DOCSLIB.ORG

Muscle Fatigue and Muscle Weakness: What We Know and What We Wish We Did

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Muscle Fatigue and Muscle Weakness: What We Know and What We Wish We Did EDITORIAL published: 30 May 2013 doi: 10.3389/fphys.2013.00125 Muscle fatigue and muscle weakness: what we know and what we wish we did Christina Karatzaferi 1,2* and P.Bryant Chase 3 1 Department of Physical Education and Sports Science, University of Thessaly, Trikala, Greece 2 Department of Kinesiology, Center for Research and Technology Thessaly, Trikala, Greece 3 Department of Biological Science, The Florida State University, Tallahassee, FL, USA *Correspondence: [email protected] Edited by: Peter J. Reiser, Ohio State University, USA Reviewed by: Peter J. Reiser, Ohio State University, USA This Research Topic on muscle fatigue and muscle weakness 1996; Karatzaferi et al., 2003, 2008). These effects may be due presents the latest ideas, arguments, and evidence from investi- to direct binding to proteins, or due to a more global alteration gations at the molecular level to macroscopic observations on of cellular energetics (GATP )inthemyocyte(Karatzaferi et al., whole animals including humans, in an effort to identify criti- 2004). cal factors underlying fatigue and weakness in health and disease. In this Research Topic, Debold (2012) consolidates the most Skeletal muscles confer movement to the human body using recent information, including single molecule assays and molec- vast amounts of energy provided through complex metabolic ular biological approaches, about the mechanisms by which Pi, pathways such that whole body mobility and energy balance H+, and ADP inhibit actomyosin cross-bridge cycling and thin are largely dictated by muscle activity. Conversely, muscle func- filament Ca2+-activation. Allen and Trajanovska (2012) provide tion reflects overall health status as exercise history and chronic a synthesis on the multiple roles of Pi in fatigue, including conditions affect either or both muscle quality, including pro- novel results from their group, showing that Pi is even more tein and fat content, and muscle mass. In health, muscle fatigue detrimental when its effects on Ca2+ release are combined with is temporary and recovery occurs rapidly, and recreational or inhibition of actomyosin force generation and Ca2+ activation. competitive athletes are always pursuing the next best fatigue In addition to activity-driven changes in metabolites and cellular “fix.” However, after inactivity—whether due to lifestyle choices, energetics, mutations in sarcomeric proteins have been associ- injury or chronic disease—muscle fatigue may occur prema- ated with prolonged muscle weakness in myopathies. Moving turely and persist, endangering a person’s safety because weak- away from actomyosin events, Ottenheijm et al. (2012) consider ness can lead to falls that may result in loss of independence. the role of nebulin in sarcomere function, and how transgenic Individuals are then trapped in a self-perpetuating, vicious cycle mouse models can inform us about mutations in the giant fila- of inactivity, disuse muscle atrophy/weakness, and metabolic mentous protein nebulin, and mutations in other thin filament disturbance that compounds morbidity (i.e., causing metabolic and closely related proteins that are associated with nemaline syndrome, obesity, hypertension, cachexia) and eventually pre- myopathy. mature death. Such issues transcend many scientific disciplines To fully test our understanding of muscle fatigue, appropri- and it becomes evident that not only recognizing fundamen- ately detailed models of muscle function will be necessary. Röhrle tal factors in muscle fatigue and muscle weakness is necessary, et al. (2012) make major advances in that arena by presenting a but also evaluating their interaction with factors outside of the multi-scale, finite element model of the human tibialis anterior. muscle is essential if we aspire to design better interventions Their model has the advantage of allowing simulation of fatigue that improve muscle function and thus improve quality of life at the cellular and motor unit levels, and can incorporate altered and life prognosis for the ageing population and chronic disease recruitment patterns of motor units due to central components of patients. fatigue. Thus their model can serve an invaluable role as we bridge Fatigue and weakness may stem from changes within myocytes our understanding between the cellular and tissue levels. that affect cross-bridge function or Ca2+ activation, to changes Muscle’s plasticity is most readily evident in its adaptation within the circulation