Special Issue "Muscle Structure and Function"

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (15 May 2014)

Special Issue Editor

Guest Editor
Prof. Dr. Jim O. Vigoreaux

Department of Biology, University of Vermont, USA
Website | E-Mail
Interests: insect flight muscle; thick filaments; myosin binding proteins; molecular evolution; proteomics

Special Issue Information

Dear Colleagues,

Muscle is amazingly adaptable. Over a long time scale, a variety of muscle types have evolved to perform distinct and specialized functions based on a well conserved design of interdigitating myofilaments. Over a short time scale, muscle adapts to exercise and training by undergoing biochemical, metabolic, and structural remodeling. Muscle relies on different mechanisms to supply energy for contractile and homeostatic processes and increasing evidence suggests a variety of strategies by which energy production and transfer is regulated in different muscles and in muscles subjected to acute exercise and training. Cell biology research over the past decade has increasingly demonstrated a high degree of cytoplasmic compartmentalization defined not by structural boundaries, but by transient molecular interactions among pathway components and cellular structures. For this special issue, we welcome original research and review articles that examine muscle metabolism, in health and disease, in light of the emerging paradigm of the cytoplasm as an interconnected network of microdomains.

Prof. Dr. Jim O. Vigoreaux
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 650 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolism
  • glycolysis
  • compartmentalization
  • energy transfer
  • phosphagens
  • aerobic pathways
  • adaptation
  • exercise

Published Papers (9 papers)

View options order results:
result details:
Displaying articles 1-9
Export citation of selected articles as:

