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Artykuły w czasopismach na temat "Muscle-brain axis"
1
Sikiric, Predrag, Slaven Gojkovic, Ivan Krezic, Ivan Maria Smoday, Luka Kalogjera, Helena Zizek, Katarina Oroz i in. "Stable Gastric Pentadecapeptide BPC 157 May Recover Brain–Gut Axis and Gut–Brain Axis Function". Pharmaceuticals 16, nr 5 (30.04.2023): 676. http://dx.doi.org/10.3390/ph16050676.
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Conceptually, a wide beneficial effect, both peripherally and centrally, might have been essential for the harmony of brain–gut and gut–brain axes’ function. Seen from the original viewpoint of the gut peptides’ significance and brain relation, the favorable stable gastric pentadecapeptide BPC 157 evidence in the brain–gut and gut–brain axes’ function might have been presented as a particular interconnected network. These were the behavioral findings (interaction with main systems, anxiolytic, anticonvulsive, antidepressant effect, counteracted catalepsy, and positive and negative schizophrenia symptoms models). Muscle healing and function recovery appeared as the therapeutic effects of BPC 157 on the various muscle disabilities of a multitude of causes, both peripheral and central. Heart failure was counteracted (including arrhythmias and thrombosis), and smooth muscle function recovered. These existed as a multimodal muscle axis impact on muscle function and healing as a function of the brain–gut axis and gut–brain axis as whole. Finally, encephalopathies, acting simultaneously in both the periphery and central nervous system, BPC 157 counteracted stomach and liver lesions and various encephalopathies in NSAIDs and insulin rats. BPC 157 therapy by rapidly activated collateral pathways counteracted the vascular and multiorgan failure concomitant to major vessel occlusion and, similar to noxious procedures, reversed initiated multicausal noxious circuit of the occlusion/occlusion-like syndrome. Severe intracranial (superior sagittal sinus) hypertension, portal and caval hypertensions, and aortal hypotension were attenuated/eliminated. Counteracted were the severe lesions in the brain, lungs, liver, kidney, and gastrointestinal tract. In particular, progressing thrombosis, both peripherally and centrally, and heart arrhythmias and infarction that would consistently occur were fully counteracted and/or almost annihilated. To conclude, we suggest further BPC 157 therapy applications.
2
Sanjay Kalra, Saurabh Arora i Nitin Kapoor. "The Mood-Muscle Meta Bridge (Brain Muscle Axis)". Journal of the Pakistan Medical Association 74, nr 4 (11.02.2024): 589–90. http://dx.doi.org/10.47391/jpma.24-16.
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Psychological well-being is essential for the maintenance of good metabolic health. Modern management of most chronic metabolic disorders rightly focusses on improving the health-related quality of life of persons living with disease. In this brief communication we describe the bidirectional association between muscle function and mood (psychological health), explore the various pathways that link these aspects of health, and underscore their clinical implications. This paper emphasizes the importance of maintaining good mental health through exercise and vice a versa.
Keywords: Muscle function, muscle strength, sarcopenia, dysthymia, depression, physical activity.
3
Burtscher, Johannes, Grégoire P. Millet, Nicolas Place, Bengt Kayser i Nadège Zanou. "The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection". International Journal of Molecular Sciences 22, nr 12 (17.06.2021): 6479. http://dx.doi.org/10.3390/ijms22126479.
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Regular exercise is associated with pronounced health benefits. The molecular processes involved in physiological adaptations to exercise are best understood in skeletal muscle. Enhanced mitochondrial functions in muscle are central to exercise-induced adaptations. However, regular exercise also benefits the brain and is a major protective factor against neurodegenerative diseases, such as the most common age-related form of dementia, Alzheimer’s disease, or the most common neurodegenerative motor disorder, Parkinson’s disease. While there is evidence that exercise induces signalling from skeletal muscle to the brain, the mechanistic understanding of the crosstalk along the muscle–brain axis is incompletely understood. Mitochondria in both organs, however, seem to be central players. Here, we provide an overview on the central role of mitochondria in exercise-induced communication routes from muscle to the brain. These routes include circulating factors, such as myokines, the release of which often depends on mitochondria, and possibly direct mitochondrial transfer. On this basis, we examine the reported effects of different modes of exercise on mitochondrial features and highlight their expected benefits with regard to neurodegeneration prevention or mitigation. In addition, knowledge gaps in our current understanding related to the muscle–brain axis in neurodegenerative diseases are outlined.
