Trimax/Phenogen Rebound - wtf?

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    Trimax/Phenogen Rebound - wtf?


    Finished my Trimax/Phenogen/M5AA cycle last Friday.
    Final weight was 188, down from 197.
    Weighed myself yesterday at the gym and I'm back up to 193.

    Eating at maintenance (was a little below during cycle), cardio is the same, taking Rebound XT, Syntrax MM4 & Beta3 for pct. What the hell happened?

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    It could be as simple as your muscles picking up more glycogen. Trimax speeds the rate at witch your muscles use nutrients (including glycogen). It can flatten you out some. This is often mistaken for catabolism IMO. Keep your nutrition and cardio in check. You'll be fine.
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    Thanks. I know Phenogen is notorious for this also, but didn't think the muscles could hold that much.
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    My experience is limimted to two cycles, one with MDien and one with M1T. After both, my weight went up for a few days, then leveled off, and then dropped back close to the end of cycle weight. the first cycle I started taking creatine right after the cycle and that may have contributed to some gain (water) right away. At the end of both cycles I could tell I was "flat" and after a few days I had gained some weight back, but felt I looked better overall than at the very end, and strength began to pick back up. The fat I lost around my waist seemed to stay off even though there was an overall increase in my weight after the first few days. Don't lose hope yet. The payoff for me was that after a month or so I had not regained the fat lost during the cycle, even though my overall weight wasn't as low as at the end of the cycle.
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    the more glycogen in the muscle, the more water it will hold...Dim
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    Quote Originally Posted by WhutEvr
    Thanks. I know Phenogen is notorious for this also, but didn't think the muscles could hold that much.
    ****, muscles have a huge capacity to store water/glycogen. Where do you think the weight comes from when someone picks up 10 to 15 lbs in 2 weeks on SD or M1T?

    5lbs is nothing when talking glycogen. It comes and goes...
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    I am just finishing my extreme cutter on Saturday (no androgens) and I will be moving into a short lean bulker. Right now I am down about 23 lbs in 6 weeks. Wait till I start eating some carbs again and drop the Phenogen and Trimax. I figure I will gain back 8-10 lbs in a week easily.
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    on UD2 my weight pre and post carbup can differ by about 7-8lbs. My guess is that you have gained some extra cellular water because you stopped the M5AA, and the rest is glycogen resynthesis after stopping phengen/trimax. Are any of the products in your PCT creatine based? That is advised after using phenogen.
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    I am going to be kicking in Clout and Body Octane on Saturday.



    Quote Originally Posted by meathead1987
    on UD2 my weight pre and post carbup can differ by about 7-8lbs. My guess is that you have gained some extra cellular water because you stopped the M5AA, and the rest is glycogen resynthesis after stopping phengen/trimax. Are any of the products in your PCT creatine based? That is advised after using phenogen.
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    Quote Originally Posted by meathead1987
    on UD2 my weight pre and post carbup can differ by about 7-8lbs. My guess is that you have gained some extra cellular water because you stopped the M5AA, and the rest is glycogen resynthesis after stopping phengen/trimax. Are any of the products in your PCT creatine based? That is advised after using phenogen.
    Not using creatine, I'm a non-responder.
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    I usually am also but I keep going back tot he well with each of the new cretines that come out.



    Quote Originally Posted by WhutEvr
    Not using creatine, I'm a non-responder.
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    I've tried them all, no luck.
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    When coming off pheno, creatine is good non responder or not. GPA is basically anticreatine and depletes ATP stores in the muscle. You may not respond to creatine in certain situations but after coming off phenogen you definately will.
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    Quote Originally Posted by meathead1987
    When coming off pheno, creatine is good non responder or not. GPA is basically anticreatine and depletes ATP stores in the muscle. You may not respond to creatine in certain situations but after coming off phenogen you definately will.
    This makes no sense to me.
    Do you have any studies to back this up?
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    No, but I have heard both spook and Par advocate this over at the avant boards.

    I'd just get 100g CEE and run 3g a day for a month. Thats only ~$6 so you cant really go wrong. You should get a very nice strength rebound from it.
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    Quote Originally Posted by meathead1987
    No, but I have heard both spook and Par advocate this over at the avant boards.