Research

Jump to: Review, Other

Open AccessArticle In Vivo Molecular Responses of Fast and Slow Muscle Fibers to Lipopolysaccharide in a Teleost Fish, the Rainbow Trout (Oncorhynchus mykiss)
Biology 2015, 4(1), 67-87; https://doi.org/10.3390/biology4010067
Received: 27 November 2014 / Revised: 6 January 2015 / Accepted: 28 January 2015 / Published: 4 February 2015
Cited by 3 | PDF Full-text (676 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The physiological consequences of the activation of the immune system in skeletal muscle in fish are not completely understood. To study the consequences of the activation of the immune system by bacterial pathogens on skeletal muscle function, we administered lipopolysaccharide (LPS), an active
[...] Read more.
The physiological consequences of the activation of the immune system in skeletal muscle in fish are not completely understood. To study the consequences of the activation of the immune system by bacterial pathogens on skeletal muscle function, we administered lipopolysaccharide (LPS), an active component of Gram-negative bacteria, in rainbow trout and performed transcriptomic and proteomic analyses in skeletal muscle. We examined changes in gene expression in fast and slow skeletal muscle in rainbow trout at 24 and 72 h after LPS treatment (8 mg/kg) by microarray analysis. At the transcriptional level, we observed important changes in metabolic, mitochondrial and structural genes in fast and slow skeletal muscle. In slow skeletal muscle, LPS caused marked changes in the expression of genes related to oxidative phosphorylation, while in fast skeletal muscle LPS administration caused major changes in the expression of genes coding for glycolytic enzymes. We also evaluated the effects of LPS administration on the fast skeletal muscle proteome and identified 14 proteins that were differentially induced in LPS-treated trout, primarily corresponding to glycolytic enzymes. Our results evidence a robust and tissue-specific response of skeletal muscle to an acute inflammatory challenge, affecting energy utilization and possibly growth in rainbow trout. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Open AccessArticle The Effect of Nutritional Status in the Pathogenesis of Critical Illness Myopathy (CIM)
Biology 2014, 3(2), 368-382; https://doi.org/10.3390/biology3020368
Received: 10 February 2014 / Revised: 22 May 2014 / Accepted: 27 May 2014 / Published: 30 May 2014
Cited by 1 | PDF Full-text (159 KB) | HTML Full-text | XML Full-text
Abstract
The muscle wasting and loss of specific force associated with Critical Illness Myopathy (CIM) is, at least in part, due to a preferential loss of the molecular motor protein myosin. This acquired myopathy is common in critically ill immobilized and mechanically ventilated intensive
[...] Read more.
The muscle wasting and loss of specific force associated with Critical Illness Myopathy (CIM) is, at least in part, due to a preferential loss of the molecular motor protein myosin. This acquired myopathy is common in critically ill immobilized and mechanically ventilated intensive care patients (ICU). There is a growing understanding of the mechanisms underlying CIM, but the role of nutritional factors triggering this serious complication of modern intensive care remains unknown. This study aims at establishing the effect of nutritional status in the pathogenesis of CIM. An experimental ICU model was used where animals are mechanically ventilated, pharmacologically paralysed post-synaptically and extensively monitored for up to 14 days. Due to the complexity of the experimental model, the number of animals included is small. After exposure to this ICU condition, animals develop a phenotype similar to patients with CIM. The results from this study show that the preferential myosin loss, decline in specific force and muscle fiber atrophy did not differ between low vs. eucaloric animals. In both experimental groups, passive mechanical loading had a sparing effect of muscle weight independent on nutritional status. Thus, this study confirms the strong impact of the mechanical silencing associated with the ICU condition in triggering CIM, overriding any potential effects of caloric intake in triggering CIM. In addition, the positive effects of passive mechanical loading on muscle fiber size and force generating capacity was not affected by the nutritional status in this study. However, due to the small sample size these pilot results need to be validated in a larger cohort. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Open AccessArticle High Intensity Training Improves Health and Physical Function in Middle Aged Adults
Biology 2014, 3(2), 333-344; https://doi.org/10.3390/biology3020333
Received: 27 February 2014 / Revised: 30 April 2014 / Accepted: 1 May 2014 / Published: 12 May 2014
Cited by 5 | PDF Full-text (199 KB) | HTML Full-text | XML Full-text
Abstract
High intensity training (HIT) is effective at improving health; however, it is unknown whether HIT also improves physical function. This study aimed to determine whether HIT improves metabolic health and physical function in untrained middle aged individuals. Fourteen (three male and eleven female)
[...] Read more.
High intensity training (HIT) is effective at improving health; however, it is unknown whether HIT also improves physical function. This study aimed to determine whether HIT improves metabolic health and physical function in untrained middle aged individuals. Fourteen (three male and eleven female) untrained individuals were recruited (control group n = 6: age 42 ± 8 y, weight 64 ± 10 kg, BMI 24 ± 2 kg·m−2 or HIT group n = 8: age 43 ± 8 y, weight 80 ± 8 kg, BMI 29 ± 5 kg·m−2). Training was performed twice weekly, consisting of 10 × 6-second sprints with a one minute recovery between each sprint. Metabolic health (oral glucose tolerance test), aerobic capacity (incremental time to exhaustion on a cycle ergometer) and physical function (get up and go test, sit to stand test and loaded 50 m walk) were determined before and after training. Following eight weeks of HIT there was a significant improvement in aerobic capacity (8% increase in VO2 peak; p < 0.001), physical function (11%–27% respectively; p < 0.05) and a reduction in blood glucose area under the curve (6% reduction; p < 0.05). This study demonstrates for the first time the potential of HIT as a training intervention to improve skeletal muscle function and glucose clearance as we age. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Review

Jump to: Research, Other

Open AccessReview The Intriguing Dual Lattices of the Myosin Filaments in Vertebrate Striated Muscles: Evolution and Advantage
Biology 2014, 3(4), 846-865; https://doi.org/10.3390/biology3040846
Received: 5 September 2014 / Revised: 20 November 2014 / Accepted: 25 November 2014 / Published: 3 December 2014
Cited by 3 | PDF Full-text (1867 KB) | HTML Full-text | XML Full-text
Abstract
Myosin filaments in vertebrate striated muscle have a long roughly cylindrical backbone with cross-bridge projections on the surfaces of both halves except for a short central bare zone. In the middle of this central region the filaments are cross-linked by the M-band which
[...] Read more.
Myosin filaments in vertebrate striated muscle have a long roughly cylindrical backbone with cross-bridge projections on the surfaces of both halves except for a short central bare zone. In the middle of this central region the filaments are cross-linked by the M-band which holds them in a well-defined hexagonal lattice in the muscle A-band. During muscular contraction the M-band-defined rotation of the myosin filaments around their long axes influences the interactions that the cross-bridges can make with the neighbouring actin filaments. We can visualise this filament rotation by electron microscopy of thin cross-sections in the bare-region immediately adjacent to the M-band where the filament profiles are distinctly triangular. In the muscles of teleost fishes, the thick filament triangular profiles have a single orientation giving what we call the simple lattice. In other vertebrates, for example all the tetrapods, the thick filaments have one of two orientations where the triangles point in opposite directions (they are rotated by 60° or 180°) according to set rules. Such a distribution cannot be developed in an ordered fashion across a large 2D lattice, but there are small domains of superlattice such that the next-nearest neighbouring thick filaments often have the same orientation. We believe that this difference in the lattice forms can lead to different contractile behaviours. Here we provide a historical review, and when appropriate cite recent work related to the emergence of the simple and superlattice forms by examining the muscles of several species ranging back to primitive vertebrates and we discuss the functional differences that the two lattice forms may have. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1a

