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      Exercise Fat Oxidation Is Positively Associated with Body Fatness in Men with Obesity: Defying the Metabolic Flexibility Paradigm

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          Abstract

          Obesity is thought to be associated with a reduced capacity to increase fat oxidation in response to physical exercise; however, scientific evidence supporting this paradigm remains scarce. This study aimed to determine the interrelationship of different submaximal exercise metabolic flexibility (Metflex) markers and define its association with body fatness on subjects with obesity. Twenty-one male subjects with obesity performed a graded-intensity exercise protocol (Test 1) during which cardiorespiratory fitness (CRF), maximal fat oxidation (MFO) and its corresponding exercise intensity (FATmax) were recorded. A week afterward, each subject performed a 60-min walk (treadmill) at FATmax (Test 2), and the resulting fat oxidation area under the curve (TFO) and maximum respiratory exchange ratio (RER peak) were recorded. Blood lactate (LA b) levels was measured during both exercise protocols. Linear regression analysis was used to study the interrelationship of exercise Metflex markers. Pearson’s correlation was used to evaluate all possible linear relationships between Metflex and anthropometric measurement, controlling for CRF). The MFO explained 38% and 46% of RER peak and TFO’s associated variance ( p < 0.01) while TFO and RER peak were inversely related ( R 2 = 0.54, p < 0.01). Body fatness positively correlated with MFO ( r = 0.64, p < 0.01) and TFO ( r = 0.63, p < 0.01) but inversely related with RER peak ( r = −0.67, p < 0.01). This study shows that MFO and RER peak are valid indicators of TFO during steady-state exercise at FATmax. The fat oxidation capacity is directly associated with body fatness in males with obesity.

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              Mechanisms for insulin resistance: common threads and missing links.

              Insulin resistance is a complex metabolic disorder that defies explanation by a single etiological pathway. Accumulation of ectopic lipid metabolites, activation of the unfolded protein response (UPR) pathway, and innate immune pathways have all been implicated in the pathogenesis of insulin resistance. However, these pathways are also closely linked to changes in fatty acid uptake, lipogenesis, and energy expenditure that can impact ectopic lipid deposition. Ultimately, these cellular changes may converge to promote the accumulation of specific lipid metabolites (diacylglycerols and/or ceramides) in liver and skeletal muscle, a common final pathway leading to impaired insulin signaling and insulin resistance. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                29 June 2021
                July 2021
                : 18
                : 13
                : 6945
                Affiliations
                [1 ]Chemical Biological Sciences PhD Graduate Program, Department of Chemical Sciences, Biomedical Sciences Institute, Ciudad Juarez Autonomous University, Chihuahua 32310, Mexico; isaac.chavez@ 123456uacj.mx (I.A.C.-G.); awall@ 123456uacj.mx (A.W.-M.); alberto.perez@ 123456uacj.mx (J.A.P.-L.)
                [2 ]Faculty of Physical Culture Sciences, Autonomous University of Chihuahua, Chihuahua 31000, Mexico; rhernant@ 123456uach.mx
                [3 ]Faculty of Sports, Autonomous University of Baja California, Mexicali, Baja California 21289, Mexico; marina.trejo@ 123456uabc.edu.mx
                [4 ]Faculty of Medicine and Biomedical Sciences, Autonomous University of Chihuahua, Circuito Universitario, Campus II, Chihuahua 31109, Mexico; evegonzal@ 123456uach.mx (E.G.-R.); vmoreno@ 123456uach.mx (V.M.-B.)
                Author notes
                [* ]Correspondence: aramos@ 123456uacj.mx ; Tel.: +52-656-167-9309
                Author information
                https://orcid.org/0000-0001-9773-5043
                https://orcid.org/0000-0003-1772-5836
                https://orcid.org/0000-0003-0401-0073
                https://orcid.org/0000-0002-6196-3607
                https://orcid.org/0000-0002-9148-2054
                https://orcid.org/0000-0002-4347-6725
                Article
                ijerph-18-06945
                10.3390/ijerph18136945
                8297250
                34209545
                4f8542ba-80e9-4f3b-b498-edcb653b7150
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                : 03 June 2021
                : 25 June 2021
                Categories
                Article

                Public health
                energy metabolism,indirect calorimetry,physical exercise,antiobesity agents,aerobic exercise

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