or function of the nervous system. Within to repeated exercise, and conversely to inactivity that may be myocytes, metabolic products of ATP hydrolysis in the cytoplasm associated with various injuries and disease states. Bogdanis such as inorganic phosphate (Pi), protons (H+ or pH), and ADP (2012) reviews the long-term changes in muscle at the molec- have often been considered as agents that could disrupt force ular, cellular, and tissue levels, as well as the corresponding generation at the sarcomere level (Fabiato and Fabiato, 1978; functional changes that are associated with these adaptations to Cooke and Pate, 1985; Metzger and Moss, 1987; Nosek et al., activity level history. Fatigability is a key functional character- 1987, 1990; Chase and Kushmerick, 1988, 1995; Cooke et al., istic of different muscle fiber types, and can vary greatly with 1988; Godt and Nosek, 1989; Pate and Cooke, 1989; Metzger activity, or inactivity, and Bogdanis evaluates the utility of high- and Moss, 1990a,b; Pate et al., 1995, 1998; Wiseman et al., intensity bouts of exercise for modulating fatigability by training, www.frontiersin.org May 2013 | Volume 4 | Article 125 | 1 Karatzaferi and Chase Research topic: muscle fatigue or as a component in therapy. Bogdanis’ section on effects of reac- the view that fatigue, as experienced by patients undergo- tive oxygen species (ROS) sets the stage for the succinct review ing routine hemodialysis, might be better addressed by care- on antioxidants by Hernández et al. (2012).Despitethepop- givers as a syndrome and not with isolated measures since ularity of antioxidants as nutritional supplements, Hernández its apparent complexity requires a cross-disciplinary therapeu- et al. report that their utility for either minimizing or speeding tic approach. While hemodialysis and some other patients may recovery from fatigue appears to be limited to specific mus- be afflicted with specific syndromes, the rest of us have all cle types. Moreover, Bogdanis’ (2012) section on neural fac- heard the expression “mind over matter.” Does it apply to tors opens the discussion on the role of non-muscle factors in muscle? Noakes (2012) concludes the series with a challenging fatigue and serves as a bridge to the articles by Kobilo and review, partly historical in nature, arguing that the key com- van Praag (2012), Sakkas and Karatzaferi (2012),andNoakes ponent in fatigue is central. The author discusses the accepted (2012). models on the limits of human exercise performance, and What is the extent to which muscle activity and fatigue presents his central governor model of exercise regulation, argu- influence the function of other physiological systems of the ing that fatigue is brain-derived, being an important homeo- body, particularly the nervous system upon which skeletal mus- static mechanism that protects an organism from catastrophic cle depends for activation, and how much of fatigability is overexertion. determined centrally? In the commentary by Kobilo and van It is our sincere hope that this Research Topic will not Praag (2012), pharmacological activation of AMP-activated pro- only provide readers with new insights and viewpoints on tein kinase (AMPK)—a metabolic regulator that is activated the issue of muscle fatigue and weakness, but will also stim- during exercise—is shown to alter performance in a test of ulate novel ideas, experiments, and further advances in this spatial memory and hippocampal neurogenesis in mice in a research field. time-dependent manner. How can diseases and treatments mod- ify the experience and presentation of fatigue? In their opin- ACKNOWLEDGMENTS ion article, Sakkas and Karatzaferi (2012) consider available We thank all authors and reviewers for their invaluable contribu- evidence on the complex symptomatology of fatigue in renal tions in this Research Topic. Christina Karatzaferi is supported by patients on hemodialysis treatment. By drawing analogies to NSRF 2007–2013, European Social Fund (University of Thessaly- Chronic Fatigue Syndrome, Sakkas and Karatzaferi (2012) present 4525, MIS 377260). REFERENCES Debold, E. P. (2012). Recent insights that mimic fatigue. Am. J. Physiol. Noakes, T. D. (2012). Fatigue is a Allen, D. G., and Trajanovska, S. (2012). into muscle fatigue at the cross- Regul. Integr. Comp. Physiol. 294, brain-derived emotion that reg- The multiple roles of phosphate bridge level. Front. Physiol. R948–R955. doi: 10.1152/ajpregu. ulates the exercise behavior to in muscle fatigue. Front. Physiol. 3:151. doi: 10.3389/fphys.2012. 00541.2007 ensure the protection of whole 3:463. doi: 10.3389/fphys.2012. 00151 Karatzaferi, C., Myburgh, K. H., Chinn, body homeostasis. Front. Physiol. 