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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Exercise also promotes neovascularization in skeletal muscle. Exercise-induced angiogenesis is a physiological process, in contrast to most post-development angiogenesis (e.g., neoplasms, retinal diseases). Exercise also remains the most efficacious intervention for peripheral artery disease. Understanding exercise-induced angiogenesis could thus inform novel approaches for the treatment of peripheral artery disease. Until recently, the prevailing paradigm had been that metabolic demands created by exercising muscle cause a supply/demand mismatch, leading to activation of ischemic sensors like AMPK and HIF-1α. Recent data with genetically modified mice, however, do not support this notion. Mice lacking AMPK activity in skeletal muscle have intact exercise-induced angiogenesis,181 and mice lacking HIF-1α in skeletal muscle have more, rather than fewer microvessels.182 On the other hand, mice lacking PGC-1α in skeletal muscle lack the capacity for exercise-induced angiogenesis183 (although, interestingly, not for exercise-induced mitochondrial biogenesis).184,185 Conversely, mice transgenitically overexpressing PGC-1 in skeletal muscle have dramatic increases in microvascular density and are protected in a hind limb ischemia model of peripheral artery disease. Β-Adrenergic and other signals induce PGC-1α in skeletal muscle, and PGC-1α directly activates the expression of VE growth factor, a canonical angiogenic factor, in an HIF-independent fashion.186 Physiological angiogenesis in muscle is thus likely triggered more preemptively by nerve activity than reactively by ischemia.
Higher sirt1 is associated with a better body composition in master sprinters and untrained peers
Published in European Journal of Sport Science, 2023
Patrício Lopes de Araújo Leite, Larissa Alves Maciel, Patrick Anderson Santos, Lucas Pinheiro Barbosa, Sara Duarte Gutierrez, Hugo de Luca Corrêa, Lysleine Alves de Deus, Marcia Cristina Araújo, Samuel da Silva Aguiar, Thiago dos Santos Rosa, John E. Lewis, Herbert Gustavo Simões
Another important finding of the current study was that MS showed attenuation of the usual age-related decline in Sirt1. Lifelong exercise seems to preserve Sirt1 for master athletes, which in turn may be related to attenuated biological aging, given that telomere length is maintained in this population (Aguiar et al., 2021; Simoes et al., 2017). Other studies have shown the importance of exercise training in increasing circulating levels of Sirt (Aguiar et al., 2022; Pucci et al., 2013; Vargas-Ortiz et al., 2019). Some mechanisms have been proposed to explain the activation of Sirt through exercise. Exercise training depends on a continuous supply of energy for muscle performance, which can be provided through increased levels of NAD+, leading to the activation of the deacetylation mechanism of Sirt1. This last process may in turn lead to mitochondrial biogenesis and improved oxidative capacity through the pathway of PGC-1α. Thus, increased NAD may be pivotal (Pucci et al., 2013; Vargas-Ortiz et al., 2019).
Biochanin A prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced adipocyte dysfunction in cultured 3T3-L1 cells
Published in Journal of Environmental Science and Health, Part A, 2019
Eun Mi Choi, Kwang Sik Suh, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Suk Chon
Adipocyte browning is an attractive therapeutic target against metabolic disorders. The brown adipocyte-like phenotype appears in white adipocytes upon exposure to physiological stimuli.[35] Various pharmacological and dietary compounds induce the brown adipocyte-like phenotype, marked by an increase in thermogenesis.[36] One of the characteristics of beige adipocyte tissue is enhanced mitochondrial biogenesis.[37] PGC-1α, the main regulator of mitochondrial biogenesis, positively regulates catabolic metabolism, and is abundantly expressed in oxidative tissues, such as brown adipose tissue, muscle, and liver.[38] Ectopic expression of PGC-1α in white adipocytes induces the brite phenotype.[39] The present study showed that biochanin A increased the level of PGC-1α in adipocytes in the presence of TCDD, suggesting that biochanin A induces the brite phenotype by increasing the key brown adipocyte-specific marker PGC-1α. Therefore, the increase of PGC-1α in response to biochanin A was probably related to upregulated energy metabolism in mitochondria.
Applications of omega-3 polyunsaturated fatty acid supplementation for sport performance
Published in Research in Sports Medicine, 2019
Jordan D. Philpott, Oliver C. Witard, Stuart D.R. Galloway
An important aspect of endurance exercise performance and training adaptation is the capacity to utilize substrates efficiently and maximise available energy from adenosine triphosphate (ATP) stores. The mitochondrial content of the cell aids regulation of ATP resynthesis. A key regulator of mitochondrial biogenesis, defined as the process of increasing mitochondrial volume, is Peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α). Previous studies in rodents have shown dietary n-3PUFA supplementation to increase expression of PGC-1α (Hancock et al., 2008) and increase mitochondrial biogenesis (Turner et al., 2007). However, studies investigating n-3PUFA supplementation and mitochondrial biogenesis in humans are limited. Currently, only one study has examined mitochondrial biogenesis with n-3PUFA supplementation and reported that EPA supplementation stimulated mitochondrial biogenesis in obese individuals (Laiglesia et al., 2016). Based on findings from animal studies, it is possible that n-3PUFA supplementation may increase mitochondrial biogenesis leading to improved endurance performance as mediated via the PGC-1α pathway. However, human studies in athletes are warranted in order to examine this theory.