Increased expression of fibroblast growth factors in a rabbit skeletal muscle model of exercise conditioning.

Morrow, Noelle; Kraus, William E.; Moore, James W.; Williams, R. Sanders; Swain, Judith L.

doi:10.1172/jci114640

Cited by 72 publications

(35 citation statements)

References 20 publications

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“…Release of FGF-2 by satellite cells or from membrane stores on ECM degradation may have a role to play in supporting angiogenesis and enhancing exercise-induced collateralisation of muscle. This may explain the original report of increased mitogen activity in stimulated muscle [108] if muscle damage was produced.…”

Section: Endogenous Stimulators Of Angiogenesismentioning

confidence: 80%

Invited review: activity-induced angiogenesis

Egginton

2008

Pflugers Arch - Eur J Physiol

214

231

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The dynamic biochemical and mechanical environment around blood vessels during muscle activity generates powerful stimuli for vascular remodelling. Ultimately, this must lead to a coordinated expansion of various elements of the cardiovascular system in order to support enhanced aerobic exercise. Vascular endothelial growth factor plays a central role, and understanding how this is regulated in vivo by changes in transcription and stability of mRNA, production of protein and interaction with other growth factors, is a continuing challenge. Exercise hyperaemia leads to an increase in microvascular shear stress, which stimulates endothelial release of nitric oxide, whilst proteolytic modification of the extracellular matrix is induced by mechanical deformation during cyclical contractions or muscle overload. These components of the exercise response lead to different forms of capillary growth, and subsequent expansion of the microcirculation may not have the same functional outcome. In vitro and in vivo studies have shown a complex interplay between different cytokines, receptors and mural cells in directing the necessary tissue re-organisation. The mechanisms involved in arteriogenesis are less well-understood than those of angiogenesis, but application of these data to understanding vascular remodelling in response to exercise may help resolve a range of cardiovascular dysfunction.

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Section: Endogenous Stimulators Of Angiogenesismentioning

confidence: 80%

Invited review: activity-induced angiogenesis

Egginton

2008

Pflugers Arch - Eur J Physiol

214

231

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“…acts locally and, most likely, without direct GH control in exercise-induced anabolism (28). The fibroblast growth factors Fig.…”

Section: T R a I N E D U N T R A I N E D T R A I N E D U N T R A I N E Dmentioning

confidence: 99%

Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats

et al. 1994

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ABSTRACT. Exercise training improves maximal oxygen uptake and endurance times in adult human beings and other animals. The mechanism of this improvement results in part from anabolic effects of exercise and may be mediated by growth hormone (GH). Little is known about the role of GH in the adaptation to exercise in younger, stilldeveloping organisms. To examine this role, we began a 4-wk treadmill exercise training protocol in 14-d-old female rats. GH was suppressed by passive immunization with anti-GH releasing hormone antisera. There were four experimental groups: I) GH-control (normal GH secretory capacity), untrained (n = 21); 2) GH-suppressed, untrained (n = 13); 3) GH-control, trained (n = 14); and 4) GHsuppressed; trained (n = 11). At the end of the training period, maximal oxygen uptake and treadmill endurance running time were measured. Serum GH and IGF-I were assessed using RIA, and whole hind limb musculature succinate dehydrogenase (an indicator of mitochondria1 function) was measured with standard fluorometric technique. Body weight gain was markedly reduced in GHsuppressed rats (mean, 54% of GH-controls in untrained rats and 55% in trained; p < 0.05). No apparent effect of training on linear growth was observed. As expected, serum IGF-I was markedly reduced by GH suppression, but no exercise-induced increase occurred in IGF-I as a result of training in either the GH-control or GH-suppressed rats. In GH-control rats, maximal oxygen uptake and succinate dehydrogenase were 69% and 25% greater, respectively, in trained compared with untrained rats (p < 0.05). Despite GH inhibition, similar increases were found in the trained GH-suppressed rats (68% greater than controls for maximal oxygen uptake and 34% for succinate dehydrogenase, In mature human beings and animals of many species, increased physical activity leads, to improved functional capabilities often measured as increased Vozmax or exercise endurance time. A pivotal mechanism for the improved function is the unique, naturally occurring anabolic effects of exercise ( I ) , such as skeletal and cardiac muscle hypertrophy (2), increased capillarization and mitochondria (3), and increased bone density (4). Because exercise stimulates GH secretion (5) and because GH (either directly or in combination with IGF-I) is a potent growth factor for skeletal iind heart muscle (6-9), it is not surprising that many investigations in both human beings (10, I I) and other species (12)(13)(14) indicate that GH plays an important role in the adaptation to exercise. Despite this finding, the role of GH in exerciseinduced growth is not understood, and evidence exists that exogenous GH administration does not enhance the effect of exercise training on muscle growth or strength in young, welltrained adult males ( 15-17).Far less is known about responses to repeated bouts of physical activity in the younger, developing organism where overall body growth is rapid and secretory patterns of growth factors (such as GH) are in a state of flux (18). The purpose of this ...

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“…Their results demonstrated that bFGF expression was not increased in rat skeletal muscle. Of course, several studies have reported that ES of skeletal muscle led to an increase in FGF-2 expression [25,42]. In our previous study, we reported that sensory and motor ES did not induce the release of VEGF in rat skeletal muscle [16].…”

Section: Discussionmentioning

confidence: 75%

Role of sensory and motor intensity of electrical stimulation on fibroblastic growth factor-2 expression, inflammation, vascularization, and mechanical strength of full-thickness wounds

Asadi

Torkaman

Hedayati³

et al. 2013

JRRD

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Abstract-Electrical stimulation (ES) profoundly affects angiogenesis by modulating the production of angiogenic factors. We evaluated the effect of sensory (direct current, 600 microamperes) and motor (monophasic pulse current, 2.5 to 3 milliamperes, 300-microsecond pulse duration, 100 Hz) intensities of cathodal current on the release of fibroblastic growth factor-2 (FGF-2) at the wound site and also the biomechanical and histological properties of healed skin. Ninety-six male, SpragueDawley rats were randomly assigned into one control and two experimental groups. A full-thickness skin incision was made on the dorsal region of each animal. The experimental groups received 10 sessions of ES (sensory or motor) for 1 hour per day every other day. The results showed that FGF-2 levels in the sensory group were significantly greater than in the other groups on the third day. In the motor group, FGF-2 levels were significantly decreased compared with the control group. There were no significant differences between the normalized ultimate strength and stiffness in the groups, but they tended to be higher in the motor ES group. We conclude that the application of sensory ES during the early stage of wound healing may have a beneficial effect on wound healing by inducing the release of angiogenic factors and decreasing the duration of the inflammation phase.

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Increased expression of fibroblast growth factors in a rabbit skeletal muscle model of exercise conditioning.

Cited by 72 publications

References 20 publications

Invited review: activity-induced angiogenesis

Invited review: activity-induced angiogenesis

Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats

Role of sensory and motor intensity of electrical stimulation on fibroblastic growth factor-2 expression, inflammation, vascularization, and mechanical strength of full-thickness wounds

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