Modell des Muskelwachstums @alle Med-studenten...

Polynomstapler

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und so weiter.

Gibt es ein Modell für Muskelwachstum? Durch welche Impulse/Substanzen wird Muskelwachstum ausgelöst? Anders gefragt: In welcher Verbindung steht Training mit Muskelwachstum?

Ist das erforscht?
 
A

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Re: Modell des Muskelwachstums @alle Med-studenten...
Hallo Polynomstapler,

schau mal hier:
was mit .
abstracts:


McCarthy,J.P.; Pozniak,M.A.; Agre,J.C.

Neuromuscular adaptations to concurrent strength and endurance training

PURPOSE: The purpose of this study was to examine muscle morphological and neural activation adaptations resulting from the interaction between concurrent strength and endurance training. METHODS: Thirty sedentary healthy male subjects were randomly assigned to one of three training groups that performed 10 wk of 3-d x wk(-1) high-intensity strength training (S), cycle endurance training (E), or concurrent strength and endurance training (CC). Strength, quadriceps-muscle biopsies, computed tomography scans at mid-thigh, and surface electromyogram (EMG) assessments were made before and after training. RESULTS: S and CC groups demonstrated similar increases (P < 0.0001) in both thigh extensor (12 and 14%) and flexor/adductor (7 and 6%) muscle areas. Type II myofiber areas similarly increased (P < 0.002) in both S (24%) and CC (28%) groups, whereas the increase (P < 0.004) in Type I area with S training (19%) was also similar to the nonsignificant (P = 0.041) increase with CC training (13%). Significant increases (P < 0.005) in maximal isometric knee-extension torque were accompanied by nonsignificant (P <or= 0.07) increases in root mean squared EMG amplitude of the quadriceps musculature for both S and C groups. No changes (P > 0.38) in the EMG/torque relation across 20 to 100% maximal voluntary contractions occurred in any group. A small 3% increase (P < 0.01) in thigh extensor area was the only change in any of the above variables with E training. CONCLUSIONS: Findings indicate 3-d x wk(-1) concurrent performance of both strength and endurance training does not impair adaptations in strength, muscle hypertrophy, and neural activation induced by strength training alone. Results provide a physiological basis to support several performance studies that consistently indicate 3-d x wk(-1) concurrent training does not impair strength development over the short term

Tipton,K.D.; Wolfe,R.R.
Exercise, protein metabolism, and muscle growth

Exercise has a profound effect on muscle growth, which can occur only if muscle protein synthesis exceeds muscle protein breakdown; there must be a positive muscle protein balance. Resistance exercise improves muscle protein balance, but, in the absence of food intake, the balance remains negative (i.e., catabolic). The response of muscle protein metabolism to a resistance exercise bout lasts for 24-48 hours; thus, the interaction between protein metabolism and any meals consumed in this period will determine the impact of the diet on muscle hypertrophy. Amino acid availability is an important regulator of muscle protein metabolism. The interaction of postexercise metabolic processes and increased amino acid availability maximizes the stimulation of muscle protein synthesis and results in even greater muscle anabolism than when dietary amino acids are not present. Hormones, especially insulin and testosterone, have important roles as regulators of muscle protein synthesis and muscle hypertrophy. Following exercise, insulin has only a permissive role on muscle protein synthesis, but it appears to inhibit the increase in muscle protein breakdown. Ingestion of only small amounts of amino acids, combined with carbohydrates, can transiently increase muscle protein anabolism, but it has yet to be determined if these transient responses translate into an appreciable increase in muscle mass over a prolonged training
period

Chilibeck,P.D.; Syrotuik,D.G.; Bell,G.J.
The effect of strength training on estimates of mitochondrial density and distribution throughout muscle fibres

The purpose of this study was to investigate the effect of strength training (12 weeks, 3 days/week, four lower-body exercises) of young individuals (mean age 23.6 years) on estimates of mitochondrial distribution throughout muscle fibres. A control group (mean age 21. 7 years) was followed simultaneously. Skeletal muscle biopsy samples were obtained from the vastus lateralis, pre- and post-training. The regional distribution of subsarcolemmal and intermyofibrillar mitochondrial populations was determined using quantitative histochemical staining of succinate dehydrogenase (SDH) in type I and II muscle fibres. Strength training resulted in significant increases of 26% and 28% in the cross-sectional area of type I and II fibres, respectively (P < 0.05). Overall SDH activity decreased by 13% with strength training (P < 0.05). The decrease in SDH activity with strength training between fibre types and between subsarcolemmal and intermyofibrillar regions of muscle fibres was not different. Fibre area and SDH activity was unchanged in the control group. We conclude that the muscle hypertrophy associated with strength training results in reduced density of regionally distributed mitochondria, as indicated by the reduction in the activity of SDH
 
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