Apoptoza miofibryli?

glukozamine rowniez powinienem znalezc

Bardzo dziękuję Panie Sławku za odpowiedź
I mam jeszcze pytanie, czy suplementacja samą argininą coś da? Czytałem dawno temu artykuł/wypowiedź na temat tego iż sama arginina nic nie zdziała (na sfd) lecz nie pamiętam już szczegółów podawanych na jakiej to zasadzie 'nie' działa - nikt nie zaprzeczył

Edit: Czy apoptoza komórek mięsniowych odbywa się wyłącznie za pomocą komórek kaskadowych czy biorą w tym udział również perforyny, granzymy... ?

Zmieniony przez - Skalar. w dniu 2007-08-31 09:23:02

Co do glukozaminy to jest ogromna ilość badań, bo to nie tylko suplement, ale również i lek stoswany klinicznie.

Arginina to obok kreatyny najsilniejszy, dozwolony anabolik. Jeszcze raz proponuję lekturę artykułu z SdW "Arginina, tlenek, masa", bo to obszerny temat i nie chce mi się tego powtarzać. Zamieszczę ten art też w tym dziale, ale za jakiś czas, bo taka jest umowa z redakcją. Tam jest też o regeracji mięśni.

Najprościej:
Rozwój masy mięśniowej następuje poprzez dwa mechanizmy - rozrost (hyperplasia), czyli zwiększenie liczby komórek i przerost (hypertophia), czyli zwiększenie objętości komórek. Rozrost następuje w życiu płodowym i trwa do okresu pokwitania. Bierze również udział w regeracji mięśni, jeżeli zniszczeniu ulegają całe komórki mięśniowe. Wtedy - faktycznie - konkuruje z procesem bliznowacenia, czyli przerostu tkanki mięśniowej tkanką łączną. Przerost jest głównym mechanizmem rozwoju masy w odpowiedzi na trening. Jednak, jak już pisałem, rozrost ma też swój udział w przeroście, bo wtedy wzrasta liczba komórek satelitarnych i chociaż te nie zlewają się ze sobą i nie tworzą nowych komórek mięśniowych, to jednak zlewają się ze starymi komórkami i zasileją je młodymi jądrami wydajnie prowadzącymi syntezę białek.

Ten ostatni mechanizm (zasilanie jądrami) odkryto dopiero kilka lat temu, więc może jeszcze nie być o nim informacji w podręcznikach.

jak obiecalem
jako punkt startowy do wlasnych poszukiwan


Skeletal muscle fiber hyperplasia.
Antonio J, Gonyea WJ.

Department of Cell Biology and Neurosciences, University of Texas Southwestern Medical Center, Dallas 75235-9039.

Skeletal muscle enlargement in adult animals has been ascribed primarily to changes in fiber cross-sectional area ( i.e., fiber hypertrophy); however, recent evidence from several laboratories suggests strongly that fiber hyperplasia contributes to muscle mass increases in adult animals and possibly human athletes. Scientists have used three models to study the cellular mechanisms of muscle enlargement: compensatory hypertrophy, stretch, and exercise. Each of these models has provided direct as well as indirect evidence supporting the occurrence of muscle fiber hyperplasia. Direct counts of muscle fibers using nitric acid digestion techniques have shown that both exercise and stretch overload result in significant increases (range = 9-52%) in fiber number. Indirect fiber counts using histological cross-sections have suggested fiber hyperplasia (range = 10-82%) in all three models. Additionally, the expression of embryonic myosin isoforms have provided indirect evidence for new fiber formation in stretch overloaded muscle. Furthermore, satellite cells have been shown to be involved in muscle fiber hyperplasia in stretch and exercise.


Morphological observations supporting muscle fiber hyperplasia following weight-lifting exercise in cats.
Giddings CJ, Gonyea WJ.

Department of Cell Biology and Neuroscience, University of Texas Southwestern Medical Center, Dallas 75235-9039.

