Journal articles on the topic 'Skeletal adaption'
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Yan, Zhen. "Exercise, PGC-1α, and metabolic adaptation in skeletal muscleThis paper article is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process." Applied Physiology, Nutrition, and Metabolism 34, no. 3 (June 2009): 424–27. http://dx.doi.org/10.1139/h09-030.
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Endurance exercise promotes skeletal muscle adaptation, and exercise-induced peroxisome proliferator-activated receptor γ coactivator-1α (Pgc-1α) gene expression may play a pivotal role in the adaptive processes. Recent applications of mouse genetic models and in vivo imaging in exercise studies have started to delineate the signaling-transcription pathways that are involved in the regulation of the Pgc-1α gene. These studies revealed the importance of p38 mitogen-activated protein kinase/activating transcription factor 2 and protein kinase D/histone deacetylase 5 signaling transcription axes in exercise-induced Pgc-1α transcription and metabolic adaptation in skeletal muscle. The signaling-transcription network that is responsible for exercise-induced skeletal muscle adaption remains to be fully elucidated.
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Brugger, Daniel, and Wilhelm M. Windisch. "Adaption of body zinc pools in weaned piglets challenged with subclinical zinc deficiency." British Journal of Nutrition 121, no. 8 (January 29, 2019): 849–58. http://dx.doi.org/10.1017/s0007114519000187.
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AbstractThe effects of subclinical Zn deficiency on depletion and redistribution of body Zn were studied in weaned piglets. Forty-eight weaned piglets (German-Large-White×Land-Race×Piétrain; 50 % female, 50 % male-castrated; body weight 8·5 (sd 0·27) kg) were fed restrictively (450 g/d) a basal maize–soyabean meal-based diet supplemented with varying amounts of ZnSO4.7H2O (analysed dietary Zn: 28·1, 33·6, 38·8, 42·7, 47·5, 58·2, 67·8, 88·0 mg/kg diet) for an experimental period of 8 d. Analyses comprised Zn concentrations in soft tissues. Statistical analyses included regression models and k-means cluster analysis. Jejunum and kidney Zn correlated positively with dietary Zn (P<0·05). Other Zn pools responded in a non-linear fashion by declining (colon, epidermis, spleen) or increasing (mesenteric lymph follicles, thymus, skeletal muscle) below 63·6, 48·0, 47·5, 68·0, 43·0 and 53·1 mg Zn/kg diet, respectively (P<0·01). Above these thresholds, Zn concentrations in epidermis, mesenteric lymph follicles and skeletal muscle plateaued (P<0·0001), whereas they exhibited a decrease in colon and thymus (P<0·01) as well as a numerical increase in spleen. Clustering by dietary Zn concentration indicated clusters of varying Zn supply status and pathophysiological status. Clustering by biological matrices revealed a discrimination between storage, transport and excretion media as well as soft tissues. Taken together, novel response patterns indicated compensation reactions in tissues that are essential for the acute survival of growing animals (heart, skeletal muscle, immune tissues). Furthermore, this is to our knowledge the first study that mapped the gross Zn requirement by clustering tissue Zn concentrations between treatment groups.
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Minari, André Luis Araujo, Felipe Avila, Lila Missae Oyama, and Ronaldo Vagner Thomatieli-Santos. "Skeletal muscles induce recruitment of Ly6C+ macrophage subtypes and release inflammatory cytokines 3 days after downhill exercise." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 317, no. 4 (October 1, 2019): R597—R605. http://dx.doi.org/10.1152/ajpregu.00163.2019.
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Macrophages are one of the most versatile cells of the immune system that can express distinct subtypes and functions depending on the physiological challenge. After skeletal muscle damage, inflammatory macrophage subtypes aid muscles to regenerate and are implicated in physical training adaption. Based on this information, this study aimed to evaluate two classic mice macrophage subtypes and determine whether some inflammatory cytokines might be involved in the muscle adaption process after exercise. For this purpose, mice were exposed to an intermittent experimental protocol of downhill exercise (18 bouts of running, each bout 5 min with a 2-min rest interval, slope −16°) and were euthanized before [control (CTRL)] and 1, 2 (D2), and 3 (D3) days after exercise. After euthanasia, the triceps brachii was harvested and submitted to protein extraction, immunostaining, and mononuclear digestion procedures. The muscle size, macrophage accumulation, and cytokines were determined. We observed an increase in the Ly6C+ macrophage subtype ( P ≤ 0.05) in D2 and D3 compared with CTRL, as well as a significant inverse correlation coefficient (−0.52; P ≤ 0.05) between Ly6C+ and Ly6C− macrophage subtypes. Moreover, we also observed elevation in several cytokines (IL-1β, IFN-γ, TNF-α, IL-6, and IL-13) at D3, although not IL-4, which tended to decrease at this time point ( P = 0.06). Downhill exercises preferentially recruited Ly6C+ macrophages with important proinflammatory cytokine elevation at D3. Moreover, despite the elevation of several cytokines involved with myogenesis, an increase in IL-6 and IL-13, which potentially involve muscle adaption training after acute exercise, was also observed.
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Feng, Han-Zhong, Min Chen, Lee S. Weinstein, and J. P. Jin. "Improved fatigue resistance in Gsα-deficient and aging mouse skeletal muscles due to adaptive increases in slow fibers." Journal of Applied Physiology 111, no. 3 (September 2011): 834–43. http://dx.doi.org/10.1152/japplphysiol.00031.2011.
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Genetically modified mice with deficiency of the G protein α-subunit (Gsα) in skeletal muscle showed metabolic abnormality with reduced glucose tolerance, low muscle mass, and low contractile force, along with a fast-to-slow-fiber-type switch (Chen M, Feng HZ, Gupta D, Kelleher J, Dickerson KE, Wang J, Hunt D, Jou W, Gavrilova O, Jin JP, Weinstein LS. Am J Physiol Cell Physiol 296: C930–C940, 2009). Here we investigated a hypothesis that the switching to more slow fibers is an adaptive response with specific benefit. The results showed that, corresponding to the switch of myosin isoforms, the thin-filament regulatory proteins troponin T and troponin I both switched to their slow isoforms in the atrophic soleus muscle of 3-mo-old Gsα-deficient mice. This fiber-type switch involving coordinated changes of both thick- and thin-myofilament proteins progressed in the Gsα-deficient soleus muscles of 18- to 24-mo-old mice, as reflected by the expression of solely slow isoforms of myosin and troponin. Compared with age-matched controls, Gsα-deficient soleus muscles with higher proportion of slow fibers exhibited slower contractile and relaxation kinetics and lower developed force, but significantly increased resistance to fatigue, followed by a better recovery. Gsα-deficient soleus muscles of neonatal and 3-wk-old mice did not show the increase in slow fibers. Therefore, the fast-to-slow-fiber-type switch in Gsα deficiency at older ages was likely an adaptive response. The benefit of higher fatigue resistance in adaption to metabolic deficiency and aging provides a mechanism to sustain skeletal muscle function in diabetic patients and elderly individuals.
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Mendias, Christopher L., Andrew J. Schwartz, Jeremy A. Grekin, Jonathan P. Gumucio, and Kristoffer B. Sugg. "Changes in muscle fiber contractility and extracellular matrix production during skeletal muscle hypertrophy." Journal of Applied Physiology 122, no. 3 (March 1, 2017): 571–79. http://dx.doi.org/10.1152/japplphysiol.00719.2016.
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Skeletal muscle can adapt to increased mechanical loads by undergoing hypertrophy. Transient reductions in whole muscle force production have been reported during the onset of hypertrophy, but contractile changes in individual muscle fibers have not been previously studied. Additionally, the extracellular matrix (ECM) stores and transmits forces from muscle fibers to tendons and bones, and determining how the ECM changes during hypertrophy is important in understanding the adaptation of muscle tissue to mechanical loading. Using the synergist ablation model, we sought to measure changes in muscle fiber contractility, collagen content, and cross-linking, and in the expression of several genes and activation of signaling proteins that regulate critical components of myogenesis and ECM synthesis and remodeling during muscle hypertrophy. Tissues were harvested 3, 7, and 28 days after induction of hypertrophy, and nonoverloaded rats served as controls. Muscle fiber specific force (sFo), which is the maximum isometric force normalized to cross-sectional area, was reduced 3 and 7 days after the onset of mechanical overload, but returned to control levels by 28 days. Collagen abundance displayed a similar pattern of change. Nearly a quarter of the transcriptome changed over the course of overload, as well as the activation of signaling pathways related to hypertrophy and atrophy. Overall, this study provides insight into fundamental mechanisms of muscle and ECM growth, and indicates that although muscle fibers appear to have completed remodeling and regeneration 1 mo after synergist ablation, the ECM continues to be actively remodeling at this time point. NEW & NOTEWORTHY This study utilized a rat synergist ablation model to integrate changes in single muscle fiber contractility, extracellular matrix composition, activation of important signaling pathways in muscle adaption, and corresponding changes in the muscle transcriptome to provide novel insight into the basic biological mechanisms of muscle fiber hypertrophy.