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Arosio, Beatrice, Riccardo Calvani, Evelyn Ferri, Hélio José Coelho-Junior, Angelica Carandina, Federica Campanelli, Veronica Ghiglieri, Emanuele Marzetti i Anna Picca. "Sarcopenia and Cognitive Decline in Older Adults: Targeting the Muscle–Brain Axis". Nutrients 15, nr 8 (12.04.2023): 1853. http://dx.doi.org/10.3390/nu15081853.
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Declines in physical performance and cognition are commonly observed in older adults. The geroscience paradigm posits that a set of processes and pathways shared among age-associated conditions may also serve as a molecular explanation for the complex pathophysiology of physical frailty, sarcopenia, and cognitive decline. Mitochondrial dysfunction, inflammation, metabolic alterations, declines in cellular stemness, and altered intracellular signaling have been observed in muscle aging. Neurological factors have also been included among the determinants of sarcopenia. Neuromuscular junctions (NMJs) are synapses bridging nervous and skeletal muscle systems with a relevant role in age-related musculoskeletal derangement. Patterns of circulating metabolic and neurotrophic factors have been associated with physical frailty and sarcopenia. These factors are mostly related to disarrangements in protein-to-energy conversion as well as reduced calorie and protein intake to sustain muscle mass. A link between sarcopenia and cognitive decline in older adults has also been described with a possible role for muscle-derived mediators (i.e., myokines) in mediating muscle–brain crosstalk. Herein, we discuss the main molecular mechanisms and factors involved in the muscle–brain axis and their possible implication in cognitive decline in older adults. An overview of current behavioral strategies that allegedly act on the muscle–brain axis is also provided.
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Przewłócka, Katarzyna, Daria Korewo-Labelle, Paweł Berezka, Mateusz Jakub Karnia i Jan Jacek Kaczor. "Current Aspects of Selected Factors to Modulate Brain Health and Sports Performance in Athletes". Nutrients 16, nr 12 (12.06.2024): 1842. http://dx.doi.org/10.3390/nu16121842.
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This review offers a comprehensive evaluation of current aspects related to nutritional strategies, brain modulation, and muscle recovery, focusing on their applications and the underlying mechanisms of physiological adaptation for promoting a healthy brain, not only in athletes but also for recreationally active and inactive individuals. We propose that applying the rule, among others, of good sleep, regular exercise, and a properly balanced diet, defined as “SPARKS”, will have a beneficial effect on the function and regeneration processes of the gut–brain–muscle axis. However, adopting the formula, among others, of poor sleep, stress, overtraining, and dysbiosis, defined as “SMOULDER”, will have a detrimental impact on the function of this axis and consequently on human health as well as on athletes. Understanding these dynamics is crucial for optimizing brain health and cognitive function. This review highlights the significance of these factors for overall well-being, suggesting that adopting the “SPARKS” approach may benefit not only athletes but also older adults and individuals with health conditions.
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Saponaro, Federica, Andrea Bertolini, Riccardo Baragatti, Leonardo Galfo, Grazia Chiellini, Alessandro Saba i Giuseppina D’Urso. "Myokines and Microbiota: New Perspectives in the Endocrine Muscle–Gut Axis". Nutrients 16, nr 23 (25.11.2024): 4032. http://dx.doi.org/10.3390/nu16234032.
