Abstract
Increased sympathetic outflow to the heart is associated with high heart rates and fast fiber shortening. It might, therefore, be expected that chronic, intermittently, increased sympathetic drive of heart leads to adaptational reactions at the myofibrillar level with improved potential to cope with the imposed load. Past fiber shortening can in principal be achieved either by increased transmembrane Ca2+ fluxes, or via an increase in the rate of cross bridge cycling. Altered transmembrane Ca2+ fluxes are employed primarily for acute adjustment of heart performance to given demands. The set-point of this modulation of velocity-dependent parameters is given by the isoenzyme population of myosin (1). Alterations in the myosin isoenzyme population are achieved only on a longer-term basis as can be inferred from the 5.5 days half-life of myosin (2). Intermittently increased sympathetic drive of the heart is expected to be associated possibly with an adaptive response in terms of expression of genes coding for the fast myosin isoenzyme.
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References
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© 1985 Martinus Nijhoff Publishing, Boston
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Rupp, H., Jacob, R. (1985). Ventricular Myocardium as a Fast- or Slow-Type Muscle. The Influence of Stressors and the Preventive Action of Intense Exercise. In: Beamish, R.E., Panagia, V., Dhalla, N.S. (eds) Pathogenesis of Stress-Induced Heart Disease. Developments in Cardiovascular Medicine, vol 46. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2589-5_13
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DOI: https://doi.org/10.1007/978-1-4613-2589-5_13
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