Influence of Concentric and Eccentric Resistance Training on Architectural
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Muscle Physiology Page 1 of 17
Emojevwe’s Lecture note on physiology- Muscle Physiology Page 1 of 17 MUSCLE PHYSIOLOGY (PHS 213) By Emojevwe V. Course Objectives: To familiarize students with the principles and basic facts of Human Physiology and with some of the laboratory techniques and equipment used in the acquisition of physiological data. The emphasis will be on muscles physiology. Since the course will focus on muscle physiology, some cellular and molecular mechanisms will be discussed in order to present a current view of physiological principles of muscle. Where appropriate, basic chemical and physical laws will be reviewed in order to enhance and to promote student understanding. The laboratory component of the course is designed to reinforce the topics discussed in lecture, as well as to familiarize students with some of the laboratory techniques and equipment used in muscle research Student Learning Outcomes: Upon successful completion of lecture portion of this course, the students will be able to describe, identify, and/or explain: • Structure and function of skeletal muscle, including excitation-contraction coupling, sliding filament mechanism, force generation, and isometric versus isotonic contractions. • Structure and functions of the cardiovascular system, including the mechanical and electrical properties of cardiac muscle function. • Structure and functions of smooth muscles including contraction of smooth muscle Upon successful completion of the laboratory portion of this course, the students will be able to describe, identify, explain, perform, and/or measure: • Computer simulations of the membrane potential, action potential, and synaptic neurotransmission. • Skeletal muscle mechanics, and the electromyogram (EMG). Required Course Materials: • Any textbook of physiology (human or medical) published within the last four years will be appropriate. -
SYMPOSIUM References 1
J Orthopaed Traumatol (2008): 24 November 2008 DOI 10.1007/s10195-008-0030-6 24 NOVEMBER 2008 SYMPOSIUM References 1. Pola E, Lattanzi W, Pecorini G, Logroscino CA, Robbins PD (2005) Gene therapy for in vivo bone formation: recent TISSUE ENGINEERING advances. Eur Rev Med Pharmacol Sci 9(3):167–174 2. Pola E, Gao W, Zhou Y, Pola R, Lattanzi W, Sfeir C, et al (2004) A CLINICALLY RELEVANT GENE THERAPY APPROACH Efficient bone formation by gene transfer of human LIM miner- TO INDUCE OSTEOGENESIS: STUDY OF THE NEW alization protein-3. Gene Ther 11(8):683 –693 GROWTH FACTOR LIM MINERALIZAZION PROTEIN-3 3. Lattanzi W, Parrilla C, Fetoni A, Logroscino G, Straface G, Pecorini G, Tampieri A, Bedini R, Pecci R, Michetti F, E. Pola Gambotto A, Robbins PD, Pola E (2008) Ex-vivo transduced autologous skin fibroblasts expressing human Lim Minera - Department of Orthopaedics and Traumatology, Università lization Protein-3 efficiently form new bone in animal models. Cattolica del Sacro Cuore, School of Medicine (Rome-IT) Gene Therapy [Epub ahead of print] Recombinant proteins, such as the bone morphogenetic proteins have been used to enhance repair of non-union fractures and facil- TYPE-I COLLAGEN MEMBRANE AS A SCAFFOLD FOR itate new bone formation in animal models as well as in clinical TENDON REPAIR: AN IN VITRO AND IN VIVO STUDY applications. However, a significant amount of recombinant BMP is required to promote osteogenesis and frequently the extent of A. Gigante, E. Cesari, A. Busilacchi, S. Manzotti, F. Greco new bone formation is low. In contrast, local gene transfer of BMPs has been shown to be more efficient in promoting osteogenesis in Department of Orthopaedics, Polytechnic University of Marche rodents than the use of recombinant proteins. -
Characterization of Contractile Machinery of Vascular Smooth Muscles in Hypertension
