scholarly journals Exercise training, energy metabolism, and heart failureThis paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.

2009 ◽  
Vol 34 (3) ◽  
pp. 336-339 ◽  
Author(s):  
Renée Ventura-Clapier
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Endurance Training ◽  
Cell Function ◽  
Peer Review Process ◽  
The Body ◽  
Industrialized Countries ◽  
Beneficial Effects ◽  
Intracellular Energy Transfer

Energy metabolism is at the crossroad of cell function and dysfunction. Cardiac and skeletal muscle cells, the energy metabolism of which is high, fluctuating, and adaptable to the special needs of the body, have developed sophisticated strategies for synthesizing, transferring, and utilizing energy in accordance with the needs of the body. Adaptation to endurance training mainly involves energetic remodelling in skeletal muscles, but less is known for the cardiac muscle. Alterations in energy metabolism participate in many pathophysiological processes, among which is heart failure. Because endurance training improves symptoms and quality of life and decreases mortality rate and hospitalization, it is increasingly recognized as a beneficial practice for heart failure patients. The mechanisms involved in the beneficial effects of exercise training are far from being understood. Proper evaluation of these mechanisms is thus a major health issue for populations living in industrialized countries. This review mainly focuses on oxidative metabolism and intracellular energy transfer in muscles and the heart, their alterations in heart failure, and the effects of endurance exercise training.

scholarly journals Exercise training normalizes elevated firing rate of hypothalamic presympathetic neurons in heart failure rats

2019 ◽  
Vol 316 (2) ◽  
pp. R110-R120 ◽  
Author(s):  
Yiming Shen ◽  
Jin Bong Park ◽  
So Yeong Lee ◽  
Seong Kyu Han ◽  
Pan Dong Ryu
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Firing Rate ◽  
Gaba Release ◽  
Neuronal Firing ◽  
Ventrolateral Medulla ◽  
Patch Clamp Technique ◽  
Electrophysiological Properties ◽  
Beneficial Effects ◽  
Underlying Mechanisms

Exercise training (ExT) normalizes elevated sympathetic nerve activity in heart failure (HF), but the underlying mechanisms are not well understood. In this study, we examined the effects of 3 wk of ExT on the electrical activity of the hypothalamic presympathetic neurons in the brain slice of HF rats. HF rats were prepared by ligating the left descending coronary artery. The electrophysiological properties of paraventricular nucleus neurons projecting to the rostral ventrolateral medulla (PVN-RVLM) were examined using the slice patch-clamp technique. The neuronal firing rate was elevated in HF rats, and ExT induced a reduction in the firing rate ( P < 0.01). This ExT-induced decrease in the firing rate was associated with an increased frequency of spontaneous and miniature inhibitory postsynaptic current (IPSCs; P < 0.05). There was no significant change in excitatory postsynaptic current. Replacing Ca2+ with Mg2+ in the recording solution reduced the elevated IPSC frequency in HF rats with ExT ( P < 0.01) but not in those without ExT, indicating an increase in the probability of GABA release. In contrast, ExT did not restore the reduced GABAA receptor-mediated tonic inhibitory current in HF rats. A GABAA receptor blocker (bicuculline, 20 μM) increased the firing rate in HF rats with ExT ( P < 0.01) but not in those without ExT. Collectively, these results show that ExT normalized the elevated firing activity by increasing synaptic GABA release in PVN-RVLM neurons in HF rats. Our findings provide a brain mechanism underlying the beneficial effects of ExT in HF, which may shed light on the pathophysiology of other diseases accompanied by sympathetic hyperactivation.

Beneficial effects of exercise training in heart failure are lost in male diabetic rats

2017 ◽  
Vol 123 (6) ◽  
pp. 1579-1591
Author(s):  
Dalila Boudia ◽  
Valérie Domergue ◽  
Philippe Mateo ◽  
Loubina Fazal ◽  
Mathilde Prud’homme ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Coronary Artery Ligation ◽  
Standard Diet ◽  
Beneficial Effects ◽  
Patients With Heart Failure

