Moore Sarah A, Jakovljevic Djordje G, Ford Gary A, Rochester Lynn, Trenell Michael I
Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom; Research Councils UK, Newcastle Centre for Ageing and Vitality, Newcastle upon Tyne, United Kingdom.
Arch Phys Med Rehabil. 2016 Apr;97(4):596-603. doi: 10.1016/j.apmr.2015.12.018. Epub 2016 Jan 4.
To explore the physiological factors affecting exercise-induced changes in peak oxygen consumption and function poststroke.
Single-center, single-blind, randomized controlled pilot trial.
Community stroke services.
Adults (N=40; age>50y; independent with/without stick) with stroke (diagnosed >6 mo previously) were recruited from 117 eligible participants. Twenty participants were randomized to the intervention group and 20 to the control group. No dropouts or adverse events were reported.
Intervention group: 19-week (3 times/wk) progressive mixed (aerobic/strength/balance/flexibility) community group exercise program. Control group: Matched duration home stretching program.
(1) Pre- and postintervention: maximal cardiopulmonary exercise testing with noninvasive (bioreactance) cardiac output measurements; and (2) functional outcome measures: 6-minute walk test; timed Up and Go test, and Berg Balance Scale.
Exercise improved peak oxygen consumption (18±5 to 21±5 mL/(kg⋅min); P<.01) and peak arterial-venous oxygen difference (9.2±2.7 to 11.4±2.9 mL of O2/100 mL of blood; P<.01), but did not alter cardiac output (17.2±4 to 17.7±4.2 L/min; P=.44) or cardiac power output (4.8±1.3 to 5.0±1.35 W; P=.45). A significant relation existed between change in peak oxygen consumption and change in peak arterial-venous oxygen difference (r=.507; P<.05), but not with cardiac output. Change in peak oxygen consumption did not strongly correlate with change in function.
Exercise induced peripheral muscle, but not cardiac output, adaptations after stroke. Implications for stroke clinical care should be explored further in a broader cohort.
探讨影响中风后运动诱发的峰值耗氧量变化及功能的生理因素。
单中心、单盲、随机对照试验。
社区中风服务机构。
从117名符合条件的参与者中招募了中风(诊断时间>6个月前)的成年人(N = 40;年龄>50岁;独立行走,可使用或不使用拐杖)。20名参与者被随机分配到干预组,20名被分配到对照组。未报告有退出者或不良事件。
干预组:为期19周(每周3次)的渐进式混合(有氧/力量/平衡/柔韧性)社区团体运动计划。对照组:持续时间匹配的家庭伸展计划。
(1)干预前后:采用无创(生物电阻抗)心输出量测量进行最大心肺运动测试;(2)功能结局指标:6分钟步行试验、计时起立行走试验和伯格平衡量表。
运动改善了峰值耗氧量(从18±5至21±5 mL/(kg·min);P<.01)和峰值动静脉氧差(从9.2±2.7至11.4±2.9 mL O2/100 mL血液;P<.01),但未改变心输出量(从17.2±4至17.7±4.2 L/min;P = 0.44)或心脏功率输出(从4.8±1.3至5.0±1.35 W;P = 0.45)。峰值耗氧量的变化与峰值动静脉氧差的变化之间存在显著相关性(r = 0.507;P<.05),但与心输出量无关。峰值耗氧量的变化与功能变化之间没有强烈的相关性。
中风后运动诱发了外周肌肉适应,但未诱发心输出量适应。应在更广泛的队列中进一步探讨对中风临床护理的意义。