Relevant bibliographies by topics / Anabolic response

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Anabolic response'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Anabolic response"

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Toth, Michael J., Martin M. LeWinter, Philip A. Ades, and Dwight E. Matthews. "Impaired muscle protein anabolic response to insulin and amino acids in heart failure patients: relationship with markers of immune activation." Clinical Science 119, no. 11 (August 17, 2010): 467–76. http://dx.doi.org/10.1042/cs20100110.

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Patients with chronic HF (heart failure) experience muscle atrophy during the course of the disease. The mechanisms underlying muscle atrophy in HF, however, are not understood. Thus we evaluated leg phenylalanine balance and kinetics in HF patients and controls following a brief fast (24 h) and under euglycaemic–hyperinsulinaemic–hyperaminoacidaemic conditions to determine whether HF increases muscle protein catabolism in response to nutritional deprivation and/or diminishes the anabolic response to meal-related stimuli (insulin and amino acids) and whether alterations in protein metabolism correlate to circulating cytokine levels. No differences in phenylalanine balance, rate of appearance or rate of disappearance were found between patients and controls under fasting conditions. However, the anabolic response to hyperinsulinaemia–hyperaminoacidaemia was reduced by more than 50% in patients compared with controls. The diminished anabolic response was due to reduced suppression of the leg phenylalanine appearance rate, an index of protein breakdown, in HF patients; whereas no group difference was found in the increase in the leg phenylalanine disappearance rate, an index of protein synthesis. The diminished responses of both phenylalanine balance and appearance rate to hyperinsulinaemia–hyperaminoacidaemia were related to greater circulating IL-6 (interleukin-6) levels. Our results suggest that, following a brief period of nutritional deprivation, HF patients demonstrate an impaired muscle protein anabolic response to meal-related stimuli, due to an inability to suppress muscle proteolysis, and that this diminished protein anabolic response correlates with markers of immune activation. The inability to stimulate muscle protein anabolism following periods of nutritional deficiency may contribute to muscle wasting in HF patients.
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Mitchell, W. Kyle, Bethan E. Phillips, John P. Williams, Debbie Rankin, Jonathan N. Lund, Daniel J. Wilkinson, Kenneth Smith, and Philip J. Atherton. "The impact of delivery profile of essential amino acids upon skeletal muscle protein synthesis in older men: clinical efficacy of pulse vs. bolus supply." American Journal of Physiology-Endocrinology and Metabolism 309, no. 5 (September 1, 2015): E450—E457. http://dx.doi.org/10.1152/ajpendo.00112.2015.

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Essential amino acids (EAA) are responsible for skeletal muscle anabolic effects after nutrient intake. The pattern of appearance of EAA in blood, e.g., after intake of “slow” or “fast” protein sources or in response to grazing vs. bolus feeding patterns, may impact anabolism. However, the influence of this on muscle anabolism is poorly understood, particularly in older individuals. We determined the effects of divergent feeding profiles of EAA on blood flow, anabolic signaling, and muscle protein synthesis (MPS) in older men. Sixteen men (∼70 yr) consumed EAA either as a single dose (bolus, 15 g; n = 8) or as small repeated fractions (pulse, 4 × 3.75 g every 45 min; n = 8) during 13C6 phenylalanine infusion. Repeated blood samples and muscle biopsies permitted measurement of fasting and postprandial plasma EAA, insulin, anabolic signaling, and MPS. Muscle blood flow was assessed by contrast-enhanced ultrasound (Sonovue). Bolus achieved rapid insulinemia (12.7 μiU/ml 25-min postfeed), essential aminoacidemia (∼3,000 μM, 45–65 min postfeed), and mTORC1 activity; pulse achieved attenuated insulin responses, gradual low-amplitude aminoacidemia (∼1,800 μM 80–195 min after feeding), and undetectable mTORC1 signaling. Despite this, equivalent anabolic responses were observed: fasting FSRs of 0.051 and 0.047%/h (bolus and pulse, respectively) increased to 0.084 and 0.073%/h, respectively. Moreover, pulse led to sustainment of MPS beyond 180 min, when bolus MPS had returned to basal rates. We detected no benefit of rapid aminoacidemia in this older population despite enhanced anabolic signaling and greater overall EAA exposure. Rather, apparent delayed onset of the “muscle-full” effect permitted identical MPS following low-amplitude-sustained EAA exposure.
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Mitchell, Cameron J., Randall F. D'Souza, Vandre C. Figueiredo, Alex Chan, Kirsten Aasen, Brenan Durainayagam, Sarah Mitchell, et al. "Effect of dietary arachidonic acid supplementation on acute muscle adaptive responses to resistance exercise in trained men: a randomized controlled trial." Journal of Applied Physiology 124, no. 4 (April 1, 2018): 1080–91. http://dx.doi.org/10.1152/japplphysiol.01100.2017.

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Arachidonic acid (ARA), a polyunsaturated ω-6 fatty acid, acts as precursor to a number of prostaglandins with potential roles in muscle anabolism. It was hypothesized that ARA supplementation might enhance the early anabolic response to resistance exercise (RE) by increasing muscle protein synthesis (MPS) via mammalian target of rapamycin (mTOR) pathway activation and/or the late anabolic response by modulating ribosome biogenesis and satellite cell expansion. Nineteen men with ≥1 yr of resistance-training experience were randomized to consume either 1.5 g daily ARA or a corn-soy-oil placebo in a double-blind manner for 4 wk. Participants then undertook fasted RE (8 sets each of leg press and extension at 80% 1-repetition maximum), with vastus lateralis biopsies obtained before exercise, immediately postexercise, and at 2, 4, and 48 h of recovery. MPS (measured via stable isotope infusion) was not different between groups ( P = 0.212) over the 4-h recovery period. mTOR pathway members p70 S6 kinase and S6 ribosomal protein were phosphorylated postexercise ( P < 0.05), with no difference between groups. 45S preribosomal RNA increased 48 h after exercise only in ARA ( P = 0.012). Neural cell adhesion molecule-positive satellite cells per fiber increased 48 h after exercise ( P = 0.013), with no difference between groups ( P = 0.331). Prior ARA supplementation did not alter the acute anabolic response to RE in previously resistance-trained men; however, at 48 h of recovery, ribosome biogenesis was stimulated only in the ARA group. The findings do not support a mechanistic link between ARA and short-term anabolism, but ARA supplementation in conjunction with resistance training may stimulate increases in translational capacity. NEW & NOTEWORTHY Four weeks of daily arachidonic acid supplementation in trained men did not alter their acute muscle protein synthetic or anabolic signaling response to resistance exercise. However, 48 h after exercise, men supplemented with arachidonic acid showed greater ribosome biogenesis and a trend toward greater change in satellite cell content. Chronic arachidonic acid supplementation does not appear to regulate the acute anabolic response to resistance exercise but may augment muscle adaptation in the following days of recovery.
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Abou Sawan, Sidney, Michael Mazzulla, Daniel R. Moore, and Nathan Hodson. "More than just a garbage can: emerging roles of the lysosome as an anabolic organelle in skeletal muscle." American Journal of Physiology-Cell Physiology 319, no. 3 (September 1, 2020): C561—C568. http://dx.doi.org/10.1152/ajpcell.00241.2020.

