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Journal articles on the topic 'Skeletal Adaptation'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Hibbitt, Catherine. "Using Skeleton Typograms to Explore Comparative Anatomy." American Biology Teacher 82, no. 2 (February 1, 2020): 120–22. http://dx.doi.org/10.1525/abt.2020.82.2.120.

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A highlight activity of the author's comparative anatomy class, this skeletal typogram activity challenges students to take their understanding of the skeletal system's components beyond mere memorization of bone names and locations. Each student creates a poster of a vertebrate skeleton, using the letters of the bone names to depict the actual bone shape and location. Animals are chosen by the teacher to represent a wide variety of evolutionary adaptations (swimming, flying, grazing, hunting, etc.). Students are then asked to compare the different typograms through analysis of contrasting skeletal evolutionary adaptations. The infographic nature of the project helps students understand the power of visual information, allowing for creative cross-disciplinary work. Through developing and comparing typograms, students deepen their understanding of how skeletal form fits function and the role of adaptation in vertebrate evolution.

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2

Turner, Charles H. "Skeletal Adaptation to Mechanical Loading." Clinical Reviews in Bone and Mineral Metabolism 5, no. 4 (December 2007): 181–94. http://dx.doi.org/10.1007/s12018-008-9010-x.

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3

Röckl, Katja S. C., Michael F. Hirshman, Josef Brandauer, Nobuharu Fujii, Lee A. Witters, and Laurie J. Goodyear. "Skeletal Muscle Adaptation to Exercise Training." Diabetes 56, no. 8 (May 18, 2007): 2062–69. http://dx.doi.org/10.2337/db07-0255.

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4

Mcleod, Kenneth J., Clinton T. Rubin, Mark W. Otter, and Yi-Xian Qin. "Skeletal Cell Stresses and Bone Adaptation." American Journal of the Medical Sciences 316, no. 3 (September 1998): 176–83. http://dx.doi.org/10.1016/s0002-9629(15)40398-2.

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5

Wang, Y., and J. M. Winters. "Predictive model for skeletal muscle adaptation." Journal of Biomechanics 39 (January 2006): S43. http://dx.doi.org/10.1016/s0021-9290(06)83047-2.

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6

Burton, H. W., B. M. Carlson, and J. A. Faulkner. "Microcirculatory Adaptation to Skeletal Muscle Transplantation." Annual Review of Physiology 49, no. 1 (March 1987): 439–51. http://dx.doi.org/10.1146/annurev.ph.49.030187.002255.

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7

Carter, Dennis R., and Tracy E. Orr. "Skeletal development and bone functional adaptation." Journal of Bone and Mineral Research 7, S2 (December 1992): S389—S395. http://dx.doi.org/10.1002/jbmr.5650071405.

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8

Warden, Stuart J. "Extreme Skeletal Adaptation to Mechanical Loading." Journal of Orthopaedic & Sports Physical Therapy 40, no. 3 (March 2010): 188. http://dx.doi.org/10.2519/jospt.2010.0404.

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9

McLEOD, KENNETH J., CLINTON T. RUBIN, MARK W. OTTER, and YI-XIAN QIN. "Skeletal Cell Stresses and Bone Adaptation." American Journal of the Medical Sciences 316, no. 3 (September 1998): 176–83. http://dx.doi.org/10.1097/00000441-199809000-00005.

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10

Yuan, Chong-Xi, Qiang Ji, Qing-Jin Meng, Alan R. Tabrum, and Zhe-Xi Luo. "Earliest Evolution of Multituberculate Mammals Revealed by a New Jurassic Fossil." Science 341, no. 6147 (August 15, 2013): 779–83. http://dx.doi.org/10.1126/science.1237970.

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Multituberculates were successful herbivorous mammals and were more diverse and numerically abundant than any other mammal groups in Mesozoic ecosystems. The clade also developed diverse locomotor adaptations in the Cretaceous and Paleogene. We report a new fossil skeleton from the Late Jurassic of China that belongs to the basalmost multituberculate family. Dental features of this new Jurassic multituberculate show omnivorous adaptation, and its well-preserved skeleton sheds light on ancestral skeletal features of all multituberculates, especially the highly mobile joints of the ankle, crucial for later evolutionary success of multituberculates in the Cretaceous and Paleogene.

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11

Huang, Tai-Yu, Melissa A. Linden, Scott E. Fuller, Felicia R. Goldsmith, Jacob Simon, Heidi M. Batdorf, Matthew C. Scott, Nabil M. Essajee, John M. Brown, and Robert C. Noland. "Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 320, no. 6 (June 1, 2021): E1053—E1067. http://dx.doi.org/10.1152/ajpendo.00410.2020.

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A ketogenic diet with normal protein content (NPKD) increases body weight and fat mass, increases intramuscular triglyceride storage, and upregulates pathways related to protein metabolism. In combination with exercise training, a NPKD induces additive and/or synergistic activation of AMPK, PGC-1α, mitochondrial fission/fusion genes, mitochondrial fatty acid oxidation, and peroxisomal adaptations in skeletal muscle. Collectively, results from this study provide mechanistic insight into adaptations in skeletal muscle relevant to keto-adaptation.

