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Antioxidant Supplements and Exercise Adaptations
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Shaun A. Mason, Lewan Parker, Adam J. Trewin, Glenn D. Wadley
Elevated cellular concentrations of ROS/RNS may impair selective redox-sensitive pathways of energy metabolism. For instance, hydrogen peroxide (H2O2) and peroxynitrite (ONOO–) can inhibit glyceraldehyde 3-phosphate dehydrogenase (GAPDH) activity by reacting directly with the active site thiol, thus potentially impairing glycolysis (Quijano et al., 2016). Further, ROS can impair activity of the enzyme aconitase by releasing an Fe atom from an Fe-S cluster that functions as a Lewis acid during catalysis in the tricarboxylic acid cycle, potentially diminishing the supply of reducing agents to the electron transport chain and thus diminishing the rate of ROS production (Quijano et al., 2016). Elevated ROS and RNS may also reduce beta-oxidation efficiency through the generation of nitro-fatty acids that can undergo beta-oxidation in the mitochondria (Quijano et al., 2016). Despite the known interplay between oxidants and energy metabolism, effects of elevated ROS/RNS on these pathways of energy metabolism during exercise are unclear. Moreover, effects of antioxidants on energy metabolism pathways have been scarcely explored in the context of acute exercise or exercise training adaptations. Effects of exogenous antioxidants on substrate metabolism are likely complex and will depend on the specific antioxidant compound, its bioavailability, and dosing regimen administered.
Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
Energy metabolism is an involved thermodynamic system integrating the interaction of physiological and biochemical components, the metabolic characteristics of metabolism (especially of carbohydrates and fats), and also regulatory hormonal relations.
New Understanding of the Nature and Causes of Major Depression
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
Some of the increases in oxidative and nitrosative stress in MDD may result from genetic predisposition. For example, associations have been made between depression and certain polymorphisms in genes affecting the enzymatic activities of manganese superoxide dismutase and catalase.5 Some, but not all, researchers have seen decreases in the activity of antioxidant enzymes, such as glutathione peroxidase, during episodes of depression.6 Severe chronic or repeated psychological stress increase blood levels of oxidation biomarkers, and these changes correspond to increases in salivary cortisol.7 Metabolic Syndrome is also associated with oxidative stress, due in part to disturbances in energy metabolism.8 Inflammatory conditions cause oxidative and nitrosative damage and, in turn, debris from cells damaged by oxidative stress stimulates TLR4 receptors that initiate the inflammatory cascade.9
The reliability and validity of the perceive, recall, plan and perform assessment in children with a mitochondrial disorder
Published in Disability and Rehabilitation, 2023
Marieke Lindenschot, Saskia Koene, Melissa T. Nott, Maria W. G. Nijhuis-van der Sanden, Imelda J. M. de Groot, Esther M. J. Steultjens, Maud J. L. Graff
Mitochondrial disorders are rare diseases that influence cellular energy metabolism. These disorders are one of the most common inherited errors of metabolism that can be caused by mutations in more than 230 different genes [1,2]. This genetic heterogeneity is also reflected in the large range of symptoms and impairments associated with mitochondrial disorders, varying from motor impairments (such as muscle weakness or balance problems) to cognitive impairments (such as concentration problems and intellectual disability) [3–6]. These impairments have a tremendous impact on daily functioning and influence participation in school, leisure activities, the neighborhood, and the community [6]. It is a challenge for clinicians to assess the functioning of children with mitochondrial disorders with ‘standardized’ assessments due to the heterogenicity of the population.
Interaction of bone and brain: osteocalcin and cognition
Published in International Journal of Neuroscience, 2021
Misa Nakamura, Masakazu Imaoka, Masatoshi Takeda
The positive effect of improving cognitive function can generally be recognized in exercise interventions conducted for healthy older people and those with MCI [52–56], and moderate exercise is particularly effective for dementia prevention [57]. Exercise may have a positive impact on cognition by improving vascular risk factors [58] and cerebral blood flow [59]. It has also been reported that exercise increases hippocampal volume [60]. Obesity, hypertension, hypercholesterolemia, hyperhomocysteinemia, and insulin resistance are all risk factors for potentially modifiable vascular disease via physical activity [61]. Among these factors, it has been reported that improved insulin resistance may increase synaptic plasticity and energy metabolism directly [62]. Exercise also increases mitochondrial production in neurons [63], thereby enhancing energy metabolism in the brain and ensuring the delivery of energy to the neurons. Exercise has also been reported to promote the expression of genes that regulate the production of free radical scavenging enzymes; this could help prevent free radical damage to neurons and neurodegenerative diseases [64,65]. In addition, it is thought that the myokines, BDNF, insulin-like growth factors, and vascular endothelial growth factors induced by exercise contributes to the prevention of cognitive decline. In other words, these humoral factors that proliferate as a result of exercise are thought to increase neurogenesis, angiogenesis, synaptic plasticity, and dendritic spine density in the hippocampus, thereby contribute to the maintenance and improvement of cognitive function [66].
Pathological mechanisms of abnormal iron metabolism and mitochondrial dysfunction in systemic lupus erythematosus
Published in Expert Review of Clinical Immunology, 2021
Chris Wincup, Natalie Sawford, Anisur Rahman
In conclusion, iron homeostasis is maintained by a variety of tightly regulated physiological processes. However, patients with SLE may ultimately be at risk of cellular iron deficiency due to either increased rates of absolute iron deficiency [a fundamental lack of iron within the body], or via a state of functional iron deficiency [whereby elevated levels of proinflammatory cytokines impair iron transport and prevent the release of iron from stores]. This has a number of wide-ranging consequences as iron is an essential nutrient for numerous essential cellular processes. This includes DNA synthesis, enzyme activity and, importantly, energy metabolism. Within the immune system, iron deficiency has been demonstrated to impair priming to vaccine response, whilst iron supplementation has been shown to increase the risk of infection through enabling bacterial proliferation.