Although exercise-induced muscle fiber hyperplasia has been demonstrated through direct fiber counts following nitric-acid digestion of muscle, morphological studies to determine the mechanism of hyperplasia have not been performed previously. In this study, light and electron microscopy were used to evaluate evidence of muscle fiber splitting or de novo formation of new muscle fibers. Since both fiber hypertrophy and hyperplasia may result in alterations in the muscle nuclear populations, myonuclear number and satellite cell frequency were assessed quantitatively to determine their role in regulating muscle fiber size. Ten adult cats performed weight-lifting exercise, and the right (exercised) and left (control) forelimbs were fixed by vascular perfusion. Spaced serial sections were used to evaluate muscle fiber morphology along the length of fibers, and muscle fiber areas were measured. Myonuclei and satellite cells were counted using electron microscopy. Morphological evidence supporting muscle fiber hyperplasia was observed in exercised muscles. These observations included the presence of small fibers which may signify de novo fiber formation. Myonuclear counts indicate that myonuclear density is not a primary regulator of fiber size. Satellite cell frequency was unchanged following exercise. Autoradiographic studies revealed satellite cell activation by uptake of tritiated thymidine in exercised muscles. Satellite cell activation appears to result from increased activity in exercised muscles. These findings confirm previous studies demonstrating muscle fiber hyperplasia following weight-lifting exercise, and suggest that de novo fiber formation is the major mechanism contributing to muscle fiber hyperplasia in this model.


Mechanical overload and skeletal muscle fiber hyperplasia: a meta-analysis.
Kelley G.

Department of Physical Education, Northern Illinois University, DeKalb 60115-2854, USA.

With use of the meta-analytic approach, the purpose of this study was to examine the effects of mechanical overload on skeletal muscle fiber number in animals. A total of 17 studies yielding 37 data points and 360 subjects met the initial criteria: 1) "basic" research studies published in journals, 2) animals (no humans) as subjects, 3) control group included, 4) some type of mechanical overload (stretch, exercise, or compensatory hypertrophy) used to induce changes in muscle fiber number, and 5) sufficient data to accurately calculate percent changes in muscle fiber number. Across all designs and categories, statistically significant increases were found for muscle fiber number [ 15.00 +/- 19.60% (SD), 95% confidence interval = 8.65-21.53], muscle fiber area (31.60 +/- 44.30%, 95% confidence interval = 16.83-46.37), and muscle mass (90.50 +/- 86.50%, 95% confidence interval = 61.59-119.34). When partitioned according to the fiber-counting technique, larger increases in muscle fiber number were found by using the histological vs. nitric acid digestion method (histological = 20.70%, nitric acid digestion = 11.10%; P = 0.14). Increases in fiber number partitioned according to species were greatest among those groups that used an avian vs. mammalian model (avian = 20.95%, mammalian = 7.97%; P = 0.07). Stretch overload yielded larger increases in muscle fiber number than did exercise and compensatory hypertrophy (stretch = 20.95%, exercise = 11.59%, compensatory hypertrophy = 5.44%; P = 0.06). No significant differences between changes in fiber number were found when data were partitioned according to type of control (intra-animal = 15.20%, between animal = 13.90%; P = 0.82) or fiber arrangement of muscle (parallel = 15.80%, pennate = 11.60%; P = 0.61). The results of this study suggest that in several animal species certain forms of mechanical overload increase muscle fiber number.


Changes in muscle fiber size and composition in response to heavy-resistance exercise.
Mikesky AE, Giddings CJ, Matthews W, Gonyea WJ.

Department of Cell Biology and Neuroscience, University of Texas Southwestern Medical Center, Dallas 75235-9039.

