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Holmes2006 - Hill's model of muscle contraction

ABSTRACT: Holmes2006 - Hill's model of muscle contraction This model is described in the article: Teaching from classic papers: Hill's model of muscle contraction. Holmes JW. Adv Physiol Educ 2006 Jun; 30(2): 67-72 Abstract: A. V. Hill's 1938 paper "The heat of shortening and the dynamic constants of muscle" is an enduring classic, presenting detailed methods, meticulous experiments, and the model of muscle contraction that now bears Hill's name. Pairing a simulation based on Hill's model with a reading of his paper allows students to follow his thought process to discover key principles of muscle physiology and gain insight into how to develop quantitative models of physiological processes. In this article, the experience of the author using this approach in a graduate biomedical engineering course is outlined, along with suggestions for adapting this approach to other audiences. This model is hosted on BioModels Database and identified by: BIOMD0000000677. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Camille Laibe

PROVIDER: BIOMD0000000677 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000677?filename=BIOMD0000000677-biopax2.owl	Owl
	BIOMD0000000677?filename=BIOMD0000000677-biopax3.owl	Owl
	BIOMD0000000677?filename=BIOMD0000000677-matlab.m	Other
	BIOMD0000000677?filename=BIOMD0000000677-octave.m	Other
	BIOMD0000000677?filename=BIOMD0000000677.m	Other

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Teaching from classic papers: Hill's model of muscle contraction.

Holmes Jeffrey W JW

Advances in physiology education 20060601 2

A. V. Hill's 1938 paper "The heat of shortening and the dynamic constants of muscle" is an enduring classic, presenting detailed methods, meticulous experiments, and the model of muscle contraction that now bears Hill's name. Pairing a simulation based on Hill's model with a reading of his paper allows students to follow his thought process to discover key principles of muscle physiology and gain insight into how to develop quantitative models of physiological processes. In this article, the exp ...[more]

PMID: 16709736

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Project description:Background: Niemann-Pick disease type A (NPDA), a disease caused by mutations in acid sphingomyelinase (ASM), involves severe neurodegeneration and early death. Intracellular lipid accumulation and plasma membrane alterations are implicated in the pathology. ASM is also linked to the mechanism of plasma membrane repair, so we investigated the impact of ASM deficiency in skeletal muscle, a tissue that undergoes frequent cycles of injury and repair in vivo. Methods: Utilizing the NPDA/B mouse model ASM−/− and wild type (WT) littermates, we performed excitation- contraction coupling/Ca2+ mobilization and sarcolemma injury/repair assays with isolated flexor digitorum brevis fibers, proteomic analyses with quadriceps femoris, flexor digitorum brevis, and tibialis posterior muscle and in vivo tests of the contractile force (maximal isometric torque) of the quadriceps femoris muscle before and after eccentric contraction-induced muscle injury. Results: ASM−/− flexor digitorum brevis fibers showed impaired excitation-contraction coupling compared to WT, a defect expressed as reduced tetanic [Ca2+]i in response to electrical stimulation and early failure in sustaining [Ca2+]i during repeated tetanic contractions. When injured mechanically by needle passage, ASM−/− flexor digitorum brevis fibers showed susceptibility to injury similar to WT, but a reduced ability to reseal the sarcolemma. Proteomic analyses revealed changes in a small group of skeletal muscle proteins as a consequence of ASM deficiency, with downregulation of calsequestrin occurring in the three different muscles analyzed. In vivo, the loss in maximal isometric torque of WT quadriceps femoris was similar immediately after and 2 min after injury. The loss in ASM−/− mice immediately after injury was similar to WT, but was markedly larger at 2 min after injury. Conclusions: Skeletal muscle fibers from ASM−/− mice have an impairment in intracellular Ca2+ handling that results in reduced Ca2+ mobilization and a more rapid decline in peak Ca2+ transients during repeated contraction-relaxation cycles. Isolated fibers show reduced ability to repair damage to the sarcolemma, and this is associated with an exaggerated deficit in force during recovery from an in vivo eccentric contraction- induced muscle injury. Our findings uncover the possibility that skeletal muscle functional defects may play a role in the pathology of NPDA/B disease.