Voluntary running induces fiber type-specific angiogenesis in mouse skeletal muscle

2004 ◽  
Vol 287 (5) ◽  
pp. C1342-C1348 ◽  
Author(s):  
Richard E. Waters ◽  
Svein Rotevatn ◽  
Ping Li ◽  
Brian H. Annex ◽  
Zhen Yan
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Fiber Type ◽  
Capillary Density ◽  
Adult Skeletal Muscle ◽  
Heavy Chains ◽  
Type Transformation ◽  
Type Composition ◽  
Voluntary Running ◽  
Exercise Induced

Adult skeletal muscle undergoes adaptation in response to endurance exercise, including fast-to-slow fiber type transformation and enhanced angiogenesis. The purpose of this study was to determine the temporal and spatial changes in fiber type composition and capillary density in a mouse model of endurance training. Long-term voluntary running (4 wk) in C57BL/6 mice resulted in an approximately twofold increase in capillary density and capillary-to-fiber ratio in plantaris muscle as measured by indirect immunofluorescence with an antibody against the endothelial cell marker CD31 (466 ± 16 capillaries/mm2 and 0.95 ± 0.04 capillaries/fiber in sedentary control mice vs. 909 ± 55 capillaries/mm2 and 1.70 ± 0.04 capillaries/fiber in trained mice, respectively; P < 0.001). A significant increase in capillary-to-fiber ratio was present at day 7 with increased concentration of vascular endothelial growth factor (VEGF) in the muscle, before a significant increase in percentage of type IIa myofibers, suggesting that exercise-induced angiogenesis occurs first, followed by fiber type transformation. Further analysis with simultaneous staining of endothelial cells and isoforms of myosin heavy chains (MHCs) showed that the increase in capillary contact manifested transiently in type IIb + IId/x fibers at the time ( day 7) of significant increase in total capillary density. These findings suggest that endurance training induces angiogenesis in a subpopulation of type IIb + IId/x fibers before switching to type IIa fibers.

Resident stem cells are not required for exercise-induced fiber-type switching and angiogenesis but are necessary for activity-dependent muscle growth

2006 ◽  
Vol 290 (6) ◽  
pp. C1461-C1468 ◽  
Author(s):  
Ping Li ◽  
Takayuki Akimoto ◽  
Mei Zhang ◽  
R. Sanders Williams ◽  
Zhen Yan
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Intraperitoneal Injection ◽  
Fiber Type ◽  
Muscle Growth ◽  
Plantaris Muscle ◽  
Voluntary Running ◽  
Exercise Induced ◽  
Activity Dependent

Skeletal muscle undergoes active remodeling in response to endurance exercise training, and the underlying mechanisms of this remodeling remain to be defined fully. We have recently obtained evidence that voluntary running induces cell cycle gene expression and cell proliferation in mouse plantaris muscles that undergo fast-to-slow fiber-type switching and angiogenesis after long-term exercise. To ascertain the functional role of cell proliferation in skeletal muscle adaptation, we performed in vivo 5-bromo-2′-deoxyuridine (BrdU) pulse labeling (a single intraperitoneal injection), which demonstrated a phasic increase (5- to 10-fold) in BrdU-positive cells in plantaris muscle between days 3 and 14 during 4 wk of voluntary running. Daily intraperitoneal injection of BrdU for 4 wk labeled 2.0% and 15.4% of the nuclei in plantaris muscle in sedentary and trained mice, respectively, and revealed the myogenic and angiogenic fates of the majority of proliferative cells. Ablation of resident stem cell activity by X-ray irradiation did not prevent voluntary running-induced increases of type IIa myofibers and CD31-positive endothelial cells but completely blocked the increase in muscle mass. These findings suggest that resident stem cell proliferation is not required for exercise-induced type IIb-to-IIa fiber-type switching and angiogenesis but is required for activity-dependent muscle growth. The origin of the angiogenic cells in this physiological exercise model remains to be determined.

