Angiogenesis in the Heart and Skeletal Muscle — Models for Capillary Growth

Angiogenesis ◽  
1998 ◽  
pp. 19-33 ◽  
Author(s):  
O. Hudlicka ◽  
S. Egginton ◽  
M. D. Brown
Keyword(s):  
Skeletal Muscle ◽  
Capillary Growth ◽  
Muscle Models

Angiogenesis in Skletal Muscle

Physiology ◽  
1986 ◽  
Vol 1 (5) ◽  
pp. 160-163
Author(s):  
HW Burton ◽  
JA Faulkner
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Vasoactive Agents ◽  
Adult Skeletal Muscle ◽  
Capillary Growth ◽  
Vascular Bed ◽  
Chronic Electrical Stimulation ◽  
Capillary Bed ◽  
Ischemic Muscle

Capillary growth is rarely observed in normal adult skeletal muscle, but angiogenesis may occur after injury to a capillary bed or after endurance training or chronic electrical stimulation. Revascularization of ischemic muscle may arise as inward growth from surrounding vascularized tissue, as outward growth from endothelial cells in ischemic muscle, or a combination of the two processes. A regenerated vascular bed shows diminished response to vasoactive agents and impaired regulation of blood flow during contractions.

scholarly journals Bioprinting of 3D in vitro skeletal muscle models: A review

2020 ◽  
Vol 193 ◽  
pp. 108794 ◽  
Author(s):  
Pei Zhuang ◽  
Jia An ◽  
Chee Kai Chua ◽  
Lay Poh Tan
Keyword(s):  
Skeletal Muscle ◽  
Muscle Models

Differences Between Principal Strain Directions and Muscle Fiber Directions in the Contracting Biceps Bracii Measured With CPC-MRI

2007 ◽  
Author(s):  
Hehe Zhou ◽  
John E. Novotny
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Biceps Brachii ◽  
Principal Strain ◽  
Strain Fields ◽  
Ultrasound Study ◽  
Lagrangian Strain ◽  
Novel Method ◽  
Muscle Models

Skeletal muscle exhibit non-uniform internal architectures and our research goals are to relate these to their internal mechanics during contraction to provide a better understanding of muscle function, verify muscle models and permit more sophisticated interpretation of the functional effects of injury. Our previous studies have developed a novel method to calculate 2D Lagrangian strain field of skeletal muscle from the CPC-MRI [1]. The objective of this study is to apply CPC-MRI to derive Lagrangian strain fields for the normal biceps brachii and to determine its minimum principal strain directions in vivo during contraction. We will then compare them to the muscle fiber directions or pennation angles measured by a parallel ultrasound study. If we assume the muscle force is mainly transmitted along fiber directions, we would expect that the minimum principal strain directions are the same as fiber directions. Comparisons between different regions of the muscle and flexion angles will also be made.

scholarly journals Capillary growth and regression in skeletal muscle

2014 ◽  
Vol 3 (5) ◽  
pp. 483-491 ◽  
Author(s):  
Hidemi Fujino ◽  
Hiroyo Kondo ◽  
Fumiko Nagatomo ◽  
Akihiko Ishihara
Keyword(s):  
Skeletal Muscle ◽  
Capillary Growth

scholarly journals Coupling 3D and 1D Skeletal Muscle Models

PAMM ◽  
2012 ◽  
Vol 12 (1) ◽  
pp. 111-112
Author(s):  
Michael Sprenger ◽  
Syn Schmitt ◽  
Oliver Röhrle
Keyword(s):  
Skeletal Muscle ◽  
Muscle Models

scholarly journals Model order reduction of dynamic skeletal muscle models

PAMM ◽  
2016 ◽  
Vol 16 (1) ◽  
pp. 851-852
Author(s):  
Mylena Mordhorst ◽  
Daniel Wirtz ◽  
Oliver Röhrle
Keyword(s):  
Skeletal Muscle ◽  
Model Order Reduction ◽  
Order Reduction ◽  
Model Order ◽  
Muscle Models

Vascular remodelling in human skeletal muscle

2011 ◽  
Vol 39 (6) ◽  
pp. 1628-1632 ◽  
Author(s):  
Thomas Gustafsson
Keyword(s):  
Skeletal Muscle ◽  
Cell Types ◽  
Model Systems ◽  
Limited Information ◽  
Muscle Adaptation ◽  
Multiple Systems ◽  
Sprouting Angiogenesis ◽  
Capillary Growth ◽  
Ecm Extracellular Matrix ◽  
Exercise Induced

Exercise-induced angiogenesis in skeletal muscle involves both non-sprouting and sprouting angiogenesis and results from the integrated responses of multiple systems and stimuli. VEGF-A (vascular endothelial growth factor A) levels are increased in exercised muscle and have been demonstrated to be critical for exercise-induced capillary growth. Only limited information is available regarding the role of other angiogenic and angiostatic factors in exercise, but changes in the angiopoietin family following repetitive bouts of exercise occur in a pattern that is favourable for angiogenesis. Results from other angiogenic model systems, indicate that miRNAs (microRNAs) are important factors in the regulation of angiogenesis and thus to explore their role as regulators of exercise induced angiogenesis will be an important avenue of study in the future. ECM (extracellular matrix) remodelling and activation of MMPs (matrix metalloproteinases) are, to some extent, overlooked players in skeletal muscle adaptation. Degradation of ECM proteins liberates angiogenic factors from immobilized matrix stores and make cell migration possible. In fact, it is known that MMPs become activated by a single bout of exercise in humans, rapid interstitial changes occur long before any changes in gene transcription could result in protein synthesis and inhibition of MMP activity completely abolishes sprouting angiogenesis. A growing body of evidence suggests that circulating and resident progenitor cells, in addition to other cell types located in skeletal muscle tissue, participate in skeletal muscle angiogenesis by various mechanisms. However, more studies are needed before these can be confirmed as mechanisms of exercise-induced capillary growth.

Hormetic modulation of angiogenic factors by exercise-induced mechanical and metabolic stress in human skeletal muscle

2020 ◽  
Vol 319 (4) ◽  
pp. H824-H834
Author(s):  
M. Fiorenza ◽  
L. Gliemann ◽  
N. Brandt ◽  
J. Bangsbo
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activity ◽  
Human Skeletal Muscle ◽  
Metabolic Stress ◽  
Angiogenic Factors ◽  
Capillary Growth ◽  
Exercise Induced ◽  
Molecular Signals

Skeletal muscle capillary growth is orchestrated by angiogenic factors sensitive to mechanical and metabolic signals. In this study, we employed an integrative exercise model to synergistically target, yet to different extents and for different durations, the mechanical and metabolic components of muscle activity that promote angiogenesis. Our results suggest that the magnitude of the myocellular perturbations incurred during exercise determines the amplitude of the angiogenic molecular signals, implying hormetic modulation of skeletal muscle angiogenesis by exercise-induced mechanical and metabolic stress.

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