Ervaring Kre Alkalyn Xtreme?

[jonos]

Hoi allemaal, heb vandaag me eerste creatine gekocht: kre alkalyn xtreme ( een potje met 120caps ) de vrouw uit de winkel raadde mij dit aan en mijn vraag is dus... Wat is jullie ervaring hiermee? Nadelen voordelen? Alvast heel erg bedankt!

[Falstyr]

http://forum.bodynet.nl/supplementen...e-alkalyn.html

[jonos]

Maar deze is niet van het zelfde merk? De mijne is van performance...

[Falstyr]

Kre-alkalyn is kre-alkalyn
creatine op esthers---is creatine op esthers
creatine op monohydraat---is creatine monohydraat

zit nauwelijks verschil tsusen.

[Shredmaster]

Kre-alkalyn is kre-alkalyn
creatine op esthers---is creatine op esthers
creatine op monohydraat---is creatine monohydraat

zit nauwelijks verschil tsusen.

Ikzelf merk enig verschil tussen Vitalife mono en body en fitshop mono,
Kan misschien het verschil in kwaliteit zijn.
En van vitalife kreeg ik de schijterij en van B&F niet.

[jonos]

dus falstyr je bent er niet zo enthousiast over?
heb niet veel kunnen lezen hierover
maar wat ik las was wel positief, maar toch bedankt!

[Falstyr]

Ik zou zeggen blijf bij monohydraat

Anders moet ik weer al die onderzoeken gaan aanhalen dat Alkalyn het meest van de werkende stof verlost voordat het opgenomen is door het lichaam. Dan de esthers en monohydraat is en blijft gewoon het best.

[misirlou]

Ik heb wel goeie ervaringen hiermee.
Stond in natuurwinkel aan 25euro paar weken geleden.

[Kingsley]

Creatine

Creatine Encyclopedie
Creatine "Encyclopedie"

Creatine ethyl ester - Wikipedia, the free encyclopedia
Creatine Ethyl Ester

Creatine
Alles over creatine qua artikels en onderzoeken.

Adverse effects of creatine supplementation: fact or fiction?
Poortmans JR, Francaux M.
Physiological Chemistry, Higher Institute of Physical Education and Readaptation, Free University of Brussels, Bruxelles, Belgium. [email protected]

The consumption of oral creatine monohydrate has become increasingly common among professional and amateur athletes. Despite numerous publications on the ergogenic effects of this naturally occurring substance, there is little information on the possible adverse effects of this supplement. The objectives of this review are to identify the scientific facts and contrast them with reports in the news media, which have repeatedly emphasised the health risks of creatine supplementation and do not hesitate to draw broad conclusions from individual case reports.

Exogenous creatine supplements are often consumed by athletes in amounts of up to 20 g/day for a few days, followed by 1 to 10 g/day for weeks, months and even years. Usually, consumers do not report any adverse effects, but body mass increases.

There are few reports that creatine supplementation has protective effects in heart, muscle and neurological diseases. Gastrointestinal disturbances and muscle cramps have been reported occasionally in healthy individuals, but the effects are anecdotal. Liver and kidney dysfunction have also been suggested on the basis of small changes in markers of organ function and of occasional case reports, but well controlled studies on the adverse effects of exogenous creatine supplementation are almost nonexistent.

We have investigated liver changes during medium term (4 weeks) creatine supplementation in young athletes. None showed any evidence of dysfunction on the basis of serum enzymes and urea production.

Short term (5 days), medium term (9 weeks) and long term (up to 5 years) oral creatine supplementation has been studied in small cohorts of athletes whose kidney function was monitored by clearance methods and urine protein excretion rate.

We did not find any adverse effects on renal function.

The present review is not intended to reach conclusions on the effect of creatine supplementation on sport performance, but we believe that there is no evidence for deleterious effects in healthy individuals. Nevertheless, idiosyncratic effects may occur when large amounts of an exogenous substance containing an amino group are consumed, with the consequent increased load on the liver and kidneys.

Regular monitoring is compulsory to avoid any abnormal reactions during oral creatine supplementation.

PMID: 10999421 [PubMed - indexed for MEDLINE]

Few adverse effects of long-term creatine supplementation in a placebo-controlled trial.
Groeneveld GJ, Beijer C, Veldink JH, Kalmijn S, Wokke JH, van den Berg LH.
Department of Neurology, University Medical Centre Utrecht, The Netherlands.

Although oral creatine supplementation is very popular among athletes, no prospective placebo-controlled studies on the adverse effects of long-term supplementation have yet been conducted.

