Institute for Exercise and Environmental Medicine, 7232 Greenville Avenue, Suite 435, Dallas, TX 75231, USA.
J Physiol. 2012 Aug 1;590(15):3495-505. doi: 10.1113/jphysiol.2012.233858. Epub 2012 May 28.
Recent studies have suggested the presence of cardiac atrophy as a key component of the pathogenesis of the postural orthostatic tachycardia syndrome (POTS), similar to physical deconditioning. It has also been shown that exercise intolerance is associated with a reduced stroke volume (SV) in POTS, and that the high heart rate (HR) observed at rest and during exercise in these patients is due to this low SV. We tested the hypotheses that (a) circulatory control during exercise is normal in POTS; and (b) that physical ‘reconditioning' with exercise training improves exercise performance in patients with POTS. Nineteen (18 women) POTS patients completed a 3 month training programme. Cardiovascular responses during maximal exercise testing were assessed in the upright position before and after training. Resting left ventricular diastolic function was evaluated by Doppler echocardiography. Results were compared with those of 10 well-matched healthy sedentary controls. A lower SV resulted in a higher HR in POTS at any given oxygen uptake (V(O(2))) during exercise while the cardiac output (Q(c))-V(O(2)) relationship was normal. V(O(2peak)) was lower in POTS than controls (26.1 ± 1.0 (SEM) vs. 36.3 ± 0.9 ml kg-1 min-1; P < 0.001) due to a lower peak SV (65 ± 3 vs. 80 ± 5 ml; P = 0.009). After training in POTS, HR became lower at any given due to increased SV without changes in the – relationship. V(O(2peak)) increased by 11% (P < 0.001) due to increased peak SV (P = 0.021) and was proportional to total blood volume. Peak HR was similar, but HR recovery from exercise was faster after training than before training (P = 0.036 for training and 0.009 for interaction). Resting diastolic function was mostly normal in POTS before training, though diastolic suction was impaired (P = 0.023). There were no changes in any Doppler index after training. These results suggest that short-term exercise training improves physical fitness and cardiovascular responses during exercise in patients with POTS.
最近的研究表明,心脏萎缩是体位性心动过速综合征(POTS)发病机制的一个关键组成部分,类似于身体适应性降低。研究还表明,运动不耐受与 POTS 中的每搏量(SV)降低有关,而这些患者在休息和运动期间观察到的高心率(HR)是由于 SV 降低所致。我们检验了以下假设:(a)POTS 患者运动期间循环控制正常;(b)运动训练的身体“再适应”可改善 POTS 患者的运动表现。19 名(18 名女性)POTS 患者完成了 3 个月的训练计划。在训练前后,直立位进行最大运动测试时评估心血管反应。通过多普勒超声心动图评估静息左心室舒张功能。将结果与 10 名匹配良好的健康久坐对照者进行比较。在任何给定的运动摄氧量(V(O(2)))下,POTS 中的 SV 较低导致 HR 较高,而心输出量(Q(c))-V(O(2))关系正常。POTS 的 V(O(2peak))低于对照组(26.1 ± 1.0(SEM)比 36.3 ± 0.9 ml kg-1 min-1;P < 0.001),原因是峰值 SV 较低(65 ± 3 比 80 ± 5 ml;P = 0.009)。在 POTS 患者进行训练后,由于 SV 增加,任何给定的 HR 都会降低,而关系不变。由于峰值 SV 增加(P = 0.021)和总血容量增加,V(O(2peak))增加了 11%(P < 0.001)。峰值 HR 相似,但训练后从运动中恢复的 HR 比训练前更快(训练时为 P = 0.036,交互作用时为 P = 0.009)。在训练前,POTS 中的静息舒张功能大多正常,尽管舒张抽吸受损(P = 0.023)。训练后,任何多普勒指数均无变化。这些结果表明,短期运动训练可改善 POTS 患者的身体适应性和运动期间的心血管反应。