ROLE OF RESISTANCE EXERCISE IN CONTROLLING  INSULIN-LIKE GROWTH FACTOR 1 (IGF-1) AND IT�S ASSOCIATION WITH  METABOLIC DISEASE PREVENTION

Based on data Riset Kesehatan Dasar (Riskesdas) in 2007, the people who had no or low physical activity reached 48.2 %. This condition contributes to increase number of metabolic disease cases such as: hypertension, heart disease, stroke and diabetes mellitus. Optimizing training approach especially aerobic type helps to counter metabolic diseases. Unfortunately, benefits of resistance training (RT) is less understood. RT improves muscle strength, induce muscle hypertrophy, improvement of local muscular performance, and also help to strenghtening body balance and coordination. There is interplay between training and hormone in muscle adaptation during resistance training. Hormone plays an important role in the regeneration of muscle after resistance training. The changes of hormone level cause hypertrophy. Regeneration and muscle hypertrophy are mediated by activation, proliferation and differentiation of satellite cells. It is regulated by mitotic and myogenic activity, namely insulin-like growth factor-1 (IGF-1), which serves as a paracrine or autocrine. Better understanding of homeostasis hormone during training in skeletal muscle and its ultimate purpose to counter metabolic disease will lead us to better treatment approach for the patient.

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ROLE OF RESISTANCE EXERCISE IN CONTROLLING INSULIN-LIKE GROWTH FACTOR 1 (IGF-1) AND IT’S ASSOCIATION WITH METABOLIC DISEASE PREVENTION

JURNAL ILMU FAAL OLAHRAGA INDONESIA ◽

10.51671/jifo.v2i1.106 ◽

2021 ◽

Vol 2 (1) ◽

pp. 1

Author(s):

Fitri Fadhilah ◽

Abdul Hadi Hassan ◽

Hanna Goenawan ◽

Herry Herman ◽

Aziiz Mardanarian Rosdianto ◽

...

Keyword(s):

Metabolic Disease ◽

Growth Factor ◽

Resistance Training ◽

Muscle Hypertrophy ◽

Metabolic Diseases ◽

Insulin Like Growth Factor ◽

Muscle Adaptation ◽

Proliferation And Differentiation ◽

Myogenic Activity

Based on data Riset Kesehatan Dasar (Riskesdas) in 2007, the number of people who had no or low physical activity reached 48.2 %. This condition contributes to the increasing number of metabolic disease cases such as hypertension, heart disease, stroke, and diabetes mellitus. Optimizing training approaches especially the aerobic type helps to counter metabolic diseases. Unfortunately, the benefits of resistance training (RT) are less understood. RT improves muscle strength, induces muscle hypertrophy, improvement of local muscular performance, and also helps to strengthen body balance and coordination. There is an interplay between training and hormone in muscle adaptation during resistance training. The hormone plays an important role in the regeneration of muscle after resistance training. The changes in hormone level cause hypertrophy. Regeneration and muscle hypertrophy are mediated by activation, proliferation, and differentiation of satellite cells. It is regulated by mitotic and myogenic activity, namely insulin-like growth factor-1 (IGF-1), which serves as a paracrine or autocrine. A better understanding of homeostasis hormone during training in skeletal muscle and its ultimate purpose to counter metabolic disease will lead us to a better treatment approach for the patient.

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Viral expression of insulin-like growth factor-I enhances muscle hypertrophy in resistance-trained rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00479.2003 ◽

2004 ◽

Vol 96 (3) ◽

pp. 1097-1104 ◽

Cited By ~ 130

Author(s):

Sukho Lee ◽

Elisabeth R. Barton ◽

H. Lee Sweeney ◽

Roger P. Farrar

Keyword(s):