Open AccessReview The Structural and Functional Coordination of Glycolytic Enzymes in Muscle: Evidence of a Metabolon?
Biology 2014, 3(3), 623-644; https://doi.org/10.3390/biology3030623
Received: 14 July 2014 / Revised: 5 September 2014 / Accepted: 8 September 2014 / Published: 22 September 2014
Cited by 7 | PDF Full-text (601 KB) | HTML Full-text | XML Full-text
Abstract
Metabolism sustains life through enzyme-catalyzed chemical reactions within the cells of all organisms. The coupling of catalytic function to the structural organization of enzymes contributes to the kinetic optimization important to tissue-specific and whole-body function. This coupling is of paramount importance in the
[...] Read more.
Metabolism sustains life through enzyme-catalyzed chemical reactions within the cells of all organisms. The coupling of catalytic function to the structural organization of enzymes contributes to the kinetic optimization important to tissue-specific and whole-body function. This coupling is of paramount importance in the role that muscle plays in the success of Animalia. The structure and function of glycolytic enzyme complexes in anaerobic metabolism have long been regarded as a major regulatory element necessary for muscle activity and whole-body homeostasis. While the details of this complex remain to be elucidated through in vivo studies, this review will touch on recent studies that suggest the existence of such a complex and its structure. A potential model for glycolytic complexes and related subcomplexes is introduced. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Open AccessReview Discerning Primary and Secondary Factors Responsible for Clinical Fatigue in Multisystem Diseases
Biology 2014, 3(3), 606-622; https://doi.org/10.3390/biology3030606
Received: 27 June 2014 / Revised: 21 August 2014 / Accepted: 1 September 2014 / Published: 22 September 2014
Cited by 2 | PDF Full-text (104 KB) | HTML Full-text | XML Full-text
Abstract
Fatigue is a common symptom of numerous acute and chronic diseases, including myalgic encephalomyelitis/chronic fatigue syndrome, multiple sclerosis, heart failure, cancer, and many others. In these multi-system diseases the physiological determinants of enhanced fatigue encompass a combination of metabolic, neurological, and myofibrillar adaptations.
[...] Read more.
Fatigue is a common symptom of numerous acute and chronic diseases, including myalgic encephalomyelitis/chronic fatigue syndrome, multiple sclerosis, heart failure, cancer, and many others. In these multi-system diseases the physiological determinants of enhanced fatigue encompass a combination of metabolic, neurological, and myofibrillar adaptations. Previous research studies have focused on adaptations specific to skeletal muscle and their role in fatigue. However, most have neglected the contribution of physical inactivity in assessing disease syndromes, which, through deconditioning, likely contributes to symptomatic fatigue. In this commentary, we briefly review disease-related muscle phenotypes in the context of whether they relate to the primary disease or whether they develop secondary to reduced physical activity. Knowledge of the etiology of the skeletal muscle adaptations in these conditions and their contribution to fatigue symptoms is important for understanding the utility of exercise rehabilitation as an intervention to alleviate the physiological precipitants of fatigue. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Open AccessReview Combustion, Respiration and Intermittent Exercise: A Theoretical Perspective on Oxygen Uptake and Energy Expenditure
Biology 2014, 3(2), 255-263; https://doi.org/10.3390/biology3020255
Received: 23 January 2014 / Revised: 2 March 2014 / Accepted: 5 March 2014 / Published: 28 March 2014
Cited by 2 | PDF Full-text (335 KB) | HTML Full-text | XML Full-text
Abstract
While no doubt thought about for thousands of years, it was Antoine Lavoisier in the late 18th century who is largely credited with the first “modern” investigations of biological energy exchanges. From Lavoisier’s work with combustion and respiration a scientific trend emerges that
[...] Read more.
While no doubt thought about for thousands of years, it was Antoine Lavoisier in the late 18th century who is largely credited with the first “modern” investigations of biological energy exchanges. From Lavoisier’s work with combustion and respiration a scientific trend emerges that extends to the present day: the world gains a credible working hypothesis but validity goes missing, often for some time, until later confirmed using proper measures. This theme is applied to glucose/glycogen metabolism where energy exchanges are depicted as conversion from one form to another and, transfer from one place to another made by both the anaerobic and aerobic biochemical pathways within working skeletal muscle, and the hypothetical quantification of these components as part of an oxygen (O2) uptake measurement. The anaerobic and aerobic energy exchange components of metabolism are represented by two different interpretations of O2 uptake: one that contains a glycolytic component (1 L O2 = 21.1 kJ) and one that does not (1 L O2 = 19.6 kJ). When energy exchange transfer and oxygen-related expenditures are applied separately to exercise and recovery periods, an increased energy cost for intermittent as compared to continuous exercise is hypothesized to be a direct result. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Open AccessReview McArdle Disease and Exercise Physiology
Biology 2014, 3(1), 157-166; https://doi.org/10.3390/biology3010157
Received: 5 February 2014 / Revised: 19 February 2014 / Accepted: 20 February 2014 / Published: 25 February 2014
Cited by 1 | PDF Full-text (717 KB) | HTML Full-text | XML Full-text
Abstract
McArdle disease (glycogen storage disease Type V; MD) is a metabolic myopathy caused by a deficiency in muscle glycogen phosphorylase. Since muscle glycogen is an important fuel for muscle during exercise, this inborn error of metabolism provides a model for understanding the role
[...] Read more.
McArdle disease (glycogen storage disease Type V; MD) is a metabolic myopathy caused by a deficiency in muscle glycogen phosphorylase. Since muscle glycogen is an important fuel for muscle during exercise, this inborn error of metabolism provides a model for understanding the role of glycogen in muscle function and the compensatory adaptations that occur in response to impaired glycogenolysis. Patients with MD have exercise intolerance with symptoms including premature fatigue, myalgia, and/or muscle cramps. Despite this, MD patients are able to perform prolonged exercise as a result of the “second wind” phenomenon, owing to the improved delivery of extra-muscular fuels during exercise. The present review will cover what this disease can teach us about exercise physiology, and particularly focuses on the compensatory pathways for energy delivery to muscle in the absence of glycogenolysis. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Other