Progressive resistance exercise was used to induce hypertrophy in the right palmaris longus muscle (PLM) of 16 cats. The left PLM served as the non-exercised intra-animal control. After an average 150 +/- 26.6 wk of training, left and right PLMs were removed and weighed. Muscle fibers were typed using standard histochemical techniques. Mean fiber cross-sectional area, connective tissue content, and muscle fiber length were determined. The right exercised PLM demonstrated a 24.2 +/- 6.9% increase in muscle mass. Mean muscle fiber cross-sectional area increased 11.0 +/- 7.3% in the exercised muscles. No change in connective tissue content, fiber length, or fiber type composition was observed. The results show that increases in muscle fiber cross-sectional area do not account for all the observed increases in muscle mass, and that other mechanisms, such as muscle fiber hyperplasia, may play a role in contributing to muscle mass increases.




z glukozamina bylo mi troche gorzej - bo nie mialem dostepu do nawet abstraktow wielu nowych badan - jakies takie dziwne
wiec to co mi sie udalo


Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis.
Clegg DO, Reda DJ, Harris CL, Klein MA, O'Dell JR, Hooper MM, Bradley JD, Bingham CO 3rd, Weisman MH, Jackson CG, Lane NE, Cush JJ, Moreland LW, Schumacher HR Jr, Oddis CV, Wolfe F, Molitor JA, Yocum DE, Schnitzer TJ, Furst DE, Sawitzke AD, Shi H, Brandt KD, Moskowitz RW, Williams HJ.
Division of Rheumatology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA. [email protected]
BACKGROUND: Glucosamine and chondroitin sulfate are used to treat osteoarthritis. The multicenter, double-blind, placebo- and celecoxib-controlled Glucosamine/chondroitin Arthritis Intervention Trial (GAIT) evaluated their efficacy and safety as a treatment for knee pain from osteoarthritis. METHODS: We randomly assigned 1583 patients with symptomatic knee osteoarthritis to receive 1500 mg of glucosamine daily, 1200 mg of chondroitin sulfate daily, both glucosamine and chondroitin sulfate, 200 mg of celecoxib daily, or placebo for 24 weeks. Up to 4000 mg of acetaminophen daily was allowed as rescue analgesia. Assignment was stratified according to the severity of knee pain (mild [N=1229] vs. moderate to severe [N=354]). The primary outcome measure was a 20 percent decrease in knee pain from baseline to week 24. RESULTS: The mean age of the patients was 59 years, and 64 percent were women. Overall, glucosamine and chondroitin sulfate were not significantly better than placebo in reducing knee pain by 20 percent. As compared with the rate of response to placebo ( 60.1 percent), the rate of response to glucosamine was 3.9 percentage points higher (P=0.30), the rate of response to chondroitin sulfate was 5.3 percentage points higher (P=0.17), and the rate of response to combined treatment was 6.5 percentage points higher (P=0.09). The rate of response in the celecoxib control group was 10.0 percentage points higher than that in the placebo control group (P=0.008). For patients with moderate-to-severe pain at baseline, the rate of response was significantly higher with combined therapy than with placebo ( 79.2 percent vs. 54.3 percent, P=0.002). Adverse events were mild, infrequent, and evenly distributed among the groups. CONCLUSIONS: Glucosamine and chondroitin sulfate alone or in combination did not reduce pain effectively in the overall group of patients with osteoarthritis of the knee. Exploratory analyses suggest that the combination of glucosamine and chondroitin sulfate may be effective in the subgroup of patients with moderate-to-severe knee pain.

Effects of glucosamine hydrochloride and chondroitin sulphate, alone and in combination, on normal and interleukin-1 conditioned equine articular cartilage explant metabolism.
Dechant JE, Baxter GM, Frisbie DD, Trotter GW, McIlwraith CW.

Equine Orthopaedic Research Laboratory, Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA.

REASONS FOR PERFORMING STUDY: Clinical trials in human and veterinary literature have documented the benefits of oral nutraceutical joint supplements containing glucosamine (GU) and chondroitin sulphate (CS) to treat mild to moderate osteoarthritis, but the effects of these components have not yet been conclusively determined. OBJECTIVES: To assess varying dosages of GU and CS on normal and interleukin-1alpha (IL-1) conditioned equine cartilage explants and rationalise the use of these products. HYPOTHESIS: Treatment would not be detrimental to cartilage metabolism and higher dosages and the combination of GU and CS would be more beneficial than lower dosages and. GU or CS alone. METHODS: Articular cartilage explants collected from the femoral trochlea and condyles were cultured in normal and IL-1 conditioned media. Treatment groups included 0, 12.5, 25,125 and 250 microg/ml concentrations of GU alone, CS alone, or GU+CS in combination. Glycosaminoglycan (GAG) synthesis and total GAG content in the explants and media were analysed. RESULTS: There were no detrimental effects of GU, CS or GU+CS on cartilage metabolism. High dosages of GU+CS reduced total GAG release into the media (degradation). CONCLUSIONS: Our results suggests that GU+CS may prevent cartilage GAG degradation. POTENTIAL RELEVANCE: The combination of GU and CS may be more effective in preventing or treating osteoarthritis in horses than either product alone.