life Review Characterization of Contractile Machinery of Vascular Smooth Muscles in Hypertension Qunhui Yang * and Masatoshi Hori Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-3-5841-7940; Fax: +81-3-5841-8183 Abstract: Hypertension is a key risk factor for cardiovascular disease and it is a growing public health problem worldwide. The pathophysiological mechanisms of vascular smooth muscle (VSM) contrac- tion contribute to the development of hypertension. Calcium (Ca2+)-dependent and -independent signaling mechanisms regulate the balance of the myosin light chain kinase and myosin light chain phosphatase to induce myosin phosphorylation, which activates VSM contraction to control blood pressure (BP). Here, we discuss the mechanism of the contractile machinery in VSM, especially RhoA/Rho kinase and PKC/CPI-17 of Ca2+ sensitization pathway in hypertension. The two signal- ing pathways affect BP in physiological and pathophysiological conditions and are highlighted in pulmonary, pregnancy, and salt-sensitive hypertension. Keywords: vascular smooth muscle contraction; hypertension; CPI-17 Citation: Yang, Q.; Hori, M. 1. Introduction Characterization of Contractile Three types of muscle tissues are found in vertebrates: skeletal muscle, cardiac muscle, Machinery of Vascular Smooth and smooth muscle [1]. Muscle contraction depends on the ATP-driven sliding of highly Muscles in Hypertension. Life 2021, organized arrays of actin filaments against arrays of myosin II filaments [2]. In smooth 11, 702. https://doi.org/10.3390/ muscle, phosphorylation at Thr18/Ser19 of the myosin regulatory light chain results in life11070702 myosin ATPase enzymatic activity that induces actin and myosin attachment to regulate smooth muscle contraction [3,4]. -
Arnau Soler2019.Pdf
This thesis has been submitted in fulfilment of the requirements for a postgraduate degree (e.g. PhD, MPhil, DClinPsychol) at the University of Edinburgh. Please note the following terms and conditions of use: This work is protected by copyright and other intellectual property rights, which are retained by the thesis author, unless otherwise stated. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author. The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author. When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given. Genetic responses to environmental stress underlying major depressive disorder Aleix Arnau Soler Doctor of Philosophy The University of Edinburgh 2019 Declaration I hereby declare that this thesis has been composed by myself and that the work presented within has not been submitted for any other degree or professional qualification. I confirm that the work submitted is my own, except where work which has formed part of jointly-authored publications has been included. My contribution and those of the other authors to this work are indicated below. I confirm that appropriate credit has been given within this thesis where reference has been made to the work of others. I composed this thesis under guidance of Dr. Pippa Thomson. Chapter 2 has been published in PLOS ONE and is attached in the Appendix A, chapter 4 and chapter 5 are published in Translational Psychiatry and are attached in the Appendix C and D, and I expect to submit chapter 6 as a manuscript for publication. -
Muscle Tissue
Muscle Tissue Dr. Heba Kalbouneh Associate Professor of Anatomy and Histology Functions of muscle tissue . Movement . Maintenance of posture . Joint stabilization . Heat generation Tendon Dr. Heba Kalbouneh Dr. Belly Tendon Types of Muscle Tissue . Skeletal muscle . Cardiac muscle Dr. Heba Kalbouneh Dr. Smooth muscle Skeletal Attach to and move skeleton 40% of body weight Fibers = multinucleate cells (embryonic cells fuse) Cells with obvious striations Contractions are voluntary Cardiac: only in the wall of the heart Cells are striated Contractions are involuntary Dr. Heba Kalbouneh Dr. Smooth: walls of hollow organs Lack striations Contractions are involuntary . Their cells are called fibers because they are elongated Similarities… . Contraction depends on myofilaments . Actin . Myosin . Plasma membrane is called sarcolemma . Sarkos = flesh . Lemma = sheath Skeletal muscle Cardiac muscle Smooth muscle Dr. Heba Kalbouneh Dr. Skeletal muscle Epimysium surrounds whole muscle Endomysium is around each Dr. Heba Kalbouneh Dr. muscle fiber Perimysium is around fascicle Epimysium Fascicle Fascicle Fascicle Fascicle Fascicle Dr. Heba Kalbouneh Dr. Fascicle Perimysium Cell Cell Cell Dr. Heba Kalbouneh Dr. Cell Cell Endomysium Dr. Heba Kalbouneh Dr. Muscle fiber== musclemuscle cell=cell= myofibermyofiber Skeletal muscle This big cylinder is a fiber: a cell Fibers (each is one cell) have striations Myofibril is an organelle Myofibrils are organelles of the cell, are made up of myofilaments Myofibrils are long rows of repeating Dr. Heba Kalbouneh -
