Effect of induced leg muscle fatigue on exertional dyspnea in healthy subjects.

Effect of induced leg muscle fatigue on exertional dyspnea in healthy subjects.
复制标题

诱发腿部肌肉疲劳对健康受试者劳力性呼吸困难的影响。

DOI:
--
复制
发表时间:
2015
影响因子:
3.3
通讯作者:
L. Adams
L. Adams
中科院分区:
医学2区
文献类型:
--
作者:
Pramod Sharma;N. Morris;L. Adams

文献摘要

被引文献

相似文献

呼吸困难的发生是复杂的。尽管普遍的腿部疲劳可能独立地加重呼吸困难,但它似乎与中枢呼吸驱动有关。我们假设,实验引起的腿部疲劳产生更强烈的劳力性呼吸困难,为一个给定的水平的运动驱动器。在熟悉之后,19名健康受试者(32.2 ± 7.6岁; 11名男性)在两天内进行了5分钟的跑步机测试(速度:104 km/h;等级:1025%),随机分为对照组(C)和实验诱导的腿部疲劳组(E),通过对40%体重重复膝关节伸展直至任务失败。每一次呼吸测量氧摄取量(V ~ o ~ 2,l/min)、二氧化碳排出量(V ~ co ~ 2,l/min)、通气量(V ~ e,l/min)和呼吸频率(fR)。连续记录心率(HR)和感觉呼吸困难强度(0-10数值量表)。数据在30秒间隔内取平均值。E期的呼吸困难在统计学上显著高于(E vs. C:4.2 ± 0.2 vs. 3.4 ± 0.2,P < 0.001),并伴有V tom e显著增加(E vs. C:61.7 ± 3.7 vs. 55.3 ± 2.8,P = 0.005)和fR(E vs. C:26.7 ± 1.0 vs. 24.2 ± 1.3,P = 0.036)。在考虑到V toe混杂因素后,E后的呼吸困难仍然显著较高(ANCOVA,P = 0.003)。两种条件下的Vto 2、Vtoco 2和HR无显著差异。然而,E和C之间的呼吸困难与V ~ o2和呼吸困难与V ~ e的斜率相似,这表明V ~ o2或V ~ e每单位变化的呼吸困难增加不会因腿部疲劳而改变。这些发现支持了这样的假设,即劳力性呼吸困难的强度是由来自疲劳腿部肌肉的外周传入信息加剧的。
The genesis of dyspnea is complex. It appears to be related to central respiratory drive although prevailing leg fatigue could independently potentiate dyspnea. We hypothesized that experimentally induced leg fatigue generates more intense exertional dyspnea for a given level of ventilatory drive. Following familiarization, 19 healthy subjects (32.2 ± 7.6 yr; 11 men) performed a 5-min treadmill test (speed: ∼4 km/h; grade: ∼25%) on two separate days randomized between control (C) and experimentally induced leg fatigue (E) achieved by repeated knee extension against 40% body weight until task failure. Oxygen uptake (V̇o2, l/min), carbon dioxide output (V̇co2, l/min), ventilation (V̇e, l/min), and respiratory rate (fR) were measured breath by breath. Heart rate (HR) and perceived dyspnea intensity (0-10 numerical scale) were recorded continuously. Data were averaged over 30-s intervals. Exertional dyspnea during E was statistically significantly higher (E vs. C: 4.2 ± 0.2 vs. 3.4 ± 0.2, P < 0.001) and accompanied by a significant increase in V̇e (E vs. C: 61.7 ± 3.7 vs. 55.3 ± 2.8, P = 0.005) and fR (E vs. C: 26.7 ± 1.0 vs. 24.2 ± 1.3, P = 0.036). Dyspnea following E remained significantly higher after allowing for the V̇e confound (ANCOVA, P = 0.003). V̇o2, V̇co2, and HR were not significantly different between two conditions. However, the slopes for dyspnea vs. V̇o2 and dyspnea vs. V̇e were similar between E and C, which suggested that gain in dyspnea per unit change in V̇o2 or V̇e was not altered by leg fatigue. These findings support the hypothesis that the intensity of exertional dyspnea is exacerbated by peripheral afferent information from fatigued leg muscles.