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Influence of pre exercise muscle gly...

Creer, Andrew R.

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Influence of pre exercise muscle glycogen levels on mitogenic responses to resistance training .

Record Type:	Electronic resources : Monograph/item
Title/Author:	Influence of pre exercise muscle glycogen levels on mitogenic responses to resistance training ./
Author:	Creer, Andrew R.
Description:	121 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0661.
Contained By:	Dissertation Abstracts International65-02B.
Subject:	Health Sciences, Nutrition. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3123932
ISBN:	0496712411

Influence of pre exercise muscle glycogen levels on mitogenic responses to resistance training .
Creer, Andrew R.

Influence of pre exercise muscle glycogen levels on mitogenic responses to resistance training . - 121 p.

Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0661.

Thesis (Ph.D.)--Ball State University, 2004.

The purpose of this study was to investigate the effects of muscle glycogen (MG) levels on mitogenic responses to resistance exercise. Eight subjects performed a low carbohydrate trial (LCHO) and a high carbohydrate trial (HCHO), involving 3 sets of 10 repetitions of knee extension exercise at 70% of 1 RM following a low (2%) or high (77%) carbohydrate diet. Muscle biopsies taken from the vastus Iateralis pre, post, and 10 min post exercise, were analyzed for ERK1/2, p90rsk, Akt, and mTOR phosphorylation, as well as MG and intramuscular triglyceride (IMTG) content. Blood samples were taken concurrently with each biopsy and analyzed for plasma glucose, FFA, and insulin. Pre exercise MG levels were 70% higher (p < 0.05) in HCHO vs. LCHO. MG levels decreased in both groups post exercise (p < 0.05), however, 43% more (p < 0.05) MG was used during HCHO. MG levels increased 14% from post to 10 min post (p = 0.05) in HCHO only. Pre exercise IMTG levels were 40% higher (p < 0.05) in the LCHO vs HCHO, and decreased by 21% post exercise (p < 0.05) during LCHO only. ERK1/2 and p90rsk phosphorylation increased (p < 0.05) 10 min post exercise in both the LCHO and HCHO trials, respectively (p < 0.05). Akt phosphorylation increased by 120% (p < 0.05) at 10 min post in HCHO only. mTOR phosphorylation increased (p < 0.05) immediately post exercise in both groups, with a trend (p = .097) for an increase from pre to 10 min post exercise in HCHO. mTOR Phosphorylation returned to baseline by 10 min post in LCHO. In conclusion, ERK1/2 pathway activation in response to resistance exercise was unaffected by pre exercise MG levels. In addition, resistance exercise is sufficient to increase mTOR activation independently of Akt or fuel status. Failure to increase Akt, or maintain mTOR activation during the LCHO trial suggests that these proteins may be metabolically regulated. Based on these findings, it appears that resistance exercise is sufficient stimulate mitogenic activation. However, cellular fuel status appears to regulate the degree of Akt and mTOR activation, possibly attenuating cellular growth and adaptation in response to resistance exercise in a depleted state.

ISBN: 0496712411Subjects--Topical Terms:

1017801
Health Sciences, Nutrition.

Influence of pre exercise muscle glycogen levels on mitogenic responses to resistance training .
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245 1 0 $a Influence of pre exercise muscle glycogen levels on mitogenic responses to resistance training .
300 $a 121 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0661.
500 $a Adviser: Scott W. Trappe.
502 $a Thesis (Ph.D.)--Ball State University, 2004.
520 $a The purpose of this study was to investigate the effects of muscle glycogen (MG) levels on mitogenic responses to resistance exercise. Eight subjects performed a low carbohydrate trial (LCHO) and a high carbohydrate trial (HCHO), involving 3 sets of 10 repetitions of knee extension exercise at 70% of 1 RM following a low (2%) or high (77%) carbohydrate diet. Muscle biopsies taken from the vastus Iateralis pre, post, and 10 min post exercise, were analyzed for ERK1/2, p90rsk, Akt, and mTOR phosphorylation, as well as MG and intramuscular triglyceride (IMTG) content. Blood samples were taken concurrently with each biopsy and analyzed for plasma glucose, FFA, and insulin. Pre exercise MG levels were 70% higher (p < 0.05) in HCHO vs. LCHO. MG levels decreased in both groups post exercise (p < 0.05), however, 43% more (p < 0.05) MG was used during HCHO. MG levels increased 14% from post to 10 min post (p = 0.05) in HCHO only. Pre exercise IMTG levels were 40% higher (p < 0.05) in the LCHO vs HCHO, and decreased by 21% post exercise (p < 0.05) during LCHO only. ERK1/2 and p90rsk phosphorylation increased (p < 0.05) 10 min post exercise in both the LCHO and HCHO trials, respectively (p < 0.05). Akt phosphorylation increased by 120% (p < 0.05) at 10 min post in HCHO only. mTOR phosphorylation increased (p < 0.05) immediately post exercise in both groups, with a trend (p = .097) for an increase from pre to 10 min post exercise in HCHO. mTOR Phosphorylation returned to baseline by 10 min post in LCHO. In conclusion, ERK1/2 pathway activation in response to resistance exercise was unaffected by pre exercise MG levels. In addition, resistance exercise is sufficient to increase mTOR activation independently of Akt or fuel status. Failure to increase Akt, or maintain mTOR activation during the LCHO trial suggests that these proteins may be metabolically regulated. Based on these findings, it appears that resistance exercise is sufficient stimulate mitogenic activation. However, cellular fuel status appears to regulate the degree of Akt and mTOR activation, possibly attenuating cellular growth and adaptation in response to resistance exercise in a depleted state.
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