00463 Fabiato, A., and Fabiato, F. (1978). M. K., Franks-Skiba, K., and Cooke, 3:82. doi: 10.3389/fphys.2012. Bogdanis, G. C. (2012). Effects of Effects of pH on the myofila- R. (2003). Effect of an ADP ana- 00082 physical activity and inactivity ments and the sarcoplasmic reticu- log on isometric force and ATPase Nosek,T.M.,Fender,K.Y.,and on muscle fatigue. Front. Physiol. lum of skinned cells from cardiac activity of active muscle fibers. Godt, R. E. (1987). It is diproto- 3:142. doi: 10.3389/fphys.2012. and skeletal muscles. J. Physiol. 276, Am.J.Physiol.CellPhysiol.284, nated inorganic phosphate that 00142 233–255. C816–C825. doi: 10.1152/ajpcell. depresses force in skinned skele- Chase, P. B., and Kushmerick, M. J. Godt, R. E., and Nosek, T. M. (1989). 00291.2002 tal muscle fibers. Science 236, (1988). Effects of pH on contrac- Changes in intracellular milieu with Kobilo, T., and van Praag, H. (2012). 191–193. doi: 10.1126/science. tion of rabbit fast and slow skele- fatigue or hypoxia depress con- Muscle fatigue and cognition: 3563496 tal muscle fibers.
Load more

Recommended publications
  • The Updated Training Wisdom of John Kellogg
    The Updated Training Wisdom of John Kellogg A collection of John Kellogg’s writings on training for distance runners Compiled by John Davis between May 2009 and December 2015 [email protected] www.runningwritings.com “Why do I pose as ‘Oz’? Because I know which mission to assign to help runners discover their potential. But I can't give them any results through magical powers; I'm just a human like the little carnival man from Kansas. I can only guide them. ” —John Kellogg Preface The goal of this project was to compile as many of John Kellogg’s posts on LetsRun.com as possible. I profoundly admire his training advice and his knowledge, and applying his principles to my own training brought me to new heights as a runner. Why John Kellogg, and not any of the other highly-regarded figures in the running world who have posted on LetsRun.com over the years (Renato Canova, Nobby Hashizume, Jack Daniels, et al.)? Perhaps because of his mysterious, guru-like reputation, or perhaps because of the sheer difficulty of assembling the range of posts. I also felt that it had to be done, that it would be a great loss for this knowledge to fade into obscurity over the years. John Kellogg seems to revel in the anonymity of the internet, and has posted under probably dozens of different “handles” over the years. In all likelihood, the writings here represent only a fraction of his total contribution to the online running community. Though his words sometimes fell on deaf ears, the power of the internet preserved much of his writing.
    [Show full text]
  • New Directions in Exercise Prescription: Is There a Role for Brain-Derived Parameters Obtained by Functional Near-Infrared Spectroscopy?
    brain sciences Perspective New Directions in Exercise Prescription: Is There a Role for Brain-Derived Parameters Obtained by Functional Near-Infrared Spectroscopy? Fabian Herold 1,2,* , Thomas Gronwald 3 , Felix Scholkmann 4,5, Hamoon Zohdi 5 , Dominik Wyser 4,6, Notger G. Müller 1,2,7 and Dennis Hamacher 8 1 Department of Neurology, Medical Faculty, Otto von Guericke University, Leipziger Str. 44, 39120 Magdeburg, Germany; [email protected] 2 Research Group Neuroprotection, German Center for Neurodegenerative Diseases (DZNE), Leipziger Str. 44, 39120 Magdeburg, Germany 3 Department Performance, Neuroscience, Therapy and Health, MSH Medical School Hamburg, University of Applied Sciences and Medical University, Am Kaiserkai 1, 20457 Hamburg, Germany; [email protected] 4 Department of Neonatology, Biomedical Optics Research Laboratory, University Hospital Zurich, University of Zurich, 8091 Zurich, Switzerland; [email protected] (F.S.); [email protected] (D.W.) 5 Institute for Complementary and Integrative Medicine, University of Bern, 3012 Bern, Switzerland; [email protected] 6 ETH Zurich, Rehabilitation Engineering Laboratory, Department of Health Sciences and Technology, 8092 Zurich, Switzerland 7 Center for Behavioral Brain Sciences (CBBS), Universitätsplatz 2, 39106 Magdeburg, Germany 8 German University for Health and Sports, (DHGS), Vulkanstraße 1, 10367 Berlin, Germany; [email protected] * Correspondence: [email protected] Received: 29 April 2020; Accepted: 29 May 2020; Published: 3 June 2020 Abstract: In the literature, it is well established that regular physical exercise is a powerful strategy to promote brain health and to improve cognitive performance. However, exact knowledge about which exercise prescription would be optimal in the setting of exercise–cognition science is lacking.