We performed a double-blind, placebo-controlled trial of creatine monohydrate in patients with the neurodegenerative disease amyotrophic lateral sclerosis, because of the neuroprotective effects it was shown to have in animal experiments.

The purpose of this paper is to compare the adverse effects, and to describe the effects on indirect markers of renal function of long-term creatine supplementation. 175 subjects (age = 57.7 +/- 11.1 y) were randomly assigned to receive creatine monohydrate 10 g daily or placebo during an average period of 310 days.

After one month, two months and from then on every fourth month, adverse effects were scored using dichotomous questionnaires, plasma urea concentrations were measured, and urinary creatine and albumin concentrations were determined.

No significant differences in the occurrence at any time of adverse effects due to creatine supplementation were found (23 % nausea in the creatine group, vs. 24 % in the placebo group, 19 % gastro-intestinal discomfort in the creatine group, vs. 18 % in the placebo group, 35 % diarrhoea in the creatine group, vs. 24 % in the placebo group).

After two months of treatment, oedematous limbs were seen more often in subjects using creatine, probably due to water retention. Severe diarrhoea (n = 2) and severe nausea (n = 1) caused 3 subjects in the creatine group to stop intake of creatine, after which these adverse effects subsided.

Long-term supplementation of creatine did not lead to an increase of plasma urea levels (5.69 +/- 1.47 before treatment vs. 5.26 +/- 1.44 at the end of treatment) or to a higher prevalence of micro-albuminuria (5.4 % before treatment vs. 1.8 % at the end of treatment).

PMID: 15795816 [PubMed - indexed for MEDLINE]

Voor degene die nog steeds denken dat creatine eng en gevaarlijk is of hun ouders wilt overtuigen dat het niet gevaarlijk is.

Kre-alkalyn® supplementation has no beneficial effect on creatine-to-creatinine conversion rates.

Tallon MJ1 and Child R2

1University of Northumbria, Sport Sciences, Northumbria University, Northumberland Building, Newcastle upon Tyne, United Kingdom, 2Department of Life Sciences, Kingston University, Penrhyn Rd, Kingston-upon-Thames, United Kingdom. [email protected]

All American Pharmaceutical and Natural Foods Corp. (Billings, MT, USA) claim that Kre-alkalyn® (KA) a “Buffered” creatine, is 100% stable in stomach acid and does not convert to creatinine. In contrast, they also claim that creatine monohydrate (CM) is highly pH labile with more than 90% of the creatine converting to the degradation product creatinine in stomach acids. To date, no independent or university laboratory has evaluated the stability of KA in stomach acids, assessed its possible conversion to creatinine, or made direct comparisons of acid stability with CM.

This study examined whether KA supplementation reduced the rate of creatine conversion to creatinine, relative to commercially available CM (CreapureÒ). Creatine products were analyzed by an independent commercial laboratory using testing guidelines recommended by the United States Pharmacopeia (USP). Each product was incubated in 900ml of pH 1 HCL at 37* 1oC and samples where drawn at 5, 30 and 120 minutes and immediately analyzed by HPLC (UV) for creatine and creatinine.

In contrast to the claims of All American Pharmaceutical and Natural Foods Corp., the rate of creatinine formation from CM was found to be less than 1% of the initial dose, demonstrating that CM is extremely stable under acidic conditions that replicate those of the stomach. This study also showed that KA supplementation actually resulted in 35% greater conversion of creatine to creatinine than CM. In conclusion the conversion of creatine to creatinine is not a limitation in the delivery of creatine from CM and KA is less stable than CM in the acid conditions of the stomach.

Creatine Efficacy Headlines At Sports Nutrition Meeting :: News :: Natural and Nutritional Products Industry Center

Creatine werkt niet tijdens de laadfase
Medicine & Science in Sports & Exercise:Volume 36(5) SupplementMay 2004p S334

Power Output Response during Loading Creatine Supplementation Period[Annual Meeting Abstracts: H-19 - Free Communication/Poster: Creatine]
Laks, Daniel M.; Duarte, Julia S.; Alves, Letícia A.; Neves, Carlos E.B; Santos, Edil L.

Graduate School of Physical Education, Exercise Physiology Laboratory, Estácio de Sá University, Campus Rebouças., Rio de Janeiro, Brazil.

Email: [email protected]

2299

Response to Creatine supplementation (CS) has been frequently focused on physical performance, maximal strength and power output (PO). However, few works investigated PO response during loading CS period (LCSP).

PURPOSE: To evaluate the peak (PPO), mean (MPO), variation (ΔPO) of PO and total work done (TW) during LCSP.