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12

Hamilton, Marc T., and Frank W. Booth. "Skeletal muscle adaptation to exercise: a century of progress." Journal of Applied Physiology 88, no. 1 (January 1, 2000): 327–31. http://dx.doi.org/10.1152/jappl.2000.88.1.327.

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Skeletal muscle physiology and biochemistry is an established field with Nobel Prize-winning scientists, dating back to the 1920s. Not until the mid to late 1960s did there appear a major focus on physiological and biochemical training adaptations in skeletal muscle. The study of adaptations to exercise training reveals a wide range of integrative approaches, from the systemic to the molecular level. Advances in our understanding of training adaptations have come in waves caused by the introduction of new experimental approaches. Research has revealed that exercise can be effective at preventing and/or treating some of the most common chronic diseases of the latter half of the 20th century. Endurance-trained muscle is more effective at clearing plasma triglyceride, glucose, and free fatty acids. However, at the present time, most of the mechanisms underlying the adaptation of human skeletal muscle to exercise still remain to be discovered. Little is known about the regulatory factors (e.g., trans-acting proteins or signaling pathways) directly modulating the expression of exercise-responsive genes. Because so many potential physiological and biochemical signals change during exercise, it will be an important challenge in the next century to move beyond “correlational studies” and to identify responsible mechanisms. Skeletal muscle metabolic adaptations may prove to be a critical component to preventing diseases such as coronary heart disease, type 2 diabetes, and obesity. Therefore, training studies have had an impact on setting the stage for a potential “preventive medicine reformation” in a society needing a return to a naturally active lifestyle of our ancestors.

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13

Hafen, Paul S., Coray N. Preece, Jacob R. Sorensen, Chad R. Hancock, and Robert D. Hyldahl. "Repeated exposure to heat stress induces mitochondrial adaptation in human skeletal muscle." Journal of Applied Physiology 125, no. 5 (November 1, 2018): 1447–55. http://dx.doi.org/10.1152/japplphysiol.00383.2018.

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The heat stress response is associated with several beneficial adaptations that promote cell health and survival. Specifically, in vitro and animal investigations suggest that repeated exposures to a mild heat stress (~40°C) elicit positive mitochondrial adaptations in skeletal muscle comparable to those observed with exercise. To assess whether such adaptations translate to human skeletal muscle, we produced local, deep tissue heating of the vastus lateralis via pulsed shortwave diathermy in 20 men and women ( n = 10 men; n = 10 women). Diathermy increased muscle temperature by 3.9°C within 30 min of application. Immediately following a single 2-h heating session, we observed increased phosphorylation of AMP-activated protein kinase and ERK1/2 but not of p38 MAPK or JNK. Following repeated heat exposures (2 h daily for 6 consecutive days), we observed a significant cellular heat stress response, as heat shock protein 70 and 90 increased 45% and 38%, respectively. In addition, peroxisome proliferator-activated receptor gamma, coactivator-1 alpha and mitochondrial electron transport protein complexes I and V expression were increased after heating. These increases were accompanied by augmentation of maximal coupled and uncoupled respiratory capacity, measured via high-resolution respirometry. Our data provide the first evidence that mitochondrial adaptation can be elicited in human skeletal muscle in response to repeated exposures to mild heat stress. NEW & NOTEWORTHY Heat stress has been shown to elicit mitochondrial adaptations in cell culture and animal research. We used pulsed shortwave diathermy to produce deep tissue heating and explore whether beneficial mitochondrial adaptations would translate to human skeletal muscle in vivo. We report, for the first time, positive mitochondrial adaptations in human skeletal muscle following recurrent heat stress. The results of this study have clinical implications for many conditions characterized by diminished skeletal muscle mitochondrial function.

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14

Witten, P. Eckhard, and Brian K. Hall. "Teleost Skeletal Plasticity: Modulation, Adaptation, and Remodelling." Copeia 103, no. 4 (December 2015): 727–39. http://dx.doi.org/10.1643/cg-14-140.

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15

SUZUKI, Atsushi. "Adaptation of skeletal myofiber types to arboreality." Primate Research 12, no. 2 (1996): 133–46. http://dx.doi.org/10.2354/psj.12.133.

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16

Scheidegger, Kathrin J., Marjorie H. J. G. Nelissen-Vrancken, Peter J. A. Leenders, Mat J. A. P. Daemen, Jos F. M. Smits, and Jeanette M. Wood. "Structural adaptation to ischemia in skeletal muscle." Journal of Hypertension 15, no. 12 (December 1997): 1455–61. http://dx.doi.org/10.1097/00004872-199715120-00013.

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17

Baker, Brent A., and Robert G. Cutlip. "Skeletal Muscle Injury Versus Adaptation with Aging." Exercise and Sport Sciences Reviews 38, no. 1 (January 2010): 10–16. http://dx.doi.org/10.1097/jes.0b013e3181c5cd7c.

