为1.5升;(c)频率为24次/分钟,潮气量为1.5升。在10 - 45秒内平均的心输出量分别增加了0.4升/分钟、0.5升/分钟和1.0升/分钟,呼气末二氧化碳分压分别下降了4毫米汞柱、6毫米汞柱和8毫米汞柱。六名正常受试者以24次/分钟的频率和1.4升的潮气量进行了60秒的过度通气,呼气末二氧化碳分压维持在38±2毫米汞柱。在10 - 60秒内平均的心输出量增加了1.0升/分钟。随着频率和潮气量的增加,无论是等碳酸血症还是低碳酸血症,心输出量反应都会出现过冲,在大约30秒时达到峰值。“心动力性呼吸急促”假说认为心输出量增加可能对通气有影响。通气对心输出量的影响也必须考虑。我们提出了一个涉及稳定正反馈的扩展假说。