scholarly journals Exercise training impacts the myocardial metabolism of older individuals in a gender-specific manner

2008 ◽  
Vol 295 (2) ◽  
pp. H842-H850 ◽  
Author(s):  
Pablo F. Soto ◽  
Pilar Herrero ◽  
Kenneth B. Schechtman ◽  
Alan D. Waggoner ◽  
Jeffrey M. Baumstark ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Cardiac Function ◽  
Myocardial Metabolism ◽  
Older Individuals ◽  
Myocardial Fatty Acid ◽  
Substrate Metabolism ◽  
Specific Manner ◽  
Myocardial Substrate ◽  
Gender Specific

Aging is associated with decreases in aerobic capacity, cardiac function, and insulin sensitivity as well as alterations in myocardial substrate metabolism. Endurance exercise training (EET) improves cardiac function in a gender-specific manner, and EET has been shown to improve whole body glucose tolerance, but its effects on myocardial metabolism are unclear. Accordingly, we studied the effect of EET on myocardial substrate metabolism in older men and women. Twelve healthy older individuals (age: 60–75 yr; 6 men and 6 women) underwent PET with [15O]water, [11C]acetate, [11C]glucose, and [11C]palmitate for the assessment of myocardial blood flow (MBF), myocardial O2 consumption (MV̇o2), myocardial glucose utilization (MGU), and myocardial fatty acid utilization (MFAU), respectively, at rest and during dobutamine infusion (10 μg·kg−1·min−1). Measurements were repeated after 11 mo of EET. Maximal O2 uptake (V̇o2max) increased ( P = 0.005) after EET. MBF was unaffected by training, as was resting MV̇o2; however, posttraining dobutamine MV̇o2 was significantly higher ( P = 0.05), as was MGU ( P < 0.04). Although overall dobutamine MFAU was unchanged, posttraining dobutamine MFAU increased in women ( P = 0.01) but decreased in men ( P = 0.03). Thus, EET in older individuals improves the catecholamine response of myocardial glucose metabolism. Moreover, gender differences exist in the myocardial fatty acid metabolic response to training. These findings suggest a role for altered myocardial substrate metabolism in modulating the cardiovascular benefits of EET in older individuals.

scholarly journals Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization

2010 ◽  
Vol 12 (4) ◽  
pp. 323-330 ◽  
Author(s):  
Ching-Yi Chen ◽  
Hsiu-Ching Hsu ◽  
Bai-Chin Lee ◽  
Hung-Ju Lin ◽  
Ying-Hsien Chen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Cardiac Function ◽  
Fatty Acid Utilization

scholarly journals Dietary Calanus oil recovers metabolic flexibility and rescues postischemic cardiac function in obese female mice

2019 ◽  
Vol 317 (2) ◽  
pp. H290-H299 ◽  
Author(s):  
Kirsten M. Jansen ◽  
Sonia Moreno ◽  
Pablo M. Garcia-Roves ◽  
Terje S. Larsen
Keyword(s):  
Fatty Acid ◽  
Cardiac Function ◽  
Glucose Oxidation ◽  
Myocardial Metabolism ◽  
Dietary Supplementation ◽  
Left Ventricular ◽  
Lv Function ◽  
Marine Oil ◽  
Normal Chow ◽  
Postischemic Recovery

The aim of this study was to find out whether dietary supplementation with Calanus oil (a novel marine oil) or infusion of exenatide (an incretin mimetic) could counteract obesity-induced alterations in myocardial metabolism and improve postischemic recovery of left ventricular (LV) function. Female C57bl/6J mice received high-fat diet (HFD, 45% energy from fat) for 12 wk followed by 8-wk feeding with nonsupplemented HFD, HFD supplemented with 2% Calanus oil, or HFD plus exenatide infusion (10 µg·kg−1·day−1). A lean control group was included, receiving normal chow throughout the whole period. Fatty acid and glucose oxidation was measured in ex vivo perfused hearts during baseline conditions, while LV function was assessed with an intraventricular fluid-filled balloon before and after 20 min of global ischemia. HFD-fed mice receiving Calanus oil or exenatide showed less intra-abdominal fat deposition than mice receiving nonsupplemented HFD. Both treatments prevented the HFD-induced decline in myocardial glucose oxidation. Somewhat surprising, recovery of LV function was apparently better in hearts from mice fed nonsupplemented HFD relative to hearts from mice fed normal chow. More importantly however, postischemic recovery of hearts from mice receiving HFD with Calanus oil was superior to that of mice receiving nonsupplemented HFD and mice receiving HFD with exenatide, as expressed by better pressure development, contractility, and relaxation properties. In summary, dietary Calanus oil and administration of exenatide counteracted obesity-induced derangements of myocardial metabolism. Calanus oil also protected the heart from ischemia, which could have implications for the prevention of obesity-related cardiac disease. NEW & NOTEWORTHY This article describes for the first time that dietary supplementation with a low amount (2%) of a novel marine oil (Calanus oil) in mice is able to prevent the overreliance of fatty acid oxidation for energy production during obesity. The same effect was observed with infusion of the incretin mimetic, exanatide. The improvement in myocardial metabolism in Calanus oil-treated mice was accompanied by a significantly better recovery of cardiac performance following ischemia-reperfusion. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/dietary-calanus-oil-energy-metabolism-and-cardiac-function/ .

