Key result
Life-long exercise in Masters athletes preserved dynamic Starling mechanism gain compared to sedentary elderly (0.96 vs 0.37 ml/m2/mmHg), whereas 1-year training yielded variable results (P=0.108).
Why the study?
Does exercise training improve the dynamic Starling mechanism impaired by ageing?
Observational
Does exercise training improve the dynamic Starling mechanism impaired by ageing?
Absolute Event Rate: 0.96% vs 0.37%
p-value: p=0.108
Ageing impairs the dynamic Starling mechanism, but life-long exercise training can partially preserve it, whereas late-life exercise training has a limited effect.
Lifelong exercise may preserve Starling mechanism in aging; cross-sectional data leave open whether late-life training reverses impairment.
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.
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Shibata et al. (2008) conducted an observational in Ageing and ventricular-arterial stiffening. Life-long exercise training and one-year endurance training vs. Sedentary lifestyle / Young controls was evaluated on Spectral transfer function gain between beat-to-beat changes in left ventricular end-diastolic pressure and stroke volume (p=0.108). Life-long exercise in Masters athletes preserved dynamic Starling mechanism gain compared to sedentary elderly (0.96 vs 0.37 ml/m2/mmHg), whereas 1-year training yielded variable results (P=0.108).
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