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Yang, Xiuying, Daniel Brobst, Wing Suen Chan, Margaret Chui Ling Tse, Oana Herlea-Pana, Palak Ahuja, Xinyi Bi, et al. "Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility." Science Signaling 12, no. 594 (August 13, 2019): eaau1468. http://dx.doi.org/10.1126/scisignal.aau1468.
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The ability of skeletal muscle to switch between lipid and glucose oxidation for ATP production during metabolic stress is pivotal for maintaining systemic energy homeostasis, and dysregulation of this metabolic flexibility is a dominant cause of several metabolic disorders. However, the molecular mechanism that governs fuel selection in muscle is not well understood. Here, we report that brain-derived neurotrophic factor (BDNF) is a fasting-induced myokine that controls metabolic reprograming through the AMPK/CREB/PGC-1α pathway in female mice. Female mice with a muscle-specific deficiency in BDNF (MBKO mice) were unable to switch the predominant fuel source from carbohydrates to fatty acids during fasting, which reduced ATP production in muscle. Fasting-induced muscle atrophy was also compromised in female MBKO mice, likely a result of autophagy inhibition. These mutant mice displayed myofiber necrosis, weaker muscle strength, reduced locomotion, and muscle-specific insulin resistance. Together, our results show that muscle-derived BDNF facilitates metabolic adaption during nutrient scarcity in a gender-specific manner and that insufficient BDNF production in skeletal muscle promotes the development of metabolic myopathies and insulin resistance.
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Strenzke, Maximilian, Paolo Alberton, Attila Aszodi, Denitsa Docheva, Elisabeth Haas, Christian Kammerlander, Wolfgang Böcker, and Maximilian Michael Saller. "Tenogenic Contribution to Skeletal Muscle Regeneration: The Secretome of Scleraxis Overexpressing Mesenchymal Stem Cells Enhances Myogenic Differentiation In Vitro." International Journal of Molecular Sciences 21, no. 6 (March 13, 2020): 1965. http://dx.doi.org/10.3390/ijms21061965.
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Integrity of the musculoskeletal system is essential for the transfer of muscular contraction force to the associated bones. Tendons and skeletal muscles intertwine, but on a cellular level, the myotendinous junctions (MTJs) display a sharp transition zone with a highly specific molecular adaption. The function of MTJs could go beyond a mere structural role and might include homeostasis of this musculoskeletal tissue compound, thus also being involved in skeletal muscle regeneration. Repair processes recapitulate several developmental mechanisms, and as myotendinous interaction does occur already during development, MTJs could likewise contribute to muscle regeneration. Recent studies identified tendon-related, scleraxis-expressing cells that reside in close proximity to the MTJs and the muscle belly. As the muscle-specific function of these scleraxis positive cells is unknown, we compared the influence of two immortalized mesenchymal stem cell (MSC) lines—differing only by the overexpression of scleraxis—on myoblasts morphology, metabolism, migration, fusion, and alignment. Our results revealed a significant increase in myoblast fusion and metabolic activity when exposed to the secretome derived from scleraxis-overexpressing MSCs. However, we found no significant changes in myoblast migration and myofiber alignment. Further analysis of differentially expressed genes between native MSCs and scleraxis-overexpressing MSCs by RNA sequencing unraveled potential candidate genes, i.e., extracellular matrix (ECM) proteins, transmembrane receptors, or proteases that might enhance myoblast fusion. Our results suggest that musculotendinous interaction is essential for the development and healing of skeletal muscles.
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Avenatti, R. C., K. H. McKeever, D. W. Horohov, and K. Malinowski. "Effects of age and exercise on inflammatory cytokines, HSP70 and HSP90 gene expression and protein content in Standardbred horses." Comparative Exercise Physiology 14, no. 1 (February 23, 2018): 27–46. http://dx.doi.org/10.3920/cep170020.
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We hypothesised that the cortisol response to acute exercise, markers of oxidative stress, expression of inflammatory cytokines, heat shock protein (HSP)70 and HSP90 expression in whole blood and skeletal muscle, and HSP70 and HSP90 protein concentrations in skeletal muscle are altered by age and in response to acute submaximal exercise in horses. Young (n=6; 5.5±2.8 year) and aged (n=6; 22.6±2.25 year) unconditioned Standardbred mares underwent an acute submaximal exercise test. Blood samples were collected and analysed for plasma cortisol and malondialdehyde (MDA) concentrations, and for cytokine and HSP gene expression pre- and post-exercise. Gluteus medius biopsies were obtained for analysis of cytokine and HSP gene expression pre- and at 0, 4, 24 and 48 h post-exercise. Data were analysed for main effects using a two-way ANOVA for repeated measures. Post-hoc comparisons of means were conducted using Student-Neuman-Keuls for pair-wise multiple comparisons where appropriate. Acute submaximal exercise increased plasma cortisol concentration in both young and aged mares, and the duration of the post-exercise rise in cortisol was altered in aged horses. Plasma MDA concentration and expression of tumour necrosis factor-α (TNF-α) and interleukin (IL)-6 were unchanged in blood and muscle. Exercise increased IL-1β expression in whole blood of young and aged mares, with young mares having greater exercise-induced expression at 2 (P<0.001) and 4 (P=0.019) h post-exercise. Both young and aged horses had increased HSP70 expression in whole blood following acute exercise, with young horses exhibiting 3-fold greater HSP70 expression than aged mares at 2 h post-exercise. HSP90 expression in whole blood following exercise was increased only in young horses. Both young and aged horses had increased HSP90 expression in skeletal muscle following exercise, but there was no difference due to age. However, the timing of HSP70 expression was different between young and aged horses. The age-related changes in cortisol and IL-1β expression following acute submaximal exercise can have implications for energy homeostasis and the adaption to such disturbances at a cellular and whole animal level. Quantification of HSP expression in whole blood may be a useful biomarker, with implications for cellular adaptation and survival in aged horses.
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Del Favero, Giorgia, Alois Bonifacio, Teisha J. Rowland, Shanshan Gao, Kunhua Song, Valter Sergo, Eric D. Adler, Luisa Mestroni, Orfeo Sbaizero, and Matthew R. G. Taylor. "Danon Disease-Associated LAMP-2 Deficiency Drives Metabolic Signature Indicative of Mitochondrial Aging and Fibrosis in Cardiac Tissue and hiPSC-Derived Cardiomyocytes." Journal of Clinical Medicine 9, no. 8 (July 31, 2020): 2457. http://dx.doi.org/10.3390/jcm9082457.
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Danon disease is a severe X-linked disorder caused by deficiency of the lysosome-associated membrane protein-2 (LAMP-2). Clinical manifestations are phenotypically diverse and consist of hypertrophic and dilated cardiomyopathies, skeletal myopathy, retinopathy, and intellectual dysfunction. Here, we investigated the metabolic landscape of Danon disease by applying a multi-omics approach and combined structural and functional readouts provided by Raman and atomic force microscopy. Using these tools, Danon patient-derived cardiac tissue, primary fibroblasts, and human induced pluripotent stem cells differentiated into cardiomyocytes (hiPSC-CMs) were analyzed. Metabolic profiling indicated LAMP-2 deficiency promoted a switch toward glycolysis accompanied by rerouting of tryptophan metabolism. Cardiomyocytes’ energetic balance and NAD+/NADH ratio appeared to be maintained despite mitochondrial aging. In turn, metabolic adaption was accompanied by a senescence-associated signature. Similarly, Danon fibroblasts appeared more stress prone and less biomechanically compliant. Overall, shaping of both morphology and metabolism contributed to the loss of cardiac biomechanical competence that characterizes the clinical progression of Danon disease.
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Tegtbur, U., MW Busse, and H. Meyer. "Lactate Catabolism during Exercise Induced Acidosis as an Indicator for Skeletal Muscle Adaption in Triathletes and Patients with Coronary Artery Disease (CAD)." Clinical Science 87, s1 (January 1, 1994): 16–17. http://dx.doi.org/10.1042/cs087s016.
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Iwaniec, Urszula T., and Russell T. Turner. "Influence of body weight on bone mass, architecture and turnover." Journal of Endocrinology 230, no. 3 (September 2016): R115—R130. http://dx.doi.org/10.1530/joe-16-0089.
