Journal articles: '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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Bamman, M. M., A. Goodman, G. R. Hunter, J. R. Shipp, and B. A. Gower. "ACUTE ANABOLIC HORMONE RESPONSE FOLLOWING ECCENTRIC RESISTANCE EXERCISE." Medicine & Science in Sports & Exercise 31, Supplement (May 1999): S325. http://dx.doi.org/10.1097/00005768-199905001-01626.

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Kim, Il-Young, Nicolaas E. P. Deutz, and Robert R. Wolfe. "Update on maximal anabolic response to dietary protein." Clinical Nutrition 37, no. 2 (April 2018): 411–18. http://dx.doi.org/10.1016/j.clnu.2017.05.029.

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Drummond, Micah J., Robin L. Marcus, and Paul C. LaStayo. "Targeting Anabolic Impairment in Response to Resistance Exercise in Older Adults with Mobility Impairments: Potential Mechanisms and Rehabilitation Approaches." Journal of Aging Research 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/486930.

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Muscle atrophy is associated with healthy aging (i.e., sarcopenia) and may be compounded by comorbidities, injury, surgery, illness, and physical inactivity. While a bout of resistance exercise increases protein synthesis rates in healthy young skeletal muscle, the effectiveness of resistance exercise to mount a protein synthetic response is less pronounced in older adults. Improving anabolic sensitivity to resistance exercise, thereby enhancing physical function, is most critical in needy older adults with clinical conditions that render them “low responders”. In this paper, we discuss potential mechanisms contributing to anabolic impairment to resistance exercise and highlight the need to improve anabolic responsiveness in low responders. This is followed with evidence suggesting that the recovery period of resistance exercise provides an opportunity to amplify the exercise-induced anabolic response using protein/essential amino acid ingestion. This anabolic strategy, if repeated chronically, may improve lean muscle gains, decrease time to recovery of function during periods of rehabilitation, and overall, maintain/improve physical independence and reduce mortality rates in older adults.

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Watson, Matthew D., Brett L. Cross, and Gregory J. Grosicki. "Evidence for the Contribution of Gut Microbiota to Age-Related Anabolic Resistance." Nutrients 13, no. 2 (February 23, 2021): 706. http://dx.doi.org/10.3390/nu13020706.

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Globally, people 65 years of age and older are the fastest growing segment of the population. Physiological manifestations of the aging process include undesirable changes in body composition, declines in cardiorespiratory fitness, and reductions in skeletal muscle size and function (i.e., sarcopenia) that are independently associated with mortality. Decrements in muscle protein synthetic responses to anabolic stimuli (i.e., anabolic resistance), such as protein feeding or physical activity, are highly characteristic of the aging skeletal muscle phenotype and play a fundamental role in the development of sarcopenia. A more definitive understanding of the mechanisms underlying this age-associated reduction in anabolic responsiveness will help to guide promyogenic and function promoting therapies. Recent studies have provided evidence in support of a bidirectional gut-muscle axis with implications for aging muscle health. This review will examine how age-related changes in gut microbiota composition may impact anabolic response to protein feeding through adverse changes in protein digestion and amino acid absorption, circulating amino acid availability, anabolic hormone production and responsiveness, and intramuscular anabolic signaling. We conclude by reviewing literature describing lifestyle habits suspected to contribute to age-related changes in the microbiome with the goal of identifying evidence-informed strategies to preserve microbial homeostasis, anabolic sensitivity, and skeletal muscle with advancing age.

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Woodhouse, Linda J., Suzanne Reisz-Porszasz, Marjan Javanbakht, Thomas W. Storer, Martin Lee, Hrant Zerounian, and Shalender Bhasin. "Development of models to predict anabolic response to testosterone administration in healthy young men." American Journal of Physiology-Endocrinology and Metabolism 284, no. 5 (May 1, 2003): E1009—E1017. http://dx.doi.org/10.1152/ajpendo.00536.2002.

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Considerable heterogeneity exists in the anabolic response to androgen administration; however, the factors that contribute to variation in an individual's anabolic response to androgens remain unknown. We investigated whether testosterone dose and/or any combination of baseline variables, including concentrations of hormones, age, body composition, muscle function, and morphometry or polymorphisms in androgen receptor could explain the variability in anabolic response to testosterone. Fifty-four young men were treated with a long-acting gonadotropin-releasing hormone (GnRH) agonist and one of five doses (25, 50, 125, 300, or 600 mg/wk) of testosterone enanthate (TE) for 20 wk. Anabolic response was defined as a change in whole body fat-free mass (FFM) by dual-energy X-ray absorptiometry (DEXA), appendicular FFM (by DEXA), and thigh muscle volume (by magnetic resonance imaging) during TE treatment. We used univariate and multivariate analysis to identify the subset of baseline measures that best explained the variability in anabolic response to testosterone supplementation. The three-variable model of TE dose, age, and baseline prostate-specific antigen (PSA) level explained 67% of the variance in change in whole body FFM. Change in appendicular FFM was best explained (64% of the variance) by the linear combination of TE dose, baseline PSA, and leg press strength, whereas TE dose, log of the ratio of luteinizing hormone to testosterone concentration, and age explained 66% of the variation in change in thigh muscle volume. The models were further validated by using Ridge analysis and cross-validation in data subsets. Only the model using testosterone dose, age, and PSA was a consistent predictor of change in FFM in subset analyses. The length of CAG tract was only a weak predictor of change in thigh muscle volume and lean body mass. Hence, the anabolic response of healthy, young men to exogenous testosterone administration can largely be predicted by the testosterone dose.

