Frank-Starling Mechanism Retains Recirculation Fraction of Myocardial Ca²⁺ in the Beating Heart

Modular regulation analysis of heart contraction: application to in situ demonstration of a direct mitochondrial activation by calcium in beating heart

“…This is the mechanism by which the heart adjusts to diastolic filling, i.e., the Frank-Starling response. It has been shown that the rapid increase in twitch force after muscle stretch was not associated with a rise in calcium transient (24,31) or a modification of calcium recirculation (33). In this study, the experiment was started under low pressure conditions, and the balloon was further inflated to normal pressure.…”

Exponential Fitting of Postextrasystolic Potentiation May Underestimate the Cardiac Ca2+ Recirculation Fraction: A Theoretical Analysis

“…At these physiological beat intervals, RF increases as the beat interval shortens [17] in contrast to the constant RF independent of beat intervals longer than the period of full mechanical restitution [20,21,27,28]. At present, we are not interested in such relatively long beat intervals because we have to obtain RF at the shorter beat intervals we consistently observe in our cardiac mechanoenergetics experiments [7][8][9][10][11][12]22].…”

“…Here, we used aϭ0.5, e ϭ2, and s ϭ0.8 as the representative values for regular beat intervals of 400-600 ms and extrasystolic beat intervals of 300-400 ms in our previous observations [11,12,17]. Furthermore, we increased b from 0 in steps of 0.1 and stopped it at 0.5 (ϭa) although our previous observations have shown that alternans PESPs obviously have bՆa [11,12,17]. In other words, PESPs with bϾa appeared so obvious that no one would dare to fit an exponential curve to it.…”

Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

“…The present results indicated a similar temperature dependence of RF and its Q 10 to those we observed previously without equalizing peak LVP. Thus, the temperature-dependent RF is indepenunchanged despite increasing LV volume (LVV) at normothermia [13], but it decreases with increasing temperature from 33°C to 38°C at a constant LVV [14]. However, increasing temperature simultaneously decreased ventricular contractility and thus peak isovolumic LV pressure (LVP) at a constant LVV because of the negative inotropism of warming [15][16][17][18][19][20][21][22].…”

“…Therefore, it remains unknown whether the temperature-dependently decreased LVP at a constant LVV affected the temperature-dependent RF. Based on our previous results [13,14], we hypothesized that the temperature-dependent RF would primarily be due to the temperature effect per se rather than the simultaneously changed peak LVP.…”