    I'd just get 100g CEE and run 3g a day for a month. Thats only ~$6 so you cant really go wrong. You should get a very nice strength rebound from it.
    I'll pass, strength is already back to normal.
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    Quote Originally Posted by WhutEvr
    This makes no sense to me.
    Do you have any studies to back this up?
    I cannot comment specifically on the non-responder part, because I don't think we really know what a non-responder is (i.e. defective transporter, muscles already saturated, etc.), but as far as increased uptake following creatine depletion:


    J Appl Physiol. 2003 Jun;94(6):2173-80. Epub 2003 Feb 28. Related Articles, Links


    Muscle creatine uptake and creatine transporter expression in response to creatine supplementation and depletion.

    Brault JJ, Abraham KA, Terjung RL.

    Department of Physiology, College of Medicine, University of Missouri, Columbia, Missouri 65211, USA.

    The total creatine pool size [Cr(total); creatine (Cr) + phosphocreatine (PCr)] is crucial for optimal energy utilization in skeletal muscle, especially at the onset of exercise and during intense contractions. The Cr(total) likely is controlled by long-term modulation of Cr uptake via the sodium-dependent Cr transporter (CrT). To test this hypothesis, adult male Sprague-Dawley rats were fed 1% Cr, their muscle Cr(total) was reduced by approximately 85% [1% beta-guanidinoproprionic acid (beta-GPA)], or their muscle Cr(total) was repleted (1% Cr after beta-GPA depletion). Cr uptake was assessed by skeletal muscle (14)C-Cr accumulation to Cr and PCr by using hindlimb perfusion, and CrT protein content was assessed by Western blot. Cr uptake rate decreased with dietary Cr supplementation in the white gastrocnemius (WG; 45%) only. Depletion of muscle Cr(total) to approximately 15% of normal increased Cr uptake in the soleus (21%) and red gastrocnemius (22%), corresponding to 70-150% increases in muscle CrT content. In contrast, the inherently lower Cr uptake rate in the WG was unchanged with depletion of muscle Cr(total) even though CrT band density was increased by 230%. Thus there was no direct relationship between apparent muscle CrT abundance and Cr uptake rates. However, Cr uptake rates scaled inversely with decreases in muscle Cr(total) in the high-oxidative muscle types but not in the WG. This implies that factors controlling Cr uptake are different among fiber types. These observations may help explain the influence of initial muscle Cr(total), time dependency, and variations in muscle Cr(total) accumulation during Cr supplementation.

    Am J Physiol Endocrinol Metab. 2003 Feb;284(2):E399-406. Related Articles, Links


    Creatine transporter activity and content in the rat heart supplemented by and depleted of creatine.

    Boehm E, Chan S, Monfared M, Wallimann T, Clarke K, Neubauer S.

    Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, United Kingdom. ernie.boehm@bioch.ox.ac.uk

    The intracellular creatine concentration is an important bioenergetic parameter in cardiac muscle. Although creatine uptake is known to be via a NaCl-dependent creatine transporter (CrT), its localization and regulation are poorly understood. We investigated CrT kinetics in isolated perfused hearts and, by using cardiomyocytes, measured CrT content at the plasma membrane or in total lysates. Rats were fed control diet or diet supplemented with creatine or the creatine analog beta-guanidinopropionic acid (beta-GPA). Creatine transport in control hearts followed saturation kinetics with a K(m) of 70 +/- 13 mM and a V(max) of 3.7 +/- 0.07 nmol x min(-1) x g wet wt(-1). Creatine supplementation significantly decreased the V(max) of the CrT (2.7 +/- 0.17 nmol x min(-1) x g wet wt(-1)). This was matched by an approximately 35% decrease in the plasma membrane CrT; the total CrT pool was unchanged. Rats fed beta-GPA exhibited a >80% decrease in tissue creatine and increase in beta-GPA(total). The V(max) of the CrT was increased (6.0 +/- 0.25 nmol x min(-1) x g wet wt(-1)) and the K(m) decreased (39.8 +/- 3.0 mM). The plasma membrane CrT increased about fivefold, whereas the total CrT pool remained unchanged. We conclude that, in heart, creatine transport is determined by the content of a plasma membrane isoform of the CrT but not by the total cellular CrT pool.

    PMID: 12531746 [PubMed - indexed for MEDLINE]

    PMID: 12611762 [PubMed - indexed for MEDLINE]
  

  
 

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