Methods: Ten male subjects (22.8 * 2.94 yrs; 75.3 * 7.9 kg; 12.57 * 5.16 % of fat), were divided in two groups - Creatine (CR) and placebo (Pl), taking 4 × 5g.d-1 of CR or maltodextrine, respectively.

After a familiarization test, all subjects accomplished 4 modified 60-s Wingate test (W1, W2, W3, W4). Experimental design was double blind placebo-controlled during 7-d, with 48h rest. The PPO, MPO, ΔPO (computed as the ratio between PO30s/PPO, PO60s/PPO, and PO60s/PO30s), and TW achieved in each test were compared through analysis of variance (ANOVA) two-way for each group (α=.05). Additionally, the PO response during LCSP was modeled by linear regression (least square method).

Results: The PPO attained within W1 and W4 showed a progressive but non-significant decrease - 75.6 * 12.9kpm.s-1, 71.8 * 17.4kpm.s-1 (CR) and 89.2 * 23.3 kpm.s-1 and 73.2 * 14.8 kpm.s-1 (Pl). The MPO presented similar results concerning W1 and W4 50.3 * 7.1kpm.s-1; 48.5 * 7.4 kpm.s-1, (CR); and 56 * 7.5kpm.s-1; 46.4 * 5.3kpm.s-1, (Pl) as well as TW 3018.8 * 426.3kpm.s-1; 2912.8 * 441.8kpm.s-1 (CR) and 3362.8 * 450.3 kpm.s-1; 2783.1 * 319.8 kpm.s-1. (Pl).

After modeling PO during LCSP, the angular coefficient fitted for CR was lower than for Pl (p<0.05), as expressed by the following equations: PPO = -2.1671.x + 78.892 (CR) and PPO = -5.5158.x + 94.166 (Pl), which could indicate a lower decrease rate in CR, compared to Pl.

Conclusion: Although no differences were obtained when comparing CR to Pl, in opposite to CR, Pl presented a significant decrease during LCSP. In summary, even though PO parameters have not shown an increase during LCSP, the PPO attained by CR presented a lower decrease, when compared to Pl.[/i]
Medicine & Science in Sports & Exercise - Fulltext: Volume 36(5) May 2004 p S334 Power Output Response during Loading Creatine Supplementation Period.




Uitleg door Coachsci

CREATINE DOES NOT ACT DURING THE CREATINE LOADING PERIOD

Laks, D. M., Duarte, J. S., Alves, L. A., Neves, C. E., & Santos, E. L. (2004). Power output response during loading creatine supplementation period. Medicine and Science in Sports and Exercise, 36(5), Supplement abstract 2299.



This study investigated the power output during a creatine supplement loading period. It evaluated the peak power output, mean power output, power output variation, and total work done during the loading period. Males (N = 10) were divided in two groups - creatine and placebo, taking 4 × 5gm/day of creatine or maltodextrine, respectively. After a familiarization test, Ss completed a modified 60-s Wingate test on four alternate days. Testing was over seven days with 48 hours of rest between each test.

Peak power output, mean power output, and total work performed showed a non-significant decrease over the seven days. The amount of decrease was slightly less in the creatine group than in the placebo group.

Implication. Power output does not increase during a creatine supplement loading period.
Fuel and Ergogenic Aids 4.1 - Creatine

Creatine ethyl ester rapidly degrades to creatinine in stomach acid
Child R1 and Tallon MJ2

1Department of Life Sciences, Kingston University, Penrhyn Rd, Kingston-upon-Thames, United Kingdom. 2University of Northumbria, Sport Sciences, Northumbria University, Northumberland Building, Newcastle upon Tyne, United Kingdom, [email protected]

Creatine ethyl ester (CEE) is a commercially available synthetic creatine that is now widely used in dietary supplements. It comprises of creatine with an ethyl group attached and this molecular configuration is reported to provide several advantages over creatine monohydrate (CM). The Medical Research Institute (CA, USA) claim that the CEE in their product (CE2) provides greater solubility in lipids, leading to improved absorption. Similarly San (San Corporation, CA, USA) claim that the CEE in their product (San CM2 Alpha) avoids the breakdown of creatine to creatinine in stomach acids. Ultimately it is claimed that CEE products provide greater absorption and efficacy than CM. To date, none of these claims have been evaluated by an independent, or university laboratory and no comparative data are available on CEE and CM.