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Roberts, Michael D., Matthew A. Romero, Christopher B. Mobley, Petey W. Mumford, Paul A. Roberson, Cody T. Haun, Christopher G. Vann, et al. "Skeletal muscle mitochondrial volume and myozenin-1 protein differences exist between high versus low anabolic responders to resistance training." PeerJ 6 (July 27, 2018): e5338. http://dx.doi.org/10.7717/peerj.5338.

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Background We sought to examine how 12 weeks of resistance exercise training (RET) affected skeletal muscle myofibrillar and sarcoplasmic protein levels along with markers of mitochondrial physiology in high versus low anabolic responders. Methods Untrained college-aged males were classified as anabolic responders in the top 25th percentile (high-response cluster (HI); n = 13, dual x-ray absorptiometry total body muscle mass change (Δ) = +3.1 ± 0.3 kg, Δ vastus lateralis (VL) thickness = +0.59 ± 0.05 cm, Δ muscle fiber cross sectional area = +1,426 ± 253 μm2) and bottom 25th percentile (low-response cluster (LO); n = 12, +1.1 ± 0.2 kg, +0.24 ± 0.07 cm, +5 ± 209 μm2; p < 0.001 for all Δ scores compared to HI). VL muscle prior to (PRE) and following RET (POST) was assayed for myofibrillar and sarcoplasmic protein concentrations, myosin and actin protein content, and markers of mitochondrial volume. Proteins related to myofibril formation, as well as whole lysate PGC1-α protein levels were assessed. Results Main effects of cluster (HI > LO, p = 0.018, Cohen’s d = 0.737) and time (PRE > POST, p = 0.037, Cohen’s d = −0.589) were observed for citrate synthase activity, although no significant interaction existed (LO PRE = 1.35 ± 0.07 mM/min/mg protein, LO POST = 1.12 ± 0.06, HI PRE = 1.53 ± 0.11, HI POST = 1.39 ± 0.10). POST myofibrillar myozenin-1 protein levels were up-regulated in the LO cluster (LO PRE = 0.96 ± 0.13 relative expression units, LO POST = 1.25 ± 0.16, HI PRE = 1.00 ± 0.11, HI POST = 0.85 ± 0.12; within-group LO increase p = 0.025, Cohen’s d = 0.691). No interactions or main effects existed for other assayed markers. Discussion Our data suggest myofibrillar or sarcoplasmic protein concentrations do not differ between HI versus LO anabolic responders prior to or following a 12-week RET program. Greater mitochondrial volume in HI responders may have facilitated greater anabolism, and myofibril myozenin-1 protein levels may represent a biomarker that differentiates anabolic responses to RET. However, mechanistic research validating these hypotheses is needed.

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Jonker, Renate, Nicolaas E. P. Deutz, Rajesh Harrykissoon, Anthony J. Zachria, Eugene A. Veley, and Mariëlle P. K. J. Engelen. "A critical evaluation of the anabolic response after bolus or continuous feeding in COPD and healthy older adults." Clinical Science 132, no. 1 (January 2, 2018): 17–31. http://dx.doi.org/10.1042/cs20171068.

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After bolus and continuous enteral feeding of the same protein, different digestion and absorption kinetics and anabolic responses are observed. Establishing which mode of feeding has the highest anabolic potential in patients with chronic obstructive pulmonary disease (COPD) may aid in the prevention of muscle wasting, but an important confounding factor is the duration of assessments after bolus feeding. We hypothesized that the anabolic response to bolus and continuous feeding in COPD patients is comparable when methodological issues are addressed. Twenty-one older adults (12 patients with stage II–IV COPD and 9 healthy controls) were studied after intake of a fast-absorbing hydrolyzed casein protein–carbohydrate mixture either as a single bolus or as small sips (crossover design). Whole body protein synthesis (PS), breakdown (PB), net PS (PS − PB) protein efficiency (netPSPE), net protein balance (phenylalanine (PHE) intake – PHE hydroxylation) protein efficiency (netBalPE), and splanchnic PHE extraction (SPEPHE) were assessed using stable isotope tracer methodology. Bolus feeding assessments were done at 90, 95, and 99% of the calculated duration of the anabolic response. At 99%, netBalPE was higher for sip feeding than bolus feeding in both groups (P<0.0001). Nevertheless, bolus feeding was associated with a lower SPEPHE (P<0.0001) and higher netPSPE (P<0.0001). At 90% compared with 99%, PS and netBalPE after bolus feeding was significantly overestimated. In conclusion, several factors complicate a comparison of the anabolic capacity of bolus and continuous feeding in acute studies, including the critical role of SPE calculation and assumptions, and the duration of postprandial assessments after bolus feeding.

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Dillon, E. Lichar, Shanon L. Casperson, William J. Durham, Kathleen M. Randolph, Randall J. Urban, Elena Volpi, Masood Ahmad, Michael P. Kinsky, and Melinda Sheffield-Moore. "Muscle protein metabolism responds similarly to exogenous amino acids in healthy younger and older adults during NO-induced hyperemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (November 2011): R1408—R1417. http://dx.doi.org/10.1152/ajpregu.00211.2011.

