Dietary supplementation with either saturated or unsaturated fatty acids does not affect the mechanoenergetics of the isolated rat heart

Goo, Soyeon; Han, June‐Chiew; Nisbet, Linley A.; LeGrice, Ian J.; Taberner, Andrew J.; Loiselle, Denis S.

doi:10.1002/phy2.272

Cited by 8 publications

(11 citation statements)

References 46 publications

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“…Baseline contractile function and coronary perfusion were insensitive to ALA supplementation, consistent with lack of mechano-energetic effects of PUFA supplementation in the hearts of healthy animals [104,105], despite improvements in mitochondrial function [106]. In contrast, others provide evidence n-3 PUFAs may improve function in healthy hearts [10] or promote cardiac efficiency without modifying contractility [13,107].…”

Section: Myocardial Function Ischemic Tolerance and Preconditioningmentioning

confidence: 72%

Dietary α-Linolenic Acid Counters Cardioprotective Dysfunction in Diabetic Mice: Unconventional PUFA Protection

et al. 2020

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Whether dietary omega-3 (n-3) polyunsaturated fatty acid (PUFA) confers cardiac benefit in cardiometabolic disorders is unclear. We test whether dietary -linolenic acid (ALA) enhances myocardial resistance to ischemia-reperfusion (I-R) and responses to ischemic preconditioning (IPC) in type 2 diabetes (T2D); and involvement of conventional PUFA-dependent mechanisms (caveolins/cavins, kinase signaling, mitochondrial function, and inflammation). Eight-week male C57Bl/6 mice received streptozotocin (75 mg/kg) and 21 weeks high-fat/high-carbohydrate feeding. Half received ALA over six weeks. Responses to I-R/IPC were assessed in perfused hearts. Localization and expression of caveolins/cavins, protein kinase B (AKT), and glycogen synthase kinase-3 β (GSK3β); mitochondrial function; and inflammatory mediators were assessed. ALA reduced circulating leptin, without affecting body weight, glycemic dysfunction, or cholesterol. While I-R tolerance was unaltered, paradoxical injury with IPC was reversed to cardioprotection with ALA. However, post-ischemic apoptosis (nucleosome content) appeared unchanged. Benefit was not associated with shifts in localization or expression of caveolins/cavins, p-AKT, p-GSK3β, or mitochondrial function. Despite mixed inflammatory mediator changes, tumor necrosis factor-a (TNF-a) was markedly reduced. Data collectively reveal a novel impact of ALA on cardioprotective dysfunction in T2D mice, unrelated to caveolins/cavins, mitochondrial, or stress kinase modulation. Although evidence suggests inflammatory involvement, the basis of this “un-conventional” protection remains to be identified.

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Section: Myocardial Function Ischemic Tolerance and Preconditioningmentioning

confidence: 72%

Dietary α-Linolenic Acid Counters Cardioprotective Dysfunction in Diabetic Mice: Unconventional PUFA Protection

et al. 2020

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“…Despite careful recapitulation of dietary protocols, results from trabecula experiments in the flow-through microcalorimeter showed no effect of fish oil supplementation on load-dependent cardiac efficiency (58) nor did those from isolated working whole hearts (59).…”

