Experimental and modelling evidence of shortening heat in cardiac muscle

Tran, Kenneth; Han, June‐Chiew; Crampin, Edmund J.; Taberner, Andrew J.; Loiselle, Denis S.

doi:10.1113/jp274680

Cited by 16 publications

(37 citation statements)

References 51 publications

(100 reference statements)

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“…The physiologic mode can be used to construct tension-length loops 93 that correspond to pressure-volume loops in whole ventricles ( Figure 2C). In agreement with experiments [12,13], model 94 simulations revealed a linear relationship between tension-length area (a.k.a. stress-strain area) and ATP consumption 95 during a heartbeat ( Figure 2D).…”

supporting

confidence: 88%

Model order reduction for left ventricular mechanics via congruency training

Achille¹,

Parikh²,

Khamzin

et al. 2020

PLoS ONE

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1The LO simulations make it possible to design novel cardiac muscle contraction models by following iterative approaches 2 where the consequences of model assumptions can be evaluated across scales from isolated preparation assays to whole 3 organ effects. Leveraging such capability, we constructed a new phenomenological model of muscle contraction. The new 4 myofilament model is a modified version of [1] with the addition of XB-XB cooperative effects and with a simple 5 mean-field strain formulation similar to [2]. The model equations are designed to reproduce several experimental features 6 observed in both isolated muscle and physiological measurements at the ventricle level, as described below. 7 XB kinetics and ktr-Ca dependence 8 Similar to previous models describing cooperative behavior of crossbridges (XBs) within regulatory units (RUs) (e.g., [3]), 9 we simulated XB dynamics from the perspective of XB-groups. The core model equation describes the formation and 10 collapse of XB "populations", groups of XBs featuring XB-XB cooperative effects within a group. The XB-group could 11 be interpreted as the crossbridges in a single RU, as crossbridges probably interact only within a RU [4]. Alternatively, 12 groups could be interpreted as all RUs of separate actin filaments, if we were to assume that all crossbridges in the 13 actin-activation model interact with each other. Finally, populations could be purely functional units. 14 In a typical XB-group development, force is first generated when a "primary" crossbridge is formed as a myosin head 15 binds actin at a relatively slow rate, initiating a new group. "Secondary" crossbridges are then formed at a much faster 16 rate, which results in collapsing of groups at relatively slow rates. The simplest equation for the fraction of groups G XB 17 engaged in force generation that guarantees a mono-exponential shape for the rate of force redevelopment (Ktr) curve 18 assumes the form 19 157 5. Ovchinnikov S. Max-min representation of piecewise linear functions. Contributions to Algebra and Geometry.158 2002;43(1):297-302. 159 6. Janssen P, Hunter WC. Force, not sarcomere length, correlates with prolongation of isosarcometric contraction. 160 American Journal of Physiology-Heart and Circulatory Physiology. 1995;269(2):H676-H685. 161 7. Janssen PM, Stull LB, Marbán E. Myofilament properties comprise the rate-limiting step for cardiac relaxation at 162 body temperature in the rat. American Journal of Physiology-Heart and Circulatory Physiology.163 2002;282(2):H499-H507. 164 8. Milani-Nejad N, Canan BD, Elnakish MT, Davis JP, Chung JH, Fedorov V, et al. The Frank-Starling mechanism 165involves deceleration of cross-bridge kinetics and is preserved in failing human right ventricular myocardium.

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supporting

confidence: 88%

Model order reduction for left ventricular mechanics via congruency training

Achille¹,

Parikh²,

Khamzin

et al. 2020

PLoS ONE

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“…Crossbridge cycling heat was further partitioned into shortening and non‐shortening (isometric) components (Tran et al . ; Pham et al . ).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary arterial hypertension reduces energy efficiency of right, but not left, rat ventricular trabeculae