Glucosamine sulfate in the treatment of knee osteoarthritis symptoms: a randomized, double-blind, placebo-controlled study using acetaminophen as a side comparator.
Herrero-Beaumont G, Ivorra JA, Del Carmen Trabado M, Blanco FJ, Benito P, Martín-Mola E, Paulino J, Marenco JL, Porto A, Laffon A, Araújo D, Figueroa M, Branco J.

Rheumatology Department, Fundación Jiménez Díaz-Capio, Madrid, Spain. [email protected]

OBJECTIVE: To assess the effects of the prescription formulation of glucosamine sulfate (1,500 mg administered once daily) on the symptoms of knee osteoarthritis (OA) during a 6-month treatment course. METHODS: Three hundred eighteen patients were enrolled in this randomized, placebo-controlled, double-blind trial in which acetaminophen, the currently preferred medication for symptomatic treatment of OA, was used as a side comparator. Patients were randomly assigned to receive oral glucosamine sulfate 1,500 mg once daily (n = 106), acetaminophen 3 gm/day (n = 108), or placebo (n = 104). The primary efficacy outcome measure was the change in the Lequesne index after 6 months. Secondary parameters included the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and response according to the Osteoarthritis Research Society International criteria. These outcome measures were assessed using an intent-to-treat analysis. RESULTS: At baseline, the study patients had moderately severe OA symptoms (mean Lequesne index approximately 11 points). Glucosamine sulfate was more effective than placebo in improving the Lequesne score, with a final decrease of 3.1 points, versus 1.9 with placebo (difference between glucosamine sulfate and placebo -1.2 [95% confidence interval -2.3, -0.8]) (P = 0.032). The 2.7-point decrease with acetaminophen was not significantly different from that with placebo (difference - 0.8 [95% confidence interval -1.9, 0.3]) (P = 0.18). Similar results were observed for the WOMAC. There were more responders to glucosamine sulfate (39.6%) and acetaminophen (33.3%) than to placebo (21.2%) (P = 0.004 and P = 0.047, respectively, versus placebo). Safety was good, and was comparable among groups. CONCLUSION: The findings of this study indicate that glucosamine sulfate at the oral once-daily dosage of 1,500 mg is more effective than placebo in treating knee OA symptoms. Although acetaminophen also had a higher responder rate compared with placebo, it failed to show significant effects on the algofunctional indexes.

Dziękuję za odpowiedzi

Hehe - no to Biniu zapewniłeś mi lekturę na wieczór

Tak więc w sprawie hiperplazji nadal nie ma jasności...

i podejrzewam ze szybko nie bedzie
jednak jak mawiaja starzy indianie - cos moze byc na rzeczy

Zapewne udział hiperplazji w budowaniu dodatkowej masy mięśniowej jest, ale niewielki. Zwasze ostrzegam tylko przed bardzo cięzkimi treningami nieszczącymi całe komórki mięśniowe, które były bardzo modne swojego czasu. W odbudowie takich uszkodzeń zawsze komórki satelitarne, odtwarzające nowe komórki mieśniowe, konkurują z fibroblastami zabliźniającymi uzkodzenie tkanką łączną.

tutaj rowniez sie zgadzamy

nie widze potrzeby niszczenia komorek miesnowych
wystarczy wyrwanie z homeostazy (za pomoca odpowiednio silnego bodzca (niekoniecznie zbyt silnego) - ciezaru treningowego)