Section: Cardiac Muscle Myometrymentioning

confidence: 99%

Muscle heat: a window into the thermodynamics of a molecular machine

Loiselle

Johnston

Han

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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contraction of muscle is characterized by the development of force and movement (mechanics) together with the generation of heat (metabolism). Heat represents that component of the enthalpy of ATP hydrolysis that is not captured by the microscopic machinery of the cell for the performance of work. It arises from two conceptually and temporally distinct sources: initial metabolism and recovery metabolism. Initial metabolism comprises the hydrolysis of ATP and its rapid regeneration by hydrolysis of phosphocreatine (PCr) in the processes underlying excitation-contraction coupling and subsequent cross-bridge cycling and sliding of the contractile filaments. Recovery metabolism describes those process, both aerobic (mitochondrial) and anaerobic (cytoplasmic), that produce ATP, thereby allowing the regeneration of PCr from its hydrolysis products. An equivalent partitioning of muscle heat production is often invoked by muscle physiologists. In this formulation, total enthalpy expenditure is separated into external mechanical work (W) and heat (Q). Heat is again partitioned into three conceptually distinct components: basal, activation, and force dependent. In the following mini-review, we trace the development of these ideas in parallel with the development of measurement techniques for separating the various thermal components.Microcalorimetry; muscle heat production; myothermy; thermopiles MUSCLE IS A MOLECULAR machine. It operates isothermally, isobarically, and isovolumetrically. At the microscopic level, it directly converts the Free Energy component of the enthalpy of ATP hydrolysis into cyclic attachment and detachment of actomyosin cross bridges, together with transportation of ions up their electrochemical potential gradients. At the macroscopic level, two consequences result: the generation of force and the evolution of heat. Of these two entities, heat is by far the more difficult to quantify and to interpret. In this brief review, we trace the development of techniques to measure muscle heat production from the mid-19th century to the present, providing parallel commentary on the progressive understanding of muscle function. We give particular consideration to the development of techniques of separating the metabolic cost of cross-bridge cycling from the purely "overhead" cost of its activation.

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“…Flow probes, connected to flow meters, measured the rates of aortic and coronary outflow. The fully-cannulated heart was then attached to the working-heart rig (Goo et al, 2013 , 2014b ; Loiselle et al, 2014 ) and enclosed by a water-jacketed glass chamber equilibrated to 37°C. Intrinsic heart rate was measured, followed by external pacing at 5 Hz, by placing a stimulus electrode at the sinoatrial node.…”

Section: Methodsmentioning

confidence: 99%

“…The left ventricle was subjected to a fixed preload of 17 mmHg while 8-10 different afterloads were presented in random order, ranging from 30 mmHg (at which point the coronary flow was near zero) to maximal (typically 100 mmHg, at which point the aortic flow was near zero). LV afterload was altered by changing the height of the aortic tubing (Goo et al, 2013 , 2014a , b ; Loiselle et al, 2014 ). To remove the effect of RV pressure overload, RV afterload was fixed at a low value (10 mmHg) and no Tyrode solution was allowed to flow into the RV except the coronary effluent from the LV via the coronary sinus.…”

Section: Methodsmentioning

confidence: 99%

Left-Ventricular Energetics in Pulmonary Arterial Hypertension-Induced Right-Ventricular Hypertrophic Failure

et al. 2018

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Pulmonary arterial hypertension (PAH) alters the geometries of both ventricles of the heart. While the right ventricle (RV) hypertrophies, the left ventricle (LV) atrophies. Multiple lines of clinical and experimental evidence lead us to hypothesize that the impaired stroke volume and systolic pressure of the LV are a direct consequence of the effect of pressure overload in the RV, and that atrophy in the LV plays only a minor role. In this study, we tested this hypothesis by examining the mechanoenergetic response of the atrophied LV to RV hypertrophy in rats treated with monocrotaline. Experiments were performed across multiple-scales: the whole-heart in vivo and ex vivo, and its trabeculae in vitro. Under the in vivo state where the RV was pressure-overloaded, we measured reduced systemic blood pressure and LV ventricular pressure. In contrast, under both ex vivo and in vitro conditions, where the effect of RV pressure overload was circumvented, we found that LV was capable of developing normal systolic pressure and stress. Nevertheless, LV atrophy played a minor role in that LV stroke volume remained lower, thereby contributing to lower LV mechanical work output. Concomitantly lower oxygen consumption and change of enthalpy were observed, and hence LV energy efficiency was unchanged. Our internally consistent findings between working-heart and trabecula experiments explain the rapid improvement of LV systolic function observed in patients with chronic pulmonary hypertension following surgical relief of RV pressure overload.

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Dietary supplementation with either saturated or unsaturated fatty acids does not affect the mechanoenergetics of the isolated rat heart

Cited by 8 publications

References 46 publications

Dietary α-Linolenic Acid Counters Cardioprotective Dysfunction in Diabetic Mice: Unconventional PUFA Protection

Dietary α-Linolenic Acid Counters Cardioprotective Dysfunction in Diabetic Mice: Unconventional PUFA Protection

Muscle heat: a window into the thermodynamics of a molecular machine

Left-Ventricular Energetics in Pulmonary Arterial Hypertension-Induced Right-Ventricular Hypertrophic Failure

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