Variable Gearing in Pennate Muscles
Variable gearing in pennate muscles Emanuel Azizi*, Elizabeth L. Brainerd, and Thomas J. Roberts Department of Ecology and Evolutionary Biology, Brown University, Providence, RI 02912 Edited by Ewald R. Weibel, University of Bern, Bern, Switzerland, and approved December 3, 2007 (received for review September 27, 2007) Muscle fiber architecture, i.e., the physical arrangement of fibers within a muscle, is an important determinant of a muscle’s me- chanical function. In pennate muscles, fibers are oriented at an angle to the muscle’s line of action and rotate as they shorten, becoming more oblique such that the fraction of force directed along the muscle’s line of action decreases throughout a contrac- tion. Fiber rotation decreases a muscle’s output force but increases output velocity by allowing the muscle to function at a higher gear ratio (muscle velocity/fiber velocity). The magnitude of fiber rota- tion, and therefore gear ratio, depends on how the muscle changes shape in the dimensions orthogonal to the muscle’s line of action. Here, we show that gear ratio is not fixed for a given muscle but decreases significantly with the force of contraction (P < 0.0001). We find that dynamic muscle-shape changes promote fiber rota- tion at low forces and resist fiber rotation at high forces. As a result, gearing varies automatically with the load, to favor velocity output during low-load contractions and force output for contractions against high loads. Therefore, muscle-shape changes act as an automatic transmission system allowing a pennate muscle to shift Fig. 1. A 17th century geometric examination of muscle architecture (5). -
Calcium Ion-Regulated Thin Filaments from Vascular Smooth Muscle
Biochem. J. (1980) 185, 355-365 355 Printed in Great Britain Calcium Ion-Regulated Thin Filaments from Vascular Smooth Muscle Steven B. MARSTON, Rachel M. TREVETT and Michael WALTERS Imperial Chemical Industries Limited, Pharmaceuticals Division, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, U.K. (Received 20 June 1979) Myosin and actin competition tests indicated the presence of both thin-filament and myosin-linked Ca2+-regulatory systems in pig aorta and turkey gizzard smooth-muscle actomyosin. A thin-filament preparation was obtained from pig aortas. The thin filaments had no significant ATPase activity [1.1 + 2.6 nmol/mg per min (mean + S.D.)], but they activated skeletal-muscle myosin ATPase up to 25-fold [500nmol/mg of myosin per min (mean + S.D.)] in the presence of 1O-4M free Ca2+. At 10-8M-Ca2+ the thin filaments activated myosin ATPase activity only one-third as much. Thin-filament activation of myosin ATPase activity increased markedly in the range 10-6-10-5M- Ca2+ and was half maximal at 2.7 x 10-6M (pCa2+ 5.6). The skeletal myosin-aorta-thin- filament mixture gave a biphasic ATPase-rate-versus-ATP-concentration curve at 10-8M-Ca2+ similar to the curve obtained with skeletal-muscle thin filaments. Thin fila- ments bound up to 9.5,umol of Ca2+/g in the presence of MgATP2-. In the range 0.06- 27,uM-Ca2+ binding was hyperbolic with an estimated binding constant of (0.56 + 0.07) x 106 M-1 (mean + S.D.) and maximum binding of 8.0 + 0.8,umol/g (mean + S.D.). -
Skeletal Muscle Function During Exercise—Fine-Tuning of Diverse Subsystems by Nitric Oxide