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18

Timmons, James A. "Variability in training-induced skeletal muscle adaptation." Journal of Applied Physiology 110, no. 3 (March 2011): 846–53. http://dx.doi.org/10.1152/japplphysiol.00934.2010.

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When human skeletal muscle is exposed to exercise training, the outcomes, in terms of physiological adaptation, are unpredictable. The significance of this fact has long been underappreciated, and only recently has progress been made in identifying some of the molecular bases for the heterogeneous response to exercise training. It is not only of great medical importance that some individuals do not substantially physiologically adapt to exercise training, but the study of the heterogeneity itself provides a powerful opportunity to dissect out the genetic and environmental factors that limit adaptation, directly in humans. In the following review I will discuss new developments linking genetic and transcript abundance variability to an individual's potential to improve their aerobic capacity or endurance performance or induce muscle hypertrophy. I will also comment on the idea that certain gene networks may be associated with muscle “adaptability” regardless the stimulus provided.

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19

Altan, Ekin, Alexander Zöllner, Okan Avcı, and Oliver Röhrle. "Towards modelling skeletal muscle growth and adaptation." PAMM 16, no. 1 (October 2016): 921–24. http://dx.doi.org/10.1002/pamm.201610448.

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20

Bandy, William D., Venita Lovelace-Chandler, and Beth McKitrick-Bandy. "Adaptation of Skeletal Muscle to Resistance Training." Journal of Orthopaedic & Sports Physical Therapy 12, no. 6 (December 1990): 248–55. http://dx.doi.org/10.2519/jospt.1990.12.6.248.

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21

Meulen, Marjolein C. H. van der. "Mechanics in skeletal development, adaptation and disease." Philosophical Transactions of the Royal Society of London. Series A: Mathematical, Physical and Engineering Sciences 358, no. 1766 (January 15, 2000): 565–78. http://dx.doi.org/10.1098/rsta.2000.0546.

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22

Blachley, J. D., B. P. Crider, and J. H. Johnson. "Extrarenal potassium adaptation: role of skeletal muscle." American Journal of Physiology-Renal Physiology 251, no. 2 (August 1, 1986): F313—F318. http://dx.doi.org/10.1152/ajprenal.1986.251.2.f313.

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Following the ingestion of a high-potassium-content diet for only a few days, the plasma potassium of rats rises only modestly in response to a previously lethal dose of potassium salts. This acquired tolerance, termed potassium adaptation, is principally the result of increased capacity to excrete potassium into the urine. However, a substantial portion of the acute potassium dose is not immediately excreted and is apparently translocated into cells. Previous studies have failed to show an increase in the content of potassium of a variety of tissues from such animals. Using 86Rb as a potassium analogue, we have shown that the skeletal muscle of potassium-adapted rats takes up significantly greater amounts of potassium in vivo in response to an acute challenge than does that of control animals. Furthermore, the same animals exhibit greater efflux of 86Rb following the termination of the acute infusion. We have also shown that the Na+-K+-ATPase activity and ouabain-binding capacity of skeletal muscle microsomes are increased by the process of potassium adaptation. We conclude that skeletal muscle is an important participant in potassium adaptation and acts to temporarily buffer acute increases in the extracellular concentration of potassium.

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23

Laughlin, M. Harold. "Physical activity-induced remodeling of vasculature in skeletal muscle: role in treatment of type 2 diabetes." Journal of Applied Physiology 120, no. 1 (January 1, 2016): 1–16. http://dx.doi.org/10.1152/japplphysiol.00789.2015.

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This manuscript summarizes and discusses adaptations of skeletal muscle vasculature induced by physical activity and applies this understanding to benefits of exercise in prevention and treatment of type 2 diabetes (T2D). Arteriolar trees of skeletal muscle are heterogeneous. Exercise training increases capillary exchange and blood flow capacities. The distribution of vascular adaptation to different types of exercise training are influenced by muscle fiber type composition and fiber recruitment patterns that produce different modes of exercise. Thus training-induced adaptations in vascular structure and vascular control in skeletal muscle are not homogeneously distributed throughout skeletal muscle or along the arteriolar tree within a muscle. Results summarized indicate that similar principles apply to vascular adaptation in skeletal muscle in T2D. It is concluded that exercise training-induced changes in vascular gene expression differ along the arteriolar tree and by skeletal muscle fiber type composition. Results suggest that it is unlikely that hemodynamic forces are the only exercise-induced signals mediating the regulation of vascular gene expression. In patients with T2D, exercise training is perhaps the most effective treatment of the many related symptoms. Training-induced changes in the vasculature and in insulin signaling in the muscle fibers and vasculature augment glucose and insulin delivery as well as glucose uptake. If these adaptations occur in a sufficient amount of muscle mass, exposure to hyperglycemia and hyperinsulinemia will decrease along with the risk of microvascular complications throughout the body. It is postulated that exercise sessions in programs of sufficient duration, that engage as much skeletal muscle mass as possible, and that recruit as many muscle fibers within each muscle as possible will produce the greatest benefit. The added benefit of combined resistance and aerobic training programs and of high-intensity exercise programs is not simply “more exercise is better”.

