Miura T, Miyazaki S, Guth B D, Kambayashi M, Ross J
Yamaguchi University, Japan.
Circulation. 1992 Aug;86(2):563-71. doi: 10.1161/01.cir.86.2.563.
The magnitude of the force-frequency effect on myocardial contractility in the conscious animal has been studied at rest, but it has not been assessed during exercise.
The influence of heart rate (HR) changes were evaluated during treadmill exercise in eight preinstrumented, conscious dogs in which high-fidelity left ventricular (LV) pressure, LV volume (by sonomicrometry), and aortic pressure were measured. Under resting conditions, end-systolic pressure-volume relations were obtained using inferior vena caval occlusion. Dogs were run on a treadmill, and the intrinsic exercise HR was reduced by infusion of a specific bradycardic drug (UL-FS 49 0.5 mg/kg) during continuing exercise while HR was maintained at 240 beats per minute by atrial pacing. At 6 minutes of running at a fixed, paced HR when a stable drug effect had been achieved, no effects of UL-FS 49 on measures of LV contractility were detected compared with exercise before drug administration. HR was then reduced stepwise from 240 to 210, 180, or 150 beats per minute in a random manner, returning to 240 beats per minute between steps. Progressive reductions in measures of myocardial contractility occurred as the HR was slowed, and reduction of rate from 240 to 150 beats per minute reduced the LV maximum positive dP/dt by 31% and (dP/dt)DP40 by 21% despite increases in LV end-diastolic pressure. The entire end-systolic pressure-volume could not be determined during exercise, but beat-averaged end-systolic pressure-volume points during exercise were progressively shifted to the right and downward by slowing the exercise HR. Thus, a pronounced negative inotropic influence of slowing the heart was observed during exercise, and the rate of ventricular relaxation (tau) was also significantly prolonged.
These findings indicate that force-frequency effects on the inotropic state of the intact LV are markedly enhanced by exercise.
在清醒动物中，已对静息状态下心肌收缩力的力-频率效应强度进行了研究，但尚未在运动期间进行评估。
在八只预先植入仪器的清醒犬进行跑步机运动期间，评估心率（HR）变化的影响，这些犬测量了高保真左心室（LV）压力、LV容积（通过超声心动图）和主动脉压力。在静息条件下，通过下腔静脉闭塞获得收缩末期压力-容积关系。犬在跑步机上奔跑，在持续运动期间，通过输注特定的减慢心率药物（UL-FS 49 0.5 mg/kg）降低固有运动心率，同时通过心房起搏将心率维持在每分钟240次搏动。在以固定的起搏心率跑步6分钟且达到稳定的药物效果时，与给药前的运动相比，未检测到UL-FS 49对LV收缩力测量指标有影响。然后，心率以随机方式从每分钟240次逐步降至210、180或150次搏动，在各步骤之间恢复到每分钟240次搏动。随着心率减慢，心肌收缩力测量指标逐渐降低，尽管LV舒张末期压力升高，但心率从每分钟240次降至150次使LV最大正dP/dt降低了31%，(dP/dt)DP40降低了21%。在运动期间无法确定整个收缩末期压力-容积，但通过减慢运动心率，运动期间的逐搏平均收缩末期压力-容积点逐渐向右下方移动。因此，在运动期间观察到心率减慢有明显的负性肌力影响，并且心室舒张速率（tau）也显著延长。
这些发现表明，运动可显著增强力-频率对完整LV收缩状态的影响。
