What is treppe phenomenon?

Answer 1

When the contractile frequency is increased, cardiac output is elevated through an increased number of beats per minute, as during exercise. In most species, including nonfailing human myocardium, increased frequency also leads to elevation of contractile force, an event also known as the Treppe phenomenon or the Bowditch effect (Miura et al. 1992). However, in the failing myocardium, frequency potentiation of contractile force is inverse, decreasing contractile force. The Treppe phenomenon has been suggested to result from increased transsarcolemmal Ca2+ influx leading to greater filling of the SR and therefore, a higher amount of Ca2+ available for release during systole (Pieske et al. 1995). This positive inotropic effect can be further augmented with ß-AR agonist dobutamine under resting conditions, when the heart rate is modulated by pacing (Kambayashi et al. 1992). In failing hearts, SR Ca2+ uptake was significantly reduced, suggesting a possible mechanism for inverse force-frequency relationship in CHF (Pieske et al. 1995). Altered Ca2+ handling could be explained by a depressed role of SERCA combined with enhanced cytosolic Ca2+ extrusion via NCX (Pieske et al. 1999b).

== == When the contractile frequency is increased, cardiac output is elevated through an increased number of beats per minute, as during exercise. In most species, including nonfailing human myocardium, increased frequency also leads to elevation of contractile force, an event also known as the Treppe phenomenon or the Bowditch effect (Miura et al. 1992). However, in the failing myocardium, frequency potentiation of contractile force is inverse, decreasing contractile force. The Treppe phenomenon has been suggested to result from increased transsarcolemmal Ca2+ influx leading to greater filling of the SR and therefore, a higher amount of Ca2+ available for release during systole (Pieske et al. 1995). This positive inotropic effect can be further augmented with ß-AR agonist dobutamine under resting conditions, when the heart rate is modulated by pacing (Kambayashi et al. 1992). In failing hearts, SR Ca2+ uptake was significantly reduced, suggesting a possible mechanism for inverse force-frequency relationship in CHF (Pieske et al. 1995). Altered Ca2+ handling could be explained by a depressed role of SERCA combined with enhanced cytosolic Ca2+ extrusion via NCX (Pieske et al. 1999b).

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