Enhanced left ventricular performance in endurance trained older men.

Enhanced left ventricular performance in endurance trained older men.
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DOI:
10.1161/01.cir.89.1.198
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发表时间:
1994
期刊:
影响因子:
37.8
通讯作者:
D. R. Seals;James M. Hagberg;R. Spina;Marc A. Rogers;Kenneth B. Schechtman;A. Ehsani
D. R. Seals;James M. Hagberg;R. Spina;Marc A. Rogers;Kenneth B. Schechtman;A. Ehsani
中科院分区:
医学1区
文献类型:
--
作者:
D. R. Seals;James M. Hagberg;R. Spina;Marc A. Rogers;Kenneth B. Schechtman;A. Ehsani

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背景:有氧运动能力的年龄相关性下降可通过耐力运动训练部分逆转。中等强度耐力运动训练增加有氧运动能力,部分是通过改善老年男性的每搏输出量和左心室功能来介导的。本研究旨在描述长期剧烈耐力运动对心血管适应的性质,并描述训练有素的老年耐力运动员每搏输出量和心输出量增加的机制。方法和结果9名男性运动员(MA:64 +/- 2岁,平均值+/- SEM)和9名老年久坐健康男性(对照组:63 +/- 1岁)进行了研究。采用心血池显像和超声心动图评价左室收缩功能。MA组的最大摄氧量(VO 2 max)为50.4 +/- 1.7 mL.kg-1 x min-1,对照组为29.6 +/- 1.4 mL.kg-1 x min-1(P = .0001)。两组在休息和运动时的收缩压和平均血压没有差异。峰值运动时MA组的左心室收缩功能高于久坐对照组,表现为(1)较高的左心室功能储备(Δ EF:12.4 +/- 2 vs 5.6 +/- 2.5,P = 0.05),(2)运动期间收缩末期容积大幅下降(MA:静息时为56 +/- 4 mL,运动峰值时为42 +/- 5 mL,P = 0.007;对照组:静息时为43 +/- 2 mL,运动峰值时为42 +/- 6 mL,P = 0.35)收缩压无差异,(3)运动峰值时左心室缩短分数较高(MA:52 +/- 2.6%;对照组:45 +/-1%,P = .046),收缩末期壁应力值相当(MA:56 +/- 12 g/cm 2;对照组:53 +/- 7 g/cm 2,P = 0.50),(4)MA组在运动峰值时收缩末期直径的下降幅度大于对照组(MA:-1.2 +/- 0.16 cm vs.-0.57 +/- 0.13 cm,P = 0.014),尽管运动期间收缩末期室壁应力变化之间无显著差异(MA:-15.5 +/- 7.5 g/cm 2,对照组:-11.0 +/- 9.0 g/cm 2,P = 0.6)。MA静息时舒张末期容积较大(153 +/- 6 vs 132 +/- 4 mL,P = 0.009),壁厚与半径比正常(0.34 +/- 0.02)。MA组的峰值运动每搏输出量(132 +/- 6 mL/min)高于(P = 0.023)久坐对照组(111 +/- 6 mL/min)。在MA组,每搏输出量的变化与射血分数的变化密切相关(r = 0.80,P = 0.010),但在久坐对照组则不相关(r = 0.59,P = 0.097)。此外,在MA(r = 0.78,P = 0.013)和久坐对照组(r = 0.73,P = 0.026)中,每搏输出量从静息到运动的变化与舒张末期容积的变化密切相关,提示每搏输出量依赖于舒张末期容积和前负荷。然而,对于给定的舒张末期容积的增加,运动过程中的每搏输出量的增加在MA中显著大于对照组,这在平均血压没有差异的情况下表明,独立于前负荷的增强的左心室收缩功能在高度训练的老年男性在峰值运动时维持较高的每搏输出量方面起着额外的作用。结论:老年耐力训练者心脏适应性改变的特征是左室容量超负荷性肥大和运动峰值时左室收缩功能增强。这些适应性反应有助于增强老年耐力训练男性在高峰运动时的每搏输出量。
BACKGROUND The age-associated decline in aerobic exercise capacity is partially reversible by endurance exercise training. Moderate-intensity endurance exercise training increases aerobic exercise capacity mediated, in part, by improvement of stroke volume and left ventricular performance in older men. The present study was designed to characterize the nature of cardiovascular adaptations to strenuous endurance exercise of long duration and to delineate the mechanisms underlying increased stroke volume and cardiac output in highly trained older endurance athletes. METHODS AND RESULTS Nine male master athletes (MA: 64 +/- 2 years old, mean +/- SEM) and 9 older sedentary healthy men (controls: 63 +/- 1 year) were studied. Left ventricular systolic function was evaluated with the use of cardiac blood pool imaging and echocardiography. Maximal O2 uptake (VO2max) was 50.4 +/- 1.7 mL.kg-1 x min-1 in the MA and 29.6 +/- 1.4 mL.kg-1 x min-1 (P = .0001) in controls. Systolic and mean blood pressures at rest and during exercise were not different in the two groups. Left ventricular systolic function at peak exercise was higher in the MA than in sedentary controls as evidenced by (1) a higher left ventricular functional reserve (delta EF: 12.4 +/- 2 versus 5.6 +/- 2.5, P = .05), (2) a large decrease in end-systolic volume during exercise (MA: 56 +/- 4 mL at rest and 42 +/- 5 mL at peak exercise, P = .007; controls: 43 +/- 2 mL at rest and 42 +/- 6 mL at peak exercise, P = .35) with no differences in systolic blood pressure, (3) a higher left ventricular fractional shortening at peak exercise (MA: 52 +/- 2.6%; controls: 45 +/- 1%, P = .046) at comparable values for end-systolic wall stress (MA: 56 +/- 12 g/cm2; controls: 53 +/- 7 g/cm2, P = .50), and (4) a greater decrease in end-systolic diameter at peak exercise in the MA than in controls (MA: -1.2 +/- 0.16 cm versus -0.57 +/- 0.13 cm, P = .014) despite no significant differences between the changes in end-systolic wall stress during exercise (MA: -15.5 +/- 7.5 g/cm2, controls: -11.0 +/- 9.0 g/cm2, P = .6). MA had a larger end-diastolic volume at rest (153 +/- 6 versus 132 +/- 4 mL, P = .009) with a normal wall thickness-to-radius ratio (0.34 +/- 0.02). Peak exercise stroke volume was higher (P = .023) in the MA (132 +/- 6 mL/min) than in the sedentary controls (111 +/- 6 mL/min). Changes in stroke volume correlated strongly with changes in ejection fraction in the MA (r = .80, P = .010) but not in sedentary controls (r = .59, P = .097). Further, changes in stroke volume from rest to exercise correlated strongly with changes in end-diastolic volume in both MA (r = .78, P = .013) and sedentary controls (r = .73, P = .026), suggestive of reliance of stroke volume on end-diastolic volume and preload. However, for a given increase in end-diastolic volume, the rise in stroke volume during exercise was significantly larger in the MA than in controls, which, in the absence of differences in mean blood pressures, indicates that enhanced left ventricular systolic function independent of preload plays an additional role in maintaining a higher stroke volume at peak exercise in the highly trained older men. CONCLUSIONS Cardiac adaptations in older endurance trained men are characterized by volume-overload left ventricular hypertrophy and enhancement of left ventricular systolic performance at peak exercise. These adaptive responses contribute to enhanced stroke volume at peak exercise in older endurance trained men.