Eisenhauer
New member
test test test test test sorry
Zuletzt bearbeitet:
mögliche nebenwirkungen seitens kreatin
- Ersteller Eisenhauer
- Erstellt am
A
Anzeige
schau mal hier:
nebenwirkungen von kreatin .
Eisenhauer
New member
Eisenhauer schrieb:hi
welche möglichen veränderungen auf physiologisch-biochemischer ebene und somit gesundheitlich-medizinisch möglichen Nebenwirkungen könnte eine langzeitliche kreatinsupplemention mit sich führen?
sprich: gibt es noch mehrere "side-effects" außer der receptordownregulation, die m.E eh reversibel ist, oder den h²o einlagerungen?
ich habe bereits zich papers zu kreatin gelesen und bin zu dem fazit gekommen, dass es keine langzeitstudien gibt.
@ kurt: welhce nebenwirkungen würdest Du als sportarzt noch für möglich erachten/ möglicherweise in betracht ziehen?
ps: bitte keine schlaumeier antworten, die noch weniger ahnung von der materie haben als ich, und meinen ich solle gefälligst im archiv recherchieren.
hewwelmann
New member
grüß dich eisenhauer,
hast du den artikel auf kurts hp darüber schon gelesen?
mfg christian
hast du den artikel auf kurts hp darüber schon gelesen?
mfg christian
Eisenhauer
New member
jop bereits gelesen
Eisenhauer
New member
hier nochmal studien die die positiven effecte seitens kreatin zeigen:
1
The creatine kinase system in human skin: protective effects of creatine against oxidative and UV damage in vitro and in vivo.
Lenz H, Schmidt M, Welge V, Schlattner U, Wallimann T, Elsasser HP, Wittern KP, Wenck H, Stab F, Blatt T.
Department of Cytobiology and Cytopathology, Philipps University Marburg, sport, medicine, Marburg, Germany.
Cutaneous aging is characterized by a decline in cellular energy metabolism, which is mainly caused by detrimental changes in mitochondrial function. The processes involved seem to be predominantly mediated by free radicals known to be generated by exogenous noxes, e.g., solar ultraviolet (UV) radiation. Basically, skin cells try to compensate any loss of mitochondrial energetic capacity by extra-mitochondrial pathways such as glycolysis or the creatine kinase (CK) system. Recent studies reported the presence of cytosolic and mitochondrial isoenzymes of CK, as well as a creatine transporter in human skin. In this study, we analyzed the cutaneous CK system, focusing on those cellular stressors known to play an important role in the process of skin aging. According to our results, a stress-induced decline in mitochondrial energy supply in human epidermal cells correlated with a decrease in mitochondrial CK activity. In addition, we investigated the effects of creatine supplementation on human epidermal cells as a potential mechanism to reinforce the endogenous energy supply in skin. Exogenous creatine was taken up by keratinocytes and increased CK activity, mitochondrial function and protected against free oxygen radical stress. Finally, our new data clearly indicate that human skin cells that are energetically recharged with the naturally occurring energy precursor, creatine, are markedly protected against a variety of cellular stress conditions, like oxidative and UV damage in vitro and in vivo. This may have further implications in modulating processes, which are involved in premature skin aging and skin damage.
Increased IGF mRNA in human skeletal muscle after creatine supplementation.
Deldicque L, Louis M, Theisen D, Nielens H, Dehoux M, Thissen JP, Rennie MJ, Francaux M.
Department of Physical Education and Rehabilitation, Faculty of Medicine, Catholic University of Louvain, Louvain-la-Neuve, Belgium.
PURPOSE: We hypothesized that creatine supplementation would facilitate muscle anabolism by increasing the expression of growth factors and the phosphorylation of anabolic signaling molecules; we therefore tested the responses of mRNA for IGF-I and IGF-II and the phosphorylation state of components of anabolic signaling pathways p70(s6k) and 4E-BP1 to a bout of high-intensity resistance exercise after 5 d of creatine supplementation. METHODS: In a double-blind cross-over design, muscle biopsies were taken from the m. vastus lateralis at rest and 3 and 24 h postexercise in subjects who had taken creatine or placebo for 5 d (21 g x d(-1)). For the first 3 h postexercise, the subjects were fed with a drink containing maltodextrin (0.3 g x kg(-1) body weight x h(-1)) and protein (0.08 g x kg(-1) body weight x h(-1)). RESULTS: After creatine supplementation, resting muscle expressed more mRNA for IGF-I (+30%, P < 0.05) and IGF-II (+40%, P = 0.054). Exercise caused an increase by 3 h postexercise in IGF-I (+24%, P < 0.05) and IGF-II (+48%, P < 0.05) and by 24 h postexercise in IGF-I (+29%, P < 0.05), but this effect was not potentiated by creatine supplementation. The phosphorylation states of p70(s6k) and 4E-BP1 were not affected by creatine at rest; phosphorylation of both increased (150-400%, P < 0.05) to similar levels under placebo and creatine conditions at 3 h postexercise plus feeding. However, the phosphorylation state of 4E-BP1 was higher in the creatine versus placebo condition at 24 h postexercise. CONCLUSION: The increase in lean body mass often reported after creatine supplementation could be mediated by signaling pathway(s) involving IGF and 4E-BP1.