scholarly journals L-carnitine Improved the Cardiac Function via the Effect on Myocardial Fatty Acid Metabolism in a Hemodialysis Patient

2018 ◽  
Vol 57 (24) ◽  
pp. 3593-3596 ◽  
Author(s):  
Mai Kaneko ◽  
Hirotaka Fukasawa ◽  
Kento Ishibuchi ◽  
Hiroki Niwa ◽  
Hideo Yasuda ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cardiac Function ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Hemodialysis Patient ◽  
Myocardial Fatty Acid ◽  
Myocardial Fatty Acid Metabolism

scholarly journals Impact of sex on the heart's metabolic and functional responses to diabetic therapies

2013 ◽  
Vol 305 (11) ◽  
pp. H1584-H1591 ◽  
Author(s):  
Matthew R. Lyons ◽  
Linda R. Peterson ◽  
Janet B. McGill ◽  
Pilar Herrero ◽  
Andrew R. Coggan ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Myocardial Metabolism ◽  
Metabolic Response ◽  
Lipid Lowering ◽  
Whole Body ◽  
Functional Responses ◽  
Myocardial Glucose Uptake ◽  
Substrate Metabolism ◽  
Lipid Fatty Acid ◽  
Myocardial Substrate

Increased myocardial lipid delivery is a determinant of myocardial substrate metabolism and function in animal models of type 2 diabetes (T2DM). Sex also has major effects on myocardial metabolism in the human heart. Our aims were to determine whether 1) sex affects the myocardial metabolic response to lipid lowering in T2DM, 2) altering lipid [fatty acid (FA) or triglyceride] delivery to the heart would lower the elevated myocardial lipid metabolism associated with T2DM, and 3) decreasing lipid delivery improves diastolic dysfunction in T2DM. To this end, we studied 78 T2DM patients (43 women) with positron emission tomography, echocardiography, and whole body tracer studies before and 3 mo after randomization to metformin (MET), metformin + rosiglitazone (ROSI), or metformin + Lovaza (LOV). No treatment main effects were found for myocardial substrate metabolism, partly because men and women often had different responses to a given treatment. In men, MET decreased FA clearance, which was linked to increased plasma FA levels, myocardial FA utilization and oxidation, and lower myocardial glucose utilization. In women, ROSI increased FA clearance, thereby decreasing plasma FA levels and myocardial FA utilization. Although LOV did not change triglyceride levels, it improved diastolic function, particularly in men. Group and sex also interacted in determining myocardial glucose uptake. Thus, in T2DM, different therapeutic regimens impact myocardial metabolism and diastolic function in a sex-specific manner. This suggests that sex should be taken into account when designing a patient's diabetes treatment.

Reduced synthesis of NO causes marked alterations in myocardial substrate metabolism in conscious dogs

2002 ◽  
Vol 282 (1) ◽  
pp. E197-E206 ◽  
Author(s):  
Fabio A. Recchia ◽  
Juan Carlos Osorio ◽  
Margaret P. Chandler ◽  
Xiaobin Xu ◽  
Ashish R. Panchal ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Glucose Oxidation ◽  
Acid Oxidation ◽  
Substrate Uptake ◽  
Substrate Metabolism ◽  
Malonyl Coa ◽  
Myocardial Substrate ◽  
Myocardial Biopsies ◽  
Chronically Instrumented Dogs

To test whether the acute reduction of nitric oxide (NO) synthesis causes changes in cardiac substrate metabolism and in the activity of key enzymes of fatty acid and glucose oxidation, we blocked NOS by giving N ω-nitro-l-arginine methyl ester (l-NAME; 35 mg/kg iv two times) to nine chronically instrumented dogs. [3H]oleate, [14C]glucose, and [13C]lactate were infused to measure the rate of cardiac substrate uptake and oxidation. Glyceraldehyde-3-phosphate dehydrogenase, acetyl-CoA carboxylase, and malonyl-CoA decarboxylase activities were measured in myocardial biopsies. In eight control dogs, ANG II was infused (20–40 ng · kg−1 · min−1) to mimic the hemodynamic effects of l-NAME. Afterl-NAME, significant changes occurred for fatty acid oxidation (from 9.8 ± 0.8 to 7.1 ± 1.2 μmol/min), glucose uptake (from 12.9 ± 5.5 to 45.0 ± 14.2 μmol/min), and oxidation (from 4.4 ± 1.2 to 19.9 ± 2.3 μmol/min). ANG caused only a significantly lower increase in glucose oxidation. Lactate uptake increased by more than twofold in both groups. The enzyme activities did not differ significantly between the two groups. In conclusion, the acute inhibition of NO synthesis causes marked metabolic alterations that do not involve key rate-controlling enzymes of fatty acid oxidation nor glyceraldehyde-3-phosphate dehydrogenase.

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