EvoMuse CarioTryx

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    Quote Originally Posted by xhrr View Post

    4 weeks are you serious? I'm just playing sounds good man can't wait to get my hands on some I think it would be an awesome addition to my supplements considering I do Crossfit.
    Right around the corner. I'm going to use it for my Oly training. It's going to be a good one!
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    Quote Originally Posted by domore View Post
    Right around the corner. I'm going to use it for my Oly training. It's going to be a good one!
    Do you strictly OLY lift? We do a lot of OLY at my box and of course a workout of the day afterward.
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    Quote Originally Posted by xhrr View Post

    Do you strictly OLY lift? We do a lot of OLY at my box and of course a workout of the day afterward.
    Yeah, I'm strictly an Oly lifter. I made the transition after my college ball days.

    CardioTryx will be a perfect fit for crossfit.
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    Will cardiotryx be out before the start of September??

    Too stoked
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    Quote Originally Posted by domore View Post
    Yeah, I'm strictly an Oly lifter. I made the transition after my college ball days.

    CardioTryx will be a perfect fit for crossfit.
    I am bummed, I am making my own.


    just kidding....bring this on.....
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    Quote Originally Posted by fcbarca12 View Post
    Will cardiotryx be out before the start of September??

    Too stoked
    3 more weeks for ingredients, 1 weeks for capping.
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    Quote Originally Posted by dsade View Post
    3 more weeks for ingredients, 1 weeks for capping.
    Interesting I assumed it would be a powdered product.
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    Same here but I'm sure it'll be great
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    Quote Originally Posted by xhrr View Post
    Interesting I assumed it would be a powdered product.
    Some of the ingredients taste pretty bad.
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    We decided against the tagline "run the bad taste off" and capped it for you guys.
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    PM me with any questions!
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    Quote Originally Posted by Geoforce View Post
    We decided against the tagline "run the bad taste off" and capped it for you guys.
    Fine, challenged accepted, I'll be opening the caps into water my first time.
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    Does it take longer to kick in if it's in pill form?
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    Quote Originally Posted by fcbarca12 View Post
    Does it take longer to kick in if it's in pill form?
    I may be speaking out of line, but I believe generally the cap results in a slower release because of the digestion process, but I doubt it is all that much (and timing could be done to make it a non-issue).
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    Quote Originally Posted by xhrr View Post

    Fine, challenged accepted, I'll be opening the caps into water my first time.
    If it's anything like cissus powder, it'll just float. Lol.
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    Quote Originally Posted by enhanced View Post
    If it's anything like cissus powder, it'll just float. Lol.
    been there, never again.
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    Quote Originally Posted by dsade View Post
    Ingredients in production....

    Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes.

    Chen YY, Lee MH, Hsu CC, Wei CL, Tsai YC. Source

    Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan, ROC.

    Abstract

    Methyl cinnamate, an active component of Zanthoxylum armatum , is a widely used natural flavor compound with antimicrobial and tyrosinase inhibitor activities. However, the underlying bioactivity and molecular mechanisms of methyl cinnamate on adipocyte function and metabolism remain unclear. The aim of this study was to investigate the inhibitory effect of methyl cinnamate on adipogenesis in 3T3-L1 preadipocytes. Methyl cinnamate markedly suppressed triglyceride accumulation associated with down-regulation of adipogenic transcription factor expression, including sterol regulatory element binding protein-1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), and CCAAT/enhancer-binding protein α (C/EBPα). Additionally, methyl cinnamate-inhibited PPARγ activity and adipocyte differentiation were partially reversed by the PPARγ agonist troglitazone. Furthermore, methyl cinnamate stimulated Ca(2+)/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and phospho-AMP-activated protein kinase (AMPK) expression during adipogenesis. This study first revealed methyl cinnamate has antiadipogenic activity through mechanisms mediated, in part, by the CaMKK2-AMPK signaling pathway in 3T3-L1 cells.
    PMID: 22273148 [PubMed - indexed for MEDLINE]
    Methyl cinnamate never reaches the bloodstream...however, it is metabolized to methanol and enters the blood as such: http://www.ncbi.nlm.nih.gov/pubmed/841581
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    Quote Originally Posted by mr.cooper69 View Post
    Methyl cinnamate never reaches the bloodstream...however, it is metabolized to methanol and enters the blood as such: http://www.ncbi.nlm.nih.gov/pubmed/841581
    metabolized to methanol and cinnamic acid.