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This review explores the dual role of skeletal muscle as both a mechanical and endocrine organ, highlighting its contributions to overall health and its adaptability to various inputs such as nutrition, hormones, exercise, and injuries. In addition to its role in metabolism and energy conversion, skeletal muscle secretes signalling molecules called myokines (at rest) and exerkines (during/after physical exercise), which communicate with other organs like the brain, the cardiovascular system, and the immune system. Key molecules such as interleukins, irisin, and myostatin are discussed for their roles in mediating muscle health and inter-organ communication. This work also focuses on the muscle–gut axis, emphasising the bidirectional interaction between skeletal muscle and the gut microbiota, a complex ecosystem influencing immune defence, digestion, and metabolism. Muscle activity, particularly exercise, alters the gut microbial composition, promoting beneficial species, while gut-derived metabolites like short-chain fatty acids (SCFAs) impact muscle metabolism, mitochondrial function, and insulin sensitivity. Dysbiosis, or an imbalanced microbiota, can lead to muscle atrophy, inflammation, and metabolic dysfunction. This evidence highlights emerging research into myokines and exerkines as potential therapeutic targets for managing conditions like muscle decline, ageing, and metabolic diseases through muscle–gut interactions.
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Liu, Tingting, Haojie Wu, Jingwen Li, Chaoyang Zhu i Jianshe Wei. "Unraveling the Bone–Brain Axis: A New Frontier in Parkinson’s Disease Research". International Journal of Molecular Sciences 25, nr 23 (29.11.2024): 12842. http://dx.doi.org/10.3390/ijms252312842.
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Parkinson’s disease (PD), as a widespread neurodegenerative disorder, significantly impacts patients’ quality of life. Its primary symptoms include motor disturbances, tremor, muscle stiffness, and balance disorders. In recent years, with the advancement of research, the concept of the bone–brain axis has gradually become a focal point in the field of PD research. The bone–brain axis refers to the interactions and connections between the skeletal system and the central nervous system (CNS), playing a crucial role in the pathogenesis and pathological processes of PD. The purpose of this review is to comprehensively and deeply explore the bone–brain axis in PD, covering various aspects such as the complex relationship between bone metabolism and PD, the key roles of neurotransmitters and hormones in the bone–brain axis, the role of inflammation and immunity, microRNA (miRNA) functional regulation, and potential therapeutic strategies. Through a comprehensive analysis and in-depth discussion of numerous research findings, this review aims to provide a solid theoretical foundation for a deeper understanding of the pathogenesis of PD and to offer strong support for the development of new treatment methods.
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Cutuli, Debora, Davide Decandia, Giacomo Giacovazzo i Roberto Coccurello. "Physical Exercise as Disease-Modifying Alternative against Alzheimer’s Disease: A Gut–Muscle–Brain Partnership". International Journal of Molecular Sciences 24, nr 19 (28.09.2023): 14686. http://dx.doi.org/10.3390/ijms241914686.
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Alzheimer’s disease (AD) is a common cause of dementia characterized by neurodegenerative dysregulations, cognitive impairments, and neuropsychiatric symptoms. Physical exercise (PE) has emerged as a powerful tool for reducing chronic inflammation, improving overall health, and preventing cognitive decline. The connection between the immune system, gut microbiota (GM), and neuroinflammation highlights the role of the gut–brain axis in maintaining brain health and preventing neurodegenerative diseases. Neglected so far, PE has beneficial effects on microbial composition and diversity, thus providing the potential to alleviate neurological symptoms. There is bidirectional communication between the gut and muscle, with GM diversity modulation and short-chain fatty acid (SCFA) production affecting muscle metabolism and preservation, and muscle activity/exercise in turn inducing significant changes in GM composition, functionality, diversity, and SCFA production. This gut–muscle and muscle–gut interplay can then modulate cognition. For instance, irisin, an exercise-induced myokine, promotes neuroplasticity and cognitive function through BDNF signaling. Irisin and muscle-generated BDNF may mediate the positive effects of physical activity against some aspects of AD pathophysiology through the interaction of exercise with the gut microbial ecosystem, neural plasticity, anti-inflammatory signaling pathways, and neurogenesis. Understanding gut–muscle–brain interconnections hold promise for developing strategies to promote brain health, fight age-associated cognitive decline, and improve muscle health and longevity.
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Manti, Sara, Federica Xerra, Giulia Spoto, Ambra Butera, Eloisa Gitto, Gabriella Di Rosa i Antonio Gennaro Nicotera. "Neurotrophins: Expression of Brain–Lung Axis Development". International Journal of Molecular Sciences 24, nr 8 (11.04.2023): 7089. http://dx.doi.org/10.3390/ijms24087089.
