Szmedra L, Bacharach D W, Buckenmeyer P J, Hermann D T, Ehrich D A
Exercise Science Laboratory, Bloomsburg University, PA 17815.
Int J Cardiol. 1994 Oct;46(3):209-22. doi: 10.1016/0167-5273(94)90243-7.
The purpose of this study was to investigate the response of patients with ischemic heart disease and varied left ventricular function following 6 weeks of exercise training. We studied the oxygen consumption (VO2), and central hemodynamic and metabolic responses of 14 patients with coronary artery disease (CAD) stratified by left ventricular ejection fraction (EF). There were two groups of patients: normal EF (NEF), EF = 64 +/- 9.9 (mean +/- S.E.M.); n = 7, and diminished EF (DEF), EF = 36 +/- 11.6; n = 7. The patients ranged in age from 42 to 72 years (54.9 +/- 2.2), and were evaluated prior to and then following training. Measures of VO2, cardiac output (Qt) stroke volume (SV), heart rate (HR), exercise duration (XTIME) and intensity (XI), as well as plasma lactate (LA), and the catecholamines epinephrine (E) and norepinephrine (NE) were obtained in response to maximal cycle ergometry. Subjects trained three times per week, 30 min per session, at an intensity equal to 70% of their peak oxygen consumption. Repeated measures analysis of variance (ANOVA) revealed no interaction between groups suggesting a similar training response. Significant post-training changes (P < 0.05) were observed in peak VO2 (VO2peak) NEF, 11.8% increase, (16.0 +/- 1.3 to 17.9 +/- 1.1 ml/kg/min) and DEF, 9.3% increase (15.1 +/- 1.6 to 16.5 +/- 1.2 ml/kg/min); submaximal HR, 4% decrease in the NEF (95.57 +/- 4.58 to 92 +/- 4.43 beats/min) and a 6% decrease in the DEF (107.29 +/- 7.44 to 101.43 +/- 6.77 beats/min); XTIME NEF, 11.2% increase (7.8 +/- 0.57 to 8.67 +/- 0.61 min) and DEF, 16.6% increase (7.3 +/- 0.91 to 8.51 +/- 0.69 min); and XI NEF, 19.2% increase (104.3 +/- 11.3 to 124.3 +/- 12.9 W) DEF, 21.2% increase (94.3 +/- 18.5 to 114.3 +/- 16.9 W), and a 15% decrease in resting NE (350 +/- 26 to 296.9 +/- 19 pg/ml). There were no changes in Qt, SV, LA, E, peak NE or peak HR for either group. These findings suggest short-term endurance training at 70% VO2peak provide the necessary stimulus for individuals with CAD and NEF or DEF to display an improvement in XI, XTIME, and VO2peak. The lack of a significant enhancement in Qt with short-term training may indicate that the mechanism by which both study groups were able to attain significantly higher levels of VO2peak may have been attributable to peripheral mechanisms rather than any alterations in Qt, a central mechanism.
本研究的目的是调查缺血性心脏病且左心室功能各异的患者在进行6周运动训练后的反应。我们研究了14例根据左心室射血分数（EF）分层的冠状动脉疾病（CAD）患者的耗氧量（VO2）、中心血流动力学和代谢反应。患者分为两组：正常EF（NEF）组，EF = 64±9.9（平均值±标准误）；n = 7，以及EF降低（DEF）组，EF = 36±11.6；n = 7。患者年龄在42至72岁之间（54.9±2.2），在训练前后进行了评估。通过最大运动负荷试验获得VO2、心输出量（Qt）、每搏输出量（SV）、心率（HR）、运动持续时间（XTIME）和强度（XI），以及血浆乳酸（LA）、儿茶酚胺肾上腺素（E）和去甲肾上腺素（NE）的测量值。受试者每周训练3次，每次30分钟，强度为其峰值耗氧量的70%。重复测量方差分析（ANOVA）显示两组之间无交互作用，表明训练反应相似。训练后观察到显著变化（P < 0.05）：NEF组的峰值VO2（VO2peak）增加11.8%，（从16.0±1.3增至17.9±1.1 ml/kg/min），DEF组增加9.3%（从15.1±1.6增至16.5±1.2 ml/kg/min）；次最大心率，NEF组降低4%（从95.57±4.58降至92±4.43次/分钟），DEF组降低6%（从107.29±7.44降至101.43±6.77次/分钟）；XTIME，NEF组增加11.2%（从7.8±0.57增至8.67±0.61分钟），DEF组增加16.6%（从7.3±0.91增至8.51±0.69分钟）；XI，NEF组增加19.2%（从104.3±11.3增至124.3±12.9 W），DEF组增加21.2%（从94.3±18.5增至114.3±16.9 W），静息NE降低15%（从350±26降至296.9±19 pg/ml）。两组的Qt、SV、LA、E、峰值NE或峰值HR均无变化。这些发现表明，以70%VO2peak进行短期耐力训练为CAD合并NEF或DEF的个体提供了必要的刺激，使其在XI、XTIME和VO2peak方面有所改善。短期训练中Qt未显著增加，这可能表明两个研究组能够达到显著更高水平的VO2peak的机制可能归因于外周机制，而非作为中心机制的Qt的任何改变。