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The combination of increasing blood flow and amino acid (AA) availability provides an anabolic stimulus to the skeletal muscle of healthy young adults by optimizing both AA delivery and utilization. However, aging is associated with a blunted response to anabolic stimuli and may involve impairments in endothelial function. We investigated whether age-related differences exist in the muscle protein anabolic response to AAs between younger (30 ± 2 yr) and older (67 ± 2 yr) adults when macrovascular and microvascular leg blood flow were similarly increased with the nitric oxide (NO) donor, sodium nitroprusside (SNP). Regardless of age, SNP+AA induced similar increases above baseline ( P ≤ 0.05) in macrovascular flow (4.3 vs. 4.4 ml·min−1·100 ml leg−1 measured using indocyanine green dye dilution), microvascular flow (1.4 vs. 0.8 video intensity/s measured using contrast-enhanced ultrasound), phenylalanine net balance (59 vs. 68 nmol·min−1·100 ml·leg−1), fractional synthetic rate (0.02 vs. 0.02%/h), and model-derived muscle protein synthesis (62 vs. 49 nmol·min−1·100 ml·leg−1) in both younger vs. older individuals, respectively. Provision of AAs during NO-induced local skeletal muscle hyperemia stimulates skeletal muscle protein metabolism in older adults to a similar extent as in younger adults. Our results suggest that the aging vasculature is responsive to exogenous NO and that there is no age-related difference per se in AA-induced anabolism under such hyperemic conditions.

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Shad, Brandon J., Janice L. Thompson, and Leigh Breen. "Does the muscle protein synthetic response to exercise and amino acid-based nutrition diminish with advancing age? A systematic review." American Journal of Physiology-Endocrinology and Metabolism 311, no. 5 (November 1, 2016): E803—E817. http://dx.doi.org/10.1152/ajpendo.00213.2016.

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The precise role of age-related muscle anabolic resistance in the progression of sarcopenia and functional decline in older individuals is unclear. The present aim was to assess whether the muscle protein synthesis (MPS) response to acute exercise (endurance or resistance) and/or amino acid-based nutrition is attenuated in older compared with young individuals. A systematic review was conducted on studies that directly examined the influence of age on the MPS response to exercise and/or amino acid-based nutrition. Each study arm was synthesized and reported as providing sufficient or insufficient “evidence of age-related muscle anabolic resistance”. Subsequently, three models were established to compare age-related differences in the MPS response to 1) exercise alone, 2) amino acid-based nutrition alone, or 3) the combination of exercise and amino acid-based nutrition. Following exercise alone, 8 of the 17 study arms provided sufficient evidence of age-related muscle anabolic resistance, while in response to amino acid-based nutrition alone, 8 of the 21 study arms provided sufficient evidence of age-related muscle anabolic resistance. When exercise and amino acid-based nutrition were combined, only 2 of the 10 study arms provided sufficient evidence of age-related muscle anabolic resistance. Our results highlight that optimization of exercise and amino acid-based nutrition is sufficient to induce a comparable MPS response between young and older individuals. However, the exercise volume completed and/or the amino acid/protein dose and leucine content must exceed a certain threshold to stimulate equivalent MPS rates in young and older adults, below which age-related muscle anabolic resistance may become apparent.

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Ziadlou, Barbero, Stoddart, Wirth, Li, Martin, Wang, Qin, Alini, and Grad. "Regulation of Inflammatory Response in Human Osteoarthritic Chondrocytes by Novel Herbal Small Molecules." International Journal of Molecular Sciences 20, no. 22 (November 15, 2019): 5745. http://dx.doi.org/10.3390/ijms20225745.

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In this study, 34 Traditional Chinese Medicine (TCM) compounds were screened for potential anabolic and anti-inflammatory properties on human osteoarthritic (OA) chondrocytes. The anabolic effects were assessed by measuring the glycosaminoglycan (GAG) relative to the DNA content using a 3D pellet culture model. The most chondrogenic compounds were tested in an inflammatory model consisting of 3 days of treatment with cytokines (IL-1β/TNF-α) with or without supplementation of TCM compounds. The anti-inflammatory effects were assessed transcriptionally, biochemically and histologically. From the 34 compounds, Vanilic acid (VA), Epimedin A (Epi A) and C (Epi C), 2′′-O-rhamnosylicariside II (2-O-rhs II), Icariin, Psoralidin (PS), Protocatechuicaldehyde (PCA), 4-Hydroxybenzoic acid (4-HBA) and 5-Hydroxymethylfurfural (5-HMF) showed the most profound anabolic effects. After induction of inflammation, pro-inflammatory and catabolic genes were upregulated, and GAG/DNA was decreased. VA, Epi C, PS, PCA, 4-HBA and 5-HMF exhibited anti-catabolic and anti-inflammatory effects and prevented the up-regulation of pro-inflammatory markers including metalloproteinases and cyclooxygenase 2. After two weeks of treatment with TCM compounds, the GAG/DNA ratio was restored compared with the negative control group. Immunohistochemistry and Safranin-O staining confirmed superior amounts of cartilaginous matrix in treated pellets. In conclusion, VA, Epi C, PS, PCA, 4-HBA and 5-HMF showed promising anabolic and anti-inflammatory effects.

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Weekers, Frank, and Greet Van den Berghe. "Endocrine modifications and interventions during critical illness." Proceedings of the Nutrition Society 63, no. 3 (August 2004): 443–50. http://dx.doi.org/10.1079/pns2004373.

