DESIGN AND PHYSIOLOGY OF THE HEART | Cardiac Cellular Length–Tension Relationship

H. A. Shiels

doi:10.1016/B978-0-12-374553-8.00177-5

DESIGN AND PHYSIOLOGY OF THE HEART | Cardiac Cellular Length–Tension Relationship

H. A. Shiels^*

^*Corresponding author for this work

Research output: Chapter in Book/Conference proceeding › Chapter › peer-review

Abstract

Fish use stroke volume to adjust cardiac output. Changes in stroke volume stretch the chambers of the fish heart and invoke the Frank–Starling mechanism. This mechanism ensures the heart contracts more forcefully when it is filled with larger volumes of blood, thus propelling the blood into the circulation. Stretch of the whole heart is transduced to the individual cardiac myocytes and their composite myofilaments. Cellular stretching results in an increase in cellular contractile force due to changes in myofilament overlap and to length-dependent increases in myofilament Ca sensitivity. Fish myofilaments are more sensitive to Ca than mammalian myofilaments and demonstrate a greater length dependence of this Ca sensitivity. This property allows fish myocytes to beat forcefully at the long sarcomere lengths required to volume-modulate cardiac output of the whole heart.

Original language	English
Title of host publication	Encyclopedia of Fish Physiology
Subtitle of host publication	From Genome to Environment: Volume 1-3
Publisher	Elsevier Masson s.r.l.
Pages	1060-1066
Number of pages	7
Volume	1-3
ISBN (Electronic)	9780123745453
ISBN (Print)	9780080923239
DOIs	https://doi.org/10.1016/B978-0-12-374553-8.00177-5
Publication status	Published - 1 Jan 2011

Keywords

Actin
Active tension
Cardiac output
Frank–Starling relationship
Myofilament overlap
Myosin
Passive tension
Stretch
Titin

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/B978-0-12-374553-8.00177-5

Cite this

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title = "DESIGN AND PHYSIOLOGY OF THE HEART | Cardiac Cellular Length–Tension Relationship",

abstract = "Fish use stroke volume to adjust cardiac output. Changes in stroke volume stretch the chambers of the fish heart and invoke the Frank–Starling mechanism. This mechanism ensures the heart contracts more forcefully when it is filled with larger volumes of blood, thus propelling the blood into the circulation. Stretch of the whole heart is transduced to the individual cardiac myocytes and their composite myofilaments. Cellular stretching results in an increase in cellular contractile force due to changes in myofilament overlap and to length-dependent increases in myofilament Ca sensitivity. Fish myofilaments are more sensitive to Ca than mammalian myofilaments and demonstrate a greater length dependence of this Ca sensitivity. This property allows fish myocytes to beat forcefully at the long sarcomere lengths required to volume-modulate cardiac output of the whole heart.",

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AU - Shiels, H. A.

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N2 - Fish use stroke volume to adjust cardiac output. Changes in stroke volume stretch the chambers of the fish heart and invoke the Frank–Starling mechanism. This mechanism ensures the heart contracts more forcefully when it is filled with larger volumes of blood, thus propelling the blood into the circulation. Stretch of the whole heart is transduced to the individual cardiac myocytes and their composite myofilaments. Cellular stretching results in an increase in cellular contractile force due to changes in myofilament overlap and to length-dependent increases in myofilament Ca sensitivity. Fish myofilaments are more sensitive to Ca than mammalian myofilaments and demonstrate a greater length dependence of this Ca sensitivity. This property allows fish myocytes to beat forcefully at the long sarcomere lengths required to volume-modulate cardiac output of the whole heart.

AB - Fish use stroke volume to adjust cardiac output. Changes in stroke volume stretch the chambers of the fish heart and invoke the Frank–Starling mechanism. This mechanism ensures the heart contracts more forcefully when it is filled with larger volumes of blood, thus propelling the blood into the circulation. Stretch of the whole heart is transduced to the individual cardiac myocytes and their composite myofilaments. Cellular stretching results in an increase in cellular contractile force due to changes in myofilament overlap and to length-dependent increases in myofilament Ca sensitivity. Fish myofilaments are more sensitive to Ca than mammalian myofilaments and demonstrate a greater length dependence of this Ca sensitivity. This property allows fish myocytes to beat forcefully at the long sarcomere lengths required to volume-modulate cardiac output of the whole heart.

KW - Actin

KW - Active tension

KW - Cardiac output

KW - Frank–Starling relationship

KW - Myofilament overlap

KW - Myosin

KW - Passive tension

KW - Stretch

KW - Titin

UR - https://www.scopus.com/pages/publications/84882501136

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DO - 10.1016/B978-0-12-374553-8.00177-5

M3 - Chapter

AN - SCOPUS:84882501136

SN - 9780080923239

VL - 1-3

SP - 1060

EP - 1066

BT - Encyclopedia of Fish Physiology

PB - Elsevier Masson s.r.l.

ER -

DESIGN AND PHYSIOLOGY OF THE HEART | Cardiac Cellular Length–Tension Relationship

Abstract

Keywords

UN SDGs

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