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Weight-dependent loading of the skeleton plays an important role in establishing and maintaining bone mass and strength. This review focuses on mechanical signaling induced by body weight as an essential mechanism for maintaining bone health. In addition, the skeletal effects of deviation from normal weight are discussed. The magnitude of mechanical strain experienced by bone during normal activities is remarkably similar among vertebrates, regardless of size, supporting the existence of a conserved regulatory mechanism, or mechanostat, that senses mechanical strain. The mechanostat functions as an adaptive mechanism to optimize bone mass and architecture based on prevailing mechanical strain. Changes in weight, due to altered mass, weightlessness (spaceflight), and hypergravity (modeled by centrifugation), induce an adaptive skeletal response. However, the precise mechanisms governing the skeletal response are incompletely understood. Furthermore, establishing whether the adaptive response maintains the mechanical competence of the skeleton has proven difficult, necessitating the development of surrogate measures of bone quality. The mechanostat is influenced by regulatory inputs to facilitate non-mechanical functions of the skeleton, such as mineral homeostasis, as well as hormones and energy/nutrient availability that support bone metabolism. Although the skeleton is very capable of adapting to changes in weight, the mechanostat has limits. At the limits, extreme deviations from normal weight and body composition are associated with impaired optimization of bone strength to prevailing body size.
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Bye, Anja, Morten A. Høydal, Daniele Catalucci, Mette Langaas, Ole Johan Kemi, Vidar Beisvag, Lauren G. Koch, Steven L. Britton, Øyvind Ellingsen, and Ulrik Wisløff. "Gene expression profiling of skeletal muscle in exercise-trained and sedentary rats with inborn high and low VO2max." Physiological Genomics 35, no. 3 (November 2008): 213–21. http://dx.doi.org/10.1152/physiolgenomics.90282.2008.
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The relationship between inborn maximal oxygen uptake (VO2max) and skeletal muscle gene expression is unknown. Since low VO2max is a strong predictor of cardiovascular mortality, genes related to low VO2max might also be involved in cardiovascular disease. To establish the relationship between inborn VO2max and gene expression, we performed microarray analysis of the soleus muscle of rats artificially selected for high- and low running capacity (HCR and LCR, respectively). In LCR, a low VO2max was accompanied by aggregation of cardiovascular risk factors similar to the metabolic syndrome. Although sedentary HCR were able to maintain a 120% higher running speed at VO2max than sedentary LCR, only three transcripts were differentially expressed (FDR ≤ 0.05) between the groups. Sedentary LCR expressed high levels of a transcript with strong homology to human leucyl-transfer RNA synthetase, of whose overexpression has been associated with a mutation linked to mitochondrial dysfunction. Moreover, we studied exercise-induced alterations in soleus gene expression, since accumulating evidence indicates that long-term endurance training has beneficial effects on the metabolic syndrome. In terms of gene expression, the response to exercise training was more pronounced in HCR than LCR. HCR upregulated several genes associated with lipid metabolism and fatty acid elongation, whereas LCR upregulated only one transcript after exercise training. The results indicate only minor differences in soleus muscle gene expression between sedentary HCR and LCR. However, the inborn level of fitness seems to influence the transcriptional adaption to exercise, as more genes were upregulated after exercise training in HCR than LCR.
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Treff, G., K. Winkert, and JM Steinacker. "Olympic Rowing – Maximum Capacity over 2000 Meters." Deutsche Zeitschrift für Sportmedizin/German Journal of Sports Medicine 72, no. 4 (June 20, 2021): 203–11. http://dx.doi.org/10.5960/dzsm.2021.485.
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Olympic rowing in its current form is a high-intensity boat race covering a distance of 2000 m with fastest race times ranging ~5.5-7.5 min, depending on boat class, sex, and environmental factors. To realize such race times, rowers need strength and endurance, which is physiologically evident in an oxidative Adaption of the skeletal muscles, a high aerobic capacity, and the ability to contribute and sustain a relatively high percentage of anaerobic energy for several minutes. Anthropometrically, male and female rowers are characterized by relatively large body measurements. Biomechanics & Physiology: The sitting position of the rower, the involvement of a large muscle mass and the structure of the rowing cycle, consisting of drive and recovery phase where the rower slides back and forth on a sliding seat, affect the cardiovascular and the respiratory system in a unique manner. In Addition to these physiological and anthropometric characteristics, this brief review outlines the extreme metabolic implications of the sport during racing and training and mentions rarely-discussed topics such as established testing procedures, summarizes data on training intensity distribution in elite rowing and includes a short section on heat stress during training and racing in hot and humid conditions expected for the Olympic Games 2021 in Tokyo.
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Crespillo, Ana, Juan Suárez, Francisco J. Bermúdez-Silva, Patricia Rivera, Margarita Vida, Monica Alonso, Ana Palomino, et al. "Expression of the cannabinoid system in muscle: effects of a high-fat diet and CB1 receptor blockade." Biochemical Journal 433, no. 1 (December 15, 2010): 175–85. http://dx.doi.org/10.1042/bj20100751.
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The ECS (endocannabinoid system) plays an important role in the onset of obesity and metabolic disorders, implicating central and peripheral mechanisms predominantly via CB1 (cannabinoid type 1) receptors. CB1 receptor antagonist/inverse agonist treatment improves cardiometabolic risk factors and insulin resistance. However, the relative contribution of peripheral organs to the net beneficial metabolic effects remains unclear. In the present study, we have identified the presence of the endocannabinoid signalling machinery in skeletal muscle and also investigated the impact of an HFD (high-fat diet) on lipid-metabolism-related genes and endocannabinoid-related proteins. Finally, we tested whether administration of the CB1 inverse agonist AM251 restored the alterations induced by the HFD. Rats were fed on either an STD (standard/low-fat diet) or an HFD for 10 weeks and then treated with AM251 (3 mg/kg of body weight per day) for 14 days. The accumulated caloric intake was progressively higher in rats fed on the HFD than the STD, resulting in a divergence in body weight gain. AM251 treatment reduced accumulated food/caloric intake and body weight gain, being more marked in rats fed on the HFD. CB2 (cannabinoid type 2) receptor and PPARα (peroxisome-proliferator-activated receptor α) gene expression was decreased in HFD-fed rats, whereas MAGL (monoglyceride lipase) gene expression was up-regulated. These data suggest an altered endocannabinoid signalling as a result of the HFD. AM251 treatment reduced CB2 receptor, PPARγ and AdipoR1 (adiponectin receptor 1) gene expression in STD-fed rats, but only partially normalized the CB2 receptor in HFD-fed rats. Protein levels corroborated gene expression results, but also showed a decrease in DAGL (diacylglycerol) β and DAGLα after AM251 treatment in STD- and HFD-fed rats respectively. In conclusion, the results of the present study indicate a diet-sensitive ECS in skeletal muscle, suggesting that blockade of CB1 receptors could work towards restoration of the metabolic adaption imposed by diet.
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Feng, Han-Zhong, Xuequn Chen, Moh H. Malek, and J. P. Jin. "Slow recovery of the impaired fatigue resistance in postunloading mouse soleus muscle corresponding to decreased mitochondrial function and a compensatory increase in type I slow fibers." American Journal of Physiology-Cell Physiology 310, no. 1 (January 1, 2016): C27—C40. http://dx.doi.org/10.1152/ajpcell.00173.2015.
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Unloading or disuse rapidly results in skeletal muscle atrophy, switching to fast-type fibers, and decreased resistance to fatigue. The recovery process is of major importance in rehabilitation for various clinical conditions. Here we studied mouse soleus muscle during 60 days of reloading after 4 wk of hindlimb suspension. Unloading produced significant atrophy of soleus muscle with decreased contractile force and fatigue resistance, accompanied by switches of myosin isoforms from IIa to IIx and IIb and fast troponin T to more low-molecular-weight splice forms. The total mass, fiber size, and contractile force of soleus muscle recovered to control levels after 15 days of reloading. However, the fatigue resistance showed a trend of worsening during this period with significant infiltration of inflammatory cells at days 3 and 7, indicating reloading injuries that were accompanied by active regeneration with upregulations of filamin-C, αB-crystallin, and desmin. The fatigue resistance partially recovered after 30–60 days of reloading. The expression of peroxisome proliferator-activated receptor γ coactivator 1α and mitofusin-2 showed changes parallel to that of fatigue resistance after unloading and during reloading, suggesting a causal role of decreased mitochondrial function. Slow fiber contents in the soleus muscle were increased after 30–60 days of reloading to become significantly higher than the normal level, indicating a secondary adaption to compensate for the slow recovery of fatigue resistance.