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24

Englund, Davis A., Kevin A. Murach, Cory M. Dungan, Vandré C. Figueiredo, Ivan J. Vechetti, Esther E. Dupont-Versteegden, John J. McCarthy, and Charlotte A. Peterson. "Depletion of resident muscle stem cells negatively impacts running volume, physical function, and muscle fiber hypertrophy in response to lifelong physical activity." American Journal of Physiology-Cell Physiology 318, no. 6 (June 1, 2020): C1178—C1188. http://dx.doi.org/10.1152/ajpcell.00090.2020.

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To date, studies that have aimed to investigate the role of satellite cells during adult skeletal muscle adaptation and hypertrophy have utilized a nontranslational stimulus and/or have been performed over a relatively short time frame. Although it has been shown that satellite cell depletion throughout adulthood does not drive skeletal muscle loss in sedentary mice, it remains unknown how satellite cells participate in skeletal muscle adaptation to long-term physical activity. The current study was designed to determine whether reduced satellite cell content throughout adulthood would influence the transcriptome-wide response to physical activity and diminish the adaptive response of skeletal muscle. We administered vehicle or tamoxifen to adult Pax7-diphtheria toxin A (DTA) mice to deplete satellite cells and assigned them to sedentary or wheel-running conditions for 13 mo. Satellite cell depletion throughout adulthood reduced balance and coordination, overall running volume, and the size of muscle proprioceptors (spindle fibers). Furthermore, satellite cell participation was necessary for optimal muscle fiber hypertrophy but not adaptations in fiber type distribution in response to lifelong physical activity. Transcriptome-wide analysis of the plantaris and soleus revealed that satellite cell function is muscle type specific; satellite cell-dependent myonuclear accretion was apparent in oxidative muscles, whereas initiation of G protein-coupled receptor (GPCR) signaling in the glycolytic plantaris may require satellite cells to induce optimal adaptations to long-term physical activity. These findings suggest that satellite cells play a role in preserving physical function during aging and influence muscle adaptation during sustained periods of physical activity.

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25

Hawley, John A., Louise M. Burke, Stuart M. Phillips, and Lawrence L. Spriet. "Nutritional modulation of training-induced skeletal muscle adaptations." Journal of Applied Physiology 110, no. 3 (March 2011): 834–45. http://dx.doi.org/10.1152/japplphysiol.00949.2010.

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Skeletal muscle displays remarkable plasticity, enabling substantial adaptive modifications in its metabolic potential and functional characteristics in response to external stimuli such as mechanical loading and nutrient availability. Contraction-induced adaptations are determined largely by the mode of exercise and the volume, intensity, and frequency of the training stimulus. However, evidence is accumulating that nutrient availability serves as a potent modulator of many acute responses and chronic adaptations to both endurance and resistance exercise. Changes in macronutrient intake rapidly alter the concentration of blood-borne substrates and hormones, causing marked perturbations in the storage profile of skeletal muscle and other insulin-sensitive tissues. In turn, muscle energy status exerts profound effects on resting fuel metabolism and patterns of fuel utilization during exercise as well as acute regulatory processes underlying gene expression and cell signaling. As such, these nutrient-exercise interactions have the potential to activate or inhibit many biochemical pathways with putative roles in training adaptation. This review provides a contemporary perspective of our understanding of the molecular and cellular events that take place in skeletal muscle in response to both endurance and resistance exercise commenced after acute and/or chronic alterations in nutrient availability (carbohydrate, fat, protein, and several antioxidants). Emphasis is on the results of human studies and how nutrient provision (or lack thereof) interacts with specific contractile stimulus to modulate many of the acute responses to exercise, thereby potentially promoting or inhibiting subsequent training adaptation.

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26

Akimoto, Takayuki, Kanako Okuhira, Katsuji Aizawa, Shogo Wada, Hiroaki Honda, Toru Fukubayashi, and Takashi Ushida. "Skeletal muscle adaptation in response to mechanical stress in p130cas−/− mice." American Journal of Physiology-Cell Physiology 304, no. 6 (March 15, 2013): C541—C547. http://dx.doi.org/10.1152/ajpcell.00243.2012.

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Mammalian skeletal muscles undergo adaptation in response to changes in the functional demands upon them, involving mechanical-stress-induced cellular signaling called “mechanotransduction.” We hypothesized that p130Cas, which is reported to act as a mechanosensor that transduces mechanical extension into cellular signaling, plays an important role in maintaining and promoting skeletal muscle adaptation in response to mechanical stress via the p38 MAPK signaling pathway. We demonstrate that muscle-specific p130Cas−/− mice express the contractile proteins normally in skeletal muscle. Furthermore, muscle-specific p130Cas−/− mice show normal mechanical-stress-induced muscle adaptation, including exercise-induced IIb-to-IIa muscle fiber type transformation and hypertrophy. Finally, we provide evidence that exercise-induced p38 MAPK signaling is not impaired by the muscle-specific deletion of p130Cas. We conclude that p130Cas plays a limited role in mechanical-stress-induced skeletal muscle adaptation.

