Exercise Metabolism in Health and Disease

Philippou, Αnastassios; Chryssanthopοulos, Costas; Maridaki, Maria; Dimitriadis, George; Koutsilieris, Michael

doi:10.1007/978-3-030-04816-7_5

Cited by 10 publications

(8 citation statements)

References 270 publications

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“…In accordance with previous literature [38], AA catabolism was activated as an alternative means of producing energy during the marathon (Figure 2). This is supported by a reduction in concentrations of AAs (leucine, isoleucine, valine, lysine, and proline) and the elevation of the various observed serum AA catabolism intermediates (3-methyl-2oxovaleric acid and 3-hydroxyisobutyric acid).…”

Section: Discussionsupporting

confidence: 91%

Characterizing Marathon-Induced Metabolic Changes Using 1H-NMR Metabolomics

et al. 2021

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Although physical activity is a health-promoting, popular global pastime, regular engagement in strenuous exercises, such as long-distance endurance running races, has been associated with a variety of detrimental physiological and immunological health effects. The resulting altered physiological state has previously been associated with fluctuations in various key metabolite concentrations; however, limited literature exists pertaining to the global/holistic metabolic changes that are induced by such. This investigation subsequently aims at elucidating the metabolic changes induced by a marathon by employing an untargeted proton nuclear magnetic resonance (1H-NMR) spectrometry metabolomics approach. A principal component analysis (PCA) plot revealed a natural differentiation between pre- and post-marathon metabolic profiles of the 30-athlete cohort, where 17 metabolite fluctuations were deemed to be statistically significant. These included reduced concentrations of various amino acids (AA) along with elevated concentrations of ketone bodies, glycolysis, tricarboxylic acid (TCA) cycle, and AA catabolism intermediates. Moreover, elevated concentrations of creatinine and creatine in the post-marathon group supports previous findings of marathon-induced muscle damage. Collectively, the results of this investigation characterize the strenuous metabolic load induced by a marathon and the consequential regulation of main energy-producing pathways to accommodate this, and a better description of the cause of the physiological changes seen after the completion of a marathon.

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Section: Discussionsupporting

confidence: 91%

Characterizing Marathon-Induced Metabolic Changes Using 1H-NMR Metabolomics

et al. 2021

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“…Kahn et al [300] provided experimental support to this hypothesis showing that the β-cells and insulin sensitive tissues interact in a tightly regulated manner: when insulin sensitivity is high, insulin release is low and vice versa. Within this context, lifestyle interventions, such as optimal regulation of body weight and increased physical activity/exercise, are important to improve the sensitivity of tissues to insulin, and hence avoid marked hyperglycemia and hyperinsulinemia under fasting or postprandial conditions [301][302][303][304][305].…”

Section: The Importance Of Insulin Sensitivitymentioning

confidence: 99%

Regulation of Postabsorptive and Postprandial Glucose Metabolism by Insulin-Dependent and Insulin-Independent Mechanisms: An Integrative Approach

et al. 2021

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Glucose levels in blood must be constantly maintained within a tight physiological range to sustain anabolism. Insulin regulates glucose homeostasis via its effects on glucose production from the liver and kidneys and glucose disposal in peripheral tissues (mainly skeletal muscle). Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. After meals, several mechanisms (sequence/composition of meals, gastric emptying/intestinal glucose absorption, gastrointestinal hormones, hyperglycemia mass action effects, insulin/glucagon secretion/action, de novo lipogenesis and glucose disposal) operate in concert for optimal regulation of postprandial glucose fluctuations. The contribution of the liver in postprandial glucose homeostasis is critical. The liver is preferentially used to dispose over 50% of the ingested glucose and restrict the acute increases of glucose and insulin in the bloodstream after meals, thus protecting the circulation and tissues from the adverse effects of marked hyperglycemia and hyperinsulinemia.

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“…With exercise, not only skeletal muscle but also all other organs are modulated. It has therapeutic effects on conditions such as autoimmune and neurodegenerative diseases, and cancer with multiple molecular events and adaptations, as well as increasing the power of oxygen use with exercise, increased attenuation corrected perfusion, changes in muscles, and functional capacity and performance 5,6 .…”

Section: Introductionmentioning

confidence: 99%