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Skeletal muscle is a highly plastic tissue capable of remodeling in response to a range of physiological stimuli, including nutrients and exercise. Historically, the lysosome has been considered an essentially catabolic organelle contributing to autophagy, phagocytosis, and exo-/endocytosis in skeletal muscle. However, recent evidence has emerged of several anabolic roles for the lysosome, including the requirement for autophagy in skeletal muscle mass maintenance, the discovery of the lysosome as an intracellular signaling hub for mechanistic target of rapamycin complex 1 (mTORC1) activation, and the importance of transcription factor EB/lysosomal biogenesis-related signaling in the regulation of mTORC1-mediated protein synthesis. We, therefore, propose that the lysosome is an understudied organelle with the potential to underpin the skeletal muscle adaptive response to anabolic stimuli. Within this review, we describe the molecular regulation of lysosome biogenesis and detail the emerging anabolic roles of the lysosome in skeletal muscle with particular emphasis on how these roles may mediate adaptations to chronic resistance exercise. Furthermore, given the well-established role of amino acids to support muscle protein remodeling, we describe how dietary proteins “labeled” with stable isotopes could provide a complementary research tool to better understand how lysosomal biogenesis, autophagy regulation, and/or mTORC1-lysosomal repositioning can mediate the intracellular usage of dietary amino acids in response to anabolic stimuli. Finally, we provide avenues for future research with the aim of elucidating how the regulation of this important organelle could mediate skeletal muscle anabolism.
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Murton, Andrew J. "Muscle protein turnover in the elderly and its potential contribution to the development of sarcopenia." Proceedings of the Nutrition Society 74, no. 4 (March 31, 2015): 387–96. http://dx.doi.org/10.1017/s0029665115000130.

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The underlying aetiology of sarcopenia appears multifaceted and not yet fully defined, but ultimately involves the gradual loss of muscle protein content over time. The present evidence suggests that the loss of lean tissue in the elderly is exacerbated by low dietary protein intake. Moreover, acute stable-isotope-based methodologies have demonstrated that the muscle anabolic response to a given amount of protein may decline with age, a phenomenon that has been termed anabolic resistance. Although the mechanism responsible for the inability of muscle to mount a satisfactory anabolic response to protein provision with increasing age is presently unknown, it does not appear due to impaired digestion or absorption of dietary protein. Rather, the issue could reside with any combination of: a diminished delivery of amino acids to peripheral tissues, impaired uptake of amino acids into muscle cells, or an inability of amino acids to elicit intracellular events pivotal for anabolism to occur. Despite the presence of anabolic resistance to dietary protein, present evidence suggests that protein supplementation may be able to overcome these issues, particularly when combined with resistance exercise programmes. As such, protein supplementation may prove to be an effective approach to delay the loss of muscle mass with age and has led to calls for the recommended daily intake of protein to be increased for the elderly population.
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Belfiore, F., A. M. Rabuazzo, S. Iannello, R. Campione, and D. Vasta. "Anabolic response of some tissues to diabetes." Biochemical Medicine and Metabolic Biology 35, no. 2 (April 1986): 149–55. http://dx.doi.org/10.1016/0885-4505(86)90069-1.

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Dardevet, Dominique, Didier Rémond, Marie-Agnès Peyron, Isabelle Papet, Isabelle Savary-Auzeloux, and Laurent Mosoni. "Muscle Wasting and Resistance of Muscle Anabolism: The “Anabolic Threshold Concept” for Adapted Nutritional Strategies during Sarcopenia." Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/269531.

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Skeletal muscle loss is observed in several physiopathological situations. Strategies to prevent, slow down, or increase recovery of muscle have already been tested. Besides exercise, nutrition, and more particularly protein nutrition based on increased amino acid, leucine or the quality of protein intake has generated positive acute postprandial effect on muscle protein anabolism. However, on the long term, these nutritional strategies have often failed in improving muscle mass even if given for long periods of time in both humans and rodent models. Muscle mass loss situations have been often correlated to a resistance of muscle protein anabolism to food intake which may be explained by an increase of the anabolic threshold toward the stimulatory effect of amino acids. In this paper, we will emphasize how this anabolic resistance may affect the intensity and the duration of the muscle anabolic response at the postprandial state and how it may explain the negative results obtained on the long term in the prevention of muscle mass. Sarcopenia, the muscle mass loss observed during aging, has been chosen to illustrate this concept but it may be kept in mind that it could be extended to any other catabolic states or recovery situations.
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Klein, Gordon L. "The Role of Bone in Muscle Wasting." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 392. http://dx.doi.org/10.3390/ijms22010392.

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This review describes the role of bone resorption in muscle atrophy as well as in muscle protein anabolism. Both catabolic and anabolic pathways involve components of the proinflammatory cytokine families and release of factors stored in bone during resorption. The juxtaposition of the catabolic and anabolic resorption-dependent pathways raises new questions about control of release of factors from bone, quantity of release in a variety of conditions, and relation of factors released from bone. The catabolic responses involve release of calcium from bone into the circulation resulting in increased inflammatory response in intensity and/or duration. The release of transforming growth factor beta (TGF-β) from bone suppresses phosphorylation of the AKT/mTOR pathway and stimulates ubiquitin-mediated breakdown of muscle protein. In contrast, muscle IL-6 production is stimulated by undercarboxylated osteocalcin, which signals osteoblasts to produce more RANK ligand, stimulating resorptive release of undercarboxylated osteocalcin, which in turn stimulates muscle fiber nutrient uptake and an increase in muscle mass.
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Tipton, Kevin D., Tabatha A. Elliott, Arny A. Ferrando, Asle A. Aarsland, and Robert R. Wolfe. "Stimulation of muscle anabolism by resistance exercise and ingestion of leucine plus protein." Applied Physiology, Nutrition, and Metabolism 34, no. 2 (April 2009): 151–61. http://dx.doi.org/10.1139/h09-006.

