title: 'Dynamic' Starling mechanism: effects of ageing and physical fitness on ventricular-arterial coupling.
abstract: 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.
authors.affiliation: Institute for Exercise and Environmental Medicine, 7232 Greenville Ave, Suite 435, Dallas, TX 75231, USA.
authors.forename: Shigeki
authors.initials: S
authors.lastname: Shibata
authors.forename: Jeff L
authors.initials: JL
authors.lastname: Hastings
authors.forename: Anand
authors.initials: A
authors.lastname: Prasad
authors.forename: Qi
authors.initials: Q
authors.lastname: Fu
authors.forename: Kazunobu
authors.initials: K
authors.lastname: Okazaki
authors.forename: M Dean
authors.initials: MD
authors.lastname: Palmer
authors.forename: Rong
authors.initials: R
authors.lastname: Zhang
authors.forename: Benjamin D
authors.initials: BD
authors.lastname: Levine
mesh_terms: D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D001158:Arteries / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004548:Elasticity; D015444:Exercise / Q000502:physiology; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology; D010807:Physical Endurance / Q000502:physiology; D010809:Physical Fitness / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology*; D016276:Ventricular Function