Cardiac function and modulation of sarcomeric function by length

The Frank–Starling relationship provides beat-to-beat regulation of ventricular function by matching ventricular input and output. This review addresses the subcellular mechanisms by which the ventricle adjusts its output (i.e. stroke volume) by changes in end-diastolic volume. The subcellular proce...

Full description

Saved in:
Bibliographic Details
Published in:Cardiovascular research 2008-03, Vol.77 (4), p.627-636
Main Authors: Hanft, Laurin M., Korte, Fredrick S., McDonald, Kerry S.
Format: Article
Language:English
Subjects:
Actin Cytoskeleton - metabolism
Animals
Cardiac cycle
Cardiac myocyte
Cardiac myofilaments
Cell Shape
Heart Failure - metabolism
Heart Failure - physiopathology
Humans
Models, Cardiovascular
Muscle Strength
Myocardial Contraction
Myocardium - cytology
Myocardium - metabolism
Myocytes, Cardiac - metabolism
Myofibrils - metabolism
Sarcomere length
Sarcomeres - metabolism
Stroke Volume
Ventricular Function, Left
Ventricular Pressure
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The Frank–Starling relationship provides beat-to-beat regulation of ventricular function by matching ventricular input and output. This review addresses the subcellular mechanisms by which the ventricle adjusts its output (i.e. stroke volume) by changes in end-diastolic volume. The subcellular processes are placed in the context of the four phases of the cardiac cycle with emphasis on the sarcomeric properties that mediate the number of force-generating cross-bridges recruited during pressure development. Additional mechanistic insight is provided regarding the factors that regulate myocyte loaded shortening speeds, which are paramount for dictating ejection volume. Emphasis is placed on the interplay between cross-bridge-induced cooperative activation of the thin filament and cooperative deactivation of the thin filament induced by muscle shortening. The balance of these two properties seems to determine systolic haemodynamics, and how this balance is modulated by sarcomere length, in part, underlies the Frank–Starling relationship.
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/cvm099