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The ongoing hypermetabolic response in patients with prolonged critical illness leads to the loss of lean tissue mass. Since the cachexia of prolonged illness is usually associated with low concentrations of anabolic hormones, hormonal intervention has been thought to be beneficial. However, most interventions have been shown to be ineffective and their indiscriminate use even causes harm. Before considering endocrine intervention in these frail patients, a detailed understanding of the neuroendocrinology of the stress response is warranted. It is now clear that the acute phase and the later phase of critical illness behave differently from an endocrinological point of view. The acute stress reponse consists primarily of an actively-secreting pituitary in the presence of low circulating peripheral anabolic hormones, suggesting resistance of the peripheral tissues to the effects of anterior pituitary hormones. However, when the disease process becomes prolonged, there is a uniformly-reduced pulsatile secretion of anterior pituitary hormones with proportionally reduced concentrations of peripheral anabolic hormones. The origin of this suppressed pituitary secretion is located in the hypothalamus, as hypothalamic secretagogues can reactivate the anterior pituitary and restore pulsatile secretion. The reactivated pituitary secretion is accompanied by an increase in peripheral target hormones, indicating at least partial sensitivity of these tissues to anterior pituitary hormones in this chronic phase of illness. Thus, endocrine intervention with a combination of hypothalamic secretagogues that more completely reactivate the anterior pituitary could be a more physiological and effective strategy for inducing anabolism in patients with prolonged critical illness.

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Smith, Gordon I., Philip Atherton, Dominic N. Reeds, B. Selma Mohammed, Debbie Rankin, Michael J. Rennie, and Bettina Mittendorfer. "Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to hyperinsulinaemia–hyperaminoacidaemia in healthy young and middle-aged men and women." Clinical Science 121, no. 6 (May 27, 2011): 267–78. http://dx.doi.org/10.1042/cs20100597.

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Increased dietary LCn−3PUFA (long-chain n−3 polyunsaturated fatty acid) intake stimulates muscle protein anabolism in individuals who experience muscle loss due to aging or cancer cachexia. However, it is not known whether LCn−3PUFAs elicit similar anabolic effects in healthy individuals. To answer this question, we evaluated the effect of 8 weeks of LCn−3PUFA supplementation (4 g of Lovaza®/day) in nine 25–45-year-old healthy subjects on the rate of muscle protein synthesis (by using stable isotope-labelled tracer techniques) and the activation (phosphorylation) of elements of the mTOR (mammalian target of rapamycin)/p70S6K (p70 S6 kinase) signalling pathway during basal post-absorptive conditions and during a hyperinsulinaemic–hyperaminoacidaemic clamp. We also measured the concentrations of protein, RNA and DNA in muscle to obtain indices of the protein synthetic capacity, translational efficiency and cell size. Neither the basal muscle protein fractional synthesis rate nor basal signalling element phosphorylation changed in response to LCn−3PUFA supplementation, but the anabolic response to insulin and amino acid infusion was greater after LCn−3PUFA [i.e. the muscle protein fractional synthesis rate during insulin and amino acid infusion increased from 0.062±0.004 to 0.083±0.007%/h and the phospho-mTOR (Ser2448) and phospho-p70S6K (Thr389) levels increased by ∼50%; all P<0.05]. In addition, the muscle protein concentration and the protein/DNA ratio (i.e. muscle cell size) were both greater (P<0.05) after LCn−3PUFA supplementation. We conclude that LCn−3PUFAs have anabolic properties in healthy young and middle-aged adults.

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Kraemer, William J., Nicholas A. Ratamess, and Bradley C. Nindl. "Recovery responses of testosterone, growth hormone, and IGF-1 after resistance exercise." Journal of Applied Physiology 122, no. 3 (March 1, 2017): 549–58. http://dx.doi.org/10.1152/japplphysiol.00599.2016.

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The complexity and redundancy of the endocrine pathways during recovery related to anabolic function in the body belie an oversimplistic approach to its study. The purpose of this review is to examine the role of resistance exercise (RE) on the recovery responses of three major anabolic hormones, testosterone, growth hormone(s), and insulin-like growth factor 1. Each hormone has a complexity related to differential pathways of action as well as interactions with binding proteins and receptor interactions. Testosterone is the primary anabolic hormone, and its concentration changes during the recovery period depending on the upregulation or downregulation of the androgen receptor. Multiple tissues beyond skeletal muscle are targeted under hormonal control and play critical roles in metabolism and physiological function. Growth hormone (GH) demonstrates differential increases in recovery with RE based on the type of GH being assayed and workout being used. IGF-1 shows variable increases in recovery with RE and is intimately linked to a host of binding proteins that are essential to its integrative actions and mediating targeting effects. The RE stress is related to recruitment of muscle tissue with the glandular release of hormones as signals to target tissues to support homeostatic mechanisms for metabolism and tissue repair during the recovery process. Anabolic hormones play a crucial role in the body’s response to metabolism, repair, and adaptive capabilities especially in response to anabolic-type RE. Changes of these hormones following RE during recovery in the circulatory biocompartment of blood are reflective of the many mechanisms of action that are in play in the repair and recovery process.

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Gentileschi, P., G. Palmieri, A. Perfetti, P. Sileri, G. Sica, M. Venza, D. Benavoli, and A. L. Gaspari. "Anabolic Steroid Nandrolone Augments Hepatic Regenerative Response in Rats." Transplantation Proceedings 37, no. 10 (December 2005): 4563–66. http://dx.doi.org/10.1016/j.transproceed.2005.10.123.