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27

AXELROD, CHRISTOPHER L., CIARAN E. FEALY, ANNY MULYA, EMILY HUANG, HISASHI FUJIOKA, BARTOLOME BURGUERA, CHARLES L. HOPPEL, and JOHN P. KIRWAN. "Mitochondrial Adaptation in Insulin Resistant Human Skeletal Muscle." Diabetes 67, Supplement 1 (May 2018): 1915—P. http://dx.doi.org/10.2337/db18-1915-p.

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28

Knorr, Alexa. "Positive and negative skeletal adaptation in young gymnasts." Nurse Practitioner 39, no. 5 (May 2014): 38–47. http://dx.doi.org/10.1097/01.npr.0000445782.10109.1c.

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29

Kirby, Tyler J., and John J. McCarthy. "MicroRNAs in skeletal muscle biology and exercise adaptation." Free Radical Biology and Medicine 64 (September 2013): 95–105. http://dx.doi.org/10.1016/j.freeradbiomed.2013.07.004.

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30

DELROSSI, A. "Skeletal muscle adaptation for long-term dynamic aortomyoplasty." Journal of Molecular and Cellular Cardiology 24 (June 1992): S36. http://dx.doi.org/10.1016/0022-2828(92)92964-e.

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31

Jokl, Elliot J., and Gonzalo Blanco. "Disrupted autophagy undermines skeletal muscle adaptation and integrity." Mammalian Genome 27, no. 11-12 (August 2, 2016): 525–37. http://dx.doi.org/10.1007/s00335-016-9659-2.

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32

Ohira, Y., W. Yasui, F. Kariya, T. Wakatsuki, K. Nakamura, T. Asakura, and V. R. Edgerton. "Metabolic adaptation of skeletal muscles to gravitational unloading." Acta Astronautica 33 (July 1994): 113–17. http://dx.doi.org/10.1016/0094-5765(94)90115-5.

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33

Poole, David C., and O. Mathieu-Costello. "Skeletal muscle capillary geometry: adaptation to chronic hypoxia." Respiration Physiology 77, no. 1 (July 1989): 21–29. http://dx.doi.org/10.1016/0034-5687(89)90026-1.

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34

Molenaar, Peter C., P. C. Molenaar, G. Th H. Van Kempen, and B. S. Oen. "Transsymaptic adaptation in skeletal muscle of “myasthenic” rats." Journal of Autoimmunity 2, no. 6 (December 1989): 917–18. http://dx.doi.org/10.1016/0896-8411(89)90048-6.

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35

Keller, T. S., A. M. Strauss, T. H. Hansson, and D. M. Spengler. "Skeletal adaptation in space: Is there a limit?" Journal of Biomechanics 23, no. 4 (January 1990): 374. http://dx.doi.org/10.1016/0021-9290(90)90098-n.

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36

Jessen, Niels, Elias I. O. Sundelin, and Andreas Buch Møller. "AMP kinase in exercise adaptation of skeletal muscle." Drug Discovery Today 19, no. 7 (July 2014): 999–1002. http://dx.doi.org/10.1016/j.drudis.2014.03.009.

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37

Chambers, Rebecca L., and John C. McDermott. "Molecular Basis of Skeletal Muscle Regeneration." Canadian Journal of Applied Physiology 21, no. 3 (June 1, 1996): 155–84. http://dx.doi.org/10.1139/h96-014.

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Skeletal muscle regeneration is a vital process with important implications for various muscle myopathies and adaptations to physiological overload. Few of the molecular regulatory proteins controlling this process have so far been identified. Several growth factors have defined effects on myogenic precursor cells and appear to also be involved during regeneration. In addition, factors that may be released by cells of the immune system may activate satellite cells during regeneration. Many of these growth factors are associated with signalling cascades which transmit information to the nucleus. The nuclear "receptors" that receive the incoming signals are transcription factors that interact with DNA regulatory sequences in order to modulate gene expression. Of the nuclear factors isolated so far, the immediate-early genes are associated with muscle precursor cell proliferation. This review aims to synthesize the extensive research on myogenic differentiation and relate this to research concerning the molecular regulation of skeletal muscle regeneration. Key words: satellite cells, growth factors, signal transduction, transcription factors, gene regulation, overload adaptation

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38

Wijngaarden, Marjolein A., Leontine E. H. Bakker, Gerard C. van der Zon, Peter A. C. 't Hoen, Ko Willems van Dijk, Ingrid M. Jazet, Hanno Pijl, and Bruno Guigas. "Regulation of skeletal muscle energy/nutrient-sensing pathways during metabolic adaptation to fasting in healthy humans." American Journal of Physiology-Endocrinology and Metabolism 307, no. 10 (November 15, 2014): E885—E895. http://dx.doi.org/10.1152/ajpendo.00215.2014.