    [Show full text]
  • The Process and Effects of Ultrarunning
    Bowling Green State University ScholarWorks@BGSU Honors Projects Honors College Summer 8-21-2020 The Process and Effects of Ultrarunning Ellis Ulery [email protected] Follow this and additional works at: https://scholarworks.bgsu.edu/honorsprojects Part of the Exercise Science Commons, Other Kinesiology Commons, and the Sports Sciences Commons Repository Citation Ulery, Ellis, "The Process and Effects of Ultrarunning" (2020). Honors Projects. 562. https://scholarworks.bgsu.edu/honorsprojects/562 This work is brought to you for free and open access by the Honors College at ScholarWorks@BGSU. It has been accepted for inclusion in Honors Projects by an authorized administrator of ScholarWorks@BGSU. 1 The Process and Effects of Ultrarunning Ellis Ulery Bowling Green State University HNRS 4990: Honors Project Dr. Jessica Kiss and Dr. Matthew Kutz August 21, 2020 2 Table of Contents Phase 1: Pre Run (September 1, 2019 - March 29, 2020)… 4 Research on Ultrarunning… 4 My Personal Training… 5 Nutrition Research… 6 Daily Calorie Burn and Caloric Deficit (Exercise Induced)... 6 Hydration… 6 Electrolytes and Macronutrient Imbalances… 7 Personal Physiological Results and Research Information (VO2max and Lactate Threshold Information)… 7 Recovery Techniques… 9 Stretching… 9 Foam Rolling … 9 Sauna… 10 Dry Needling… 10 Motivating Factors & Forming the Event… 11 Phase 2: The Run (March 30, 2020)… 11 The Course and Set-Up… 11 My Running Plan (Expectations)… 12 Hydration & Caloric Intake (Expectations)… 13 The Official Results… 14 Chart of Performance Throughout The 12 Hours… 15 Hydration/Caloric Intake Results… 15 3 Observations Recorded During the Run… 15 Phase 3: Post Run/Conclusion… 15 The Personal Experience After the Run (Injuries)… 15 Question 1: What does it take to run an ultramarathon?… 16 Question 2: What did I learn through this experience?..
    [Show full text]
  • Multiple Models Can Concurrently Explain Fatigue During Human Performance
    Multiple Models Can Concurrently Explain Fatigue During Human Performance C. MATTHEW LAURENT†1, and J. MATT GREEN‡2 1Department of Kinesiology, St. Ambrose University, Davenport, IA, USA; 2Department of Health, Physical Education and Recreation, The University of North Alabama, Florence, AL, USA †Denotes graduate student author, ‡denotes professional author ABSTRACT Int J Exerc Sci 2(4): 280-293, 2009. One of the most commonly and thoroughly studied paradigms of human performance is fatigue. However, despite volumes of research there remains considerable controversy among scientists regarding definitive conclusions about the specific mechanism(s) contributing to fatigue. Within the literature there are three primary yet distinctly different governing ideas of fatigue; the traditionally referenced central model and peripheral model as well as the emerging central governor model (CGM). The CGM has recently been advocated by a limited number of researchers and is suggestive of a more integrative model of fatigue when compared the traditional peripheral and central models. However, more work is needed to determine the specific and perhaps synergistic roles of each paradigm during exercise or sport activity. This article contains three components; (1) a brief overview of the problems associated with defining fatigue, (2) a description of the models governing interpretation of fatigue and, (3) a presentation of multiple interpretations of selected data to demonstrate that some results can be reasonably explained using multiple models of fatigue, often concurrently. The purposes of this paper are to reveal that a) perhaps it is not the results that suggest a certain paradigm of regulation, yet that it may be a product of an a priori definition that is being employed and b) an integrative model of central and peripheral fatigue may present a plausible explanation for fatigue vs.