Skeletal muscle adaptation in response to mechanical stress in p130cas−/− mice

2013 ◽  
Vol 304 (6) ◽  
pp. C541-C547 ◽  
Author(s):  
Takayuki Akimoto ◽  
Kanako Okuhira ◽  
Katsuji Aizawa ◽  
Shogo Wada ◽  
Hiroaki Honda ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mechanical Stress ◽  
P38 Mapk ◽  
Fiber Type ◽  
Cellular Signaling ◽  
Mapk Signaling ◽  
Muscle Adaptation ◽  
Type Transformation ◽  
Exercise Induced ◽  
Specific Deletion

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.

scholarly journals An inducible knockout of Dicer in adult mice does not affect endurance exercise-induced muscle adaptation

2019 ◽  
Vol 316 (2) ◽  
pp. C285-C292 ◽  
Author(s):  
Satoshi Oikawa ◽  
Minjung Lee ◽  
Norio Motohashi ◽  
Seiji Maeda ◽  
Takayuki Akimoto
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Citrate Synthase ◽  
Wheel Running ◽  
Fiber Type ◽  
Tamoxifen Treatment ◽  
Muscle Adaptation ◽  
Adult Skeletal Muscle ◽  
Significant Difference ◽  
Exercise Induced

The contractile and metabolic properties of adult skeletal muscle change in response to endurance exercise. The mechanisms of transcriptional regulation in exercise-induced skeletal muscle adaptation, including fiber-type switching and mitochondrial biogenesis, have been investigated intensively, whereas the role of microRNA (miRNA)-mediated posttranscriptional gene regulation is less well understood. We used tamoxifen-inducible Dicer1 knockout (iDicer KO) mice to reduce the global expression of miRNAs in adult skeletal muscle and subjected these mice to 2 wk of voluntary wheel running. Dicer mRNA expression was completely depleted in fast-twitch plantaris muscle after tamoxifen injection. However, several muscle-enriched miRNAs, including miR-1 and miR-133a, were reduced by only 30–50% in both the slow and fast muscles. The endurance exercise-induced changes that occurred for many parameters (i.e., fast-to-slow fiber-type switch and increases in succinate dehydrogenase, respiratory chain complex II, and citrate synthase activity) in wild type (WT) also occurred in the iDicer KO mice. Protein expression of myosin heavy chain IIa, peroxisome proliferator-activated receptor-γ coactivator-1α, and cytochrome c complex IV was also increased in the iDicer KO mice by the voluntary running. Furthermore, there was no significant difference in oxygen consumption rate in the isolated mitochondria between the WT and iDicer KO mice. These data indicate that muscle-enriched miRNAs were detectable even after 4 wk of tamoxifen treatment and there was no apparent specific endurance-exercise-induced muscle phenotype in the iDicer KO mice.

Dynamic exercise training in foxhounds. II. Analysis of skeletal muscle

1985 ◽  
Vol 59 (1) ◽  
pp. 190-197 ◽  
Author(s):  
D. Parsons ◽  
T. I. Musch ◽  
R. L. Moore ◽  
G. C. Haidet ◽  
G. A. Ordway
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Fiber Type ◽  
Staining Intensity ◽  
Capillary Density ◽  
Treadmill Running ◽  
Type I ◽  
Type Ii ◽  
Glycerophosphate Dehydrogenase ◽  
Before And After

The purpose of this study was to determine whether 8–12 wk of endurance training produces biochemical and histochemical adaptations in skeletal muscle in foxhounds. Analyses were performed on samples removed from gastrocnemius, triceps, and semitendinosus muscles of foxhounds before and after a treadmill running program. Biochemical analysis showed that training did not alter the activities of phosphofructokinase, beta-hydroxyacyl-CoA dehydrogenase, succinate dehydrogenase, or total phosphorylase. Histochemical analysis of myofibrillar actomyosin ATPase demonstrated three distinct classes of type II fibers and one type I fiber in the semitendinosus and triceps muscles and two type II and two type I fibers in the gastrocnemius muscle. Fiber type distribution and oxidative and glycolytic potentials, as indicated by nicotinamide adenine dinucleotide tetrazolium reductase or alpha-glycerophosphate dehydrogenase staining intensity, were unaltered by training. Similarly, capillary density, capillary-to-fiber ratios, and capillary area-to-fiber area ratios did not change with training. Thus, unlike humans and other mammals (i.e., rat), these foxhounds did not manifest biochemical or histochemical adaptations in skeletal muscle as the result of endurance training. This is consistent with the results of the study in which endurance training produced a 27% increase in maximal cardiac output and a 4% increase in maximal arteriovenous O2 extraction in foxhounds.

scholarly journals PGC-1α plays a functional role in exercise-induced mitochondrial biogenesis and angiogenesis but not fiber-type transformation in mouse skeletal muscle

