CARDIORESPIRATORY RESPONSES TO EXERCISE TRAINING AFTER ORTHOTOPIC CARDIAC TRANSPLANTATION
CARDIORESPIRATORY RESPONSES TO EXERCISE TRAINING AFTER ORTHOTOPIC CARDIAC TRANSPLANTATION
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DOI：
10.1161/01.cir.77.1.162
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发表时间：
1988-01-01
期刊：
影响因子：
37.8
通讯作者：
SAWYER, P
中科院分区：
文献类型：
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作者：
KAVANAGH, T;YACOUB, MH;SAWYER, P
我们已经测试了2年（平均16 .+-）的可行性和有效性。36例男性原位心脏移植患者（21 ~ 57岁）术后2 ~ 23个月进行步行/慢跑运动。将最初的运动测试结果与45名年龄匹配的正常男性的结果进行比较，结果显示患者的瘦体重较低（55.6 +-）。7 vs 63。8 kg, p < .001)，静息心率更高(104 .+-。12 vs 77。14次/分，p < .001)，收缩压（138 .+-）。16 vs 129 .+-。17 mm Hg, p < 0.001)和舒张压（95 .+-）。14比84，+-。10 mm Hg, p < 0.001)。峰值输出功率小于正常(101 .+-。27 vs 219。41 W, p < .001)，峰值心率(136。15 vs 176, +-。13次/分，p < 0.001)，峰值摄氧量（p < 0.001）。VO2max)(22 .+-。5比34。6毫升。cntdot。Min-1, p < .001)，绝对无氧阈值(1.18。0.40 vs 2.04。0.40升。cntdot。最低为1,.cntdot。P < 0.001)。峰值通气量当量较高(48。9 vs 37。6 1.1-1, p < .001)。心输出量。Q)，根据CO2再呼吸法估计，在休息时略高于正常水平（p < 0.01），但在两个次最大工作速率下低于正常水平。该组的平均每周训练距离为24公里，其中8名高度依从的患者每周训练距离达到32公里或更多。训练后，瘦组织增加（+2.4 .+-）。1.3 kg, p < .001)，静息值因心率降低(-4。11次/分，p < 0.05)，收缩压(-13。20 mm Hg, p < .001)，舒张压(-9。17 mm Hg, p < 0.001)。每分钟通气的次最大值显著降低。VE)，感知劳累等级和同等工作负荷下的舒张压。功率输出峰值增加(+49 .+-。34 W, p < 0.001), .ovrhdot。VO2max(+ 4.0 .+-。6.0 ml .cntdot。公斤.cntdot。Min-1, p < .001), .ovrhdot。+20 .+-。20 .cntdot。Min-1, p < .001)，心率(+ 13。17次/分，p < 0.001)，舒张压降低(- 8。15 mm Hg, p < 0.001)。在8名高度依从的患者中，静息心率下降幅度更大(-11。5次/分钟，p < .001)和次最大心率（每次功率输出时减少5至10次/分钟），峰值功率输出增加更大(+68。42 W,p < .001), .ovrhdot。VO2max(+11 .+-。6毫升。cntdot。公斤.cntdot。Min-1, p < 0.001)。导数q /导数的斜率。VO2线未受训练影响。没有任何患者心脏神经再支配的证据。我们的结论是，运动康复是合理的，因为它能够提高心脏移植患者的工作能力，从而提高生活质量。
We have tested the feasibility and effectiveness of a 2 year (average 16 .+-. 7 months) walk/jog exercise program on 36 male orthotopic cardiac transplant patients (21 to 57 years old) seen initially 2 to 23 months after surgery. Comparison of initial exercise test results with those in 45 age-matched normal men showed the patients to have a lesser lean body mass (56 .+-. 7 vs 63 .+-. 8 kg, p < .001), with a higher resting heart rate (104 .+-. 12 vs 77 .+-. 14 beats/min, p < .001) and systolic (138 .+-. 16 vs 129 .+-. 17 mm Hg, p < .001) and diastolic (95 .+-. 14 vs 84 .+-. 10 mm Hg, p < .001) blood pressures. Peak power output was less than normal (101 .+-. 27 vs 219 .+-. 41 W, p < .001), as was peak heart rate (136 .+-. 15 vs 176 .+-. 13 beats/min, p < .001), peak oxygen intake (.ovrhdot.VO2max) (22 .+-. 5 vs 34 .+-. 6 ml .cntdot. min-1, p < .001), and absolute anaerobic threshold (1.18 .+-. 0.40 vs 2.04 .+-. 0.40 liters .cntdot. min-1, .cntdot. p < .001). Peak ventilatory equivalent was higher (48 .+-. 9 vs 37 .+-. 6 1.1-1, p < .001). Cardiac output (.ovrhdot.Q), as estimated by the CO2 rebreathing method, was slightly above normal at rest (p < .01), but below normal at two submaximal work rates. The group''s average weekly training distance was 24 km, with eight highly compliant patients progressing to 32 km or more weekly. After training, lean tissue increased (+2.4 .+-. 1.3 kg, p < .001), and resting values were reduced for heart rate (-4 .+-. 11 beats/min, p < .05), systolic (-13 .+-. 20 mm Hg, p < .001), and diastolic (-9 .+-. 17 mm Hg, p < .001) blood pressures. There were significant reductions in submaximal values for minute ventilation (.ovrhdot.VE), ratings of perceived exertion, and diastolic blood pressure at equivalent workloads. Peak values increased for power output (+49 .+-. 34 W, p < .001), .ovrhdot.VO2max (+ 4.0 .+-. 6.0 ml .cntdot. kg .cntdot. min-1, p < .001), .ovrhdot.VE (+20 .+-. 20 l .cntdot. min-1, p < .001), and heart rate (+ 13 .+-. 17 beats/min, p < .001), and decreased for diastolic blood pressure (- 8 .+-. 15 mm Hg, p < .001). In the eight highly compliant patients a greater decrease occurred in resting heart rate (-11 .+-. 5 beats/min, p < .001) and submaximal heart rate (range 5 to 10 beats/min less at each power output), with a greater increase in peak power output (+68 .+-. 42 W,p < .001), and .ovrhdot.VO2max (+11 .+-. 6 ml .cntdot. kg .cntdot. min-1, p < .001). The slope of the .ovrhdot.Q/.ovrhdot.VO2 line was unchanged by training. There was no evidence of cardiac reinnervation in any patient. We conclude that exercise rehabilitation is justified because of its ability to increase working capacity and thus quality of life in cardiac transplant patients.