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Neurotrophins (NTs) are a group of soluble growth factors with analogous structures and functions, identified initially as critical mediators of neuronal survival during development. Recently, the relevance of NTs has been confirmed by emerging clinical data showing that impaired NTs levels and functions are involved in the onset of neurological and pulmonary diseases. The alteration in NTs expression at the central and peripheral nervous system has been linked to neurodevelopmental disorders with an early onset and severe clinical manifestations, often named "synaptopathies" because of structural and functional synaptic plasticity abnormalities. NTs appear to be also involved in the physiology and pathophysiology of several airway diseases, neonatal lung diseases, allergic and inflammatory diseases, lung fibrosis, and even lung cancer. Moreover, they have also been detected in other peripheral tissues, including immune cells, epithelium, smooth muscle, fibroblasts, and vascular endothelium. This review aims to provide a comprehensive description of the NTs as important physiological and pathophysiological players in brain and lung development.
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Igual Gil, Carla, Bethany M. Coull, Wenke Jonas, Rachel N. Lippert, Susanne Klaus i Mario Ost. "Mitochondrial stress-induced GFRAL signaling controls diurnal food intake and anxiety-like behavior". Life Science Alliance 5, nr 11 (6.09.2022): e202201495. http://dx.doi.org/10.26508/lsa.202201495.
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Growth differentiation factor 15 (GDF15) is a mitochondrial stress-induced cytokine that modulates energy balance in an endocrine manner. However, the importance of its brainstem-restricted receptor GDNF family receptor alpha-like (GFRAL) to mediate endocrine GDF15 signaling to the brain upon mitochondrial dysfunction is still unknown. Using a mouse model with muscle-specific mitochondrial dysfunction, we here show that GFRAL is required for activation of systemic energy metabolism via daytime-restricted anorexia but not responsible for muscle wasting. We further find that muscle mitochondrial stress response involves a GFRAL-dependent induction of hypothalamic corticotropin-releasing hormone, without elevated corticosterone levels. Finally, we identify that GFRAL signaling governs an anxiety-like behavior in male mice with muscle mitochondrial dysfunction, with females showing a less robust GFRAL-dependent anxiety-like phenotype. Together, we here provide novel evidence of a mitochondrial stress-induced muscle–brain crosstalk via the GDF15-GFRAL axis to modulate food intake and anxiogenic behavior.
Rozprawy doktorskie na temat "Muscle-brain axis"
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Cao, Jingxian. "Brain-Derived Neurotrophic Factor (BDNF) as a diagnostic and prognostic biomarker in anorexia nervosa". Electronic Thesis or Diss., Université Paris Cité, 2024. http://www.theses.fr/2024UNIP5290.
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L'anorexie mentale (AM) est un trouble alimentaire complexe caractérisé par une restriction calorique sévère, une perte de poids extrême et une image corporelle déformée. Cette thèse examine le rôle du facteur neurotrophique dérivé du cerveau (BDNF) dans l'AM à travers les dimensions neurobiologiques, métaboliques et psychologiques. En utilisant un modèle animal chronique, la recherche explore comment la signalisation du BDNF interagit avec les circuits de récompense et cognitifs, ainsi que ses implications pour l'axe muscle-cerveau et le rôle des autres neurotrophines dans l'AM. Chapitre 1 aborde les dimensions neurobiologiques et métaboliques de l'AM. Il se concentre sur la façon dont les dynamiques de la signalisation du BDNF sont affectées par la restriction chronique, la réalimentation et les comportements de boulimie, spécifiquement au sein des structures cérébrales associées aux circuits de récompense et cognitifs. En utilisant un modèle animal chronique, ce chapitre explore les altérations de la signalisation du BDNF dans des régions cérébrales clés, notamment le striatum dorsal (DS), le cortex préfrontal (PFC), le noyau accumbens (NAc) et la zone