Int. J. Mol. Sci. 2013, 14, 7109-7139; doi:10.3390/ijms14047109 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Review Skeletal Muscle Function during Exercise—Fine-Tuning of Diverse Subsystems by Nitric Oxide Frank Suhr, Sebastian Gehlert, Marijke Grau and Wilhelm Bloch * Institute of Cardiovascular Research and Sport Medicine, Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Am Sportpark Müngersdorf 6, 50933 Cologne, Germany; E-Mails: [email protected] (F.S.); [email protected] (S.G.); [email protected] (M.G.) * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +49-221-4982-5380; Fax: +49-221-4982-8370. Received: 31 January 2013; in revised form: 17 March 2013 / Accepted: 19 March 2013 / Published: 28 March 2013 Abstract: Skeletal muscle is responsible for altered acute and chronic workload as induced by exercise. Skeletal muscle adaptations range from immediate change of contractility to structural adaptation to adjust the demanded performance capacities. These processes are regulated by mechanically and metabolically induced signaling pathways, which are more or less involved in all of these regulations. Nitric oxide is one of the central signaling molecules involved in functional and structural adaption in different cell types. It is mainly produced by nitric oxide synthases (NOS) and by non-enzymatic pathways also in skeletal muscle. The relevance of a NOS-dependent NO signaling in skeletal muscle is underlined by the differential subcellular expression of NOS1, NOS2, and NOS3, and the alteration of NO production provoked by changes of workload. -
WO 2011/084768 Al
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date _ . ... _ . 14 July 2011 (14.07.2011) WO 2011/084768 Al (51) International Patent Classification: Ridge, Loveland, OH 45 140 (US). ARONHALT, Tay¬ A61B 17/00 (2006.01) A61B 19/10 (2006.01) lor, W. [US/US]; 306 Beech Road, Loveland, OH 45140 (US). (21) International Application Number: PCT/US20 10/06 1422 (74) Agents: JOHNSON, Philip, S. et al; Johnson & John son, 1 Johnson & Johnson Plaza, New Brunswick, NJ (22) International Filing Date: 08933 (US). 2 1 December 2010 (21 .12.2010) (81) Designated States (unless otherwise indicated, for every (25) Filing Language: English kind of national protection available): AE, AG, AL, AM, (26) Publication Langi English AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (30) Priority Data: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, 61/288,375 2 1 December 2009 (21 .12.2009) US HN, HR, HU, ID, JL, IN, IS, JP, KE, KG, KM, KN, KP, 12/971,249 17 December 2010 (17.12.2010) US KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, (71) Applicant (for all designated States except US): ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, ETHICON ENDO-SURGERY, INC. [US/US]; 4545 NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, Creek Road, Cincinnati, OH 45242 (US). -
Association of Smooth Muscle Myosin and Its Carboxyl Isoforms with Actin Isoforms in Aorta Smooth Muscle Jason Edward Black
Marshall University Marshall Digital Scholar Theses, Dissertations and Capstones 1-1-2007 Association of Smooth Muscle Myosin and its Carboxyl Isoforms with Actin Isoforms in Aorta Smooth Muscle Jason Edward Black Follow this and additional works at: http://mds.marshall.edu/etd Part of the Musculoskeletal, Neural, and Ocular Physiology Commons Recommended Citation Black, Jason Edward, "Association of Smooth Muscle Myosin and its Carboxyl Isoforms with Actin Isoforms in Aorta Smooth Muscle" (2007). Theses, Dissertations and Capstones. Paper 489. This Dissertation is brought to you for free and open access by Marshall Digital Scholar. It has been accepted for inclusion in Theses, Dissertations and Capstones by an authorized administrator of Marshall Digital Scholar. For more information, please contact [email protected]. Association of Smooth Muscle Myosin and its Carboxyl Isoforms with Actin Isoforms in Aorta Smooth Muscle By Jason Edward Black Dissertation submitted to the Graduate College of Marshall University in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences Approved by Elizabeth C. Bryda Todd L. Green William McCumbee Michael Moore Gary L. Wright, Committee Chairperson Department of Pharmacology, Physiology, and Toxicology ABSTRACT Association of Smooth Muscle Myosin and its Carboxyl Isoforms with Actin Isoforms in Aorta Smooth Muscle By Jason Edward Black The contraction mechanism of smooth muscle is not fully understood. The primary interaction that leads to the formation of tension, the myosin-actin crossbridge, has been studied extensively. However, even this aspect of the contraction has proven not to be as simple as it might seem. There are several isoforms of smooth muscle myosin and actin, and the differences in the activities of these isoforms and their interactions during the contractile process are largely unknown. -