Creatine supplementation normalizes mutagenesis of mitochondrial DNA as well as functional consequences.
Berneburg M, Gremmel T, Kurten V, Schroeder P, Hertel I, von Mikecz A, Wild S, Chen M, Declercq L, Matsui M, Ruzicka T, Krutmann J.
Molecular Oncology and Aging, Department of Dermatology, Eberhard Karls University, Tuebingen, Germany.
Mutations of mitochondrial (mt) DNA play a role in neurodegeneration, normal aging, premature aging of the skin (photoaging), and tumors. We and others could demonstrate that mtDNA mutations can be induced in skin cells in vitro and in normal human skin in vivo by repetitive, sublethal ultraviolet (UV)-A-irradiation. These mutations are mediated by singlet oxygen and persist in human skin as long-term biomarkers of UV exposure. Although mtDNA exclusively encodes for the respiratory chain, involvement of the energy metabolism in mtDNA mutagenesis and a protective role of the energy precursor creatine have thus far not been shown. We assessed the amount of a marker mutation of mtDNA, the so-called common deletion, by real-time PCR. Induction of the common deletion was paralleled by a measurable decrease of oxygen consumption, mitochondrial membrane potential, and ATP content, as well as an increase of matrix metalloproteinase-1. Mitochondrial mutagenesis as well as functional consequences could be normalized by increasing intracellular creatine levels. These data indicate that increase of the energy precursor creatine protects from functionally relevant, aging-associated mutations of mitochondrial DNA.
Durch Kreatin wird man sogar schlauer :
Supplementation with oral creatine monohydrate significantly
increased intelligence (as measured by RAPMs
done under time pressure, figure 1a) compared with
placebo (F3 ,33 = 32.3, p , 0.0001; repeated-measures
ANOVA).
Zitat Wirkprinzip:
ATP is strongly buffered in the brain by conversion via
creatine kinase catalysed reaction to phosphocreatine, the
phosphorylated analogue of the guanidino amino acid creatine.
ATP can be resynthesized from phosphocreatine 12
times faster than via oxidative phosphorylation and more
than 70 times faster than de novo pathways (Wallimann et
al. 1992).
Siehe hier:Indeed, creatine has been shown to be
neuroprotective in various neurological conditions
(Wyss & Schulze 2002).
Und hier,..noch etwas zu seinen Eigenschaften:Recently, brain creatine levels in
humans have been shown to increase in response to mental
training (Valenzuela et al. 2003), and acute oral creatine
supplementation has been shown to reduce mental
fatigue and decrease task-responsive oxygen delivery
(demand) to activated areas on performance of a serial
gruß
1
The creatine kinase system in human skin: protective effects of creatine against oxidative and UV damage in vitro and in vivo.
Lenz H, Schmidt M, Welge V, Schlattner U, Wallimann T, Elsasser HP, Wittern KP, Wenck H, Stab F, Blatt T.
Department of Cytobiology and Cytopathology, Philipps University Marburg, sport, medicine, Marburg, Germany.
Cutaneous aging is characterized by a decline in cellular energy metabolism, which is mainly caused by detrimental changes in mitochondrial function. The processes involved seem to be predominantly mediated by free radicals known to be generated by exogenous noxes, e.g., solar ultraviolet (UV) radiation. Basically, skin cells try to compensate any loss of mitochondrial energetic capacity by extra-mitochondrial pathways such as glycolysis or the creatine kinase (CK) system. Recent studies reported the presence of cytosolic and mitochondrial isoenzymes of CK, as well as a creatine transporter in human skin. In this study, we analyzed the cutaneous CK system, focusing on those cellular stressors known to play an important role in the process of skin aging. According to our results, a stress-induced decline in mitochondrial energy supply in human epidermal cells correlated with a decrease in mitochondrial CK activity. In addition, we investigated the effects of creatine supplementation on human epidermal cells as a potential mechanism to reinforce the endogenous energy supply in skin. Exogenous creatine was taken up by keratinocytes and increased CK activity, mitochondrial function and protected against free oxygen radical stress. Finally, our new data clearly indicate that human skin cells that are energetically recharged with the naturally occurring energy precursor, creatine, are markedly protected against a variety of cellular stress conditions, like oxidative and UV damage in vitro and in vivo. This may have further implications in modulating processes, which are involved in premature skin aging and skin damage.
Increased IGF mRNA in human skeletal muscle after creatine supplementation.
Deldicque L, Louis M, Theisen D, Nielens H, Dehoux M, Thissen JP, Rennie MJ, Francaux M.
Department of Physical Education and Rehabilitation, Faculty of Medicine, Catholic University of Louvain, Louvain-la-Neuve, Belgium.