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Steiner, Jennifer L., and Charles H. Lang. "Sepsis Attenuates the Anabolic Response to Skeletal Muscle Contraction." Shock 43, no. 4 (April 2015): 344–51. http://dx.doi.org/10.1097/shk.0000000000000304.

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Brownson, C., and PT Loughna. "Alterations in Muscle Phenotype in Response to Anabolic Stimuli." Clinical Science 87, s1 (January 1, 1994): 103. http://dx.doi.org/10.1042/cs087s103.

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Herndon, David N., and Marc G. Jeschke. "Administration of anabolic agents improve the postburn hypermetabolic response." Shock 12, Supplement (November 1999): 48. http://dx.doi.org/10.1097/00024382-199911001-00149.

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JESCHKE, MARC G. "EFFECT OF ANABOLIC AGENTS ON THE ACUTE-PHASE-RESPONSE." Shock 21, Supplement (March 2004): 85. http://dx.doi.org/10.1097/00024382-200403001-00340.

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Wanek, Sandra, and Steven E. Wolf. "Metabolic response to injury and role of anabolic hormones." Current Opinion in Clinical Nutrition and Metabolic Care 10, no. 3 (May 2007): 272–77. http://dx.doi.org/10.1097/mco.0b013e3280f31b17.

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Banerjee, Camellia, Jagadish Ulloor, Edgar L. Dillon, Qusai Dahodwala, Brittani Franklin, Thomas Storer, Paola Sebastiani, et al. "Identification of serum biomarkers for aging and anabolic response." Immunity & Ageing 8, no. 1 (2011): 5. http://dx.doi.org/10.1186/1742-4933-8-5.

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Cartaña, Jordi, and Michael J. Stock. "Effects of digoxin on the anabolic response to clenbuterol." Metabolism 43, no. 8 (July 1994): 959–64. http://dx.doi.org/10.1016/0026-0495(94)90174-0.

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Garma, T., C. Kobayashi, F. Haddad, G. R. Adams, P. W. Bodell, and K. M. Baldwin. "Similar acute molecular responses to equivalent volumes of isometric, lengthening, or shortening mode resistance exercise." Journal of Applied Physiology 102, no. 1 (January 2007): 135–43. http://dx.doi.org/10.1152/japplphysiol.00776.2006.

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The present study was undertaken to test the hypothesis that the contraction mode of action [static-isometric (Iso), shortening-concentric (Con), or lengthening-eccentric (Ecc)] used to stress the muscle provides a differential mechanical stimulus eliciting greater or lesser degrees of anabolic response at the initiation of a resistance training program. We performed an acute resistance training study in which different groups of rodents completed four training sessions in either the Iso, Con, or Ecc mode of contraction under conditions of activation and movement specifically designed to elicit equivalent volumes of force accumulation. The results of this experiment indicate that the three modes of contraction produced nearly identical cell signaling, indicative of an anabolic response involving factors such as increased levels of mRNA for IGF-I, procollagen III α1, decreased myostatin mRNA, and increased total RNA concentration. The resulting profiles collectively provide evidence that pure mode of muscle action, in and of itself, does not appear to be a primary variable in determining the efficacy of increased loading paradigms with regard to the initiation of selected muscle anabolic responses.

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Gardner, Frank H. "Anabolic steroids in aplastic anemia." Acta Endocrinologica 110, no. 3_Suppla (December 1985): S87—S96. http://dx.doi.org/10.1530/acta.0.109s0087.

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Abstract. Despite the successful recovery of young patients with aplastic anemia following bone marrow transplants, additional patients have had benefit from immune suppression therapy, predominantly antithymus globulin (ATG). There exists a large residual pool of patients who have not been able to benefit from these modalities because of 1) lack of compatible siblings, 2) age, 3) duration of illness prior to diagnosis. Historically oral androstanes have been helpful in the treatment of chronic aplastic anemia. The long-range survival in large cooperative groups of patients treated with androstanes have indicated that both severe and chronic aplastic anemia have had responses similar to immune suppressive therapy. There is a need to have further investigations to seek the most effective anabolic agents. Many group studies have shortened treatment schedules when an erythropoietic response has been obtained, rather than continue therapy until the maximum platelet count is achieved. Such abbreviation of therapy may hasten a hematological relapse. Clinics also should evaluate parenteral androstanes since they appear to be more hematopoietic. Also the investigation of different androstane metabolites, i.e. etiocholanolone, should be pursued to determined if a more effective stimulus of stem cell proliferation can be achieved. In the recovery phase of the aplastic anemia patients treated with immune suppression or androstanes the peripheral blood reflects an altered proliferation of the marrow stem cell. The majority of these patients continue to have abnormalities in red cells (macrocytosis) and decreased platelet size.

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Uzych, Leo. "Anabolic-Androgenic Steroids and Psychiatric-Related Effects: A Review*." Canadian Journal of Psychiatry 37, no. 1 (February 1992): 23–28. http://dx.doi.org/10.1177/070674379203700106.

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Anabolic-androgenic steroid use may have a wide range of adverse psychiatric and behavioural effects. The available data, however, are often inconsistent and inconclusive concerning possible effects of anabolic-androgenic steroids on libido in men, in women and also the way in which they affect libido differently in males and females. Anabolic-androgenic steroids may both relieve and cause depression. Cessation or diminished use of anabolic-androgenic steroids may also result in depression. More study is required to determine whether or not the disparate data on depression are consistent clinical observations. The level of testosterone appears to be positively associated with “aggression”, particularly in response to provocation! Various psychotic symptoms and manic episodes may be associated with anabolic-androgenic steroids. The possibility of hypomania induced by synthetic androgens must also be considered.

