Skeletal Muscle Hypertrophy after Aerobic Exercise Training
Posted: 21 February 2014 12:43 PM   [ Ignore ]  
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Exerc Sport Sci Rev. 2014 Feb 13.
Skeletal Muscle Hypertrophy after Aerobic Exercise Training.
Konopka AR1, Harber MP.

Pretty interesting. I would like to see how this could be different if we did a interval type cardio. I have posted the conclusion of the article below:

Conclusion
This review provides considerable evidence to support that aerobic exercise training can produce skeletal muscle hypertrophy. Multiple investigations demonstrate alterations in skeletal muscle molecular regulation and protein metabolism that is conducive for increased myofiber and whole muscle size after aerobic exercise training in sedentary individuals (Figure 4). Cross talk between pathways regulating mitochondrial homeostasis and skeletal muscle protein metabolism may play a role in the ability of aerobic exercise to stimulate skeletal muscle hypertrophy. Collectively these data warrant that aerobic exercise training should be acknowledged to increase skeletal muscle mass and be considered an effective countermeasure for muscle loss with advancing age. More research is needed to understand the complete influence of aerobic exercise as well as adjunct therapies (i.e., diet, nutriceuticals, and non-traditional exercise) on skeletal muscle size, function and quality across various age group and clinical populations

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Posted: 21 February 2014 12:45 PM   [ Ignore ]   [ # 1 ]  
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J Appl Physiol (1985). 2014 Jan 9.
Exercise induced AMPK activation does not interfere with muscle hypertrophy in response to resistance training in men.
Lundberg TR1, Fernandez-Gonzalo R, Tesch PA.

Abstract
As aerobic exercise (AE) may interfere with adaptations to resistance exercise (RE), this study explored acute and chronic responses to consecutive AE (~45 min cycling) and RE (4 x 7 maximal knee extensions), vs. RE only. Ten men performed acute unilateral AE+RE interspersed by 15 min recovery. The contralateral leg was subjected to RE. This exercise paradigm was then implemented in a 5-wk training program. Protein phosphorylation, gene expression and glycogen content were assessed in biopsies obtained from m. vastus lateralis of both legs immediately before and 3 h after acute RE. Quadricep muscle size and in vivo torque were measured, and muscle samples analyzed for citrate synthase activity and glycogen concentration, before and after training. Acute AE reduced glycogen content (32%; P < 0.05) and increased (P < 0.05) phosphorylation of AMPK (1.5-fold) and rpS6 (1.3-fold). Phosphorylation of p70S6K and 4E-BP1 remained unchanged. Myostatin gene expression was downregulated after acute AE+RE but not RE. Muscle size showed greater (P < 0.05) increase after AE+RE (6%) than RE (3%) training. Citrate synthase activity (18%) and endurance performance (22%) increased (P < 0.05) after AE+RE but not RE. While training increased (P < 0.05) in vivo muscle strength in both legs, normalized and concentric torque increased after RE only. Thus, AE activates AMPK, reduces glycogen stores, and impairs the progression of concentric force, yet muscle hypertrophic responses to chronic RE training appears not to be compromised.

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