    Phone Sucks, I will post other studies. I wanted to wait to post the rest of the ingredient list until we were in production actual.
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    Quote Originally Posted by mr.cooper69 View Post
    Methyl cinnamate never reaches the bloodstream...however, it is metabolized to methanol and enters the blood as such: http://www.ncbi.nlm.nih.gov/pubmed/841581
    metabolized to methanol and cinnamic acid.

    Phone Sucks, I will post other studies. I wanted to wait to post the rest of the ingredient list until we were in production actual.
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    How long till production?
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    Quote Originally Posted by dsade View Post
    metabolized to methanol and cinnamic acid.

    Phone Sucks, I will post other studies. I wanted to wait to post the rest of the ingredient list until we were in production actual.
    Ah ok. Sorry if i was pre-emptive. You make special products so they get special attention
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    Quote Originally Posted by mr.cooper69 View Post
    Ah ok. Sorry if i was pre-emptive. You make special products so they get special attention
    I always appreciate the challenge. Don't ever let me get away with not beig questioned!
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    Bioorg Med Chem Lett. 2013 Aug 1;23(15):4441-6. doi: 10.1016/j.bmcl.2013.05.079. Epub 2013 Jun 1.
    Effects of (-)-epicatechin and derivatives on nitric oxide mediated induction of mitochondrial proteins.
    Moreno-Ulloa A, Cid A, Rubio-Gayosso I, Ceballos G, Villarreal F, Ramirez-Sanchez I.
    Source

    University of California, San Diego, Department of Medicine, La Jolla, CA 92093-0613, USA; Escuela Superior de Medicina, Instituto Politecnico Nacional, Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Plan de San Luis y, Diaz Miron S/N Casco de Santo Tomas, Del. M. Hidalgo Mexico, DF 11340, Mexico.
    Abstract

    Impaired mitochondrial function represents an early manifestation of endothelial dysfunction and likely contributes to the development of cardiovascular diseases (CVD). The stimulation of mitochondrial function and/or biogenesis is seen as a means to improve the bioenergetic and metabolic status of cells and thus, reduce CVD. In this study we examined the capacity of the flavanol (-)-epicatechin and two novel derivatives to enhance mitochondrial function and protein levels in cultured bovine coronary artery endothelial cells. As nitric oxide production by endothelial cells is suspected in mediating mitochondria effects (including biogenesis), we also examined the dependence of responses on this molecule using an inhibitor of nitric oxide synthase. Results indicate that the flavanol (-)-epicatechin and derivatives are capable of stimulating mitochondrial function as assessed by citrate synthase activity as well as induction of structural (porin, mitofilin) and oxidative phosporylation protein levels (complex I and II). Effects were blocked by the use of the chemical inhibitor of the synthase thus, evidencing a role for nitric oxide in mediating these effects. The results observed indicate that the three agents are effective in enhancing mitochondria function and protein content. The effects noted for (-)-epicatechin may serve to explain the healthy effects on cardiometabolic risk ascribed to the consumption of cocoa products.

    Copyright © 2013 Elsevier Ltd. All rights reserved.