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Hodson, Nathan, Daniel W. D. West, Andrew Philp, Nicholas A. Burd, and Daniel R. Moore. "Molecular regulation of human skeletal muscle protein synthesis in response to exercise and nutrients: a compass for overcoming age-related anabolic resistance." American Journal of Physiology-Cell Physiology 317, no. 6 (December 1, 2019): C1061—C1078. http://dx.doi.org/10.1152/ajpcell.00209.2019.

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Skeletal muscle mass, a strong predictor of longevity and health in humans, is determined by the balance of two cellular processes, muscle protein synthesis (MPS) and muscle protein breakdown. MPS seems to be particularly sensitive to changes in mechanical load and/or nutritional status; therefore, much research has focused on understanding the molecular mechanisms that underpin this cellular process. Furthermore, older individuals display an attenuated MPS response to anabolic stimuli, termed anabolic resistance, which has a negative impact on muscle mass and function, as well as quality of life. Therefore, an understanding of which, if any, molecular mechanisms contribute to anabolic resistance of MPS is of vital importance in formulation of therapeutic interventions for such populations. This review summarizes the current knowledge of the mechanisms that underpin MPS, which are broadly divided into mechanistic target of rapamycin complex 1 (mTORC1)-dependent, mTORC1-independent, and ribosomal biogenesis-related, and describes the evidence that shows how they are regulated by anabolic stimuli (exercise and/or nutrition) in healthy human skeletal muscle. This review also summarizes evidence regarding which of these mechanisms may be implicated in age-related skeletal muscle anabolic resistance and provides recommendations for future avenues of research that can expand our knowledge of this area.

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Zdanowicz, Martin M. "Use of Growth Hormone and Insulin-like Growth Factor 1 for Treatment of Tissue Wasting in Catabolic Conditions." Hospital Pharmacy 35, no. 2 (February 2000): 163–68. http://dx.doi.org/10.1177/001857870003500219.

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Trauma, surgery, burn injury, sepsis, prolonged bed rest, cancer, and AIDS are examples of catabolic states that can lead to a significant loss of lean body tissues and skeletal muscle. The physiologic stresses associated with these catabolic conditions can impair immune function, alter drug response, and delay the recovery process. Although enhanced nutritional supplementation is a mainstay for treating tissue wasting in these conditions, it is of limited effectiveness in reversing skeletal muscle protein loss or enhancing anabolism in lean body tissues. The use of anabolic hormones such as Growth Hormone (GH) or Insulin-Like Growth Factor 1 (IGF-1) to limit lean body wasting and preserve muscle mass in these conditions has been widely investigated. This article was designed to give pharmacists and patient care professionals an overview of recent literature involving anabolic hormone treatment of tissue wasting. The use of these agents in the clinical setting may undergo significant expansion in the near future.

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Kim, Il-Young, Sanghee Park, Ellen T. H. C. Smeets, Scott Schutzler, Gohar Azhar, Jeanne Y. Wei, Arny A. Ferrando, and Robert R. Wolfe. "Consumption of a Specially-Formulated Mixture of Essential Amino Acids Promotes Gain in Whole-Body Protein to a Greater Extent than a Complete Meal Replacement in Older Women with Heart Failure." Nutrients 11, no. 6 (June 17, 2019): 1360. http://dx.doi.org/10.3390/nu11061360.

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Heart failure in older individuals is normally associated with a high body mass index and relatively low lean body mass due to, in part, a resistance to the normal anabolic effect of dietary protein. In this study we have investigated the hypothesis that consumption of a specially-formulated composition of essential amino acids (HiEAAs) can overcome anabolic resistance in individuals with heart failure and stimulate the net gain of body protein to a greater extent than a commercially popular protein-based meal replacement beverage with greater caloric but lower essential amino acid (EAA) content (LoEAA). A randomized cross-over design was used. Protein kinetics were determined using primed continuous infusions of L-(2H5)phenylalanine and L-(2H2)tyrosine in the basal state and for four hours following consumption of either beverage. Both beverages induced positive net protein balance (i.e., anabolic response). However, the anabolic response was more than two times greater with the HiEAA than the LoEAA (p < 0.001), largely through a greater suppression of protein breakdown (p < 0.001). Net protein accretion (g) was also greater in the HiEAA when data were normalized for either amino acid or caloric content (p < 0.001). We conclude that a properly formulated EAA mixture can elicit a greater anabolic response in individuals with heart failure than a protein-based meal replacement. Since heart failure is often associated with obesity, the minimal caloric value of the HiEAA formulation is advantageous.

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Rivas, Donato A., Nicholas P. Rice, Yassine Ezzyat, Devin J. McDonald, Brittany E. Cooper, and Roger A. Fielding. "Sphingosine-1-phosphate analog FTY720 reverses obesity but not age-induced anabolic resistance to muscle contraction." American Journal of Physiology-Cell Physiology 317, no. 3 (September 1, 2019): C502—C512. http://dx.doi.org/10.1152/ajpcell.00455.2018.