Exercise training has been demonstrated to have beneficial effects in patients with heart failure (HF) or diabetes. However, it is unknown whether diabetic patients with HF will benefit from exercise training. Male Wistar rats were fed either a standard (Sham, n = 53) or high-fat, high-sucrose diet ( n = 66) for 6 mo. After 2 mo of diet, the rats were already diabetic. Rats were then randomly subjected to either myocardial infarction by coronary artery ligation (MI) or sham operation. Two months later, heart failure was documented by echocardiography and animals were randomly subjected to exercise training with treadmill for an additional 8 wk or remained sedentary. At the end, rats were euthanized and tissues were assayed by RT-PCR, immunoblotting, spectrophotometry, and immunohistology. MI induced a similar decrease in ejection fraction in diabetic and lean animals but a higher premature mortality in the diabetic group. Exercise for 8 wk resulted in a higher working power developed by MI animals with diabetes and improved glycaemia but not ejection fraction or pathological phenotype. In contrast, exercise improved the ejection fraction and increased adaptive hypertrophy after MI in the lean group. Trained diabetic rats with MI were nevertheless able to develop cardiomyocyte hypertrophy but without angiogenic responses. Exercise improved stress markers and cardiac energy metabolism in lean but not diabetic-MI rats. Hence, following HF, the benefits of exercise training on cardiac function are blunted in diabetic animals. In conclusion, exercise training only improved the myocardial profile of infarcted lean rats fed the standard diet. NEW & NOTEWORTHY Exercise training is beneficial in patients with heart failure (HF) or diabetes. However, less is known of the possible benefit of exercise training for HF patients with diabetes. Using a rat model where both diabetes and MI had been induced, we showed that 2 mo after MI, 8 wk of exercise training failed to improve cardiac function and metabolism in diabetic animals in contrast to lean animals.

scholarly journals Cardiac and skeletal muscle energy metabolism in heart failure: beneficial effects of voluntary activity

2002 ◽  
Vol 56 (2) ◽  
pp. 260-268 ◽  
Author(s):  
E DESOUSA ◽  
P LECHENE ◽  
D FORTIN ◽  
B NGUESSAN ◽  
S BELMADANI ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Voluntary Activity ◽  
Beneficial Effects ◽  
Muscle Energy ◽  
Muscle Energy Metabolism

scholarly journals Impairment of microcirculation and energy metabolism in intermittent claudication: beneficial effects of exercise training

2016 ◽  
Vol 72 (3) ◽  
Author(s):  
Eugenio Laurenzano ◽  
Lucrezia Spadera ◽  
Mario De Laurentis ◽  
Gregorio Brevetti
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Intermittent Claudication ◽  
Large Body ◽  
Arterial Disease ◽  
Walking Ability ◽  
Beneficial Effects ◽  
Relevant Role ◽  
Peripheral Arterial

Although in peripheral arterial disease (PAD) the primary determinant of inadequate blood supply to the affected limb during exercise is a flow-limiting lesion of a conduit artery, there is a large body of evidence that impairment of microcirculation and skeletal muscle energy metabolism play a relevant role in the reduced working ability of affected individuals. This review was conceived to cast some light on this topic, paying special attention to the functional benefits of exercise training (ET) in the treatment of claudicant patients. In PAD, the ischemia induced by maximal exercise increases oxidative stress, inflammation and endothelial dysfunction. Perturbation of the endothelial homeostasis results in increased adhesiveness of leukocytes and platelets, and in reduced vasodilator capability. These events, expression of the interplay between inflammation and endothelium, provoke an obstacle in the microcirculation with a reduction in the nutritive blood flow, leading to acidosis and impaired energy metabolism in skeletal muscle, with consequent reduced exercise tolerance. ET counteracts these effects by improving walking ability and quality of life in patients with intermittent claudication, thus representing the gold standard in the treatment of PAD.

scholarly journals Cellular Energetics of Mast Cell Development and Activation

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 524
Author(s):  
Ryan P. Mendoza ◽  
Dylan H. Fudge ◽  
Jared M. Brown
Keyword(s):  
Mast Cell ◽  
Energy Metabolism ◽  
Mast Cells ◽  
Cell Function ◽  
Cell Metabolism ◽  
Cell Development ◽  
The Body ◽  
Mast Cell Activation ◽  
Wide Range ◽  
Ige Mediated

Mast cells are essential first responder granulocytes in the innate immune system that are well known for their role in type 1 immune hypersensitivity reactions. Although mostly recognized for their role in allergies, mast cells have a range of influences on other systems throughout the body and can respond to a wide range of agonists to properly prime an appropriate immune response. Mast cells have a dynamic energy metabolism to allow rapid responsiveness to their energetic demands. However, our understanding of mast cell metabolism and its impact on mast cell activation and development is still in its infancy. Mast cell metabolism during stimulation and development shifts between both arms of metabolism: catabolic metabolism—such as glycolysis and oxidative phosphorylation—and anabolic metabolism—such as the pentose phosphate pathway. The potential for metabolic pathway shifts to precede and perhaps even control activation and differentiation provides an exciting opportunity to explore energy metabolism for clues in deciphering mast cell function. In this review, we discuss literature pertaining to metabolic environments and fluctuations during different sources of activation, especially IgE mediated vs. non-IgE mediated, and mast cell development, including progenitor cell types leading to the well-known resident mast cell.