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During fasting, rapid metabolic adaptations are required to maintain energy homeostasis. This occurs by a coordinated regulation of energy/nutrient-sensing pathways leading to transcriptional activation and repression of specific sets of genes. The aim of the study was to investigate how short-term fasting affects whole body energy homeostasis and skeletal muscle energy/nutrient-sensing pathways and transcriptome in humans. For this purpose, 12 young healthy men were studied during a 24-h fast. Whole body glucose/lipid oxidation rates were determined by indirect calorimetry, and blood and skeletal muscle biopsies were collected and analyzed at baseline and after 10 and 24 h of fasting. As expected, fasting induced a time-dependent decrease in plasma insulin and leptin levels, whereas levels of ketone bodies and free fatty acids increased. This was associated with a metabolic shift from glucose toward lipid oxidation. At the molecular level, activation of the protein kinase B (PKB/Akt) and mammalian target of rapamycin pathways was time-dependently reduced in skeletal muscle during fasting, whereas the AMP-activated protein kinase activity remained unaffected. Furthermore, we report some changes in the phosphorylation and/or content of forkhead protein 1, sirtuin 1, and class IIa histone deacetylase 4, suggesting that these pathways might be involved in the transcriptional adaptation to fasting. Finally, transcriptome profiling identified genes that were significantly regulated by fasting in skeletal muscle at both early and late time points. Collectively, our study provides a comprehensive map of the main energy/nutrient-sensing pathways and transcriptomic changes during short-term adaptation to fasting in human skeletal muscle.

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39

Kinjo, Sonoko, Tsuyoshi Uehara, Ikuko Yazaki, Yoshihisa Shirayama, and Hiroshi Wada. "Morphological diversity of larval skeletons in the sea urchin family Echinometridae (Echinoidea: Echinodermata)." Journal of the Marine Biological Association of the United Kingdom 86, no. 4 (June 15, 2006): 799–816. http://dx.doi.org/10.1017/s0025315406013725.

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To clarify the morphological variety of larval skeletons, a detailed morphological comparison among the species of the family Echinometridae was performed. Through conspecific comparison of larval skeletons among different ages, we found five skeletal characters of the body skeleton that are stable in the four-armed pluteus and thus useful in homologous comparison among the species. The morphological variation was summarized as the difference in the number of spines and posteroventral transverse rods, and differences in the shape of the body skeleton. Significant correlations were found between some skeletal characters, such as between upper body length and bottom width of body skeleton and between lower body length and the number of spines. We found that the larval skeletons of tropical species tend to have fewer spines and rods than those of temperate species, which is consistent with the hypothesis that a reduction in skeletal elements decreases the specific gravity of larvae as an adaptation to tropical waters.

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40

Adams, Gregory R., Vincent J. Caiozzo, and Kenneth M. Baldwin. "Skeletal muscle unweighting: spaceflight and ground-based models." Journal of Applied Physiology 95, no. 6 (December 2003): 2185–201. http://dx.doi.org/10.1152/japplphysiol.00346.2003.

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Long-term manned spaceflight requires that flight crews be exposed to extended periods of unweighting of antigravity skeletal muscles. This exposure will result in adaptations in these muscles that have the potential to debilitate crew members on return to increased gravity environments. Therefore, the development of countermeasures to prevent these unwanted adaptations is an important requirement. The limited access to microgravity environments for the purpose of studying muscle adaptation and evaluating countermeasure programs has necessitated the use of ground-based models to conduct both basic and applied muscle physiology research. In this review, the published results from ground-based models of muscle unweighting are presented and compared with the results from related spaceflight research. The models of skeletal muscle unweighting with a sufficient body of literature included bed rest, cast immobilization, and unilateral lower limb suspension. Comparisons of changes in muscle strength and size between these models in the context of the limited results available from spaceflight suggest that each model may be useful for the investigation of certain aspects of the skeletal muscle unweighting that occur in microgravity.

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41

McAllister, Richard M., Sean C. Newcomer, and M. Harold Laughlin. "Vascular nitric oxide: effects of exercise training in animals." Applied Physiology, Nutrition, and Metabolism 33, no. 1 (February 2008): 173–78. http://dx.doi.org/10.1139/h07-146.

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Exercise training is known to induce several adaptations in the cardiovascular system, one of which is increased skeletal muscle blood flow at maximal exercise. Improved muscle blood flow, in turn, could in part be accounted for by augmented endothelium-dependent, nitric oxide (NO)-mediated vasodilation. Studies have indeed demonstrated that endothelium-dependent, NO-mediated dilation of conductance-type vessels is augmented after endurance exercise training; recently, this adaptation has been extended into resistance-type vessels within rodent skeletal muscle. With the latter, however, it appears that only resistance vessels supplying muscle active during training sessions exhibit this adaptation. These findings in rats are in contrast to those from human studies, in which increased endothelium-dependent dilation has been observed in vasculatures not associated with elevated blood flow during exercise. Increased expression of endothelial NO synthase (eNOS) appears to underlie enhanced endothelium-dependent, NO-mediated dilation of both conductance and resistance vessels. Greater eNOS expression may also underlie the preventive and (or) rehabilitative effect(s) of exercise training on atherosclerosis, given that NO inhibits several steps of the atherosclerotic disease process. Thus, exercise training may induce adaptations that benefit both vasodilation and vascular health.