Structure and Function of Smooth Muscle with Special Reference to Mast Cells
Chapter 15 Structure and Function of Smooth Muscle with Special Reference to Mast Cells Angel Vodenicharov Additional information is available at the end of the chapter http://dx.doi.org/10.5772/48566 1. Introduction The structure of the smooth muscle tissue is quite different from that of other muscle tissue subtypes. The primary smooth muscle structural and functional unit – the smooth muscle myocyte (Myocytus nonstriatus) has unique structure, arrangement and innervation. The spindle shape of the mononucleated smooth muscle cell permits a close contact among cells in the splanchnic and vascular walls. Regardless of its location in the body, the communication between tightly packed adjacent spindle-shaped mononucleated smooth muscle cells occurs via a specific junction, referred to as Macula communicans (nexus, gap junction). The space between the different macular connexons is about 2 nm, which allows low-molecular compounds to pass from one cell to another. This type of junction is analogous to the plasmodesma (pl. plasmodesmata), encountered in cells of plants. The basement membrane covering each smooth muscle cell, is absent at gap junction sites. The contractility, proper of smooth muscle cells, is influenced by the autonomic nervous system, hormones and local metabolites, which alter the contractility in a way that adapts to the new functional requirements. Smooth muscle cell contraction could be modulated via surface receptors, activating internal second messenger systems. The expression of a variety of receptors accounts for the response of smooth muscle cells in different areas to a number of hormones [1]. It is known that for the major part of smooth musculature (except for the iris, vas deferens and large blood vessels) one autonomic nerve fibre innervates a group of 15-20 smooth muscle cells, as the stimulus to one cell is transmitted via nexus contacts to the other [2] assuming a simultaneous contraction of the pack of cells. -
Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders
1521-0081/68/2/476–532$25.00 http://dx.doi.org/10.1124/pr.115.010652 PHARMACOLOGICAL REVIEWS Pharmacol Rev 68:476–532, April 2016 Copyright © 2016 The Author(s) This is an open access article distributed under the CC-BY Attribution 4.0 International license. ASSOCIATE EDITOR: STEPHANIE W. WATTS Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders F.V. Brozovich, C.J. Nicholson, C.V. Degen, Yuan Z. Gao, M. Aggarwal, and K.G. Morgan Department of Health Sciences, Boston University, Boston, Massachusetts (C.J.N., Y.Z.G., M.A., K.G.M.); Department of Medicine, Mayo Clinic, Rochester, Minnesota (F.V.B.); and Paracelsus Medical University Salzburg, Salzburg, Austria (C.V.D.) Abstract ...................................................................................478 I. Introduction . ..............................................................................478 A. Scope and Limitations..................................................................478 B. Overview of Regulation of Blood Pressure/Vascular Tone. ...............................478 1. Guyton View of Regulation Blood Pressure, Kidney Role, Volume Regulation. .......478 2. Recent Direct Confirmation of Changes in Vascular Tone/Resistance Related to Changes in Systemic Vascular Resistance and Blood Pressure and Downloaded from the Importance of Vascular Smooth Muscle Contraction in both Normal Physiology and Pathophysiology—Hypertension......................................479 3. Racial Differences/Personalized