PURPOSE: We hypothesized that creatine supplementation would facilitate muscle anabolism by increasing the expression of growth factors and the phosphorylation of anabolic signaling molecules; we therefore tested the responses of mRNA for IGF-I and IGF-II and the phosphorylation state of components of anabolic signaling pathways p70(s6k) and 4E-BP1 to a bout of high-intensity resistance exercise after 5 d of creatine supplementation. METHODS: In a double-blind cross-over design, muscle biopsies were taken from the m. vastus lateralis at rest and 3 and 24 h postexercise in subjects who had taken creatine or placebo for 5 d (21 g x d(-1)). For the first 3 h postexercise, the subjects were fed with a drink containing maltodextrin (0.3 g x kg(-1) body weight x h(-1)) and protein (0.08 g x kg(-1) body weight x h(-1)). RESULTS: After creatine supplementation, resting muscle expressed more mRNA for IGF-I (+30%, P < 0.05) and IGF-II (+40%, P = 0.054). Exercise caused an increase by 3 h postexercise in IGF-I (+24%, P < 0.05) and IGF-II (+48%, P < 0.05) and by 24 h postexercise in IGF-I (+29%, P < 0.05), but this effect was not potentiated by creatine supplementation. The phosphorylation states of p70(s6k) and 4E-BP1 were not affected by creatine at rest; phosphorylation of both increased (150-400%, P < 0.05) to similar levels under placebo and creatine conditions at 3 h postexercise plus feeding. However, the phosphorylation state of 4E-BP1 was higher in the creatine versus placebo condition at 24 h postexercise. CONCLUSION: The increase in lean body mass often reported after creatine supplementation could be mediated by signaling pathway(s) involving IGF and 4E-BP1.
Creatine supplementation normalizes mutagenesis of mitochondrial DNA as well as functional consequences.
Berneburg M, Gremmel T, Kurten V, Schroeder P, Hertel I, von Mikecz A, Wild S, Chen M, Declercq L, Matsui M, Ruzicka T, Krutmann J.
Molecular Oncology and Aging, Department of Dermatology, Eberhard Karls University, Tuebingen, Germany.
Mutations of mitochondrial (mt) DNA play a role in neurodegeneration, normal aging, premature aging of the skin (photoaging), and tumors. We and others could demonstrate that mtDNA mutations can be induced in skin cells in vitro and in normal human skin in vivo by repetitive, sublethal ultraviolet (UV)-A-irradiation. These mutations are mediated by singlet oxygen and persist in human skin as long-term biomarkers of UV exposure. Although mtDNA exclusively encodes for the respiratory chain, involvement of the energy metabolism in mtDNA mutagenesis and a protective role of the energy precursor creatine have thus far not been shown. We assessed the amount of a marker mutation of mtDNA, the so-called common deletion, by real-time PCR. Induction of the common deletion was paralleled by a measurable decrease of oxygen consumption, mitochondrial membrane potential, and ATP content, as well as an increase of matrix metalloproteinase-1. Mitochondrial mutagenesis as well as functional consequences could be normalized by increasing intracellular creatine levels. These data indicate that increase of the energy precursor creatine protects from functionally relevant, aging-associated mutations of mitochondrial DNA.
Durch Kreatin wird man sogar schlauer :
Supplementation with oral creatine monohydrate significantly
increased intelligence (as measured by RAPMs
done under time pressure, figure 1a) compared with
placebo (F3 ,33 = 32.3, p , 0.0001; repeated-measures
ANOVA).
Zitat Wirkprinzip:
ATP is strongly buffered in the brain by conversion via
creatine kinase catalysed reaction to phosphocreatine, the
phosphorylated analogue of the guanidino amino acid creatine.
ATP can be resynthesized from phosphocreatine 12
times faster than via oxidative phosphorylation and more
than 70 times faster than de novo pathways (Wallimann et
al. 1992).
Siehe hier:Indeed, creatine has been shown to be
neuroprotective in various neurological conditions
(Wyss & Schulze 2002).
Und hier,..noch etwas zu seinen Eigenschaften:Recently, brain creatine levels in
humans have been shown to increase in response to mental
training (Valenzuela et al. 2003), and acute oral creatine
supplementation has been shown to reduce mental
fatigue and decrease task-responsive oxygen delivery
(demand) to activated areas on performance of a serial
gruß
deadlifter
New member
@Eisenhauer:Bist du der Einsenhauer,der auch im Zint Forum schreibt?
Eisenhauer
New member
zint? ka^^ kenne das forum nicht
ka^^ kenne das forum nichtdeadlifter
New member
Der Eisenhauer,der in Lauchhamer gestartet ist,bei der Junioren DM im KDK? Wenn ja:Wieso hast du nicht volles Euipment benutzt?
Wenn ja:Wieso hast du nicht volles Euipment benutzt?Eisenhauer
New member
nene bin wohl nen anderer
A
Anzeige
schau mal hier:
nebenwirkungen von kreatin .