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Sarcopenia, the age-associated loss of skeletal muscle mass and function, is coupled with declines in physical functioning leading to subsequent higher rates of disability, frailty, morbidity, and mortality. Aging and obesity independently contribute to muscle atrophy that is assumed to be a result of the activation of mutual physiological pathways. Understanding mechanisms contributing to the induction of skeletal muscle atrophy with aging and obesity is important for determining targets that may have pivotal roles in muscle loss in these conditions. We find that aging and obesity equally induce an anabolic resistance to acute skeletal muscle contraction as observed with decreases in anabolic signaling activation after contraction. Furthermore, treatment with the sphingosine-1-phosphate analog FTY720 for 4 wk increased lean mass and strength, and the anabolic signaling response to contraction was improved in obese but not older animals. To determine the role of chronic inflammation and different fatty acids on anabolic resistance in skeletal muscle cells, we overexpressed IKKβ with and without exposure to saturated fatty acid (SFA; palmitic acid), polyunsaturated fatty acid (eicosapentaenoic acid), and monounsaturated fatty acid (oleic acid). We found that IKKβ overexpression increased inflammation markers in muscle cells, and this chronic inflammation exacerbated anabolic resistance in response to SFA. Pretreatment with FTY720 reversed the inflammatory effects of palmitic acid in the muscle cells. Taken together, these data demonstrate chronic inflammation can induce anabolic resistance, SFA aggravates these effects, and FTY720 can reverse this by decreasing ceramide accumulation in skeletal muscle.

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Robling, Alexander G., Rajendra Kedlaya, Shana N. Ellis, Paul J. Childress, Joseph P. Bidwell, Teresita Bellido, and Charles H. Turner. "Anabolic and Catabolic Regimens of Human Parathyroid Hormone 1–34 Elicit Bone- and Envelope-Specific Attenuation of Skeletal Effects in Sost-Deficient Mice." Endocrinology 152, no. 8 (June 7, 2011): 2963–75. http://dx.doi.org/10.1210/en.2011-0049.

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PTH is a potent calcium-regulating factor that has skeletal anabolic effects when administered intermittently or catabolic effects when maintained at consistently high levels. Bone cells express PTH receptors, but the cellular responses to PTH in bone are incompletely understood. Wnt signaling has recently been implicated in the osteo-anabolic response to the hormone. Specifically, the Sost gene, a major antagonist of Wnt signaling, is down-regulated by PTH exposure. We investigated this mechanism by treating Sost-deficient mice and their wild-type littermates with anabolic and catabolic regimens of PTH and measuring the skeletal responses. Male Sost+/+ and Sost−/− mice were injected daily with human PTH 1–34 (0, 30, or 90 μg/kg) for 6 wk. Female Sost+/+ and Sost−/− mice were continuously infused with vehicle or high-dose PTH (40 μg/kg · d) for 3 wk. Dual energy x-ray absorptiometry-derived measures of intermittent PTH (iPTH)-induced bone gain were impaired in Sost−/− mice. Further probing revealed normal or enhanced iPTH-induced cortical bone formation rates but concomitant increases in cortical porosity among Sost−/− mice. Distal femur trabecular bone was highly responsive to iPTH in Sost−/− mice. Continuous PTH (cPTH) infusion resulted in equal bone loss in Sost+/+ and Sost−/− mice as measured by dual energy x-ray absorptiometry. However, distal femur trabecular bone, but not lumbar spine trabecular bone, was spared the bone-wasting effects of cPTH in Sost−/− mice. These results suggest that changes in Sost expression are not required for iPTH-induced anabolism. iPTH-induced resorption of cortical bone might be overstimulated in Sost-deficient environments. Furthermore, Sost deletion protects some trabecular compartments, but not cortical compartments, from bone loss induced by high-dose PTH infusion.

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Pratsinis, Harris, Stylianos Tsagarakis, Irene Zervolea, Dimitri Stathakos, Nikos Thalassinos, and Dimitris Kletsas. "The Unexpected Anabolic Phenotype and Extended Longevity of Skin Fibroblasts after Chronic Glucocorticoid Excess." Dose-Response 4, no. 2 (April 2006): dose—response.0. http://dx.doi.org/10.2203/dose-response.05-007.pratsinis.

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Stoitsev, Georgi J., Veselin Gavrilov, Georgi Manchev, Boyan Markov, Valya Goranovska, Boris Tsankov, and Vassil Gegouskov. "Therapy with L-thyroxine and Omnadren after Cardiac Surgery. A Case Report." Folia Medica 61, no. 4 (December 31, 2019): 650–54. http://dx.doi.org/10.3897/folmed.61.e47962.

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Background: Cardiopulmonary bypass in cardiac surgery produces systemic inflammatory response and catabolic state. Severe stress frequently causes abnormalities in thyroid hormones in the absence of primary thyroid disease, defined as sick euthyroid syndrome (SES). Materials and methods: Supplementation therapy with thyroid and anabolic hormones in combination with an adequate nutritional support has been used to improve outcome in critically ill patient after cardiac surgery. Results: Administration of thyroid and anabolic hormones significantly improved patient’s condition. Conclusions: Supplementation therapy with thyroid and anabolic hormones in combination with an adequate nutritional support could be used to improve hemodynamics, achieve transition to anabolic metabolism and enhance recovery, which could eventually help for a reduction in post-operative morbidity and mortality.

