Shibata Shigeki, Hastings Jeff L, Prasad Anand, Fu Qi, Okazaki Kazunobu, Palmer M Dean, Zhang Rong, Levine Benjamin D
Institute for Exercise and Environmental Medicine, 7232 Greenville Ave, Suite 435, Dallas, TX 75231, USA.
J Physiol. 2008 Apr 1;586(7):1951-62. doi: 10.1113/jphysiol.2007.143651. Epub 2008 Feb 7.
Cardiovascular diseases increase with advancing age, associated with left ventricular and arterial stiffening in humans. In contrast, daily exercise training prevents and/or improves both ventricular and arterial stiffening with ageing. We propose a new approach to quantify the dynamics of the Starling mechanism, namely the beat-to-beat modulation of stroke volume (SV) caused by beat-to-beat alterations in left ventricular filling, which we propose reflects the complex interaction between ventricular and arterial stiffness. We hypothesized that the dynamic Starling mechanism would be impaired with ageing, and that this impairment would be prevented and restored by daily exercise training. Two different approaches were employed: (1) a cross-sectional study to assess the effects of ageing and life-long exercise training; and (2) a longitudinal study to assess the effects of one-year endurance training in the elderly. Spectral transfer function gain between beat-to-beat changes in left ventricular end-diastolic pressure and SV was used as an index of the dynamic Starling mechanism. Gain was significantly lower in the sedentary elderly (70 +/- 3 years) than in both young individuals (27 +/- 6 years) and Masters athletes (68 +/- 3 years), and it was significantly lower in Masters athletes than in young controls (elderly: 0.37 +/- 0.11; Masters athletes: 0.96 +/- 0.55; young: 1.52 +/- 0.42 ml m(-2) mmHg(-1), mean +/- s.d.). Gain increased by 65% after one-year exercise training in the elderly, although the response was quite variable (P = 0.108). These findings suggest that the dynamic Starling mechanism is impaired with human ageing possibly due to ventricular-arterial stiffening. Life-long daily exercise training may minimize this impairment, although the effect may be limited particularly when started later in life.
心血管疾病随年龄增长而增加,这与人类左心室和动脉僵硬有关。相比之下,日常运动训练可预防和/或改善衰老过程中的心室和动脉僵硬。我们提出了一种新方法来量化心脏的斯塔林机制的动力学,即由左心室充盈的逐搏变化引起的每搏输出量(SV)的逐搏调节,我们认为这反映了心室和动脉僵硬度之间的复杂相互作用。我们假设动态斯塔林机制会随着衰老而受损,并且这种损伤可以通过日常运动训练来预防和恢复。我们采用了两种不同的方法:(1)一项横断面研究,以评估衰老和终身运动训练的影响;(2)一项纵向研究,以评估老年人群一年耐力训练的影响。左心室舒张末期压力和SV的逐搏变化之间的频谱传递函数增益被用作动态斯塔林机制的指标。久坐不动的老年人(70±3岁)的增益显著低于年轻人(27±6岁)和大师级运动员(68±3岁),并且大师级运动员的增益显著低于年轻对照组(老年人:0.37±0.11;大师级运动员:0.96±0.55;年轻人:1.52±0.42 ml m(-2) mmHg(-1),平均值±标准差)。老年人进行一年运动训练后,增益增加了65%,尽管反应差异很大(P = 0.108)。这些发现表明,动态斯塔林机制可能由于心室-动脉僵硬而在人类衰老过程中受损。终身日常运动训练可能会使这种损伤最小化,尽管这种效果可能有限,尤其是在生命后期开始训练时。