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Zernicke, Ronald, Christopher MacKay, and Caeley Lorincz. "Mechanisms of bone remodeling during weight-bearing exercise." Applied Physiology, Nutrition, and Metabolism 31, no. 6 (December 2006): 655–60. http://dx.doi.org/10.1139/h06-051.
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Exercise-induced mechanical loading can have potent effects on skeletal form and health. Both intrinsic and extrinsic factors contribute to bone structure and function. Mechanical simuli (e.g., strain magnitude, frequency, rate, and gradients, as well as fluid flow and shear stress) have potent influences on bone-cell cytoskeleton and associated signalling pathways. Although the immature skeleton may be more able to benefit from exercise, a skeletally mature population can also benefit from exercise programs aimed at increasing the functional loads to which the skeleton is exposed. The definitive explanation of mechanical-loading and (or) bone-cell mechanotransductive phenomena, however, remains elusive. Here, we briefly review the structural and anatomical foundation for bone adaptation, focusing on mechanical loading effects on bone, linked to the roles of integrins, cytoskeleton, membrane channels, and auto- and paracrine factors in bone modeling and remodeling.
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Vogel, Johanna, Daniel Niederer, Georg Jung, and Kerstin Troidl. "Exercise-Induced Vascular Adaptations under Artificially Versus Pathologically Reduced Blood Flow: A Focus Review with Special Emphasis on Arteriogenesis." Cells 9, no. 2 (January 31, 2020): 333. http://dx.doi.org/10.3390/cells9020333.
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Background: The vascular effects of training under blood flow restriction (BFR) in healthy persons can serve as a model for the exercise mechanism in lower extremity arterial disease (LEAD) patients. Both mechanisms are, inter alia, characterized by lower blood flow in the lower limbs. We aimed to describe and compare the underlying mechanism of exercise-induced effects of disease- and external application-BFR methods. Methods: We completed a narrative focus review after systematic literature research. We included only studies on healthy participants or those with LEAD. Both male and female adults were considered eligible. The target intervention was exercise with a reduced blood flow due to disease or external application. Results: We identified 416 publications. After the application of inclusion and exclusion criteria, 39 manuscripts were included in the vascular adaption part. Major mechanisms involving exercise-mediated benefits in treating LEAD included: inflammatory processes suppression, proinflammatory immune cells, improvement of endothelial function, remodeling of skeletal muscle, and additional vascularization (arteriogenesis). Mechanisms resulting from external BFR application included: increased release of anabolic growth factors, stimulated muscle protein synthesis, higher concentrations of heat shock proteins and nitric oxide synthase, lower levels in myostatin, and stimulation of S6K1. Conclusions: A main difference between the two comparators is the venous blood return, which is restricted in BFR but not in LEAD. Major similarities include the overall ischemic situation, the changes in microRNA (miRNA) expression, and the increased production of NOS with their associated arteriogenesis after training with BFR.
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Kinjo, Sonoko, Tsuyoshi Uehara, Ikuko Yazaki, Yoshihisa Shirayama, and Hiroshi Wada. "Morphological diversity of larval skeletons in the sea urchin family Echinometridae (Echinoidea: Echinodermata)." Journal of the Marine Biological Association of the United Kingdom 86, no. 4 (June 15, 2006): 799–816. http://dx.doi.org/10.1017/s0025315406013725.
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To clarify the morphological variety of larval skeletons, a detailed morphological comparison among the species of the family Echinometridae was performed. Through conspecific comparison of larval skeletons among different ages, we found five skeletal characters of the body skeleton that are stable in the four-armed pluteus and thus useful in homologous comparison among the species. The morphological variation was summarized as the difference in the number of spines and posteroventral transverse rods, and differences in the shape of the body skeleton. Significant correlations were found between some skeletal characters, such as between upper body length and bottom width of body skeleton and between lower body length and the number of spines. We found that the larval skeletons of tropical species tend to have fewer spines and rods than those of temperate species, which is consistent with the hypothesis that a reduction in skeletal elements decreases the specific gravity of larvae as an adaptation to tropical waters.
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Hu, Chunxiu, Miriam Hoene, Peter Plomgaard, Jakob S. Hansen, Xinjie Zhao, Jia Li, Xiaolin Wang, et al. "Muscle-Liver Substrate Fluxes in Exercising Humans and Potential Effects on Hepatic Metabolism." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (December 11, 2019): 1196–209. http://dx.doi.org/10.1210/clinem/dgz266.
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Abstract Context The liver is crucial to maintain energy homeostasis during exercise. Skeletal muscle-derived metabolites can contribute to the regulation of hepatic metabolism. Objective We aim to elucidate which metabolites are released from the working muscles and taken up by the liver in exercising humans and their potential influence on hepatic function. Methods In two separate studies, young healthy men fasted overnight and then performed an acute bout of exercise. Arterial-to-venous differences of metabolites over the hepato-splanchnic bed and over the exercising and resting leg were investigated by capillary electrophoresis- and liquid chromatography-mass spectrometry metabolomics platforms. Liver transcriptome data of exercising mice were analyzed by pathway analysis to find a potential overlap between exercise-regulated metabolites and activators of hepatic transcription. Results During exercise, hepatic O2 uptake and CO2 delivery were increased two-fold. In contrast to all other free fatty acids (FFA), those FFA with 18 or more carbon atoms and a high degree of saturation showed a constant release in the liver vein and only minor changes by exercise. FFA 6:0 and 8:0 were released from the working leg and taken up by the hepato-splanchnic bed. Succinate and malate showed a pronounced hepatic uptake during exercise and were also released from the exercising leg. The transcriptional response in the liver of exercising mice indicates the activation of HIF-, NRF2-, and cAMP-dependent gene transcription. These pathways can also be activated by succinate. Conclusion Metabolites circulate between working muscles and the liver and may support the metabolic adaption to exercise by acting both as substrates and as signaling molecules.
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Van Pelt, Douglas W., Zachary R. Hettinger, and Peter W. Vanderklish. "RNA-binding proteins: The next step in translating skeletal muscle adaptations?" Journal of Applied Physiology 127, no. 2 (August 1, 2019): 654–60. http://dx.doi.org/10.1152/japplphysiol.00076.2019.
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The decline of skeletal muscle mass during illness, injury, disuse, and aging is associated with poor health outcomes. Therefore, it is important to pursue a greater understanding of the mechanisms that dictate skeletal muscle adaptation. In this review, we propose that RNA-binding proteins (RBPs) comprise a critical regulatory node in the orchestration of adaptive responses in skeletal muscle. While RBPs have broadly pleiotropic molecular functions, our discussion is constrained at the outset by observations from hibernating animals, which suggest that RBP regulation of RNA stability and its impact on translational reprogramming is a key component of skeletal muscle response to anabolic and catabolic stimuli. We discuss the limited data available on the expression and functions of RBPs in adult skeletal muscle in response to disuse, aging, and exercise. A model is proposed in which dynamic changes in RBPs play a central role in muscle adaptive processes through their differential effects on mRNA stability. While limited, the currently available data suggest that understanding how adaptive (and maladaptive) changes in the expression of RBPs regulate mRNA stability in skeletal muscle could be an informative and productive research area for finding new strategies to limit atrophy and promote hypertrophy.
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Landis, W. J. "Effects of Spaceflight on Cultured Bone Cells." Microscopy and Microanalysis 7, S2 (August 2001): 140–41. http://dx.doi.org/10.1017/s1431927600026775.
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Bone is known to alter its architecture, mass, composition, metabolic state, development and function in response to the effects of external forces applied to it, whether those forces be loading or unloading in nature (1). These adaptive changes by bone and the vertebrate skeletal system in general may be imparted by mechanical forces, gravity, buoyancy, or other such influences and manifest themselves in a number of ways. The skeleton of an animal, for example, may increase in mass through exercise and heightened activity, it may lose mass as a result of extended immobilization or weightlessness, or it may remodel during fracture repair processes. A mechanism explaining the adaptation by bone and the skeleton to the presence or absence of applied forces is not completely understood, but the changes are thought to occur ultimately at the cellular level of structure. Studies presented here have examined the relationship between forces and bone cell response in this context: Spaceflight and weightlessness have been utilized to investigate the influence of gravitational unloading on a model of cultured osteoblasts derived from normal embryonic chicken calvaria.
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Philp, Andrew, Thomas Rowland, Joaquin Perez-Schindler, and Simon Schenk. "Understanding the acetylome: translating targeted proteomics into meaningful physiology." American Journal of Physiology-Cell Physiology 307, no. 9 (November 1, 2014): C763—C773. http://dx.doi.org/10.1152/ajpcell.00399.2013.