    [Show full text]
  • The Central Governor Model and Fatigue During Exercise
    In: Regulation of Fatigue in Exercise ISBN 978-1-61209-334-5 Editor: Frank E. Marino © 2011 Nova Science Publishers, Inc. The exclusive license for this PDF is limited to personal website use only. No part of this digital document may be reproduced, stored in a retrieval system or transmitted commercially in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services. Chapter 1 THE CENTRAL GOVERNOR MODEL AND FATIGUE DURING EXERCISE Timothy David Noakes* UCT/MRC Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town and Sports Science Institute of South Africa, Boundary Road, Newlands, 7700, South Africa ABSTRACT In 1923 Nobel Laureate A.V. Hill proposed that maximal exercise performance is limited by the development of ischaemia of the heart leading to anaerobiosis in the exercising skeletal muscles. This anaerobiosis prevented the oxidative removal of the lactic acid that Hill believed induced skeletal muscle contraction. As a result, skeletal muscle relaxation was inhibited, impairing exercise performance and inducing fatigue. This theory has dominated teaching and research in the exercise sciences for the past 80 years. But the problem with the model is that there is little biological evidence that it is correct and much that disproves it.
    [Show full text]
  • An Organic Cause for Perceived Muscle Weakness Thangavelu Senthilvelkumar1, Thamaraiselvan Aravindan1, Ajith Sivadasan2
    doi:10.17659/01.2020.0027 Journal of Case Reports 2020;10(2):103-106 An Organic Cause for Perceived Muscle Weakness Thangavelu Senthilvelkumar1, Thamaraiselvan Aravindan1, Ajith Sivadasan2 1Department of Physical Medicine and Rehabilitation; 2Department of Neurology and Neurosciences, Christian Medical College, Vellore 632004, Tamil Nadu, India. Corresponding Author: Abstract Mr. Thangavelu Senthilvelkumar Email: [email protected] Background: Although neurological conditions present with specific clinical patterns, practitioners often encounter patients with vague symptom complexes. Delayed This is an Open Access article distributed diagnosis and unnecessary medications can lead to iatrogenic effects and poor prognosis. under the terms of the Creative Commons Case Report: This paper reports a 21-year-old girl who perceived right upper extremity Attribution License (creativecommons.org/ monoplegia following a trauma, which did not fit into the traditional neurological licenses/by/3.0). diagnosis. Her movement patterns during physiotherapy were suggestive of the central Received : March 29, 2020 fatigue related reduction of function. Focused behavioral neuro-rehabilitation approach Accepted : May 9, 2020 based training helped her to regain her upper extremity function. Conclusion: Central Published : May 20, 2020 fatigue may be considered as a differential diagnosis when atypical muscle weakness occurs following a probable physical exertion. Keywords: Differential Diagnosis, Fatigue, Muscle Weakness, Nervous System Diseases, Prognosis. Introduction meter distance. She expressed that while carrying the pot, the maximum force was exerted on her ring Although neurological conditions present with and middle finger. At the destination, she literally specific clinical patterns, practitioners often dropped the pot and experienced severe pain at encounter patients with vague symptom complexes. right metacarpo-phalangeal joint of ring and middle With few exceptions, motor weakness fits into either an upper motor neuron or lower motor finger.