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Berdeaux, Rebecca, and Randi Stewart. "cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration." American Journal of Physiology-Endocrinology and Metabolism 303, no. 1 (July 1, 2012): E1—E17. http://dx.doi.org/10.1152/ajpendo.00555.2011.

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Among organ systems, skeletal muscle is perhaps the most structurally specialized. The remarkable subcellular architecture of this tissue allows it to empower movement with instructions from motor neurons. Despite this high degree of specialization, skeletal muscle also has intrinsic signaling mechanisms that allow adaptation to long-term changes in demand and regeneration after acute damage. The second messenger adenosine 3′,5′-monophosphate (cAMP) not only elicits acute changes within myofibers during exercise but also contributes to myofiber size and metabolic phenotype in the long term. Strikingly, sustained activation of cAMP signaling leads to pronounced hypertrophic responses in skeletal myofibers through largely elusive molecular mechanisms. These pathways can promote hypertrophy and combat atrophy in animal models of disorders including muscular dystrophy, age-related atrophy, denervation injury, disuse atrophy, cancer cachexia, and sepsis. cAMP also participates in muscle development and regeneration mediated by muscle precursor cells; thus, downstream signaling pathways may potentially be harnessed to promote muscle regeneration in patients with acute damage or muscular dystrophy. In this review, we summarize studies implicating cAMP signaling in skeletal muscle adaptation. We also highlight ligands that induce cAMP signaling and downstream effectors that are promising pharmacological targets.

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Warden, Stuart J., Julie A. Hurst, Megan S. Sanders, Charles H. Turner, David B. Burr, and Jiliang Li. "Exercise-induced Bone Adaptation Significantly Increases Skeletal Fatigue Resistance." Medicine & Science in Sports & Exercise 37, Supplement (May 2005): S452. http://dx.doi.org/10.1249/00005768-200505001-02341.

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Warden, Stuart J., Julie A. Hurst, Megan S. Sanders, Charles H. Turner, David B. Burr, and Jiliang Li. "Exercise-induced Bone Adaptation Significantly Increases Skeletal Fatigue Resistance." Medicine & Science in Sports & Exercise 37, Supplement (May 2005): S452. http://dx.doi.org/10.1097/00005768-200505001-02341.

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Desplanches, D., M. H. Mayet, E. I. Ilyina-Kakueva, B. Sempore, and R. Flandrois. "Skeletal muscle adaptation in rats flown on Cosmos 1667." Journal of Applied Physiology 68, no. 1 (January 1, 1990): 48–52. http://dx.doi.org/10.1152/jappl.1990.68.1.48.

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Seven male Wistar rats were subjected to 7 days of weightlessness on the Soviet biosatellite Cosmos 1667. Muscle histomorphometry and biochemical analyses were performed on the soleus (SOL) and extensor digitorum longus (EDL) of flight rats (group F) and compared with data from three groups of terrestrial controls: one subjected to conditions similar to group F in space except for the state of weightlessness (group S) and the others living free in a vivarium (V1, V2). Relative to group V2 (its age and weight-matched control group), group F showed a greater decrease of muscle mass in SOL (23%) than in EDL (11%). In SOL a decrease in the percentage of type I fibers was counterbalanced by a simultaneous increase in type IIa fibers. The cross-sectional area of type I fiber was reduced by 24%. No statistically significant difference in capillarization and enzymatic activities was observed between the groups. In EDL a reduction in type I fiber distribution and 3-hydroxyacyl-CoA-dehydrogenase activity (27%) occurred after the flight. The small histochemical and biochemical changes reported suggest the interest in studying muscular adaptation during a flight of longer duration.

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Tidball, James G. "Mechanical signal transduction in skeletal muscle growth and adaptation." Journal of Applied Physiology 98, no. 5 (May 2005): 1900–1908. http://dx.doi.org/10.1152/japplphysiol.01178.2004.

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The adaptability of skeletal muscle to changes in the mechanical environment has been well characterized at the tissue and system levels, but the mechanisms through which mechanical signals are transduced to chemical signals that influence muscle growth and metabolism remain largely unidentified. However, several findings have suggested that mechanical signal transduction in muscle may occur through signaling pathways that are shared with insulin-like growth factor (IGF)-I. The involvement of IGF-I-mediated signaling for mechanical signal transduction in muscle was originally suggested by the observations that muscle releases IGF-I on mechanical stimulation, that IGF-I is a potent agent for promoting muscle growth and affecting phenotype, and that IGF-I can function as an autocrine hormone in muscle. Accumulating evidence shows that at least two signaling pathways downstream of IGF-I binding can influence muscle growth and adaptation. Signaling via the calcineurin/nuclear factor of activated T-cell pathway has been shown to have a powerful influence on promoting the slow/type I phenotype in muscle but can also increase muscle mass. Neural stimulation of muscle can activate this pathway, although whether neural activation of the pathway can occur independent of mechanical activation or independent of IGF-I-mediated signaling remains to be explored. Signaling via the Akt/mammalian target of rapamycin pathway can also increase muscle growth, and recent findings show that activation of this pathway can occur as a response to mechanical stimulation applied directly to muscle cells, independent of signals derived from other cells. In addition, mechanical activation of mammalian target of rapamycin, Akt, and other downstream signals is apparently independent of autocrine factors, which suggests that activation of the mechanical pathway occurs independent of muscle-mediated IGF-I release.