2010 ◽  
Vol 298 (3) ◽  
pp. C572-C579 ◽  
Author(s):  
Tuoyu Geng ◽  
Ping Li ◽  
Mitsuharu Okutsu ◽  
Xinhe Yin ◽  
Jyeyi Kwek ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Mitochondrial Biogenesis ◽  
Knockout Mice ◽  
Functional Role ◽  
Fiber Type ◽  
Mitochondrial Morphology ◽  
Mouse Skeletal Muscle ◽  
Type Transformation ◽  
Exercise Induced

Endurance exercise stimulates peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) expression in skeletal muscle, and forced expression of PGC-1α changes muscle metabolism and exercise capacity in mice. However, it is unclear if PGC-1α is indispensible for endurance exercise-induced metabolic and contractile adaptations in skeletal muscle. In this study, we showed that endurance exercise-induced expression of mitochondrial enzymes (cytochrome oxidase IV and cytochrome c) and increases of platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31)-positive endothelial cells in skeletal muscle, but not IIb-to-IIa fiber-type transformation, were significantly attenuated in muscle-specific Pgc-1α knockout mice. Interestingly, voluntary running effectively restored the compromised mitochondrial integrity and superoxide dismutase 2 (SOD2) protein expression in skeletal muscle in Pgc-1α knockout mice. Thus, PGC-1α plays a functional role in endurance exercise-induced mitochondrial biogenesis and angiogenesis, but not IIb-to-IIa fiber-type transformation in mouse skeletal muscle, and the improvement of mitochondrial morphology and antioxidant defense in response to endurance exercise may occur independently of PGC-1α function. We conclude that PGC-1α is required for complete skeletal muscle adaptations induced by endurance exercise in mice.

scholarly journals Regulation of exercise-induced fiber type transformation, mitochondrial biogenesis, and angiogenesis in skeletal muscle

2011 ◽  
Vol 110 (1) ◽  
pp. 264-274 ◽  
Author(s):  
Zhen Yan ◽  
Mitsuharu Okutsu ◽  
Yasir N. Akhtar ◽  
Vitor A. Lira
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Contractile Activity ◽  
Fiber Type ◽  
Genetically Engineered ◽  
Type Transformation ◽  
Muscle Adaptations ◽  
Exercise Induced ◽  
Skeletal Muscle Adaptations ◽  
Muscle Contractile

Skeletal muscle exhibits superb plasticity in response to changes in functional demands. Chronic increases of skeletal muscle contractile activity, such as endurance exercise, lead to a variety of physiological and biochemical adaptations in skeletal muscle, including mitochondrial biogenesis, angiogenesis, and fiber type transformation. These adaptive changes are the basis for the improvement of physical performance and other health benefits. This review focuses on recent findings in genetically engineered animal models designed to elucidate the mechanisms and functions of various signal transduction pathways and gene expression programs in exercise-induced skeletal muscle adaptations.

Exercise-enhanced satellite cell proliferation and new myonuclear accretion in rat skeletal muscle

2001 ◽  
Vol 90 (4) ◽  
pp. 1407-1414 ◽  
Author(s):  
Heather K. Smith ◽  
Linda Maxwell ◽  
Carol D. Rodgers ◽  
Nancy H. McKee ◽  
Michael J. Plyley
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Normal Activity ◽  
Adult Skeletal Muscle ◽  
Vastus Intermedius ◽  
Muscle Loading ◽  
Satellite Cell Proliferation ◽  
Exercise Induced

The effects of increased functional loading on early cellular regenerative events after exercise-induced injury in adult skeletal muscle were examined with the use of in vivo labeling of replicating myofiber nuclei and immunocyto- and histochemical techniques. Satellite cell proliferation in the soleus (Sol) of nonexercised rats (0.4 ± 0.2% of fibers) was unchanged after an initial bout of declined treadmill exercise but was elevated after two (1.0 ± 0.2%, P ≤ 0.01), but not four or seven, daily bouts of the same task. Myonuclei produced over the 7-day period comprised 0.9–1.9% of myonuclei in isolated fibers of Sol, tibialis anterior, and vastus intermedius of nonexercised rats. The accretion of new myonuclei was enhanced ( P ≤ 0.05) in Sol and vastus intermedius by the initial exercise followed by normal activity (to 3.1–3.4% of myonuclei) and more so by continued daily exercise (4.2–5.3%). Observed coincident with a lower incidence of histological fiber injury and unchanged fiber diameter and myonuclei per millimeter, the greater new myonuclear accretion induced by continued muscle loading may contribute to an enhanced fiber repair and regeneration after exercise-induced injury.

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