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Leucine is known to stimulate muscle protein synthesis and anabolism. However, evidence for the efficacy of additional leucine to enhance the response of muscle anabolism to resistance exercise and protein ingestion is unclear. Thus, we investigated the response of net muscle protein balance to ingestion of additional leucine with protein in association with resistance exercise. Two groups of untrained subjects performed an intense bout of leg resistance exercise following ingestion of 1 of 2 drinks: flavored water (PL); or 16.6 g of whey protein + 3.4 g of leucine (W+L). Arteriovenous amino acid balance across the leg was measured to assess the anabolic response of muscle in each group. Arterial amino acid concentrations increased in response to ingestion of W+L. Amino acid concentrations peaked between 60 and 120 min after ingestion, and then declined to baseline values. Valine concentration decreased to levels significantly lower than baseline. Net balance of leucine, threonine, and phenylalanine did not change following PL ingestion, but increased and remained elevated above baseline for 90–120 min following W+L ingestion. Leucine (138 ± 37 and –23 ± 23 mg), phenylalanine (58 ± 28 and –38 ± 14 mg), and threonine (138 ± 37 and –23 ± 23 mg) uptake was greater for W+L than for PL over the 5.5 h following drink ingestion. Our results indicate that the whey protein plus leucine in healthy young volunteers results in an anabolic response in muscle that is not greater than the previously reported response to whey protein alone.
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Nilsson, Mats I., Nicholas P. Greene, Justin P. Dobson, Michael P. Wiggs, Heath G. Gasier, Brandon R. Macias, Kevin L. Shimkus, and James D. Fluckey. "Insulin resistance syndrome blunts the mitochondrial anabolic response following resistance exercise." American Journal of Physiology-Endocrinology and Metabolism 299, no. 3 (September 2010): E466—E474. http://dx.doi.org/10.1152/ajpendo.00118.2010.

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Metabolic risk factors associated with insulin resistance syndrome may attenuate augmentations in skeletal muscle protein anabolism following contractile activity. The purpose of this study was to investigate whether or not the anabolic response, as defined by an increase in cumulative fractional protein synthesis rates (24-h FSR) following resistance exercise (RE), is blunted in skeletal muscle of a well-established rodent model of insulin resistance syndrome. Four-month-old lean ( Fa/?) and obese ( fa/fa) Zucker rats engaged in four lower body RE sessions over 8 days, with the last bout occurring 16 h prior to muscle harvest. A priming dose of deuterium oxide (2H2O) and 2H2O-enriched drinking water were administered 24 h prior to euthanization for assessment of cumulative FSR. Fractional synthesis rates of mixed (−5%), mitochondrial (−1%), and cytosolic (+15%), but not myofibrillar, proteins (−16%, P = 0.012) were normal or elevated in gastrocnemius muscle of unexercised obese rats. No statistical differences were found in the anabolic response of cytosolic and myofibrillar subfractions between phenotypes, but obese rats were not able to augment 24-h FSR of mitochondria to the same extent as lean rats following RE (+14% vs. +28%, respectively). We conclude that the mature obese Zucker rat exhibits a mild, myofibrillar-specific suppression in basal FSR and a blunted mitochondrial response to contractile activity in mixed gastrocnemius muscle. These findings underscore the importance of assessing synthesis rates of specific myocellular subfractions to fully elucidate perturbations in basal protein turnover rates and differential adaptations to exercise stimuli in metabolic disease.
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Dissertations / Theses on the topic "Anabolic response"

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Bird, Randy Lee. "The Effect of Post Exercise Nutrition on Anabolic Response to Resistance Exercise." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/31585.

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Purpose: To determine the effect of four postexercise beverages, differing in macronutrient content, on metabolic response to an acute resistance exercise bout.

Methods: Forty male subjects performed five sets of eight repetitions at 80% 1RM for leg press and leg extension, and then consumed one of four postexercise beverages (Placebo, PL: a carbohydrate-electrolyte beverage, CE; or one of two milk-based beverages, MILK 1: 1% chocolate milk; MILK 2: a high protein milk beverage). Indicators of muscle protein synthesis (MPS) were assessed before and 1-hr after consuming a postexercise beverage. Muscle protein degradation (MPD) was examined the day before and the day of exercise.

Results: No significant differences were found among groups in MPS. The resistance exercise bout increased the amount of eIF4E-eIF4G by 4.5% 1-hr postexercise (p<0.05) without affecting the amount of eIF4E-4E-BP1. One hour after beverage consumption, serum total amino acid concentration increased for MILK 1 (p=0.003) and MILK 2 (p<0.001) but decreased for CE (p=0.028) and PL (p=0.276). Consumption of MILK 1, MILK 2, and CE significantly increased circulating levels of serum insulin (p<0.001). Serum growth hormone increased 3-fold as a result of the exercise bout but fell to baseline for all groups by 60 min (p<0.001).

Conclusion: The resistance exercise bout was anabolic as shown by the increase in the active eIF4E-eIF4G complex and serum growth hormone. Consumption of MILK 2 led to the most optimal environment for muscle anabolism; however, none of the experimental beverages influenced the measured indicators of muscle protein translation 1-hr after ingestion.
Master of Science

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Banerjee, Camellia Tina. "Muscle ageing and anabolic response in the context of healthy and chronically HIV infected individuals." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12275.