    [Show full text]
  • A Novel Model of Integrative Central Neural Regulation of Effort And
    120 Br J Sports Med: first published as 10.1136/bjsm.2003.010330 on 21 January 2005. Downloaded from EDUCATION From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions T D Noakes, A St Clair Gibson, E V Lambert ............................................................................................................................... Br J Sports Med 2005;39:120–124. doi: 10.1136/bjsm.2003.010330 It is hypothesised that physical activity is controlled by a maintained. The decisive studies of Kayser,2 Nybo and Nielsen,4 and Gonzalez-Alonso et al6 central governor in the brain and that the human body would now appear to confirm this interpretation, functions as a complex system during exercise. Using feed at least for exercise at altitude and in the heat. forward control in response to afferent feedback from Even during maximal exercise of short dura- tion, which, according to the Hill cardiovascular/ different physiological systems, the extent of skeletal muscle anaerobic/catastrophic model, is limited by a recruitment is controlled as part of a continuously altering severe uncompensated metabolic acidosis, arter- pacing strategy, with the sensation of fatigue being the ial blood pH seldom falls below about 7.1 and muscle pH below 6.6.11 12 However, when isolated conscious interpretation of these homoeostatic, central perfused skeletal muscle was tetanically stimu- governor control mechanisms. lated to similar pH levels (,6.8) in vitro
    [Show full text]
  • Models to Explain Fatigue During Prolonged Endurance Cycling
    Sports Med 2005; 35 (10): 865-898 REVIEW ARTICLE 0112-1642/05/0010-0865/$34.95/0 2005 Adis Data Information BV. All rights reserved. Models to Explain Fatigue during Prolonged Endurance Cycling Chris R. Abbiss and Paul B. Laursen School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia Contents Abstract ....................................................................................866 1. Defining Fatigue ........................................................................867 2. Cardiovascular/Anaerobic Model ........................................................868 2.1 Oxygen Delivery .....................................................................868 2.1.1 Cardiac Output ................................................................868 2.1.2 Red Blood Cell Mass and Plasma Volume ........................................869 2.1.3 Muscle Blood Flow Occlusion ....................................................869 2.2 Oxygen Utilisation ....................................................................870 2.3 Metabolite Accumulation ............................................................870 2.3.1 Lactate .......................................................................870 2.4 Summary of the Cardiovascular/Anaerobic Model ......................................872 3. Energy Supply/Energy Depletion Model ...................................................872 3.1 Energy Supply/Metabolic Capacity ....................................................872 3.2
    [Show full text]
  • Muscle Fatigue and Muscle Weakness: What We Know and What We Wish We Did
    MUSCLE FATIGUE AND MUSCLE WEAKNESS: WHAT WE KNOW AND WHAT WE WISH WE DID Topic Editors P. Bryant Chase and Christina Karatzaferi PHYSIOLOGY FRONTIERS COPYRIGHT STATEMENT ABOUT FRONTIERS © Copyright 2007-2013 Frontiers is more than just an open-access publisher of scholarly articles: it is a pioneering Frontiers Media SA. All rights reserved. approach to the world of academia, radically improving the way scholarly research is managed. All content included on this site, The grand vision of Frontiers is a world where all people have an equal opportunity to seek, share such as text, graphics, logos, button and generate knowledge. Frontiers provides immediate and permanent online open access to all icons, images, video/audio clips, downloads, data compilations and its publications, but this alone is not enough to realize our grand goals. software, is the property of or is licensed to Frontiers Media SA (“Frontiers”) or its licensees and/or subcontractors. The copyright in the FRONTIERS JOURNAL SERIES text of individual articles is the property of their respective authors, The Frontiers Journal Series is a multi-tier and interdisciplinary set of open-access, online subject to a license granted to Frontiers. journals, promising a paradigm shift from the current review, selection and dissemination The compilation of articles processes in academic publishing. constituting this e-book, as well as All Frontiers journals are driven by researchers for researchers; therefore, they constitute a service all content on this site is the exclusive property of Frontiers. to the scholarly community. At the same time, the Frontiers Journal Series operates on a revo- Images and graphics not forming lutionary invention, the tiered publishing system, initially addressing specific communities of part of user-contributed materials may not be downloaded or copied scholars, and gradually climbing up to broader public understanding, thus serving the interests without permission.
    [Show full text]
  • Why Is There Still So Much Confusion About VO2 Plateau? a Re- Examination of the Work of A.V
    University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Masters Theses Graduate School 6-2011 Why is there still so much confusion about VO2 plateau? A re- examination of the work of A.V. Hill Richard Vincent Castle [email protected] Follow this and additional works at: https://trace.tennessee.edu/utk_gradthes Part of the Exercise Physiology Commons, Exercise Science Commons, and the Other Analytical, Diagnostic and Therapeutic Techniques and Equipment Commons Recommended Citation Castle, Richard Vincent, "Why is there still so much confusion about VO2 plateau? A re-examination of the work of A.V. Hill. " Master's Thesis, University of Tennessee, 2011. https://trace.tennessee.edu/utk_gradthes/955 This Thesis is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Masters Theses by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a thesis written by Richard Vincent Castle entitled "Why is there still so much confusion about VO2 plateau? A re-examination of the work of A.V. Hill." I have examined the final electronic copy of this thesis for form and content and recommend that it be accepted in partial fulfillment of the equirr ements for the degree of Master of Science, with a major in Kinesiology. David R. Bassett, Jr., Major Professor We have read this thesis and recommend its acceptance: Dixie L. Thompson, Dawn P. Coe Accepted for the Council: Carolyn R.
