Vatner S F, Franklin D, Higgins C B, Patrick T, Braunwald E
J Clin Invest. 1972 Dec;51(12):3052-60. doi: 10.1172/JCI107132.
The left ventricular response to severe exercise was studied by telemetering direct measurements of left ventricular diameter (D) and pressure (P) and aortic blood flow from healthy dogs running at speeds up to 30 mph in the field. Severe exercise increased cardiac output from 101 to 478 ml/kg per min, heart rate from 95 to 297 beats/min, stroke volume from 31 to 44 ml, left ventricular isolength (iso) systolic pressure from 120 to 186 mm Hg, left ventricular end diastolic pressure from 6 to 18 mm Hg, and left ventricular end diastolic diameter from 58.9 to 60.1 mm, while end systolic diameter decreased from 53.0 to 52.2 mm. Two indices of myocardial contractility, (dP/dt)/P increased from 37 to 92 sec(-1), while dD/dt, the velocity of myocardial fiber shortening at isolength, rose from 54 to 119 mm/sec. All of these changes were statistically significant. When, in resting dogs, heart rate was first raised to exercise levels by electrical stimulation, severe exercise subsequently increased left ventricular end diastolic diameter more profoundly, from 55.7 to 59.7 mm, while end systolic diameter remained constant and the increases in left ventricular pressure, (dP/dt)/P and velocity(iso) were roughly comparable to those occurring during exercise in spontaneous rhythm. After propranolol, 1.0 mg/kg, severe exercise resulted in significantly smaller increases in cardiac output (from 82 to 240 ml/kg), in heart rate (from 87 to 186 beats/min), in left ventricular pressure(iso) (from 122 to 150 mm Hg), in (dP/dt)/P (from 32 to 44 sec(-1)), in velocity(iso) (from 47 to 59 mm/sec), and in slightly greater increases in end diastolic diameter, from 59.8 to 62.0 mm and pressure from 8 to 22 mm Hg, while end systolic diameter did not change significantly.Thus, the left ventricle responds to severe exercise with near maximal increases in heart rate and contractility, while significant increases in end diastolic diameter (Frank-Starling mechanism) and stroke volume occur as well. When heart rate was held constant severe exercise produced similar increases in contractility but end systolic size failed to diminish and the increases in end diastolic size were greater. Beta adrenergic receptor blockade interfered with the chronotropic and particularly the inotropic response to severe exercise and while the participation of the Frank-Starling mechanism was somewhat greater, the latter was not sufficient to increase cardiac output normally.
通过遥测直接测量健康犬在野外以高达每小时30英里的速度奔跑时的左心室直径（D）、压力（P）和主动脉血流量，研究了左心室对剧烈运动的反应。剧烈运动使心输出量从每分钟101毫升/千克增加到478毫升/千克，心率从每分钟95次增加到297次，每搏量从31毫升增加到44毫升，左心室等长（iso）收缩压从120毫米汞柱增加到186毫米汞柱，左心室舒张末期压力从6毫米汞柱增加到18毫米汞柱，左心室舒张末期直径从58.9毫米增加到60.1毫米，而收缩末期直径从53.0毫米降至52.2毫米。心肌收缩性的两个指标，（dP/dt）/P从37秒⁻¹增加到92秒⁻¹，而dD/dt，即等长时心肌纤维缩短速度，从54毫米/秒升至119毫米/秒。所有这些变化均具有统计学意义。在静息犬中，当首先通过电刺激将心率提高到运动水平时，随后的剧烈运动使左心室舒张末期直径增加更为显著，从55.7毫米增加到59.7毫米，而收缩末期直径保持不变，左心室压力、（dP/dt）/P和速度（iso）的增加与自发节律运动时大致相当。给予1.0毫克/千克普萘洛尔后，剧烈运动导致心输出量（从82毫升/千克增加到240毫升/千克）、心率（从每分钟87次增加到186次）、左心室压力（iso）（从122毫米汞柱增加到150毫米汞柱）、（dP/dt）/P（从32秒⁻¹增加到44秒⁻¹）、速度（iso）（从47毫米/秒增加到59毫米/秒）的增加显著减小，而舒张末期直径的增加略大，从59.8毫米增加到62.0毫米，压力从8毫米汞柱增加到22毫米汞柱，而收缩末期直径无显著变化。因此，左心室对剧烈运动的反应是心率和收缩性近乎最大程度增加，同时舒张末期直径（Frank-Starling机制）和每搏量也显著增加。当心率保持恒定时，剧烈运动使收缩性产生类似增加，但收缩末期大小未能减小，舒张末期大小的增加更大。β肾上腺素能受体阻断干扰了对剧烈运动的变时性反应，尤其是变力性反应，虽然Frank-Starling机制的参与度有所增加，但后者不足以正常增加心输出量。