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It is well established that exercise elicits a finely tuned adaptive response in skeletal muscle, with contraction frequency, duration, and recovery shaping skeletal muscle plasticity. Given the power of physical activity to regulate metabolic health, numerous research groups have focused on the molecular mechanisms that sense, interpret, and translate this contractile signal into postexercise adaptation. While our current understanding is that contraction-sensitive allosteric factors (e.g., Ca2+, AMP, NAD+, and acetyl-CoA) initiate signaling changes, how the muscle translates changes in these factors into the appropriate adaptive response remains poorly understood. During the past decade, systems biology approaches, utilizing “omics” screening techniques, have allowed researchers to define global processes of regulation with incredible sensitivity and specificity. As a result, physiologists are now able to study substrate flux with stable isotope tracers in combination with metabolomic approaches and to coordinate these functional changes with proteomic and transcriptomic analysis. In this review, we highlight lysine acetylation as an important posttranslational modification in skeletal muscle. We discuss the evolution of acetylation research and detail how large proteomic screens in diverse metabolic systems have led to the current hypothesis that acetylation may be a fundamental mechanism to fine-tune metabolic adaptation in skeletal muscle.
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Hibbitt, Catherine. "Using Skeleton Typograms to Explore Comparative Anatomy." American Biology Teacher 82, no. 2 (February 1, 2020): 120–22. http://dx.doi.org/10.1525/abt.2020.82.2.120.
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A highlight activity of the author's comparative anatomy class, this skeletal typogram activity challenges students to take their understanding of the skeletal system's components beyond mere memorization of bone names and locations. Each student creates a poster of a vertebrate skeleton, using the letters of the bone names to depict the actual bone shape and location. Animals are chosen by the teacher to represent a wide variety of evolutionary adaptations (swimming, flying, grazing, hunting, etc.). Students are then asked to compare the different typograms through analysis of contrasting skeletal evolutionary adaptations. The infographic nature of the project helps students understand the power of visual information, allowing for creative cross-disciplinary work. Through developing and comparing typograms, students deepen their understanding of how skeletal form fits function and the role of adaptation in vertebrate evolution.
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Yuan, Chong-Xi, Qiang Ji, Qing-Jin Meng, Alan R. Tabrum, and Zhe-Xi Luo. "Earliest Evolution of Multituberculate Mammals Revealed by a New Jurassic Fossil." Science 341, no. 6147 (August 15, 2013): 779–83. http://dx.doi.org/10.1126/science.1237970.
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Multituberculates were successful herbivorous mammals and were more diverse and numerically abundant than any other mammal groups in Mesozoic ecosystems. The clade also developed diverse locomotor adaptations in the Cretaceous and Paleogene. We report a new fossil skeleton from the Late Jurassic of China that belongs to the basalmost multituberculate family. Dental features of this new Jurassic multituberculate show omnivorous adaptation, and its well-preserved skeleton sheds light on ancestral skeletal features of all multituberculates, especially the highly mobile joints of the ankle, crucial for later evolutionary success of multituberculates in the Cretaceous and Paleogene.
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Kawano, Fuminori. "Histone Modification: A Mechanism for Regulating Skeletal Muscle Characteristics and Adaptive Changes." Applied Sciences 11, no. 9 (April 26, 2021): 3905. http://dx.doi.org/10.3390/app11093905.
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Epigenetics is getting increased attention in the analysis of skeletal muscle adaptation to physiological stimuli. In this review, histone modifications in skeletal muscles and their role in the regulation of muscle characteristics and adaptive changes are highlighted. The distribution of active histone modifications, such as H3K4me3 and H3 acetylation, largely differs between fast- and slow-twitch muscles. It is also indicated that the transcriptional activity in response to exercise differs in these muscle types. Histone turnover activated by exercise training leads to loosening of nucleosomes, which drastically enhances gene responsiveness to exercise, indicating that the exercise training transforms the chromatin structure to an active status. Furthermore, histone modifications play a critical role in preserving the stem cell lineage in skeletal muscle. Lack of lysine-specific demethylase 1 in satellite cells promotes the differentiation into brown adipocytes during muscle regeneration after injury. H4K20me2, which promotes the formation of heterochromatin, is necessary to repress MyoD expression in the satellite cells. These observations indicate that histone modification is a platform that characterizes skeletal muscles and may be one of the factors regulating the range of adaptive changes in these muscles.
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Ballmann, Christopher, Yawen Tang, Zachary Bush, and Glenn C. Rowe. "Adult expression of PGC-1α and -1β in skeletal muscle is not required for endurance exercise-induced enhancement of exercise capacity." American Journal of Physiology-Endocrinology and Metabolism 311, no. 6 (December 1, 2016): E928—E938. http://dx.doi.org/10.1152/ajpendo.00209.2016.
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Exercise has been shown to be the best intervention in the treatment of many diseases. Many of the benefits of exercise are mediated by adaptions induced in skeletal muscle. The peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family of transcriptional coactivators has emerged as being key mediators of the exercise response and is considered to be essential for many of the adaptions seen in skeletal muscle. However, the contribution of the PGC-1s in skeletal muscle has been evaluated by the use of either whole body or congenital skeletal muscle-specific deletion. In these models, PGC-1s were never present, thereby opening the possibility to developmental compensation. Therefore, we generated an inducible muscle-specific deletion of PGC-1α and -1β (iMyo-PGC-1DKO), in which both PGC-1α and -β can be deleted specifically in adult skeletal muscle. These iMyo-PGC-1DKO animals were used to assess the role of both PGC-1α and -1β in adult skeletal muscle and their contribution to the exercise training response. Untrained iMyo-PGC-1DKO animals exhibited a time-dependent decrease in exercise performance 8 wk postdeletion, similar to what was observed in the congenital muscle-specific PGC-1DKOs. However, after 4 wk of voluntary training, the iMyo-PGC-1DKOs exhibited an increase in exercise performance with a similar adaptive response compared with control animals. This increase was associated with an increase in electron transport complex (ETC) expression and activity in the absence of PGC-1α and -1β expression. Taken together these data suggest that PGC-1α and -1β expression are not required for training-induced exercise performance, highlighting the contribution of PGC-1-independent mechanisms.
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D’Lugos, Andrew C., Shivam H. Patel, Jordan C. Ormsby, Donald P. Curtis, Christopher S. Fry, Chad C. Carroll, and Jared M. Dickinson. "Prior acetaminophen consumption impacts the early adaptive cellular response of human skeletal muscle to resistance exercise." Journal of Applied Physiology 124, no. 4 (April 1, 2018): 1012–24. http://dx.doi.org/10.1152/japplphysiol.00922.2017.
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Resistance exercise (RE) is a powerful stimulus for skeletal muscle adaptation. Previous data demonstrate that cyclooxygenase (COX)-inhibiting drugs alter the cellular mechanisms regulating the adaptive response of skeletal muscle. The purpose of this study was to determine whether prior consumption of the COX inhibitor acetaminophen (APAP) alters the immediate adaptive cellular response in human skeletal muscle after RE. In a double-blinded, randomized, crossover design, healthy young men ( n = 8, 25 ± 1 yr) performed two trials of unilateral knee extension RE (8 sets, 10 reps, 65% max strength). Subjects ingested either APAP (1,000 mg/6 h) or placebo (PLA) for 24 h before RE (final dose consumed immediately after RE). Muscle biopsies (vastus lateralis) were collected at rest and 1 h and 3 h after exercise. Mammalian target of rapamycin (mTOR) complex 1 signaling was assessed through immunoblot and immunohistochemistry, and mRNA expression of myogenic genes was examined via RT-qPCR. At 1 h p-rpS6Ser240/244 was increased in both groups but to a greater extent in PLA. At 3 h p-S6K1Thr389 was elevated only in PLA. Furthermore, localization of mTOR to the lysosome (LAMP2) in myosin heavy chain (MHC) II fibers increased 3 h after exercise only in PLA. mTOR-LAMP2 colocalization in MHC I fibers was greater in PLA vs. APAP 1 h after exercise. Myostatin mRNA expression was reduced 1 h after exercise only in PLA. MYF6 mRNA expression was increased 1 h and 3 h after exercise only in APAP. APAP consumption appears to alter the early adaptive cellular response of skeletal muscle to RE. These findings further highlight the mechanisms through which COX-inhibiting drugs impact the adaptive response of skeletal muscle to exercise. NEW & NOTEWORTHY The extent to which the cellular reaction to acetaminophen impacts the mechanisms regulating the adaptive response of human skeletal muscle to resistance exercise is not well understood. Consumption of acetaminophen before resistance exercise appears to suppress the early response of mTORC1 activity to acute resistance exercise. These data also demonstrate, for the first time, that resistance exercise elicits fiber type-specific changes in the intracellular colocalization of mTOR with the lysosome in human skeletal muscle.