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Stevens, L., Y. Mounier, and X. Holy. "Functional adaptation of different rat skeletal muscles to weightlessness." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 4 (April 1, 1993): R770—R776. http://dx.doi.org/10.1152/ajpregu.1993.264.4.r770.

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The adaptation to weightlessness of two postural muscles, the slow soleus (SOL) and the fast gastrocnemius lateralis (GL), and a fast muscle used in movements, the extensor digitorum longus (EDL), was studied on five adult Wistar rats. The animals exposed to 14-day spaceflight aboard COSMOS 2044, designated as flight (F), were compared with synchronous (S) animals. The experiments were performed on single skinned fibers whose functional properties were studied. After weightlessness, the SOL exhibited two populations of fibers according to their Sr2+ affinities: 40% remained slow (Fs) and 60% acquired fast-type properties (Ff). Both S and F GL and EDL showed a single distributed population of fast fibers. SOL fibers atrophied insofar as they showed a significant reduction in fiber diameter and absolute maximal tension Po (mg) but not in Po expressed in kg/cm2. GL fibers showed no change in fiber diameter but a decrease in Po in mg and kg/cm2. EDL fibers were not atrophied by weightlessness. The tension/Ca concentration relationships of the Ff SOL and F GL fibers were shifted to the right, indicating a decrease in their Ca2+ affinity. An increase in the contraction kinetics was described for the SOL fibers after weightlessness, whereas no significant modification was found for the GL and EDL. Collectively, the data suggested that the adaptive changes subsequent to weightlessness were more dependent on the muscle function than on the fiber type, since both postural SOL and GL were modified.

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Spangenburg, Espen E., Jay H. Williams, Roland R. Roy, and Robert J. Talmadge. "Skeletal muscle calcineurin: influence of phenotype adaptation and atrophy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 4 (April 1, 2001): R1256—R1260. http://dx.doi.org/10.1152/ajpregu.2001.280.4.r1256.

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Calcineurin (CaN) has been implicated as a signaling molecule that can transduce physiological stimuli (e.g., contractile activity) into molecular signals that initiate slow-fiber phenotypic gene expression and muscle growth. To determine the influence of muscle phenotype and atrophy on CaN levels in muscle, the levels of soluble CaN in rat muscles of varying phenotype, as assessed by myosin heavy chain (MHC)-isoform proportions, were determined by Western blotting. CaN levels were significantly greater in the plantaris muscle containing predominantly fast (IIx and IIb) MHC isoforms, compared with the soleus (predominantly type I MHC) or vastus intermedius (VI, contains all 4 adult MHC isoforms). Three months after a complete spinal cord transection (ST), the CaN levels in the VI muscle were significantly reduced, despite a significant increase in fast MHC isoforms. Surprisingly, the levels of CaN in the VI were highly correlated with muscle mass but not MHC isoform proportions in ST and control rats. These data demonstrate that CaN levels in skeletal muscle are highly correlated to muscle mass and that the normal relationship with phenotype is lost after ST.

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KORZENIEWSKI, Bernard, and Jerzy A. ZOLADZ. "Training-induced adaptation of oxidative phosphorylation in skeletal muscles." Biochemical Journal 374, no. 1 (August 15, 2003): 37–40. http://dx.doi.org/10.1042/bj20030526.

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Muscle training/conditioning improves the adaptation of oxidative phosphorylation in skeletal muscles to physical exercise. However, the mechanisms underlying this adaptation are still not understood fully. By quantitative analysis of the existing experimental results, we show that training-induced acceleration of oxygen-uptake kinetics at the onset of exercise and improvement of ATP/ADP stability due to physical training are mainly caused by an increase in the amount of mitochondrial proteins and by an intensification of the parallel activation of ATP usage and ATP supply (increase in direct stimulation of oxidative phosphorylation complexes accompanying stimulation of ATP consumption) during exercise.

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Sibonga, Jean D., Peter R. Cavanagh, Thomas F. Lang, Adrian D. LeBlanc, Victor S. Schneider, Linda C. Shackelford, Scott M. Smith, and Laurence Vico. "Adaptation of the Skeletal System During Long-Duration Spaceflight." Clinical Reviews in Bone and Mineral Metabolism 5, no. 4 (December 2007): 249–61. http://dx.doi.org/10.1007/s12018-008-9012-8.

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