Contractile and calcium regulating capacities of myocardia of different sized mammals scale with resting heart rate

Hamilton, N.; Ianuzzo, C. D.

doi:10.1007/bf00230179

Cited by 61 publications

(38 citation statements)

References 27 publications

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“…In various organs, capacities for membrane ion pumping, i.e. V max values for Na + -K + -ATPase (Couture and Hulbert, 1995) and Ca 2+ -ATPase (Hamilton and Ianuzzo, 1991) decline with increasing mass. Allometry in V max values for citrate synthase, a Krebs cycle enzyme that serves as an index of oxidative capacity, is observed in the skeletal muscles of mammals (Emmett and Hochachka, 1981) and fishes Somero and Childress, 1990).…”

Section: Causation In Metabolic Scalingmentioning

confidence: 99%

Multi-level regulation and metabolic scaling

Suarez

Darveau

2005

Journal of Experimental Biology

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Metabolic rates scale allometrically, such that a unit mass of elephant has a metabolic rate much less than that of a unit mass of mouse. To empiricists, the question 'what causes the allometric scaling of metabolic rates?' is one that is inextricably linked to the question 'what determines metabolic rates?' This is because whatever phenomena determine metabolic rates should presumably play major roles in driving their allometric scaling. The fundamental importance of both questions has been recognized by biologists for a century, and studies addressing them have had long and illustrious histories. Introductions to the phenomenon of metabolic scaling and accounts of the historical development of ideas and studies devoted to the subject can be found in excellent books (Calder, 1984;Schmidt-Nielsen, 1984) and reviews (Calder, 1981;Hoppeler et al., 1980;Porter, 2001;Taylor, 1987;Weibel, 1987) and are beyond the scope of this article. Here, we discuss some empirical data from the literature of comparative physiology to address the issue of what determines metabolic rates in animals. We relate this information to the allometric scaling of metabolic rates and comment on recently proposed models for metabolic scaling. Animals as the sum of their partsWhen data for basal metabolic rate, BMR, are plotted against body mass, M b , on logarithmic coordinates, the slope of the linear relationship, referred to as the allometric exponent, b, in the equation:is significantly less than 1.0, where a is the vertical intercept (Schmidt-Nielsen, 1984 Metabolic control analysis has revealed that flux through pathways is the consequence of system properties, i.e. shared control by multiple steps, as well as the kinetic effects of various pathways and processes over each other. This implies that the allometric scaling of flux rates must be understood in terms of properties that pertain to the regulation of flux rates. In contrast, proponents of models considering the scaling of branching or fractal-like systems suggest that supply rates determine metabolic rates. Therefore, the allometric scaling of supply alone provides a sufficient explanation for the allometric scaling of metabolism. Examination of empirical data from the literature of comparative physiology reveals that basal metabolic rates (BMR) are driven by rates of energy expenditure within internal organs and that the allometric scaling of BMR can be understood in terms of the scaling of the masses and metabolic rates of internal organs. Organ metabolic rates represent the sum of tissue metabolic rates while, within tissues, cellular metabolic rates are the outcome of shared regulation by multiple processes. Maximal metabolic rates (MMR, measured as maximum rates of O 2 consumption, V O ∑ max ) during exercise also scale allometrically, are also subject to control by multiple processes, but are due mainly to O 2 consumption by locomotory muscles. Thus, analyses of the scaling of MMR must consider the scaling of both muscle mass and muscle energy expenditure. Consistent with t...