tegmentale ventrale (VTA). Il examine comment ces changements affectent le traitement des récompenses, les fonctions cognitives et l'homéostasie métabolique globale dans le contexte de l'AM. Le chapitre aborde également les implications plus larges de ces résultats pour comprendre les mécanismes neurobiologiques du trouble et ses traitements. Chapitre 2 étudie les dynamiques de la signalisation du BDNF et sa relation avec les gènes impliqués dans l'axe muscle-cerveau. Ce chapitre examine comment le BDNF interagit avec les fibres musculaires rapides et lentes et explore les connexions entre les muscles et les régions cérébrales clés, notamment l'hippocampe et l'hypothalamus. La recherche met en évidence comment ces interactions influencent les processus neurobiologiques et métaboliques dans l'AM. En éclaircissant le rôle du BDNF dans la communication muscle-cerveau, ce chapitre contribue à une compréhension plus profonde des mécanismes physiologiques sous-jacents à l'AM et de leurs implications potentielles pour les stratégies thérapeutiques. Chapitre 3 explore le rôle des autres neurotrophines, spécifiquement NTF3, NTF5 et NGF, dans les régions cérébrales associées à l'AM. Ce chapitre examine comment ces neurotrophines sont régulées et leur impact sur les structures cérébrales liées à l'AM. En étudiant l'expression et la fonction de NTF3, NTF5 et NGF, la recherche fournit des éclairages sur leurs contributions aux processus neurobiologiques sous-jacents à l'AMAnorexia nervosa (AN) is a multifaceted eating disorder marked by severe caloric restriction, extreme weight loss, and distorted body image. This thesis investigates the role of brain-derived neurotrophic factor (BDNF) in AN through the lens of neurobiological, metabolic, and psychological factors. Using a chronic animal model, the research examines how BDNF signaling intersects with reward and cognitive circuits, as well as its implications for the muscle-brain axis and the role of other neurotrophins in AN. Chapter 1 delves into the neurobiological and metabolic dimensions of AN. It focuses on how BDNF signaling dynamics are affected by chronic restriction, refeeding, and binge behaviors, specifically within brain structures associated with reward and cognitive circuits. Utilizing a chronic animal model, this chapter explores alterations in BDNF signaling across key brain regions, including the dorsal striatum (DS), prefrontal cortex (PFC), nucleus accumbens (NAc), and ventral tegmental area (VTA). It examines how these changes impact reward processing, cognitive functions, and overall metabolic homeostasis in the context of AN. The chapter also addresses the broader implications of these findings for understanding the neurobiological underpinnings of the disorder and its treatment. Chapter 2 investigates the dynamics of BDNF signaling and its relationship with genes implicated in the muscle-brain axis. This chapter examines how BDNF interacts with both rapid and slow muscle fibers and explores the connections between muscle and key brain regions, including the hippocampus and hypothalamus. The research highlights how these interactions influence neurobiological and metabolic processes in AN. By elucidating the role of BDNF in muscle-brain communication, this chapter contributes to a deeper understanding of the physiological mechanisms underlying AN and their potential implications for treatment strategies. Chapter 3 explores the role of other neurotrophins, specifically NTF3, NTF5, and NGF, in brain regions associated with AN. This chapter investigates how these neurotrophins are regulated and their impact on AN-related brain structures. By examining the expression and function of NTF3, NTF5, and NGF, the research provides insights into their contributions to the neurobiological processes underlying AN
Książki na temat "Muscle-brain axis"
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
Pełny tekst źródłaStreszczenie:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
3
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
Pełny tekst źródłaStreszczenie:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
4
Kleiner, Susan M., i Maggie Greenwood-Robinson. The New Power Eating. Human Kinetics, 2019. http://dx.doi.org/10.5040/9781718214101.
