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      Exercise Physiology [Working Title] 

      From Exercise Physiology to Network Physiology of Exercise

      edited-book
      , , ,
      IntechOpen

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          Abstract

          Exercise physiology (EP) and its main research directions, strongly influenced by reductionism from its origins, have progressively evolved toward Biochemistry, Molecular Biology, Genetics, and OMICS technologies. Although these technologies may be based on dynamic approaches, the dominant research methodology in EP, and recent specialties such as Molecular Exercise Physiology and Integrative Exercise Physiology, keep focused on non-dynamical bottom-up statistical inference techniques. Inspired by the new field of Network Physiology and Complex Systems Science, Network Physiology of Exercise emerges to transform the theoretical assumptions, the research program, and the practical applications of EP, with relevant consequences on health status, exercise, and sport performance. Through an interdisciplinary work with diverse disciplines such as bioinformatics, data science, applied mathematics, statistical physics, complex systems science, and nonlinear dynamics, Network Physiology of Exercise focuses the research efforts on improving the understanding of different exercise-related phenomena studying the nested dynamics of the vertical and horizontal physiological network interactions. After reviewing the EP evolution during the last decades and discussing their main theoretical and methodological limitations from the lens of Complex Networks Science, we explain the potential impact of the emerging field of Network Physiology of Exercise and the most relevant data analysis techniques and evaluation tools used until now.

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          Network biology: understanding the cell's functional organization.

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            Epigenetic plasticity and the hallmarks of cancer

            Chromatin and associated epigenetic mechanisms stabilize gene expression and cellular states while also facilitating appropriate responses to developmental or environmental cues. Genetic, environmental, or metabolic insults can induce overly restrictive or overly permissive epigenetic landscapes that contribute to pathogenesis of cancer and other diseases. Restrictive chromatin states may prevent appropriate induction of tumor suppressor programs or block differentiation. By contrast, permissive or "plastic" states may allow stochastic oncogene activation or nonphysiologic cell fate transitions. Whereas many stochastic events will be inconsequential "passengers," some will confer a fitness advantage to a cell and be selected as "drivers." We review the broad roles played by epigenetic aberrations in tumor initiation and evolution and their potential to give rise to all classic hallmarks of cancer.
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              Muscle as an endocrine organ: focus on muscle-derived interleukin-6.

              Skeletal muscle has recently been identified as an endocrine organ. It has, therefore, been suggested that cytokines and other peptides that are produced, expressed, and released by muscle fibers and exert paracrine, autocrine, or endocrine effects should be classified as "myokines." Recent research demonstrates that skeletal muscles can produce and express cytokines belonging to distinctly different families. However, the first identified and most studied myokine is the gp130 receptor cytokine interleukin-6 (IL-6). IL-6 was discovered as a myokine because of the observation that it increases up to 100-fold in the circulation during physical exercise. Identification of IL-6 production by skeletal muscle during physical activity generated renewed interest in the metabolic role of IL-6 because it created a paradox. On one hand, IL-6 is markedly produced and released in the postexercise period when insulin action is enhanced but, on the other hand, IL-6 has been associated with obesity and reduced insulin action. This review focuses on the myokine IL-6, its regulation by exercise, its signaling pathways in skeletal muscle, and its role in metabolism in both health and disease.
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                Author and book information

                Book Chapter
                November 30 2022
                10.5772/intechopen.102756
                9cc6f4a5-6d05-4a04-852a-838bd652bbd0
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