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Musci, Robert V., Karyn L. Hamilton, and Melissa A. Linden. "Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension." Sports 7, no. 7 (July 11, 2019): 170. http://dx.doi.org/10.3390/sports7070170.
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Oxidative damage is one mechanism linking aging with chronic diseases including the progressive loss of skeletal muscle mass and function called sarcopenia. Thus, mitigating oxidative damage is a potential avenue to prevent or delay the onset of chronic disease and/or extend healthspan. Mitochondrial hormesis (mitohormesis) occurs when acute exposure to stress stimulates adaptive mitochondrial responses that improve mitochondrial function and resistance to stress. For example, an acute oxidative stress via mitochondrial superoxide production stimulates the activation of endogenous antioxidant gene transcription regulated by the redox sensitive transcription factor Nrf2, resulting in an adaptive hormetic response. In addition, acute stresses such as aerobic exercise stimulate the expansion of skeletal muscle mitochondria (i.e., mitochondrial biogenesis), constituting a mitohormetic response that protects from sarcopenia through a variety of mechanisms. This review summarized the effects of age-related declines in mitochondrial and redox homeostasis on skeletal muscle protein homeostasis and highlights the mitohormetic mechanisms by which aerobic exercise mitigates these age-related declines and maintains function. We discussed the potential efficacy of targeting the Nrf2 signaling pathway, which partially mediates adaptation to aerobic exercise, to restore mitochondrial and skeletal muscle function. Finally, we highlight knowledge gaps related to improving redox signaling and make recommendations for future research.
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Naimo, Marshall A., Erik P. Rader, James Ensey, Michael L. Kashon, and Brent A. Baker. "Reduced frequency of resistance-type exercise training promotes adaptation of the aged skeletal muscle microenvironment." Journal of Applied Physiology 126, no. 4 (April 1, 2019): 1074–87. http://dx.doi.org/10.1152/japplphysiol.00582.2018.
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The purpose of this study was to characterize the growth and remodeling molecular signaling response in aged skeletal muscle following 1 mo of “resistance-type exercise” training. Male Fischer 344 × Brown Norway hybrid rats aged 3 (young) and 30 mo (old) underwent stretch-shortening contraction (SSC) loading 2 or 3 days/wk; muscles were removed 72 h posttraining. Young rats SSC loaded 3 (Y3x) or 2 days/wk (Y2x) adapted via increased work performance. Old rats SSC loaded 3 days/wk (O3x) maladapted via decreased negative work; however, old rats SSC loaded 2 days/wk (O2x) adapted through improved negative and positive work. Y3x, Y2x, and O2x, but not O3x, displayed hypertrophy via larger fiber area and myonuclear domains. Y3x, Y2x, and O2x differentially expressed 19, 30, and 8 phosphatidylinositol 3-kinase-Akt genes, respectively, whereas O3x only expressed 2. Bioinformatics analysis revealed that rats in the adapting groups presented growth and remodeling processes (i.e., increased protein synthesis), whereas O3x demonstrated inflammatory signaling. In conclusion, reducing SSC-loading frequency in aged rodents positively influences the molecular signaling microenvironment, promoting muscle adaptation. NEW & NOTEWORTHY Decreasing resistance-type exercise training frequency in old rodents led to adaptation through enhancements in performance, fiber areas, and myonuclear domains. Modifying frequency influenced the molecular environment through improvements in phosphatidylinositol 3-kinase-Akt pathway-specific expression and bioinformatics indicating increased protein synthesis. Reducing training frequency may be appropriate in older individuals who respond unfavorably to higher frequencies (i.e., maladaptation); overall, modifying the parameters of the exercise prescription can affect the cellular environment, ultimately leading to adaptive or maladaptive outcomes.
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Englund, Davis A., Kevin A. Murach, Cory M. Dungan, Vandré C. Figueiredo, Ivan J. Vechetti, Esther E. Dupont-Versteegden, John J. McCarthy, and Charlotte A. Peterson. "Depletion of resident muscle stem cells negatively impacts running volume, physical function, and muscle fiber hypertrophy in response to lifelong physical activity." American Journal of Physiology-Cell Physiology 318, no. 6 (June 1, 2020): C1178—C1188. http://dx.doi.org/10.1152/ajpcell.00090.2020.
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To date, studies that have aimed to investigate the role of satellite cells during adult skeletal muscle adaptation and hypertrophy have utilized a nontranslational stimulus and/or have been performed over a relatively short time frame. Although it has been shown that satellite cell depletion throughout adulthood does not drive skeletal muscle loss in sedentary mice, it remains unknown how satellite cells participate in skeletal muscle adaptation to long-term physical activity. The current study was designed to determine whether reduced satellite cell content throughout adulthood would influence the transcriptome-wide response to physical activity and diminish the adaptive response of skeletal muscle. We administered vehicle or tamoxifen to adult Pax7-diphtheria toxin A (DTA) mice to deplete satellite cells and assigned them to sedentary or wheel-running conditions for 13 mo. Satellite cell depletion throughout adulthood reduced balance and coordination, overall running volume, and the size of muscle proprioceptors (spindle fibers). Furthermore, satellite cell participation was necessary for optimal muscle fiber hypertrophy but not adaptations in fiber type distribution in response to lifelong physical activity. Transcriptome-wide analysis of the plantaris and soleus revealed that satellite cell function is muscle type specific; satellite cell-dependent myonuclear accretion was apparent in oxidative muscles, whereas initiation of G protein-coupled receptor (GPCR) signaling in the glycolytic plantaris may require satellite cells to induce optimal adaptations to long-term physical activity. These findings suggest that satellite cells play a role in preserving physical function during aging and influence muscle adaptation during sustained periods of physical activity.
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LaMothe, Jeremy M., and Ronald F. Zernicke. "Rest insertion combined with high-frequency loading enhances osteogenesis." Journal of Applied Physiology 96, no. 5 (May 2004): 1788–93. http://dx.doi.org/10.1152/japplphysiol.01145.2003.
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Mechanical loading can significantly affect skeletal adaptation. High-frequency loading can be a potent osteogenic stimulus. Additionally, insertion of rest periods between consecutive loading bouts can be a potent osteogenic stimulus. Thus we investigated whether the insertion of rest-periods between short-term high-frequency loading bouts would augment adaptation in the mature murine skeleton. Right tibiae of skeletally mature (16 wk) female C57BL/6 mice were loaded in cantilever bending at peak of 800 μϵ, 30 Hz, 5 days/wk for 3 wk. Left tibiae were the contralateral control condition. Mice were randomly assigned into one of two groups: continuous high-frequency (CT) stimulation for 100 s ( n = 9), or 1-s pulses of high-frequency stimuli followed by 10 s of rest (RI) for 100 s ( n = 9). Calcein labels were administered on days 1 and 21; label incorporation was used to histomorphometrically assess periosteal and endosteal indexes of adaptation. Periosteal surface referent bone formation rate (pBFR/BS) was significantly enhanced in CT (>88%) and RI (>126%) loaded tibiae, relative to control tibiae. Furthermore, RI tibiae had significantly greater pBFR/BS, relative to CT tibiae (>72%). The endosteal surface was not as sensitive to mechanical loading as the periosteal surface. Thus short-term high-frequency loading significantly elevated pBFR/BS, relative to control tibiae. Furthermore, despite the 10-fold reduction in cycle number, the insertion of rest periods between bouts of high-frequency stimuli significantly augmented pBFR/BS, relative to tibiae loaded continually. Optimization of osteogenesis in response to mechanical loading may underpin the development of nonpharmacological regiments designed to increase bone strength in individuals with compromised bone structures.
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Summermatter, Serge, Raphael Thurnheer, Gesa Santos, Barbara Mosca, Oliver Baum, Susan Treves, Hans Hoppeler, Francesco Zorzato, and Christoph Handschin. "Remodeling of calcium handling in skeletal muscle through PGC-1α: impact on force, fatigability, and fiber type." American Journal of Physiology-Cell Physiology 302, no. 1 (January 2012): C88—C99. http://dx.doi.org/10.1152/ajpcell.00190.2011.