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Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
In the last thirty years of the HIV epidemic, HIV has transitioned from a deadly to a chronic, manageable disease wherein infected individuals are living longer. However, despite the efficacy of antiretroviral therapy in suppressing viral burden, the quality of life is still impacted. HIV-infected individuals display symptoms associated with the elderly including a frailty related phenotype, declines in muscle and bone mass, and notably, a host response resulting in gradual increases in systemic inflammation. This physiological dysregulation leads to increased morbidity and mortality in the HIV positive population. Anabolic therapies targeting muscle loss have demonstrated the efficacy of androgen supplementation, particularly testosterone, in increasing muscle mass in both younger and older individuals, as well as in HIV positive patients. In this thesis, we drew from previous studies on aging and muscle biology to understand HIV associated decreases in muscle function. We evaluated changes in serum biomarkers between older and younger men at baseline and in response to testosterone to identify possible pathways for age related declines in muscle and testosterone response. We then evaluated genomic data from muscle biopsy tissues from HIV infected individuals, older men and younger men to identify pathways that are common to infection and aging and that may underlie declines in muscle mass and function. Finally, we characterized the identified human aging pathways in two animal models of HIV infection, the HIV transgenic rat and the SIV infected rhesus macaque. Here, we provided data on nine independent serum biomarkers related to aging and observed a subset of those that change with age to be affected by testosterone treatment. Furthermore, we found a ten gene signature in muscle that differed between young and old and showed premature expression of this signature in HIV infected people. Because the signature and biomarkers implicated TGFβ associated senescence and fibrotic pathways, we explored these pathways and phenotypes in models of HIV infection, and found suggestions of accelerated aging in muscle of HIV infected individuals. Overall, this thesis provides insights into natural aging pathways co-opted by HIV and how these pathways might play a role in declines in muscle mass and function.
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Redmond, Emily Ja Young. "The protein metabolic response to ingestion of a complete meal in sarcopenic women and the potential anabolic effect of a leucine-rich meal: a pilot study." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106253.

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Sarcopenia – muscle loss that occurs with aging – is a growing concern affecting physical strength and function. This thesis assessed whether 1) the anabolic response of protein metabolism to a meal is impaired in older sarcopenic women – a phenomenon we believe to be largely responsible for the daily imbalance between protein synthesis (S) and breakdown that ultimately causes muscle loss, 2) meal supplementation with leucine (LEU), an essential amino acid which has been shown to stimulate protein S, improves the protein anabolic response to a meal, and 3) a LEU-rich meal affects meal thermogenesis or satiety. Using tracer methodology, whole-body LEU balance was measured, as well as energy expenditure, blood hormone, nutrient and appetite profiles, and activity of muscle intracellular pathways of protein S, in both healthy control (n = 4; body mass index: 24.9 ± 1.5 kg/m2; lean body mass (LBM): 39.4 ± 2.1 kg) and sarcopenic (n = 5; 22.6 ± 1 kg/m2; 34.7 ± 0.4 kg) older women (≥ 61y) after ingestion of a LEU-rich and non-LEU-rich meal in random crossover design. Preliminary results by kg LBM reveal no difference in whole-body LEU balance between groups. The LEU-rich meal achieved greater net balance in both groups without affecting thermogenesis and appetite. Muscle immunoblot data (N = 6) do not suggest blunted activation of mTORC1 and its downstream substrates PRAS40, 4E-BP1, S6K1 and rpS6 in older sarcopenic women, however additional subjects are necessary to draw any conclusions. Future longitudinal supplementation studies assessing postprandial rates of muscle protein synthesis (MPS) in the sarcopenic population will also be necessary to confirm any immunoblot results.
La sarcopénie – perte musculaire associée au vieillissement – est une source de préoccupation, puisqu'elle affecte la force physique et le fonctionnement. Cette thèse a évalué si 1) la réponse anabolique du métabolisme protéique au repas est déficiente chez la femme âgée sarcopénique – un phénomène que nous estimons être largement responsable du déséquilibre entre la synthèse (S) et le catabolisme protéique qui résulte ultérieurement en la perte musculaire, 2) un repas enrichi en leucine (LEU), un acide aminé essentiel avec lequel il fut démontré qu'il stimule la S protéique, améliore la réponse anabolique au repas et 3) un repas enrichi-LEU affecte la thermogénèse et l'appétit. Nous avons procédé à la mesure du bilan en LEU corporel à l'aide d'un traceur isotopique, de même qu'à la dépense énergétique, aux profils des hormones sanguines, nutriments et appétit, et à l'activité intracellulaire de la voie de transduction de la S protéique musculaire, chez des femmes âgées > 61 ans, témoins en santé [n = 4; indice de masse corporelle : 24.9 ± 1.5 kg/m2; masse maigre (MM) : 39.4 ± 2.1 kg] et chez des femmes sarcopéniques (n = 5; 22.6 ± 1 kg/m2; 34.7 ± 0.4 kg), après ingestion d'un repas enrichi-LEU et non-enrichi-LEU dans un devis aléatoire, pairé et croisé. Les résultats préliminaires en kg MMC ne démontrent aucune différence entre les groupes dans le bilan en LEU corporel pour l'un ou l'autre des repas. Cependant le repas enrichi-LEU a stimulé d'avantage le bilan net sans affecter la thermogénèse et l'appétit. Les données musculaires obtenues par immunoblots (n = 6) ne démontrent pas d'activité réduite du mTORC1 et de ses substrat en aval PRAS40, 4E-BP1, S6K1 et rpS6 chez les femmes sarcopéniques. Il est par contre nécessaire d'obtenir plus de sujets avant de pouvoir formuler des conclusions. Des études longitudinales avec des suppléments LEU évaluant les taux de S protéique musculaire (SPM) postprandiaux chez les femmes sarcopéniques seront aussi nécessaires pour confirmer ces résultats.
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Consitt, Leslie A. N. "Comparison of anabolic hormone responses to aerobic and resistance exercise in physically active premenopausal females." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ65480.pdf.

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Alsaqer, Saqer. "LOXL2 in anabolic response to chondrodysplasia mice progressive TMJ and knee osteoarthritis." Thesis, 2019. https://hdl.handle.net/2144/37013.