    [Show full text]
  • Standard-For-Graded-Exercise-Testing
    Hindawi Publishing Corporation Journal of Sports Medicine Volume 2016, Article ID 3968393, 12 pages http://dx.doi.org/10.1155/2016/3968393 Review Article Graded Exercise Testing Protocols for the Determination of VO2max: Historical Perspectives, Progress, and Future Considerations Nicholas M. Beltz,1 Ann L. Gibson,1 Jeffrey M. Janot,2 Len Kravitz,1 Christine M. Mermier,1 and Lance C. Dalleck3 1 Health,Exercise&SportsSciencesDepartment,University of New Mexico, Albuquerque, NM, USA 2Department of Kinesiology, University of Wisconsin-Eau Claire, Eau Claire, WI, USA 3Recreation, Exercise & Sports Science Department, Western State Colorado University, Gunnison, CO, USA Correspondence should be addressed to Nicholas M. Beltz; [email protected] Received 2 August 2016; Revised 14 October 2016; Accepted 31 October 2016 Academic Editor: Andrew Bosch Copyright © 2016 Nicholas M. Beltz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Graded exercise testing (GXT) is the most widely used assessment to examine the dynamic relationship between exercise and integrated physiological systems. The information from GXT can be applied across the spectrum of sport performance, occupational safety screening, research, and clinical diagnostics. The suitability of GXT to determine a valid maximal oxygen consumption (VO2max) has been under investigation for decades. Although a set of recommended criteria exists to verify attainment of VO2max, the methods that originally established these criteria have been scrutinized. Many studies do not apply identical criteria or fail to consider individual variability in physiological responses. As an alternative to using traditional criteria, recent research efforts have been directed toward using a supramaximal verification protocol performed after a GXT to confirm attainment2 ofVO max.
    [Show full text]
  • Focus on Guillain–Barré Syndrome and Pompe Disease
    Cell. Mol. Life Sci. (2010) 67:701–713 DOI 10.1007/s00018-009-0184-2 Cellular and Molecular Life Sciences REVIEW Fatigue in neuromuscular disorders: focus on Guillain–Barre´ syndrome and Pompe disease J. M. de Vries • M. L. C. Hagemans • J. B. J. Bussmann • A. T. van der Ploeg • P. A. van Doorn Received: 30 June 2009 / Revised: 12 October 2009 / Accepted: 13 October 2009 / Published online: 16 November 2009 Ó The Author(s) 2009. This article is published with open access at Springerlink.com Abstract Fatigue accounts for an important part of the persist, non-pharmacological interventions, such as exer- burden experienced by patients with neuromuscular disor- cise and cognitive behavioral therapy, can be initiated. ders. Substantial high prevalence rates of fatigue are reported in a wide range of neuromuscular disorders, such Keywords Fatigue Á Neuromuscular disease Á as Guillain–Barre´ syndrome and Pompe disease. Fatigue Experienced fatigue Á Physiological fatigue Á can be subdivided into experienced fatigue and physio- Guillain–Barre´ syndrome Á Pompe disease logical fatigue. Physiological fatigue in turn can be of central or peripheral origin. Peripheral fatigue is an important contributor to fatigue in neuromuscular disor- Introduction ders, but in reaction to neuromuscular disease fatigue of central origin can be an important protective mechanism to Everybody experiences periods of fatigue, but these usually restrict further damage. In most cases, severity of fatigue can be mended by taking a rest or enjoying a good night’s seems to be related with disease severity, possibly with the sleep. In a wide range of diseases, however, fatigue is a well- exception of fatigue occurring in a monophasic disorder known chronic symptom.
    [Show full text]