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Transform your body as you build muscle, lose fat, and maximize performance with The New Power Eating. Author Susan Kleiner delivers the proven strategies she’s used with male and female professional athletes and Olympians in one practical, effective resource that gives you the know-how to reach your personal goals. In The New Power Eating, Kleiner brings together the latest scientific research on nutrition planning and explains not just what to eat but also when and how to adjust eating plans for your body and specific energy needs. Whether it’s a heavy or light training day, in peak season or off-season, you’ll learn how to achieve your physique and performance goals safely, legally, and effectively. New recipes pack a nutritional punch into every meal or snack, and sample meal plans for each meal of the day help you easily put it all together―you’ll even find a food group template to help you customize your own menus. Plus, updated details on safe supplements guide you through the maze of marketing claims to help you select the best options in view of the scientific evidence. Dr. Kleiner also walks you through how she evaluates products and brands based on testing for purity, potency, digestibility, and absorption. Based on the author’s research, you’ll also find fascinating facts that explain how your relationship with food and the gut-to-brain axis can affect your physical and emotional health and performance. Both males and females will discover gender-specific guidance and strategies to help you take advantage of your body’s benefits and overcome unhealthy triggers or habits to create and maintain an effective power eating program. Incorporate The New Power Eating into your training and find out what thousands of athletes already know: The New Power Eating is more than a book. It’s your path to power excellence.
Części książek na temat "Muscle-brain axis"
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Daneshzand, Mohammad, Lucia I. Navarro de Lara, Qinglei Meng, Sergey Makarov, Işıl Uluç, Jyrki Ahveninen, Tommi Raij i Aapo Nummenmaa. "Experimental Verification of a Computational Real-Time Neuronavigation System for Multichannel Transcranial Magnetic Stimulation". W Brain and Human Body Modelling 2021, 61–73. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15451-5_4.
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AbstractMultichannel Transcranial Magnetic Stimulation (mTMS) provides the capability of stimulating multiple cortical areas simultaneously or in rapid succession by electronic shifting of the E-field hotspots. However, in order to target the desired brain region with intended intensity, the intracranial E-field distribution for all coil elements needs to be determined and subsequently combined to electronically synthesize a ‘hot spot’. Here, we assessed the performance of a computational TMS navigation system that was used to track the position of a 2×3-axis TMS coil array with respect to subject’s head and was integrated with a real-time high-resolution E-field calculation engine to predict the activated cortical regions as the array is moved around the subject’s head. For fast evaluation of the E-fields with high-resolution head models, we employed our previously proposed Magnetic Stimulation Profile (MSP) approach. Our preliminary tests demonstrated the capability of this system to precisely calculate and render E-fields with a frame rate of 6 Hz (6 frames/second). Furthermore, we utilized two z-elements from the 3-axis coils to form a figure of eight coil type and utilized it for suprathreshold stimulation of the hand first dorsal interosseous (FDI) muscle on a healthy human. The recorded motor evoked potentials (MEPs) showed clear activation of the FDI muscle comparable to the activation elicited by a commercial TMS coil. The estimated cortical E-field distributions showed a good agreement between the commercial TMS coil and the two z-elements of the 2×3-axis array.
2
Schlegel, Petr, Michal Novotny, Blanka Klimova i Martin Valis. "“Muscle-Gut-Brain Axis”: Can Physical Activity Help Patients with Alzheimer’s Disease Due to Microbiome Modulation?" W Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220006.
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Alzheimer’s disease (AD) is one of the most common forms of dementia, which cannot be cured at the moment. Therefore, researchers also look for the alternative approaches to its treatment. It is suggested that changes in human gut microbiome mediated by exercise could influence the development and progression of AD and a new term “muscle-gut-brain axis” is introduced. There is much evidence to support this assumption. The gut microbiology is closely related to a wide range of diseases of the nervous system and therefore any negative qualitative and quantitative changes in the composition of the gut microbiota can potentially contribute to the pathophysiology of AD. Research shows that the treatment of intestinal dysbiosis with probiotics/synbiotics/eubiotics can prevent or alleviate the symptoms of these chronic neurological diseases. Studies also point to the positive effects of movement on the health of seniors. A positive correlation can be found between cognitive functions and physical stress, both in the elderly and in AD patients. Even short-term interventions with a relatively low frequency seem to produce positive results, while physical activities can be performed by using relatively simple and cost-effective means. In addition, physical activity can significantly modulate gut microbiome. Thus, it can be concluded that physical activity in humans seems to correlate with gut microbiome, which can prevent the incidence and development of AD.
3
Straub, Rainer H. "Neuroendocrine system and chronic autoimmune rheumatic diseases". W Oxford Textbook of Rheumatology, 162–71. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_004.