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Osteoarthritis (OA) is a degenerative joint disease that affects an estimated 9.6 % of men and 18 % of women over 60 years of age. However, there is no chondroprotective agent that is approved for clinical application. We showed that LOXL2 is elevated in the regenerative response during fracture healing in mice and has a critical role in chondrogenic differentiation. Indeed, LOXL2 is an anabolic effector that attenuates pro-inflammatory signaling in OA cartilage of the TMJ and knee joint, induces chondroprotective and regenerative responses. The goal of the present study was to evaluate if LOXL2 adenovirus in vivo promotes protective and anabolic responses in the knee and TMJ-OA cartilage. We employed (Cho/+) OA mouse model to assess knee and TMJ-OA, which is a genetic model that develops progressive TMJ-OA due to a mutation in the Col11a1 gene. Intraperitoneal injection every 2 weeks of Adv-RFP-LOXL2 in four-month-old Cho/+ male and female mice for 16 weeks upregulated Sox9, aggrecan (Acan) and other anabolic genes in the knee and TMJ. Next, to evaluate if LOXL2 expression occurred in degenerative lesions in human clinical TMJ-OA, immunofluorescence and confocal image analysis were performed. LOXL2 has the potential to induce anabolic gene expression in the progressive knee and TMJ-OA mouse model. We showed for the first time that LOXL2-related functions could be useful for anabolic therapies for Cho/+ mice progressive knee and TMJ-OA. Thus, these data show that LOXL2 could have clinical translational applications in the future for OA-related anabolic therapies.
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Nilsson, Mats I. "Influence of Insulin Resistance on Contractile Activity-Induced Anabolic Response of Skeletal Muscle." 2009. http://hdl.handle.net/1969.1/ETD-TAMU-2009-12-7291.

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Although the long-term therapeutic benefits of exercise are indisputable, contractile activity may induce divergent adaptations in insulin-resistant vs. insulin-sensitive skeletal muscle. The purpose of this study was to elucidate if the anabolic response following resistance exercise (RE) is altered in myocellular sub-fractions in the face of insulin resistance. Lean (Fa/?) and obese (fa/fa) Zucker rats were assigned to sedentary and RE groups and engaged in either cage rest or four lower-body RE sessions over an 8-d period. Despite obese Zucker rats having significantly smaller hindlimb muscles when compared to age-matched lean rats, basal 24-h fractional synthesis rates (FSR) of mixed protein pools were near normal in distally located muscle groups (gastrocnemius, plantaris, and soleus) and even augmented in those located more proximally (P<0.05; quadriceps). Although 2 x 2 ANOVA indicated a significant main effect of phenotype on mixed FSR in gastrocnemius and soleus (P < 0.05), phenotypic differences were partially accounted for by an exercise effect in the lean phenotype. Interestingly, obese rats exhibited a significant suppression of myofibrillar FSR compared to their lean counterparts (P<0.05; gastrocnemius), while synthesis rates of mitochondrial and cytosolic proteins were normal (gastrocnemius and quadriceps), suggesting a mechanism whereby translation of specific mRNA pools encoding for metabolic enzymes may be favored over other transcripts (e.g., contractile proteins) to cope with nutrient excess in the insulin-resistant state. Immunoblotting of the cytosolic fraction in gastrocnemius muscle indicated an augmented phosporylation of eIF4EBP1 (+ 9%) and p70s6k (+85%) in obese vs. lean rats, but a more potent baseline inhibition of polypeptide-chain elongation as evidenced by an increased phospho/total ratio of eEF2 (+78%) in the obese phenotype. Resistance exercise did not improve synthesis rates of myofibrillar, cytosolic, or mitochondrial proteins to the same extent in obese vs. lean rats, suggesting a desensitization to contractile-induced anabolic stimuli in the insulin-resistant state. We conclude that insulin resistance has diverse effects on protein metabolism, which may vary between muscle groups depending on fiber type distribution, location along the proximodistal body axis, and myocellular sub-fraction, and may blunt the anabolic response to voluntary resistance exercise.
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Hum, Julia M. "Signaling mechanisms that suppress the anabolic response of osteoblasts and osteocytes to fluid shear stress." Thesis, 2014. http://hdl.handle.net/1805/4652.

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Indiana University-Purdue University Indianapolis (IUPUI)
Bone is a dynamic organ that responds to its external environment. Cell signaling cascades are initiated within bone cells when changes in mechanical loading occur. To describe these molecular signaling networks that sense a mechanical signal and convert it into a transcriptional response, we proposed the mechanosome model. “GO” and “STOP” mechansomes contain an adhesion-associated protein and a nucleocytoplasmic shuttling transcription factor. “GO” mechanosomes functions to promote the anabolic response of bone to mechanical loading, while “STOP” mechanosomes function to suppress the anabolic response of bone to mechanical loading. While much work has been done to describe the molecular mechanisms that enhance the anabolic response of bone to loading, less is known about the signaling mechanisms that suppress bone’s response to loading. We studied two adhesion-associated proteins, Src and Pyk2, which may function as “STOP” mechanosomes. Src kinase is involved in a number of signaling pathways that respond to changes in external loads on bone. An inhibition of Src causes an increase in the expression of the anabolic bone gene osteocalcin. Additionally, mechanical stimulation of osteoblasts and osteocytes by fluid shear stress further enhanced expression of osteocalcin when Src activity was inhibited. Importantly, fluid shear stress stimulated an increase in nuclear Src activation and activity. The mechanism by which Src participates in attenuating anabolic gene transcription remains unknown. The studies described here suggest Src and Pyk2 increase their association in response to fluid shear stress. Pyk2, a protein-tyrosine kinase, exhibits nucleocytoplasmic shuttling, increased association with methyl-CpG-binding protein 2 (MBD2), and suppression of osteopontin expression in response to fluid shear stress. MBD2, known to be involved in DNA methylation and interpretation of DNA methylation patterns, may aid in fluid shear stress-induced suppression of anabolic bone genes. We conclude that both Src and Pyk2 play a role in regulating bone mass, possibly through a complex with MBD2, and function to limit the anabolic response of bone cells to fluid shear stress through the suppression of anabolic bone gene expression. Taken together, these data support the hypothesis that “STOP” mechanosomes exist and their activity is simulated in response to fluid shear stress.
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Alshenibr, Weam. "Novel role of LOXL2 in TMJ and knee OA cartilage in vitro and in vivo." Thesis, 2018. https://hdl.handle.net/2144/32945.