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Section: Causation In Metabolic Scalingmentioning

confidence: 99%

Multi-level regulation and metabolic scaling

Suarez

Darveau

2005

Journal of Experimental Biology

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“…The action potential of the mouse ventricular myocardium has an extremely short duration that causes early termination of the Ca 2+ current, resulting in less dependence of contraction on trans-sarcolemmal Ca 2+ influx (3). On the other hand, the mouse myocardium was reported to have a high sarcoplasmic reticulum (SR) content and Ca 2+ -ATPase activity per unit myocardial mass (4), and its contraction is more highly dependent on Ca 2+ released from SR than other experimental animal species (2). Such characteristics of the mouse myocardium support its rapid contraction and relaxation under high heart rate.…”

Section: Introductionmentioning

confidence: 99%

Developmental Changes in Excitation–Contraction Mechanisms of the Mouse Ventricular Myocardium as Revealed by Functional and Confocal Imaging Analyses

et al. 2013

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Abstract. Developmental changes in excitation-contraction mechanisms were examined in the ventricular myocardium from fetal, neonatal, and 1-, 2-, and 4-week-old mice. In isolated tissue, the negative inotropic effect of nifedipine decreased, while that of ryanodine increased with age. Action potential duration decreased with age, especially during the late fetal period. In ventricular cardiomyocytes, fluorescence imaging revealed that the sarcoplasmic reticulum increases progressively during pre-and postnatal development. t-Tubules were absent in the fetus and neonate, were observed only in the subsarcolemmal region at 1 week after birth, and were present throughout the cytoplasm at 2 and 4 weeks after birth. The amplitude of Ca 2+ transients, as well as its ryanodine-sensitive component, increased with age. In the neonate and 1-week-old mice, Ca 2+ at the cell center showed slower rise than the subsarcolemmal region, but in 2-and 4-week-old mice, Ca 2+ increased simultaneously across the entire width of the cell. These results suggest that in the mouse ventricular myocardium, the shortening of the action potential during the late fetal period and the development of t-tubule-sarcoplasmic reticulum coupling during the second postnatal week largely contribute to the developmental increase in the dependence of contraction on sarcoplasmic reticulum function.

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“…In this regard, the swine model has proven useful because its cardiac biochemistry and collateral coronary circulation are remarkably similar to that of the human (1)(2)(3). In particular, the slower contracting β-myosin heavy chain is the predominant isoform in the swine heart as it is in the human heart; this contrasts the rodent heart in which the faster contracting α-myosin heavy chain predominates (7). Correspondingly, the kinetics of contraction and relaxation in the swine heart and human heart are much slower than those in the rodent heart.…”

Section: Introductionmentioning

confidence: 99%

Effects of gradual coronary artery occlusion and exercise training on gene expression in swine heart

et al. 2006

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Gradual occlusion (O) of the swine left circumflex coronary artery (LCX) with an ameroid occluder results in complete O within 3 weeks, collateral vessel development, and compensatory hypertrophy. The purpose of this investigation was to determine the independent and combined effects of O and exercise training (E) on gene expression in the swine heart. Adult Yucatan miniature swine were assigned to one of the following groups (n = 6-9/group): sedentary control (S), exercise-trained (E), sedentary swine subjected to LCX occlusion (SO), and exercise-trained swine with LCX occlusion (EO). Exercise consisted of progressive treadmill running conducted 5 d/wk for 16 weeks. Gene expression was studied in myocardium isolated from the collateral-dependent left ventricle free wall (LV) and the collateral-independent septum (SEP) by RNA blotting. E and O each stimulated cardiac hypertrophy independently (p < 0.001) with no interaction. O but not E increased atrial natriuretic factor expression in the LV, but not in the SEP. E decreased the expression of β-myosin heavy chain in the LV, but not in the SEP. E retarded the expression of collagen III mRNA in SEP; but not in the LV. Exercise training and coronary artery occlusion each stimulate cardiac hypertrophy independently and induce different patterns of gene expression.

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Contractile and calcium regulating capacities of myocardia of different sized mammals scale with resting heart rate

Cited by 61 publications

References 27 publications

Multi-level regulation and metabolic scaling

Multi-level regulation and metabolic scaling

Developmental Changes in Excitation–Contraction Mechanisms of the Mouse Ventricular Myocardium as Revealed by Functional and Confocal Imaging Analyses

Effects of gradual coronary artery occlusion and exercise training on gene expression in swine heart

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