Pełny tekst źródłaStreszczenie:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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A. Ochola, Lucy, i Eric M. Guantai. "Prevention of Hyperglycemia". W Metformin - Pharmacology and Drug Interactions. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99342.
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Hyperglycemia is the elevation of blood glucose concentrations above the normal range. Prolonged uncontrolled hyperglycemia is associated with serious life-threatening complications. Hyperglycemia arises from an imbalance between glucose production and glucose uptake and utilization by peripheral tissues. Disorders that compromise pancreatic function or affect the glucose counter-regulatory hormones cause hyperglycemia. Acute or serious illness or injury may also bring about hyperglycemia, as can many classes of drugs. Metformin lowers blood glucose levels by inhibiting the production of glucose by the liver whilst enhancing uptake of circulating glucose and its utilization in peripheral tissues such as muscle and adipose tissue. Metformin suppresses hepatic gluconeogenesis by inhibiting mitochondrial respiration and causing a reduction of cellular ATP levels. Metformin may also modulate the gut-brain-liver axis, resulting in suppression of hepatic glucose production. Metformin also opposes the hyperglycemic action of glucagon and may ameliorate pancreatic cell dysfunction associated with hyperglycemia. Metformin is therefore recommended for use in the prevention of hyperglycemia, including drug-induced hyperglycemia, in at risk patients. The benefits of metformin in the prevention of hyperglycemia are unmatched despite its contraindications.
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Atkinson, Martin E. "Introduction and surface anatomy". W Anatomy for Dental Students. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199234462.003.0029.
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The head and neck contain the structures that are the most significant to the practice of dental surgery. These regions are not as easy to study from dissection as other areas because an ‘onion skin’ approach has to be adopted. Layers are dissected from the most superficial subcutaneous structures to the deepest internal structures, the brain, and spinal cord; structures that appear at one level may not show up again until the dissection has advanced to much deeper layers. It is important to have a general understanding of the structures forming the head and neck to build up a coherent picture of their relationship to each other. The skull is the structural basis of the head. The skull comprises the cranium, formed from 27 bones joined together by fibrous joints known as sutures, and the separate mandible that articulates with the cranium at the temporomandibular joints (TMJ). The skull houses and protects the brain in the cranial cavity. It also protects other delicate structures vital for the reception of the special senses; the orbital cavities contain the eyes and dense bones in the cranial base house the internal ears. The entrance to the respiratory tract is the bony and cartilaginous nasal cavity; it can also be accessed together with the gastrointestinal tract through the oral cavity between the cranium and mandible. The major skeletal component of the neck is the cervical part of the vertebral column formed by seven vertebrae. The lower five cervical vertebrae conform to the general pattern of vertebrae outlined in Section 10.1.1, but the upper two cervical vertebrae are specialized; the atlas articulates with the underside of the skull for nodding movements and the second vertebra, the axis, articulates with the atlas for shaking movements of the head. The hyoid bone in the upper anterior neck and the laryngeal cartilages below it form the laryngeal skeleton. There are several important muscle groups in the head. The muscles of facial expression are small superficial muscles beneath the skin of the face; they alter facial expression in response to emotion, but also play a part in chewing, swallowing, and speech.
Streszczenia konferencji na temat "Muscle-brain axis"
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Pasha, Y., S. Taylor-Robinson, R. Leech, I. Ribeiro, N. Cook, M. Crossey i H. Marcinkowski. "PWE-091 L-ornithine L-aspartate in minimal hepatic encephalopathy: possible effects on the brain-muscle axis?" W British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.233.
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Funkenstein, Bruria, i Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, marzec 2009. http://dx.doi.org/10.32747/2009.7696530.bard.
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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.
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Funkenstein, Bruria, i Cunming Duan. GH-IGF Axis in Sparus aurata: Possible Applications to Genetic Selection. United States Department of Agriculture, listopad 2000. http://dx.doi.org/10.32747/2000.7580665.bard.