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BACKGROUND: Osteoarthritis (OA) is the most common degenerative joint disease which affects the joint structures leading to disability. Studies in the last 20 years have documented the increased prevalence of knee pain and symptomatic knee OA. Similarly, of temporomandibular joint (TMJ) disorders OA is the most common. Lysyl oxidase like-2 (LOXL2) is a copper-dependent amine oxidase. previous studies showed that LOXL2 is elevated during mouse fracture healing. Our hypothesis that LOXL2 acts as a specific anabolic factor in chondrocytes METHODS: The activity of LOXL2 in human articular and TMJ chondrocytes was assessed by cell-based assays and RT-qPCR, and LOXL2-mediated activation of NF-κB and extracellular signal-related kinase (ERK) signaling pathways was measured by western blotting. To examine LOXL2-induced effect in vivo, we implanted Matrigel-imbedded human chondrocytes into nude mice and exposed them to exogenous LOXL2 for 6 weeks. We also examined if LOXL2 induces the proliferation of OA chondrocytes. RESULTS: LOXL2 staining was detected in damaged regions of human TMJ, hip and knee joints affected by OA. Stimulation with transforming growth factor (TGF)-β1 upregulated LOXL2 expression, while pro-inflammatory cytokines IL-1β and TNF-α downregulated LOXL2, in human chondrocytes. LOXL2 expression also inhibited IL-1β-induced phospho-NF-κB/p65 and TGF-β1-induced ERK1/2 phosphorylation. Matrigel constructs of human chondrocytes from the knee joint and TMJ implanted in nude mice showed anabolic responses after LOXL2 transduction, including increased expression of SOX9, ACAN, and COL2A1. We have found that LOXL2 does not induce the proliferation of human TMJ or knee OA chondrocytes. CONCLUSIONS: We showed that LOXL2 induces differentiation and attenuates OA related catabolic signaling pathways.
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Quan, Brenton Sim Yim, and 沈奕全. "Effect of Rhodiola crenulata and Cordyceps sinensis supplementation with Aerobic Exercise Training on Anabolic Hormone Response and Exercise Performance." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/fnnsp5.

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碩士
臺北市立大學
運動健康科學系碩士班
107
this study was to investigate the effects of aerobic exercise training combined with Rhodiola and Cordyceps Sinensis supplementation on synthetic hormones and motor performance. This study enrolled 14 young male and female subjects (height 167.9 ± 8.2 cm, weight 68.6 ± 12.6 kg, age 21.6 ± 1 year old), divided into according to gender, body weight, and maximum oxygen uptake (VO2max): (Exercise training with placebo, EP, = 7) and (exercise training combined with Rhodiola crenulata plus Cordyceps Sinensis supplementation RCE = 7). Subjects were supplemented with placebo and RC during the 8-week experimental intervention, with a daily supplement of 20 mg/kg, supplemented for morning and evening supplements. Subjects were measured for changes in maximal oxygen uptake, lower extremity explosive force, lower limb reactive capacity, and synthetic hormone concentrations (DHEA-S, cortisol, D/C ratio, testosterone) before and after the intervention. The results of the study showed that the maximum oxygen uptake and DHEA-S increased significantly after eight weeks of aerobic exercise, but there was no difference between groups. There was no significant difference in the lower extremity explosive force, lower limb reaction ability, cortisol, D/C ratio and testosterone between the two groups after training. Conclusion: The results of this study found that aerobic exercise training can increase maximal oxygen uptake and DHEA-S, but the intervention of Rhodiola and Cordyceps sinensis did not significantly improve exercise performance and hormone concentration.
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Books on the topic "Anabolic response"

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Jürimäe, Jaak. Hormones and training. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0033.

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Physical exercise regulates energy balance and is important to growth and maturation. These processes are regulated by the endocrine system. Endocrine mechanisms in the response to sport training include growth hormone-insulin-like growth factor-1 (GH-IGF-1), hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes, and peripheral markers of energy homeostasis. Physical performance is associated with anabolic adaptations of the GH-IGF-1 system in child athletes alongside spontaneous growth, while heavy training does not affect basal testosterone levels. In female adolescent athletes, the major factor altering reproductive hormone secretion is energy deficiency, rather than exercise stress or increase in exercise energy expenditure. Ghrelin is another indicator of energy imbalance across the menstrual cycle. Pubertal onset decreases ghrelin, and leptin levels are reduced and may remain unchanged between prepuberty and maturation in athletes. To better understand the influence of high training load on hormonal markers responsible for overall growth and energy homeostasis, growing athletes should be monitored often.
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Book chapters on the topic "Anabolic response"

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Thissen, Jean-Paul. "Anabolic Resistance." In The Stress Response of Critical Illness: Metabolic and Hormonal Aspects, 45–60. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27687-8_5.

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Hue, L., V. Gaussin, and U. Krause. "Anabolic Response to Cell Swelling in the Liver." In Contributions of Physiology to the Understanding of Diabetes, 10–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60475-1_2.

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Millward, D. J. "The Endocrine Response to Dietary Protein: the Anabolic Drive on Growth." In Milk Proteins, 49–61. Heidelberg: Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-642-85373-9_5.

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Sundell, Jan. "Anabolic Training Response and Clinical Implications." In Nutrition and Enhanced Sports Performance, 419–21. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813922-6.00035-7.

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Sundell, Jan. "Anabolic Training Response and Clinical Implications." In Nutrition and Enhanced Sports Performance, 351–53. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-396454-0.00035-7.

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Herndon, David N., Celeste C. Finnerty, and Rene Przkora. "Hypermetabolic response to burns." In Burns (OSH Surgery), 29–34. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199699537.003.0004.

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Large burns are one of the most disastrous injuries today. The survivor experiences a tremendous metabolic response that does not resolve with burn wound healing. This response is seen in patients with burns over more than 30% of the total body surface area (TBSA). Two phases are observed: the 'ebb' phase starts immediately after a burn, lasts for 2–3 days, and is characterized by a “shock state” with decreases in cardiac output and metabolism; the ‘flow’ phase starts approximately 5 days after a burn. This phase can last up to 3 years in paediatric patients with >30% TBSA. The flow phase is characterized by persistent hypermetabolic and inflammatory responses, leading to catabolism and loss of function. Early interventions, including excision and grafting of wounds, enteral feeding, treatment of infections, pharmacological interventions (eg. anabolic hormones, adrenergic receptor antagonists), and exercise, can successfully attenuate this deleterious response.
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Tsay, J., RW Grady, PJ Giardina, AL Boskey, and MG Vogiatzi. "Impaired Bone Anabolic Response to PTH Therapy in the Th3/+ Mouse Model of Thalassemia." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–144—P1–144. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p3.p1-144.

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Gioia, Gianfranco, Alessio Molfino, Filippo Rossi Fanelli, and Maurizio Muscaritoli. "From nutritional screening to assessment and nutritional planning in community, acute, and long-term care." In Oxford Textbook of Geriatric Medicine, 479–86. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0063.