This study assessed the availability of creatine from three commercial creatine products during degradation in acidic conditions similar to those that occur in the stomach. They comprised of two products containing CEE (San CM2 Alpha and CE2) and commercially available CM (CreapureÒ). An independent laboratory, using testing guidelines recommended by the United States Pharmacopeia (USP), performed the analysis. Each product was incubated in 900ml of pH 1 HCL at 37* 1oC and samples where drawn at 5, 30 and 120 minutes. Creatine availability was assessed by immediately assaying for free creatine, CEE and the creatine breakdown product creatinine, using HPLC (UV)



After 30 minutes incubation only 73% of the initial CEE present was available from CE2, while the amount of CEE available from San CM2 Alpha was even lower at only 62%. In contrast, more than 99% of the creatine remained available from the CM product. These reductions in CEE availability were accompanied by substantial creatinine formation, without the appearance of free creatine. After 120minutes incubation 72% of the CEE was available from CE2 with only 11% available from San CM2 Alpha, while more than 99% of the creatine remained available from CM.

CEE is claimed to provide several advantages over CM because of increased solubility and stability. In practice, the addition of the ethyl group to creatine actually reduces acid stability and accelerates its breakdown to creatinine. This substantially reduces creatine availability in its esterified form and as a consequence creatines such as San CM2 and CE2 are inferior to CM as a source of free creatine.
Creatine Efficacy Headlines At Sports Nutrition Meeting :: News :: Natural and Nutritional Products Industry Center

What is the best creatine for muscle development?
by Alfredo Franco-Obregón, PhD



Background
Many commercially available nutritional supplements are marketed on the promise that they will potentiate muscle development in response to exercise. That is, many manufacturers would have you believe that your efforts in the gym will be rewarded sooner by taking their products…. However, when examined in controlled scientific studies, most of these putative anabolic agents fail to promote muscle growth.

Much of the muscle growth that ensues with training arises from the re-initiation of the developmental program that originally ran during fetal development, a process known as myogenesis. Specifically, myogenesis consists of two phases: First, previously dormant muscle stem cells awaken from stasis and start to divide, greatly increasing their numbers. These activated stem cells are now known as myoblasts. Next, myoblasts fuse with existing muscle fibers to replace damaged muscle tissue as well as to add mass and increase overall size to the existing muscle.


The outcome of myogenesis is subtly different when examined in the laboratory; that is, under artificial conditions using a technology known as tissue culture. When myoblasts are removed from an animal and grown in plastic tissue culture dishes devoid of adult muscle fibers, myoblasts instead first fuse with each other to form elongated myotubes (see figure below). Subsequently, after the first myotubes have been successfully established in the dish, myoblasts fuse with these as well.



Top: Individual muscle stem cells (myoblasts) aligning themselves into linear arrays in preparation for cell fusion to form myotubes, the first stage in the formation of an muscle fiber.
Bottom: Close-up of myotubes arising from the fusion of myoblasts as shown above.


So, given that myoblasts fuse with myoblasts in tissue culture, is examining myogenesis in dishes (in vitro) irrelevant? Most experts agree that myotubes are good approximations to the earliest skeletal muscle fibers produced in an animal and thus, can be taken as an indication of efficacious muscle development. Regardless, it remains unclear whether myotubes are produced at all in humans undertaking training, or if most of the new muscle that results from exercise is a consequence of myoblasts fusing with preexisting muscle fibers – a very important distinction for those working in the fields of muscle and exercise physiology. The production of new myotubes (inside the animal) would give rise to a process known as hyperplasia, whereas myoblasts fusing with preexisting muscle fibers would increase muscle size via a mechanism known as hypertrophy - two fundamentally distinct processes.

The study we are focusing on today was an initial attempt to quantify the direct myogenic effects of several popular ergogenic agents in vitro. Direct..., since muscle cells grown in tissue culture are not exposed to the hormonal environment present within the animal as well as are not subject to the mechanical forces provoked by the nervous system in initiating movement. In other words, any change in myogenic capacity measured in tissue culture would have to be a direct effect of the ergogenic agent in question and not a downstream consequence of the effect that exercise has on anabolic hormone balance - an indirect consequence of creatine supplementation.

Description of Study
This study tested the effects of several reputed ergogenic agents including two forms of creatine (monohydrate and pyruvate), an amino acid (L-glutamine), two steroidal agents (dehydroepiandrosterone (DHEA) and androstenedione) and two herbal extracts, (Ma Huang (Ephedra sinensis) and Zhi Shi (Citrus aurantium)) on muscle development in vitro.
The results of this study can be broken down to the effects that each ergogenic agent had over three key aspects of myogenesis: 1) alterations in muscle stem cell (myoblast) proliferation capacity; 2) changes in the ability of myoblasts to form myotubes and; 3) the influence of insulin over myogensis.