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He, Shuqi, Xingpeng Chen, Zilong Zhang, Zhaoyue Wang, and Mengran Hu. "The Exploration of Urban Material Anabolism Based on RS and GIS Methods: Case Study in Jinchang, China." Remote Sensing 12, no. 3 (January 23, 2020): 370. http://dx.doi.org/10.3390/rs12030370.

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As an open artificial ecosystem, the development of a city requires the continuous input and output of material and energy, which is called urban metabolism, and includes catabolic (material-flow) and anabolic (material-accumulation) processes. Previous studies have focused on the catabolic and ignored the anabolic process due to data and technology problems. The combination of remote-sensing technology and high-resolution satellite images facilitates the estimation of cumulative material amounts in urban systems. This study focused on persistent accumulation, which is the metabolic response of urban land use/urban land expansion, building stock, and road stock to land-use changes. Building stock is an extremely cost-intensive and long-lived component of cumulative metabolism. The study measured building stocks of Jinchang, China’s nickel capital by using remote-sensing images and field-research data. The development of the built environment could be analyzed by comparing the stock of buildings on maps representing different time periods. The results indicated that material anabolism in Jinchang is a distance-dependent function, where the amounts and rates of material anabolism decrease with changes in distance to the central business district (CBD) and city administration center (CAC). The cumulative metabolic rate and cumulative total metabolism were observed to be increasing, however, the growth rate has decreased.

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de Hart, Naomi M. M. P., Ziad S. Mahmassani, Paul T. Reidy, Joshua J. Kelley, Alec I. McKenzie, Jonathan J. Petrocelli, Michael J. Bridge, et al. "Acute Effects of Cheddar Cheese Consumption on Circulating Amino Acids and Human Skeletal Muscle." Nutrients 13, no. 2 (February 13, 2021): 614. http://dx.doi.org/10.3390/nu13020614.

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Cheddar cheese is a protein-dense whole food and high in leucine content. However, no information is known about the acute blood amino acid kinetics and protein anabolic effects in skeletal muscle in healthy adults. Therefore, we conducted a crossover study in which men and women (n = 24; ~27 years, ~23 kg/m2) consumed cheese (20 g protein) or an isonitrogenous amount of milk. Blood and skeletal muscle biopsies were taken before and during the post absorptive period following ingestion. We evaluated circulating essential and non-essential amino acids, insulin, and free fatty acids and examined skeletal muscle anabolism by mTORC1 cellular localization, intracellular signaling, and ribosomal profiling. We found that cheese ingestion had a slower yet more sustained branched-chain amino acid circulation appearance over the postprandial period peaking at ~120 min. Cheese also modestly stimulated mTORC1 signaling and increased membrane localization. Using ribosomal profiling we found that, though both milk and cheese stimulated a muscle anabolic program associated with mTORC1 signaling that was more evident with milk, mTORC1 signaling persisted with cheese while also inducing a lower insulinogenic response. We conclude that Cheddar cheese induced a sustained blood amino acid and moderate muscle mTORC1 response yet had a lower glycemic profile compared to milk.

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Maeda, Eijiro, Megumi Sugimoto, Youtaro Kosato, Chi Tat Poon, Belinda Pingguan-Murphy, and Toshiro Ohashi. "Tenocyte anabolic and catabolic response to elevation in intracellular tension." Journal of Biorheology 28, no. 1 (2014): 16–20. http://dx.doi.org/10.17106/jbr.28.16.

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Naruse, Kouji, Akimitsu Miyauchi, Moritoshi Itoman, and Yuko Mikuni-Takagaki. "Distinct Anabolic Response of Osteoblast to Low-Intensity Pulsed Ultrasound." Journal of Bone and Mineral Research 18, no. 2 (February 1, 2003): 360–69. http://dx.doi.org/10.1359/jbmr.2003.18.2.360.

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RIEBE, DEBORAH, B. O. FERNHALL, and PAUL D. THOMPSON. "The blood pressure response to exercise in anabolic steroid users." Medicine & Science in Sports & Exercise 24, no. 6 (June 1992): 633???637. http://dx.doi.org/10.1249/00005768-199206000-00004.

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Conn, C. A., W. Kozak, J. McClellan, and M. J. Kluger. "445 EFFECT OF ANABOLIC STEROID ADMINISTRATION ON THE FEBRILE RESPONSE." Medicine & Science in Sports & Exercise 25, Supplement (May 1993): S79. http://dx.doi.org/10.1249/00005768-199305001-00447.

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Hosegood, J. L., and A. J. Franks. "Response of human skeletal muscle to the anabolic steroid stanozolol." BMJ 297, no. 6655 (October 22, 1988): 1028–29. http://dx.doi.org/10.1136/bmj.297.6655.1028.

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Kim, Il-Young, Yun-A. Shin, Scott E. Schutzler, Gohar Azhar, Robert R. Wolfe, and Arny A. Ferrando. "Quality of meal protein determines anabolic response in older adults." Clinical Nutrition 37, no. 6 (December 2018): 2076–83. http://dx.doi.org/10.1016/j.clnu.2017.09.025.

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Chen, Fabian, Raymond Lam, David Shaywitz, Ronald C. Hendrickson, Gregory J. Opiteck, Dana Wishengrad, Andy Liaw, et al. "Evaluation of early biomarkers of muscle anabolic response to testosterone." Journal of Cachexia, Sarcopenia and Muscle 2, no. 1 (February 26, 2011): 45–56. http://dx.doi.org/10.1007/s13539-011-0021-y.

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Journal articles on the topic 'Anabolic response'

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