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Age-related malnutrition is the result of age-related metabolic derangements. Sarcopenia in older people is also the result of malnutrition-related metabolic changes determining the lack of long-term muscle anabolic response to nutrient intake. Frailty is associated with the presence of nutritional derangements. Nutritional screening tools and nutritional assessment in ageing take into account diagnostic parameters for detecting the risk or the presence of protein-energy malnutrition in its different forms and stages. Nutritional screening represents the first step in the nutritional care process. A full nutritional assessment is necessary if the risk of malnutrition is detected during a nutritional screening. Nutritional and metabolic interventions are recommended for all those patients identified by screening and assessment as at risk for malnutrition or malnourishment. Nutritional plans offer several options to the patients according to the clinical setting (i.e. nutritional counselling, food fortification, oral nutritional supplements, and artificial nutrition).
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"Phasic Responses to Trauma (Immediate, Catabolic, and Anabolic)." In Metabolic and Endocrine Physiology, 82–83. Teton NewMedia, 2012. http://dx.doi.org/10.1201/b16175-39.

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Johnson, Bradley J., and Christopher D. Reinhardt. "Growth Promotants for Beef Production: Anabolic Steroids: Performance Responses and Mode of Action." In Food Animal Practice, 643–51. Elsevier, 2009. http://dx.doi.org/10.1016/b978-141603591-6.10124-1.

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Conference papers on the topic "Anabolic response"

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O’Conor, Christopher J., Kenneth W. Ng, Lindsay E. Kugler, Gerard A. Ateshian, and Clark T. Hung. "The Response of Tissue Engineered Cartilage to the Temporal Application of Transforming and Insulin-Like Growth Factors." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176523.

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Agarose has been used as an experimental scaffold for cartilage tissue engineering research due to its biocompatibility with chondrocytes, support of cartilage tissue development, and ability to transmit mechanical stimuli [1–3]. Tissue engineering studies have demonstrated that the temporal application of transforming growth factor (TGF) β3 for only 2 weeks elicits rapid tissue development that results in mechanical properties approaching native values [4]. However, it is not known whether this response to a 2-week exposure to growth factors is unique to TGF-β3. Therefore, the present study characterizes the response of tissue engineered cartilage to the temporal application of the anabolic growth factors TGF-β1, TGF-β3, and insulin-like growth factor I (IGF-I).
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Taboas, J. M., S. K. Connor, and R. S. Tuan. "Constitutive Bcl-2 over-expression triggers an anabolic response in chondrocytes, with partial abatement of IL-1β catabolic effects." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967657.

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Kirschner, S. K., N. E. P. Deutz, R. Jonker, A. McNew-Wierzchowska, S. W. M. Olde Damink, R. I. Harrykissoon, A. J. Zachria, and M. P. K. J. Engelen. "Small Intestinal Dysfunction Attenuates the Anabolic Response to Feeding and Compromises Daily Functioning in Patients with Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5724.

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Qin, Yi-Xian, Tamara Kaplan, and Hoyan Lam. "Anabolic Fluid Flow as Dependent on It Dose and Frequency in Bone Formation and Inhibition of Bone Loss." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61388.

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Anabolic response of bone to interstitial fluid flow is strongly dependent on the dynamic components of the fluid pressure, implying that fluid flow is a critical regulatory component to bone mass and morphology. While the fluid stimulus can be potentially applied for therapeutic in promoting turnover, the hypothesis of fluid induced bone adaptation was evaluated in an avian ulna model using varied flow rates and magnitudes. Total of 12 one-year old male avian animals was used in this study. A sinusoidal fluid pressure was applied to the experimental ulna 10 min/day for 4 weeks. Three experimental groups of loading were performed at 1 and 30 Hz of fluid loading. The results reveal an increase of 22.7%±7.2 in trabecular volume for group of 30 Hz, 76mmHg loading, while it had only 0.5 % increase at 1Hz, 76 mmHg loading. Under physiologic fluid pressure, a higher flow rate of stimuli generates much higher remodeling response than a lower rate of loading. This implies that bone turnover may be sensitive to the dynamic components of fluid flow, thereby initiating the adaptive response.
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Nicoll, Steven B., Robert L. Mauck, Rick C. Tsay, Clark T. Hung, and Gerard A. Ateshian. "Intermittent Hydrostatic Pressurization Modulates Gene Expression in Human Dermal Fibroblasts Seeded in Three-Dimensional Polymer Scaffolds." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33604.

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Mechanical stimuli are known to regulate the morphology and differentiated function of connective tissue cells. In particular, hydrostatic pressure has been reported to alter cytoskeletal organization in osteoblast-like cells (1) and chondrocytes (2), and to modulate metabolic activity in both chondrocytes (3–5) and intervertebral disc cells (6). The cellular response to continuous hydrostatic pressure is generally catabolic (3) while intermittent hydrostatic pressure at frequencies ranging from 0.25–1.0 Hz (3–5) is anabolic, giving rise to increased expression and biosynthesis of extracellular matrix (ECM) components. Previously, human dermal fibroblasts in monolayer culture were shown to respond to hydrostatic pressure by increasing heat shock protein expression levels (7). In this study, we characterize the effects of intermittent hydrostatic pressure on gene expression in human dermal fibroblasts seeded in three-dimensional polymer scaffolds.
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Ferreri, Suzanne, and Yi-Xian Qin. "Alteration of Bone’s Nonlinear Elastic and Viscoelastic Nanomechanical Properties Is Triggered by Low Intensity Pulsed Ultrasound." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206711.

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Dynamic mechanotransduction, particularly under high frequency, low amplitude signals, has been proven effective in mediating bone loss and improving mechanical strength for tissues affected by estrogen deficient osteopenia. Ultrasound, which behaves as an alternating pressure wave in bone, may offer an effective, non-invasive technology for delivery of anabolic signals. In vitro, dynamic mechanical signals delivered using ultrasound have been shown to increase osteoblast proliferation [1], and in vivo studies have established ultrasound as an effective treatment for delayed and non-union fractures [2]. Previously, we showed that ultrasound signals similar to those currently used in a clinical setting for fracture healing were effective in mediating decreases in bone volume and mechanical strength at the millimeter length-scale in response to estrogen deficient osteopenia [3]. Due to bone’s inherent viscoelasticity and the dynamic nature of the applied ultrasound signals, it is particularly important to consider both elastic and viscous components of bone’s adaptive response to applied loads. In light of these findings, the goal of this study was to determine the role of therapeutic ultrasound signal intensity in modulating changes in bone’s nanoscale elastic and viscoelastic material properties associated with estrogen deficient osteopenia. We hypothesize that bone is sensitive to dynamic mechanical signals delivered via ultrasound and that bone’s tissue level nano-scale material properties, particularly nonlinear viscoelastic properties, are sensitive to ultrasound signal intensity.
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Keller, Benjamin V., Matthew L. Davis, Laurence E. Dahners, and Paul S. Weinhold. "Whole Body Vibration Amplitude Levels Differentially Affect Tendon and Ligament Structural Properties." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53877.