Growth Factor ◽

Resistance Training ◽

Muscle Mass ◽

Muscle Hypertrophy ◽

Insulin Like Growth Factor ◽

Effective Measure ◽

Factor I ◽

Viral Expression ◽

Igf I ◽

Growth Factor I

Muscle hypertrophy is the product of increased drive through protein synthetic pathways and the incorporation of newly divided satellite cells. Gains in muscle mass and strength can be achieved through exercise regimens that include resistance training. Increased insulin-like growth factor-I (IGF-I) can also promote hypertrophy through increased protein synthesis and satellite cell proliferation. However, it is not known whether the combined effect of IGF-I and resistance training results in an additive hypertrophic response. Therefore, rats in which viral administration of IGF-I was directed to one limb were subjected to ladder climbing to test the interaction of each intervention on muscle mass and strength. After 8 wk of resistance training, a 23.3% increase in muscle mass and a 14.4% increase in peak tetanic tension (Po) were observed in the flexor hallucis longus (FHL). Viral expression of IGF-I without resistance training produced a 14.8% increase in mass and a 16.6% increase in Po in the FHL. The combined interventions produced a 31.8% increase in muscle mass and a 28.3% increase in Po in the FHL. Therefore, the combination of resistance training and overexpression of IGF-I induced greater hypertrophy than either treatment alone. The effect of increased IGF-I expression on the loss of muscle mass associated with detraining was also addressed. FHL muscles treated with IGF-I lost only 4.8% after detraining, whereas the untreated FHL lost 8.3% muscle mass. These results suggest that a combination of resistance training and overexpression of IGF-I could be an effective measure for attenuating the loss of training-induced adaptations.

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Skeletal muscle hypertrophy, insulin-like growth factor 1, myostatin and follistatin in healthy and sarcopenic elderly men: The effect of whole-body resistance training

International Journal of Preventive Medicine ◽

10.4103/ijpvm.ijpvm_310_17 ◽

2019 ◽

Vol 10 (1) ◽

pp. 29 ◽

Cited By ~ 7

Author(s):

Raoof Negaresh ◽

Rouholah Ranjbar ◽

JulienS Baker ◽

Abdolhamid Habibi ◽

Motahare Mokhtarzade ◽

...

Keyword(s):

Skeletal Muscle ◽

Growth Factor ◽

Resistance Training ◽

Muscle Hypertrophy ◽

Whole Body ◽

Insulin Like Growth Factor ◽

Elderly Men ◽

Skeletal Muscle Hypertrophy ◽

Body Resistance

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Insulin-like growth factor-I signaling is modified during chondrocyte differentiation

Journal of Endocrinology ◽

10.1677/joe.1.05873 ◽

2004 ◽

Vol 183 (3) ◽

pp. 477-486 ◽

Cited By ~ 56

Author(s):

Chanika Phornphutkul ◽

Ke-Ying Wu ◽

Xu Yang ◽

Qian Chen ◽

Philip A Gruppuso

Keyword(s):

Growth Factor ◽

Cell Line ◽

Chondrocyte Differentiation ◽

Erk Pathway ◽

Insulin Like Growth Factor ◽

Erk Activation ◽

Atdc5 Cell ◽

Factor I ◽

Proliferation And Differentiation ◽

Igf I

Insulin-like growth factor-I (IGF-I) is a critical regulator of skeletal growth. While IGF-I has been shown to be a potent chondrocyte mitogen in vitro, its role in chondrocyte differentiation is less well characterized. We chose to study the action of IGF-I on an accepted model of chondrocyte differentiation, the ATDC5 cell line. Insulin concentrations sufficiently high to interact with the IGF-I receptor are routinely used to induce ATDC5 cells to differentiate. Therefore, we first examined the ability of IGF-I to promote chondrocyte differentiation at physiological concentrations. IGF-I could induce differentiation of these cells at concentrations below 10 nM. However, increasing IGF-I concentrations were less potent at inducing differentiation. We hypothesized that mitogenic effects of IGF-I might inhibit its differentiating effects. Indeed, the extracellular-signal-regulated kinase (ERK)-pathway inhibitor PD98059 inhibited ATDC5 cell DNA synthesis while enhancing differentiation. This suggested that the ability of IGF-I to promote both proliferation and differentiation might require that its signaling be modulated through the differentiation process. We therefore compared IGF-I-mediated ERK activation in proliferating and hypertrophic chondrocytes. IGF-I potently induced ERK activation in proliferating cells, but minimal ERK response was seen in hypertrophic cells. In contrast, IGF-I-mediated Akt activation was unchanged by differentiation, indicating intact upstream IGF-I receptor signaling. Similar findings were observed in the RCJ3.1C5.18 chondrogenic cell line and in primary chick chondrocytes. We conclude that IGF-I promotes both proliferation and differentiation of chondrocytes and that the differentiation effects of IGF-I may require uncoupling of signaling to the ERK pathway.

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