1) Creatine monohydrate generally did not interfere with the ability of myoblasts to divide and increase in number. Surprisingly, creatine pyruvate more consistently slowed the rate of cell division. On the other hand, androstenedione and DHEA killed myoblasts at a moderate concentration (micromolar) range, whereas Ma Huang and Zhi Shi proved lethal to myoblasts at all concentrations tested. In summary, creatine monohydrate was the most permissive for myoblasts proliferation of all the agents testeds.

2) Only creatine monohydrate had a positive effect over the ability of myoblasts to produce myotubes. Interestingly, the lowest dose of creatine monohydrate tested turned out to be the most efficacious at promoting myotube formation. Specifically, 0.1% (grams/liter) creatine monohydrate stimulated myotube formation, whereas 0.25%, 0.50% or 1.0% creatine monohydrate actually inhibited the formation of myotubes formation as well as slowed the proliferation of myoblasts. This result implies that overdosing with creatine may be counterproductive to muscle growth (resulting from myoblast fusion). This may be a simplistic interpretation of the data, however, as other anabolic attributes of creatine monohydrate (in conjunction with exercise) may compensate for this possible inhibitory effect.
Muscle cells in tissue culture must be supplied with a nutrient source (media) containing glucose, amino acids, and animal serum. Moreover, serum is an essential source of metabolites, hormones, currently unidentified nutrients and growth factors that permit the muscle cells to survive outside of the animal. All of the agents tested in this study were added directly to cell media containing serum, which could complicate the analysis of the results.

3) Given the success of the preliminary tests with creatine monohydrate in serum-containing media, the authors of the study next sought to identify any component of animal serum that may act in conjunction with creatine to promote muscle development. The two obvious candidates were insulin and the insulin-like growth factors – known myogenic agents. This group of researchers thus next examined the combined effects of creatine monohydrate and a special (serum-less) media formulation supplemented with insulin. The combination of insulin and creatine monohydrate was better at inducing myotube formation than the defined media containing insulin. On the other hand, somewhat surprising was the finding that creatine monohydrate without insulin was less effective than insulin alone at stimulating myotube formation, suggesting that the myogenic benefit of creatine monohydrate is strongly potentiated by insulin (or the insulin-like growth factors).
Creatine: A practical guide discusses how creatine monohydrate and the insulin-like growth factors act synergistically to promote muscle development – independently of exercise!

A Potential Criticism of the Study
Sheep myobasts were used, as they were readily available to the authors of the study. Therefore, for the sake of relevancy, these same agents should also be tested on myoblasts isolated from human muscle.


Take Home
These preliminary results would suggest that creatine monohydrate directly promotes the formation of immature muscle fibers. Oddly, creatine pyruvate instead seemed to compromise myoblast survival and undermine myotube formation. Exactly why creatine monohydrate exhibits this mysterious effect is currently not fully understood. Some hints as to what aspects of creatine monohydrate may contribute to its unique pro-myogenic effect, however, are provided in past issues of the Creatine Newsletter.


Interestingly, the other commonly used ergogenic agents, L-glutamine, DHEA, androstenedione, Ma Huang and Zhi Shi, had either no effect, or actually killed myoblasts, before they could produce myotubes - an anti-myogenic effect.
This provocative pilot study certainly merits a follow up...


Scientific References
(Ref. 1) Vierck, J. L. et al. (2003) The effects of ergogenic compounds on myogenic satellite cells. Medicine & Science in Sports & Exercise, Volume 35 (5), pages 769-776.


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Creatine Newsletter #35: What is the best creatine for muscle development?

[Kingsley]

m.a.w. volgens de wetenschap zorgt kre alkalyn creatine zelf voor de afbraak van myoblasten ipv de opbouw.

[GeneralIx]

Topstuk wat je daar hebt Kingsley.

[probodyboy]

ik gebruik kre alkalyn pro van EFX
werkt goed meer kracht en energie
wel redelijk duur 25 eu voor 60 caps

[Rico1981]

ik gebruik kre alkalyn pro van EFX
werkt goed meer kracht en energie
wel redelijk duur 25 eu voor 60 caps

Vriend die zooi is echt niet gezond voor je, En btw dit topic is igg al wel heel erg oud

[Fitness-maniak]

Vriend die zooi is echt niet gezond voor je, En btw dit topic is igg al wel heel erg oud

onderbouw.

OT: monohydraat = beste creatine