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Comparative Study
. 2008 Apr 1;586(7):1951-62.
doi: 10.1113/jphysiol.2007.143651. Epub 2008 Feb 7.

'Dynamic' Starling mechanism: effects of ageing and physical fitness on ventricular-arterial coupling

Affiliations
Comparative Study

'Dynamic' Starling mechanism: effects of ageing and physical fitness on ventricular-arterial coupling

Shigeki Shibata et al. J Physiol. .

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.

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Figures

Figure 1
Figure 1
This figure represents a physiological explanation for the dynamic Starling mechanism, the beat-to-beat dynamic relationship between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV). Each loop represents the left ventricular pressure–volume relationship during one cardiac cycle. The end-systolic pressure–volume relationship (ESPVR) reflects left ventricular (LV) end-systolic stiffness, while the end-diastolic pressure–volume relationship (EDPVR, LVEDP–LVEDV relationship) reflects LV end-diastolic stiffness. The beat-to-beat dynamic relationship between LVEDP and SV is determined by both ESPVR and EDPVR.
Figure 2A
Figure 2A
These figures represent the time series of beat-to-beat pulmonary artery diastolic pressure (PAD, upper panel) and stroke volume index (SVi, middle panel) with the respiration trace (lower panel) for one representative subject of the sedentary elderly.
Figure 2B
Figure 2B
These figures represent autospectra of beat-to-beat pulmonary artery diastolic pressure (PAD spectra, upper panel) and stroke volume index (SVi spectra, lower panel) variabilities for the same representative subject as Fig. 2A. Grey bars enhance the respiratory frequency of 0.18–0.22 Hz, where the input and output variable for the dynamic Starling mechanism was quantified.
Figure 4
Figure 4
Plots on left panel represent mean transfer function gain between pulmonary artery diastolic pressure (PAD) and stroke volume index (SVi) from all subjects at the respiratory frequency of 0.18–0.22 Hz for pre and post one year of exercise training in the elderly. Right panel represents mean +s.e.m. of individual mean of transfer function gain at the respiratory frequency of 0.18–0.22 Hz for pre and post one year of exercise training.
Figure 2C
Figure 2C
These figures represent the coherence function (upper panel), and transfer function gain (middle panel) and phase (lower panel) between pulmonary artery diastolic pressure (PAD) and stroke volume index (SVi) for the same representative subject as Fig. 2A. Grey bars enhance the respiratory frequency of 0.18–0.22 Hz whose coherence was higher than 0.5 where the gain and phase are reliable.
Figure 3
Figure 3
Plots on left panel represent mean transfer function gain between pulmonary artery diastolic pressure (PAD) and stroke volume index (SVi) from all subjects at the respiratory frequency of 0.18–0.22 Hz for the sedentary elderly (Elderly Unfit), Masters athletes (Elderly Fit) and sedentary young individuals (Young Unfit). Right panel represents mean +s.e.m. of individual mean of transfer function gain at the respiratory frequency of 0.18–0.22 Hz for Elderly Unfit, Elderly Fit and Young Unfit.

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