Jump to: Research, Review

Open AccessProject Report Elevated Circulating TNF-α in Fat-Free Mass Non-Responders Compared to Responders Following Exercise Training in Older Women
Biology 2014, 3(3), 551-559; https://doi.org/10.3390/biology3030551
Received: 24 June 2014 / Revised: 14 August 2014 / Accepted: 26 August 2014 / Published: 5 September 2014
Cited by 4 | PDF Full-text (101 KB) | HTML Full-text | XML Full-text
Abstract
The purpose of this investigation was to determine if differences in inflammatory cytokines exist between fat-free mass responders versus non-responders following a combined resistance/aerobic training program in older women. Fifty women over 60 years old, mean BMI 27 ± 4 (kg/m2)
[...] Read more.
The purpose of this investigation was to determine if differences in inflammatory cytokines exist between fat-free mass responders versus non-responders following a combined resistance/aerobic training program in older women. Fifty women over 60 years old, mean BMI 27 ± 4 (kg/m2) and physically untrained, participated in a combined training program for 16-weeks. Body composition, muscle strength, and serum inflammatory markers (TNF-α, CRP, and IL-6) were assessed at baseline and 16-weeks post-training. A significant time effect was observed for weight, %fat, fat mass, and all strength measures (p < 0.05). A group interaction was observed for TNF-α (p < 0.05), which revealed higher concentrations of circulating TNF-α at baseline (18%) and post-exercise training (24%) in non-responders compared to responders (p < 0.05). In conclusion, this study revealed a significantly greater concentration of circulating TNF-α in older women that do not increase fat-free mass following training. Full article
(This article belongs to the Special Issue Muscle Structure and Function)
Figures

Figure 1

Back to Top