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Regular endurance exercise remodels skeletal muscle, largely through the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). PGC-1α promotes fiber type switching and resistance to fatigue. Intracellular calcium levels might play a role in both adaptive phenomena, yet a role for PGC-1α in the adaptation of calcium handling in skeletal muscle remains unknown. Using mice with transgenic overexpression of PGC-1α, we now investigated the effect of PGC-1α on calcium handling in skeletal muscle. We demonstrate that PGC-1α induces a quantitative reduction in calcium release from the sarcoplasmic reticulum by diminishing the expression of calcium-releasing molecules. Concomitantly, maximal muscle force is reduced in vivo and ex vivo. In addition, PGC-1α overexpression delays calcium clearance from the myoplasm by interfering with multiple mechanisms involved in calcium removal, leading to higher myoplasmic calcium levels following contraction. During prolonged muscle activity, the delayed calcium clearance might facilitate force production in mice overexpressing PGC-1α. Our results reveal a novel role of PGC-1α in altering the contractile properties of skeletal muscle by modulating calcium handling. Importantly, our findings indicate PGC-1α to be both down- as well as upstream of calcium signaling in this tissue. Overall, our findings suggest that in the adaptation to chronic exercise, PGC-1α reduces maximal force, increases resistance to fatigue, and drives fiber type switching partly through remodeling of calcium transients, in addition to promoting slow-type myofibrillar protein expression and adequate energy supply.
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S., Shyam Sundar, and Sahith Kumar Shetty. "Bone Graft Substitutes in Maxillofacial Reconstruction - Structural and Biomechanical Perspectives." Journal of Evolution of Medical and Dental Sciences 10, no. 31 (August 2, 2021): 2369–72. http://dx.doi.org/10.14260/jemds/2021/486.
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Reconstruction of a maxillofacial skeletal defect in the recent past has witnessed a paradigm shift in the process of treatment planning. It has now become a collaboration between the surgeon and the bioengineer to provide a customised stable reconstruction. Understanding maxillofacial skeleton from an architectural and biomechanical perspective would not only guide the surgeon in planning a reconstruction but also the bioengineer to select the biomaterial and design an ideal reconstruction. This paper intended to provide an insight into scientific concepts which needed to be considered during the designing of biomaterials for reconstruction of maxillofacial skeletal defects. Any object in the world, from a mechanical perspective is seen only as a material of varying physical and chemical (organic / inorganic) properties dwelling in a dynamic three-dimensional environment. Bone continuously has been re-modelling by adapting to the dynamic loading environment through an established force distribution pattern of equilibrium. 1 Hence, for a patient requiring reconstruction of defects of varying dimensions within the craniomaxillofacial skeleton, its architectural complexity should be seen from both the surgeon’s and bioengineer’s perspective. Such multidisciplinary approach would provide a customized comprehensive reconstructive and rehabilitative solution.
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Spina, R. J., M. M. Chi, M. G. Hopkins, P. M. Nemeth, O. H. Lowry, and J. O. Holloszy. "Mitochondrial enzymes increase in muscle in response to 7-10 days of cycle exercise." Journal of Applied Physiology 80, no. 6 (June 1, 1996): 2250–54. http://dx.doi.org/10.1152/jappl.1996.80.6.2250.
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Endurance exercise training induces a significant increase in the respiratory capacity of skeletal muscle. This is reflected by a training-induced increase in mitochondrial enzyme activity. One consequence of this adaptation is that there is a decreased reliance on carbohydrate utilization with a concomitant increase in fat utilization, resulting in an improvement in endurance capacity. Recently it has been reported that 7-14 days of cycle ergometer exercise training does not induce an increase in mitochondrial enzyme levels in skeletal muscle but, nevertheless, results in smaller decreases in phosphocreatine and glycogen and smaller increases in Pi and lactate in muscle in response to the same exercise after compared with before training. However, previous studies in rats have shown that an adaptive increase in mitochondrial enzymes is already evident after only 2 days of exercise training. In view of this discrepency, the present study was performed to reevaluate the effect of short-term training (7-10 days) on mitochondrial enzymes in skeletal muscle of humans. Twelve subjects [6 men and 6 women, 27 +/- 5 (SE) yr old] underwent 7 (n = 5) or 10 days (n = 7) of cycle ergometer exercise for 2h/day at 60-70% of peak O2 consumption. Peak O2 consumption was increased by 9% (from 2.97 +/- 0.16 to 3.24 +/- 0.17 l/min) in response to training. Blood lactate levels were lower at the same absolute work rates after than before training. The activities of citrate synthase, beta-hydroxyacyl-CoA dehydrogenase, mitochondrial thiolase, and carnitine acetyltransferase were increased by approximately 30% in response to training. The results of the present study provide evidence that in humans, as in rats, the adaptive increase in mitochondrial enzymes in skeletal muscle occurs fairly rapidly in response to exercise training. They provide no support for the claim that this adaptive response is delayed for > 2 wk after the onset of training.
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Hawley, John A., Louise M. Burke, Stuart M. Phillips, and Lawrence L. Spriet. "Nutritional modulation of training-induced skeletal muscle adaptations." Journal of Applied Physiology 110, no. 3 (March 2011): 834–45. http://dx.doi.org/10.1152/japplphysiol.00949.2010.
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Skeletal muscle displays remarkable plasticity, enabling substantial adaptive modifications in its metabolic potential and functional characteristics in response to external stimuli such as mechanical loading and nutrient availability. Contraction-induced adaptations are determined largely by the mode of exercise and the volume, intensity, and frequency of the training stimulus. However, evidence is accumulating that nutrient availability serves as a potent modulator of many acute responses and chronic adaptations to both endurance and resistance exercise. Changes in macronutrient intake rapidly alter the concentration of blood-borne substrates and hormones, causing marked perturbations in the storage profile of skeletal muscle and other insulin-sensitive tissues. In turn, muscle energy status exerts profound effects on resting fuel metabolism and patterns of fuel utilization during exercise as well as acute regulatory processes underlying gene expression and cell signaling. As such, these nutrient-exercise interactions have the potential to activate or inhibit many biochemical pathways with putative roles in training adaptation. This review provides a contemporary perspective of our understanding of the molecular and cellular events that take place in skeletal muscle in response to both endurance and resistance exercise commenced after acute and/or chronic alterations in nutrient availability (carbohydrate, fat, protein, and several antioxidants). Emphasis is on the results of human studies and how nutrient provision (or lack thereof) interacts with specific contractile stimulus to modulate many of the acute responses to exercise, thereby potentially promoting or inhibiting subsequent training adaptation.
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Gordon, Kenneth R. "Adaptive Nature of Skeletal Design." BioScience 39, no. 11 (December 1989): 784–90. http://dx.doi.org/10.2307/1311184.
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Turner, Charles H. "Skeletal Adaptation to Mechanical Loading." Clinical Reviews in Bone and Mineral Metabolism 5, no. 4 (December 2007): 181–94. http://dx.doi.org/10.1007/s12018-008-9010-x.
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Raman, Ritu, Caroline Cvetkovic, Sebastien G. M. Uzel, Randall J. Platt, Parijat Sengupta, Roger D. Kamm, and Rashid Bashir. "Optogenetic skeletal muscle-powered adaptive biological machines." Proceedings of the National Academy of Sciences 113, no. 13 (March 14, 2016): 3497–502. http://dx.doi.org/10.1073/pnas.1516139113.
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Complex biological systems sense, process, and respond to their surroundings in real time. The ability of such systems to adapt their behavioral response to suit a range of dynamic environmental signals motivates the use of biological materials for other engineering applications. As a step toward forward engineering biological machines (bio-bots) capable of nonnatural functional behaviors, we created a modular light-controlled skeletal muscle-powered bioactuator that can generate up to 300 µN (0.56 kPa) of active tension force in response to a noninvasive optical stimulus. When coupled to a 3D printed flexible bio-bot skeleton, these actuators drive directional locomotion (310 µm/s or 1.3 body lengths/min) and 2D rotational steering (2°/s) in a precisely targeted and controllable manner. The muscle actuators dynamically adapt to their surroundings by adjusting performance in response to “exercise” training stimuli. This demonstration sets the stage for developing multicellular bio-integrated machines and systems for a range of applications.
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Akimoto, Takayuki, Kanako Okuhira, Katsuji Aizawa, Shogo Wada, Hiroaki Honda, Toru Fukubayashi, and Takashi Ushida. "Skeletal muscle adaptation in response to mechanical stress in p130cas−/− mice." American Journal of Physiology-Cell Physiology 304, no. 6 (March 15, 2013): C541—C547. http://dx.doi.org/10.1152/ajpcell.00243.2012.