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Many factors affect growth rate in fish: environmental, nutritional, genetics and endogenous (physiological) factors. Endogenous control of growth is very complex and many hormone systems are involved. Nevertheless, it is well accepted that growth hormone (GH) plays a major role in stimulating somatic growth. Although it is now clear that most, if not all, components of the GH-IGF axis exist in fish, we are still far from understanding how fish grow. In our project we used as the experimental system a marine fish, the gilthead sea bream (Sparus aurata), which inhabits lagoons along the Mediterranean and Atlantic coasts of Europe, and represents one of the most important fish species used in the mariculture industry in the Mediterranean region, including Israel. Production of Sparus is rapidly growing, however, in order for this production to stay competitive, the farming of this fish species has to intensify and become more efficient. One drawback, still, in Sparus extensive culture is that it grows relatively slow. In addition, it is now clear that growth and reproduction are physiological interrelated processes that affect each other. In particular sexual maturation (puberty) is known to be closely related to growth rate in fish as it is in mammals, indicating interactions between the somatotropic and gonadotropic axes. The goal of our project was to try to identify the rate-limiting components(s) in Sparus aurata GH-IGF system which might explain its slow growth by studying the ontogeny of growth-related genes: GH, GH receptor, IGF-I, IGF-II, IGF receptor, IGF-binding proteins (IGFBPs) and Pit-1 during early stages of development of Sparus aurata larvae from slow and fast growing lines. Our project was a continuation of a previous BARD project and could be divided into five major parts: i) obtaining additional tools to those obtained in the previous project that are necessary to carry out the developmental study; ii) the developmental expression of growth-related genes and their cellular localization; iii) tissue-specific expression and effect of GH on expression of growth-related genes; iv) possible relationship between GH gene structure, growth rate and genetic selection; v) the possible role of the IGF system in gonadal development. The major findings of our research can be summarized as follows: 1) The cDNAs (complete or partial) coding for Sparus IGFBP-2, GH receptor and Pit-1 were cloned. Sequence comparison reveals that the primary structure of IGFBP-2 protein is 43-49% identical to that of zebrafish and other vertebrates. Intensive efforts resulted in cloning a fragment of 138 nucleotides, coding for 46 amino acids in the proximal end of the intracellular domain of GH receptor. This is the first fish GH receptor cDNA that had been cloned to date. The cloned fragment will enable us to complete the GH - receptor cloning. 2) IGF-I, IGF-II, IGFBP-2, and IGF receptor transcripts were detected by RT-PCR method throughout development in unfertilized eggs, embryos, and larvae suggesting that these mRNAs are products of both the maternal and the embryonic genomes. Preliminary RT-PCR analysis suggest that GH receptor transcript is present in post-hatching larvae already on day 1. 3) IGF-1R transcripts were detected in all tissues tested by RT-PCR with highest levels in gill cartilage, skin, kidney, heart, pyloric caeca, and brain. Northern blot analysis detected IGF receptor only in gonads, brain and gill cartilage but not in muscle; GH increased slightly brain and gill cartilage IGF-1R mRNA levels. 4) IGFBP-2 transcript were detected only in liver and gonads, when analyzed by Northern blots; RT-PCR analysis revealed expression in all tissues studied, with the highest levels found in liver, skin, gonad and pyloric caeca. 5) Expression of IGF-I, IGF-II, IGF-1R and IGFBP-2 was analyzed during gonadal development. High levels of IGF-I and IGFBP-2 expression were found in bisexual young gonads, which decreased during gonadal development. Regardless of maturational stage, IGF-II levels were higher than those of IGF-L 6) The GH gene was cloned and its structure was characterized. It contains minisatellites of tandem repeats in the first and third introns that result in high level of genetic polymorphism. 7) Analysis of the presence of IGF-I and two types of IGF receptor by immunohistochemistry revealed tissue- and stage-specific expression during larval development. Immunohistochemistry also showed that IGF-I and its receptors are present in both testicular and ovarian cells. Although at this stage we are not able to pinpoint which is the rate-limiting step causing the slow growth of Sparus aurata, our project (together with the previous BARD) yielded a great number of experimental tools both DNA probes and antibodies that will enable further studies on the factors regulating growth in Sparus aurata. Our expression studies and cellular localization shed new light on the tissue and developmental expression of growth-related genes in fish.