scholarly journals Beta-Hydroxybutyrate, Friend or Foe for Stressed Hearts

2021 ◽  
Vol 2 ◽  
Author(s):  
Yuxin Chu ◽  
Cheng Zhang ◽  
Min Xie
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Ketone Bodies ◽  
Ischemia Reperfusion ◽  
Alternative Fuel ◽  
Diabetic Patients ◽  
Signaling Molecule ◽  
Beneficial Effects

One of the characteristics of the failing human heart is a significant alteration in its energy metabolism. Recently, a ketone body, β-hydroxybutyrate (β-OHB) has been implicated in the failing heart’s energy metabolism as an alternative “fuel source.” Utilization of β-OHB in the failing heart increases, and this serves as a “fuel switch” that has been demonstrated to become an adaptive response to stress during the heart failure progression in both diabetic and non-diabetic patients. In addition to serving as an alternative “fuel,” β-OHB represents a signaling molecule that acts as an endogenous histone deacetylase (HDAC) inhibitor. It can increase histone acetylation or lysine acetylation of other signaling molecules. β-OHB has been shown to decrease the production of reactive oxygen species and activate autophagy. Moreover, β-OHB works as an NLR family pyrin domain-containing protein 3 (Nlrp3) inflammasome inhibitor and reduces Nlrp3-mediated inflammatory responses. It has also been reported that β-OHB plays a role in transcriptional or post-translational regulations of various genes’ expression. Increasing β-OHB levels prior to ischemia/reperfusion injury results in a reduced infarct size in rodents, likely due to the signaling function of β-OHB in addition to its role in providing energy. Sodium-glucose co-transporter-2 (SGLT2) inhibitors have been shown to exert strong beneficial effects on the cardiovascular system. They are also capable of increasing the production of β-OHB, which may partially explain their clinical efficacy. Despite all of the beneficial effects of β-OHB, some studies have shown detrimental effects of long-term exposure to β-OHB. Furthermore, not all means of increasing β-OHB levels in the heart are equally effective in treating heart failure. The best timing and therapeutic strategies for the delivery of β-OHB to treat heart disease are unknown and yet to be determined. In this review, we focus on the crucial role of ketone bodies, particularly β-OHB, as both an energy source and a signaling molecule in the stressed heart and the overall therapeutic potential of this compound for cardiovascular diseases.

Exercise training improves renal excretory responses to acute volume expansion in rats with heart failure

2006 ◽  
Vol 291 (6) ◽  
pp. F1148-F1156 ◽  
Author(s):  
Hong Zheng ◽  
Yi-Fan Li ◽  
Irving H. Zucker ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Volume Expansion ◽  
Renal Sympathetic Nerve Activity ◽  
Beneficial Effects ◽  
Coronary Ligation ◽  
Ext Groups ◽  
Histological Data ◽  
Renal Responses ◽  
Renal Sympathetic

Experiments were performed to test the postulate that exercise training (ExT) improves the blunted renal excretory response to acute volume expansion (VE), in part, by normalizing the neural component of the volume reflex typically observed in chronic heart failure (HF). Diuretic and natriuretic responses to acute VE were examined in sedentary and ExT groups of rats with either HF or sham-operated controls. Experiments were performed in anesthetized (Inactin) rats 6 wk after coronary ligation surgery. Histological data indicated that there was a 34.9 ± 3.0% outer and 42.5 ± 3.2% inner infarct of the myocardium in the HF group. Sham rats had no observable damage to the myocardium. In sedentary rats with HF, VE produced a blunted diuresis (46% of sham) and natriuresis (35% of sham) compared with sham-operated control rats. However, acute VE-induced diuresis and natriuresis in ExT rats with HF were comparable to sham rats and significantly higher than sedentary HF rats. Renal denervation abolished the salutary effects of ExT on renal excretory response to acute VE in HF. Since glomerular filtration rates were not significantly different between the groups, renal hemodynamic changes may not account for the blunted renal responses in rats with HF. Additional experiments confirmed that renal sympathetic nerve activity responses to acute VE were blunted in sedentary HF rats; however, ExT normalized the renal sympathoinhibition in HF rats. These results confirm an impairment of neurally mediated excretory responses to acute VE in rats with HF. ExT restored the blunted excretory responses as well as the renal sympathoinhibitory response to acute VE in HF rats. Thus the beneficial effects of ExT on cardiovascular regulation in HF may be partly due to improvement of the neural component of volume reflex.

Sign in / Sign up

Export Citation Format

Share Document