Pham

Nisbet

Taberner

et al. 2018

The Journal of Physiology

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Pulmonary arterial hypertension (PAH) greatly increases the afterload on the right ventricle (RV), triggering RV hypertrophy, which progressively leads to RV failure. In contrast, the disease reduces the passive filling pressure of the left ventricle (LV), resulting in LV atrophy. We investigated whether these distinct structural and functional consequences to the ventricles affect their respective energy efficiencies. We studied trabeculae isolated from both ventricles of Wistar rats with monocrotaline-induced PAH and their respective Control groups. Trabeculae were mounted in a calorimeter at 37°C. While contracting at 5 Hz, they were subjected to stress-length work-loops over a wide range of afterloads. They were subsequently required to undergo a series of isometric contractions at various muscle lengths. In both protocols, stress production, length change and suprabasal heat output were simultaneously measured. We found that RV trabeculae from PAH rats generated higher activation heat, but developed normal active stress. Their peak external work output was lower due to reduced extent and velocity of shortening. Despite lower peak work output, suprabasal enthalpy was unaffected, thereby rendering suprabasal efficiency lower. Crossbridge efficiency, however, was unaffected. In contrast, LV trabeculae from PAH rats maintained normal mechano-energetic performance. Pulmonary arterial hypertension reduces the suprabasal energy efficiency of hypertrophied right ventricular tissues as a consequence of the increased energy cost of Ca cycling.

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“…Explicitly, for a given force, the heat arising from an isometric contraction is less than that from a work-loop contraction, resulting in the isometric heat-force relation lying below its work-loop counterpart. We further hypothesize that the region lying between these two contraction mode-dependent heat-force relations reflects the existence of "heat of shortening" in cardiac muscle (Tran et al, 2017). That is, the energetics equivalent of the end-systolic zone (ESZ) on the mechanics plane is the "heat of shortening" region, and this region is also expected to encompass all possible heat-force points resulting from isometric and workloop contractions.…”

Section: Introductionmentioning

confidence: 94%

“…Until recently, it was thought that the heat of shortening is a property unique to skeletal muscle (Gibbs and Chapman, 1979;Holroyd and Gibbs, 1992). However, a recent experimental and modeling study (Tran et al, 2017) has provided compelling evidence that the heat of shortening also exists in cardiac tissues. At any given force, more heat is produced from FIGURE 6 | Effects of increased contractility on velocity of shortening.…”

Section: Shortening Heatmentioning

confidence: 99%

“…An isometricallycontracting muscle transduces chemical energy entirely into heat, whereas an afterloaded shortening muscle captures some of that energy as work (Gibbs, 1978). When assessed on the heat-force plane, the mechanoenergetics of cardiac muscle likewise displays contraction-mode dependence (Pham et al, 2017;Tran et al, 2017). Explicitly, for a given force, the heat arising from an isometric contraction is less than that from a work-loop contraction, resulting in the isometric heat-force relation lying below its work-loop counterpart.…”

Section: Introductionmentioning

confidence: 99%

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Energetics Equivalent of the Cardiac Force-Length End-Systolic Zone: Implications for Contractility and Economy of Contraction

et al. 2020

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We have recently demonstrated the existence of a region on the cardiac mechanics stress-length plane, which we have designated "The cardiac end-systolic zone." The zone is defined as the area on the pressure-volume (or stress-length) plane within which all stress-length contraction profiles reach their end-systolic points. It is enclosed by three boundaries: the isometric end-systolic relation, the work-loop (shortening) endsystolic relation, and the zero-active stress isotonic end-systolic relation. The existence of this zone reflects the contraction-mode dependence of the cardiac end-systolic forcelength relations, and has been confirmed in a range of cardiac preparations at the wholeheart, tissue and myocyte levels. This finding has led us to speculate that a comparable zone prevails for cardiac metabolism. Specifically, we hypothesize the existence of an equivalent zone on the energetics plane (heat vs. stress), and that it can be attributed to the recently-revealed heat of shortening in cardiac muscle. To test these hypotheses, we subjected trabeculae to both isometric contractions and work-loop contractions over wide ranges of preloads and afterloads. We found that the heat-stress relations for work-loop contractions were distinct from those of isometric contractions, mirroring the contraction mode-dependence of the stress-length relation. The zone bounded by these contraction-mode dependent heat-stress relations reflects the heat of shortening. Isoproterenol-induced enhancement of contractility led to proportional increases in the zones on both the mechanics and energetics planes, thereby supporting our hypothesis.

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Experimental and modelling evidence of shortening heat in cardiac muscle

Cited by 16 publications

References 51 publications

Model order reduction for left ventricular mechanics via congruency training

Model order reduction for left ventricular mechanics via congruency training

Pulmonary arterial hypertension reduces energy efficiency of right, but not left, rat ventricular trabeculae

Energetics Equivalent of the Cardiac Force-Length End-Systolic Zone: Implications for Contractility and Economy of Contraction

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