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Recently there have been a large number of studies examining the potential therapeutic effects of whole body vibration (WBV). Numerous studies have shown that low magnitude, high frequency vibration (LMHFV) can be anabolic for muscle and bone. Vibration has been applied to both animals and humans with notable increases in muscle cross-sectional area as well as strength [1, 4, 7]. Both high (3 G) and low (0.3 G) vibratory stimuli have been reported to initiate an increase in bone density and subsequently bone strength [3, 5]. The effects of LMHFV on other dense connective tissue types have been relatively unexplored. Legerlotz et al. investigated the response of rat Achilles tendons to 2 G WBV and found no effect on biomechanical properties [2]. However, Legerlotz’s experiment applied between 2–7 minutes of vibration a day which is significantly less than other studies as well as clinical applications. The goal of our study was to determine the effects of vibration level on the structural and material properties of intact ligaments and tendons. We hypothesized that vibration, a passive surrogate for exercise, may contribute to ligament and tendon strengthening.
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Hart, Stephen A., and Marcelo J. Dapino. "Accelerated Bone Growth Remotely Induced by Magnetic Fields and Smart Materials." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175966.

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Bone structure is exquisitely matched to its physical loading environment. From the cartilaginous skeletal framework formed in the embryo to the aging skeleton, bone architecture is directly related to function. Bone is a dynamic system, constantly remodeling itself by absorbing old tissue and forming new tissue. This capability allows bone architecture to become optimized to the loading environment. Julius Wolff [1] first postulated that bone structure adapts to changing stress environments in 1892. Exact understanding of the process of mechanotransduction, however, has remained elusive. In addition to normal remodeling, bone growth has been shown to occur along the diaphysis, or shaft portion, of long bones such as the femur when placed in dynamic bending. Bone in this region is dense and is known as cortical bone. A bending moment placed on a long bone will cause the bone to curve creating a region of tension on one side and a region of compression on the opposing side. As the bending moment is cycled, fluid within the bone will flow from the region of compression to the region of tension creating fluid shear on cell walls within the bone which promotes the anabolic response of growth [2]. Growth from such stimuli is thought to be mediated by fluid flow around quiescent bone cells, osteocytes, and their canalicular process coursing through the bone structure [3]. Growth in this manner is directed in a latitudinal direction creating a thicker and stronger diaphysis.
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Wan, Qiaoqiao, Eunhye Cho, Seungman Park, Bumsoo Han, Hiroki Yokota, and Sungsoo Na. "Visualizing Chondrocyte Mechanotransduction in 3D." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14484.

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Chondrocytes are the only cell type present in the articular cartilage and their response to mechanical stimuli influences the maintenance and remodeling of the cartilage. Numerous studies have shown that the balance between anabolic and catabolic responses of the chondrocytes to mechanical loading is dependent on the loading intensities (reviewed in ref. [1]). Moderate, physiological loading, for instance, increases synthetic activity of the extracellular matrix (ECM) such as collagen type II, aggrecan, and proteoglycan, while decreasing the catabolic activity of degradative enzymes such as matrix metalloproteinases (MMPs) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) [2,3]. In contrast to moderate loading, static or high-intensity loading has been shown to degrade the cartilage resulting from inhibition of matrix synthesis and up-regulation of catabolic activities [3,4]. Therefore, the importance of these load-dependent signaling pathways involved in the maintenance and remodeling of the cartilage is widely accepted. However, the underlying mechanisms as to how varying magnitudes of mechanical stimuli trigger differential signaling activities that consequently lead to selective gene expression are not clear. FAK and Src are considered to be the main mechanotransduction signaling proteins at the cell-ECM adhesion sites and their activities influence various structural and signaling changes within the cell, including cytoskeletal organization, migration, proliferation, differentiation, and survival [5]. Accumulating evidence has shown that Src and FAK play crucial roles in regulating cartilage maintenance and degeneration and their activation stimulates matrix catabolic genes and activity [6,7]. Rho family GTPases such as RhoA and Rac1 play critical roles in fundamental processes including morphogenesis, polarity, movement, and cell division [8]. They also contribute to cartilage development and degradation [9,10]. Despite these studies, much remains to be elucidated on how load-induced Src and FAK participate in chondrocyte functions, and how their interactions are linked and regulated in connection to the activities of RhoA and Rac1 under different loading conditions. In this study, we use fluorescence resonance energy transfer (FRET)-based biosensors to monitor activities of Src and FAK as well as individual GTPases and evaluate the potential linkage of a network of these signaling molecules under different loading conditions.
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Zhou, Yilu, Lauren Resutek, Liyun Wang, and X. Lucas Lu. "In Situ Calcium Signaling of Chondrocytes Under Non-Serum and Serum Culture." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14624.

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Chemically defined serum-free medium has been shown to maintain the mechanical properties of cartilage allografts better than serum supplemented medium during long-term in vitro culture [1]. Little is known about this beneficial mechanism at a cellular level. Intracellular calcium ([Ca2+]i) signaling is one of the earliest responses in chondrocytes under mechanical stimulation [2]. It was recently found that calcium signaling is involved in the regulation of chondrocyte morphology changes and its short-term anabolic and catabolic responses under mechanical stimulation [3]. In this study we hypothesized that the beneficial mechanisms of serum-free culture could be indicated by the spatiotemporal features of [Ca2+]i signaling of chondrocytes in situ. We aimed to: (i) compare the in situ spontaneous [Ca2+]i responses of chondrocytes cultured in medium with and without serum; (ii) investigate the correlation between the [Ca2+]i responses of chondrocytes and the biomechanical properties of cartilage explants.
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Reports on the topic "Anabolic response"

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Kesavan, Chandrasekhar. MicroRNA, Angiogenesis and Skeletal Anabolic Response to Mechanical Strain. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581658.

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