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Mammalian skeletal muscles undergo adaptation in response to changes in the functional demands upon them, involving mechanical-stress-induced cellular signaling called “mechanotransduction.” We hypothesized that p130Cas, which is reported to act as a mechanosensor that transduces mechanical extension into cellular signaling, plays an important role in maintaining and promoting skeletal muscle adaptation in response to mechanical stress via the p38 MAPK signaling pathway. We demonstrate that muscle-specific p130Cas−/− mice express the contractile proteins normally in skeletal muscle. Furthermore, muscle-specific p130Cas−/− mice show normal mechanical-stress-induced muscle adaptation, including exercise-induced IIb-to-IIa muscle fiber type transformation and hypertrophy. Finally, we provide evidence that exercise-induced p38 MAPK signaling is not impaired by the muscle-specific deletion of p130Cas. We conclude that p130Cas plays a limited role in mechanical-stress-induced skeletal muscle adaptation.
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Wright, Traver, Randall W. Davis, Heidi C. Pearson, Michael Murray, and Melinda Sheffield-Moore. "Skeletal muscle thermogenesis enables aquatic life in the smallest marine mammal." Science 373, no. 6551 (July 8, 2021): 223–25. http://dx.doi.org/10.1126/science.abf4557.
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Basal metabolic rate generally scales with body mass in mammals, and variation from predicted levels indicates adaptive metabolic remodeling. As a thermogenic adaptation for living in cool water, sea otters have a basal metabolic rate approximately three times that of the predicted rate; however, the tissue-level source of this hypermetabolism is unknown. Because skeletal muscle is a major determinant of whole-body metabolism, we characterized respiratory capacity and thermogenic leak in sea otter muscle. Compared with that of previously sampled mammals, thermogenic muscle leak capacity was elevated and could account for sea otter hypermetabolism. Muscle respiratory capacity was modestly elevated and reached adult levels in neonates. Premature metabolic development and high leak rate indicate that sea otter muscle metabolism is regulated by thermogenic demand and is the source of basal hypermetabolism.
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Zebedin, Eva, Walter Sandtner, Stefan Galler, Julia Szendroedi, Herwig Just, Hannes Todt, and Karlheinz Hilber. "Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C2C12skeletal muscle cells." American Journal of Physiology-Cell Physiology 287, no. 2 (August 2004): C270—C280. http://dx.doi.org/10.1152/ajpcell.00015.2004.
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Each skeletal muscle of the body contains a unique composition of “fast” and “slow” muscle fibers, each of which is specialized for certain challenges. This composition is not static, and the muscle fibers are capable of adapting their molecular composition by altered gene expression (i.e., fiber type conversion). Whereas changes in the expression of contractile proteins and metabolic enzymes in the course of fiber type conversion are well described, little is known about possible adaptations in the electrophysiological properties of skeletal muscle cells. Such adaptations may involve changes in the expression and/or function of ion channels. In this study, we investigated the effects of fast-to-slow fiber type conversion on currents via voltage-gated Na+channels in the C2C12murine skeletal muscle cell line. Prolonged treatment of cells with 25 nM of the Ca2+ionophore A-23187 caused a significant shift in myosin heavy chain isoform expression from the fast toward the slow isoform, indicating fast-to-slow fiber type conversion. Moreover, Na+current inactivation was significantly altered. Slow inactivation less strongly inhibited the Na+currents of fast-to-slow fiber type-converted cells. Compared with control cells, the Na+currents of converted cells were more resistant to block by tetrodotoxin, suggesting enhanced relative expression of the cardiac Na+channel isoform Nav1.5 compared with the skeletal muscle isoform Nav1.4. These results imply that fast-to-slow fiber type conversion of skeletal muscle cells involves functional adaptation of their electrophysiological properties.
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Pérez-Schindler, Joaquín, Mary C. Esparza, James McKendry, Leigh Breen, Andrew Philp, and Simon Schenk. "Overload-mediated skeletal muscle hypertrophy is not impaired by loss of myofiber STAT3." American Journal of Physiology-Cell Physiology 313, no. 3 (September 1, 2017): C257—C261. http://dx.doi.org/10.1152/ajpcell.00100.2017.
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Although the signal pathways mediating muscle protein synthesis and degradation are well characterized, the transcriptional processes modulating skeletal muscle mass and adaptive growth are poorly understood. Recently, studies in mouse models of muscle wasting or acutely exercised human muscle have suggested a potential role for the transcription factor signal transducer and activator of transcription 3 (STAT3), in adaptive growth. Hence, in the present study we sought to define the contribution of STAT3 to skeletal muscle adaptive growth. In contrast to previous work, two different resistance exercise protocols did not change STAT3 phosphorylation in human skeletal muscle. To directly address the role of STAT3 in load-induced (i.e., adaptive) growth, we studied the anabolic effects of 14 days of synergist ablation (SA) in skeletal muscle-specific STAT3 knockout (mKO) mice and their floxed, wild-type (WT) littermates. Plantaris muscle weight and fiber area in the nonoperated leg (control; CON) was comparable between genotypes. As expected, SA significantly increased plantaris weight, muscle fiber cross-sectional area, and anabolic signaling in WT mice, although interestingly, this induction was not impaired in STAT3 mKO mice. Collectively, these data demonstrate that STAT3 is not required for overload-mediated hypertrophy in mouse skeletal muscle.
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Röckl, Katja S. C., Michael F. Hirshman, Josef Brandauer, Nobuharu Fujii, Lee A. Witters, and Laurie J. Goodyear. "Skeletal Muscle Adaptation to Exercise Training." Diabetes 56, no. 8 (May 18, 2007): 2062–69. http://dx.doi.org/10.2337/db07-0255.
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Mcleod, Kenneth J., Clinton T. Rubin, Mark W. Otter, and Yi-Xian Qin. "Skeletal Cell Stresses and Bone Adaptation." American Journal of the Medical Sciences 316, no. 3 (September 1998): 176–83. http://dx.doi.org/10.1016/s0002-9629(15)40398-2.
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Wang, Y., and J. M. Winters. "Predictive model for skeletal muscle adaptation." Journal of Biomechanics 39 (January 2006): S43. http://dx.doi.org/10.1016/s0021-9290(06)83047-2.
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Burton, H. W., B. M. Carlson, and J. A. Faulkner. "Microcirculatory Adaptation to Skeletal Muscle Transplantation." Annual Review of Physiology 49, no. 1 (March 1987): 439–51. http://dx.doi.org/10.1146/annurev.ph.49.030187.002255.
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Carter, Dennis R., and Tracy E. Orr. "Skeletal development and bone functional adaptation." Journal of Bone and Mineral Research 7, S2 (December 1992): S389—S395. http://dx.doi.org/10.1002/jbmr.5650071405.
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Warden, Stuart J. "Extreme Skeletal Adaptation to Mechanical Loading." Journal of Orthopaedic & Sports Physical Therapy 40, no. 3 (March 2010): 188. http://dx.doi.org/10.2519/jospt.2010.0404.
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McLEOD, KENNETH J., CLINTON T. RUBIN, MARK W. OTTER, and YI-XIAN QIN. "Skeletal Cell Stresses and Bone Adaptation." American Journal of the Medical Sciences 316, no. 3 (September 1998): 176–83. http://dx.doi.org/10.1097/00000441-199809000-00005.
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Druz, N. V. "ОСОБЛИВОСТІ БУДОВИ КІСТОК ТАЗОСТЕГНОВОГО СУГЛОБА ПТАХІВ, ЯК ОКРЕМОЇ ЛАНКИ ЛОКОМОТОРНОГО АПАРАТА." Scientific Messenger of LNU of Veterinary Medicine and Biotechnology 18, no. 3(70) (September 5, 2016): 88–91. http://dx.doi.org/10.15421/nvlvet7020.
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This article is dedicated to the study of the structure, ways of formation of bone structures that form the basis of locomotor organs, namely the hip joint, the elucidation of mechanisms of their development, because they provide their reliable functioning. The study of the structural features of the skeleton of birds in comparison to other animals makes it possible to understand the phylogeny as an adaptive process that is the basis of evolution at all.Theoretical generalization of structural features of birds’ hip joint that are characterized by different types of biomorphological adaptations, such as the type and speed of ground movement in the habitat, are presented in the article. This new position allows analyzing the processes of differentiation and transformation of muscles and skeletal elements of birds’ hip joint, which are functioning and developing under the influence of various external factors.The summarized results of the original systematic morpho–functional and morpho–ecological study of hip bones as the main unit of bipedal locomotion of the Class Aves, is given. A detailed comparative description of skeletal elements of birds’ hip joint, that accompanied by unique historical overview which covers more than two–thousand–year period, is provided for the first time. The analysis of some significant morphological structures, which gives clues to the reconstruction of adaptive evolution of any group of birds, is given.