    PMID:
    23791569
    [PubMed - in process]
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    J Physiol. 2011 Sep 15;589(Pt 18):4615-31. doi: 10.1113/jphysiol.2011.209924. Epub 2011 Jul 25.
    (-)-Epicatechin enhances fatigue resistance and oxidative capacity in mouse muscle.
    Nogueira L, Ramirez-Sanchez I, Perkins GA, Murphy A, Taub PR, Ceballos G, Villarreal FJ, Hogan MC, Malek MH.
    Source

    Department of Medicine, School of Medicine, University of California, San Diego, CA, USA.
    Abstract

    The flavanol (-)-epicatechin, a component of cacao (cocoa), has been shown to have multiple health benefits in humans. Using 1-year-old male mice, we examined the effects of 15 days of (-)-epicatechin treatment and regular exercise on: (1) exercise performance, (2) muscle fatigue, (3) capillarity, and (4) mitochondrial biogenesis in mouse hindlimb and heart muscles. Twenty-five male mice (C57BL/6N) were randomized into four groups: (1) water, (2) water-exercise (W-Ex), (3) (-)-epicatechin ((-)-Epi), and (4) (-)-epicatechin-exercise ((-)-Epi-Ex). Animals received 1 mg kg(-1) of (-)-epicatechin or water (vehicle) via oral gavage (twice daily). Exercise groups underwent 15 days of treadmill exercise. Significant increases in treadmill performance (∼50%) and enhanced in situ muscle fatigue resistance (∼30%) were observed with (-)-epicatechin. Components of oxidative phosphorylation complexes, mitofilin, porin, nNOS, p-nNOS, and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (-)-epicatechin treatment for hindlimb and cardiac muscles than exercise alone. In addition, there were significant increases in skeletal muscle capillarity. The combination of (-)-epicatechin and exercise resulted in further increases in oxidative phosphorylation-complex proteins, mitofilin, porin and capillarity than (-)-epicatechin alone. These findings indicate that (-)-epicatechin alone or in combination with exercise induces an integrated response that includes structural and metabolic changes in skeletal and cardiac muscles resulting in greater endurance capacity. These results, therefore, warrant the further evaluation of the underlying mechanism of action of (-)-epicatechin and its potential clinical application as an exercise mimetic
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    Why yes, this IS one of the key ingredients. How did you guess?

    Clin Sci (Lond). 2013 Jun;124(11):663-74. doi: 10.1042/CS20120469.
    (-)-Epicatechin is associated with increased angiogenic and mitochondrial signalling in the hindlimb of rats selectively bred for innate low running capacity.
    Hüttemann M, Lee I, Perkins GA, Britton SL, Koch LG, Malek MH.
    Source

    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA.
    Abstract

    Alternative approaches to reduce congenital muscle dysfunction are needed in cases where the ability to exercise is limited. (-)-Epicatechin is found in cocoa and may stimulate capillarity and mitochondrial proliferation in skeletal muscle. A total of 21 male rats bred for LCR (low running capacity) from generation 28 were randomized into three groups: vehicle for 30 days (control); (-)-epicatechin for 30 days; and (-)-epicatechin for 30 days followed by 15 days without (-)-epicatechin. Groups 2 and 3 received 1.0 mg of (-)-epicatechin/kg of body mass twice daily, whereas water was given to the control group. The plantaris muscle was harvested for protein and morphometric analyses. In addition, in vitro experiments were conducted to examine the role of (-)-epicatechin on mitochondrial respiratory kinetics at different incubation periods. Treatment for 30 days with (-)-epicatechin increased capillarity (P<0.001) and was associated with increases in protein expression of VEGF (vascular endothelial growth factor)-A with a concomitant decrease in TSP-1 (thrombospondin-1) and its receptor, which remained after 15 days of (-)-epicatechin cessation. Analyses of the p38 MAPK (mitogen-activated protein kinase) signalling pathway indicated an associated increase in phosphorylation of MKK3/6 (MAPK kinase 3/6) and p38 and increased protein expression of MEF2A (myocyte enhancer factor 2A). In addition, we observed significant increases in protein expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator 1α), PGC-1β, Tfam and cristae abundance. Interestingly, these increases associated with (-)-epicatechin treatment remained after 15 days of cessation. Lastly, in vitro experiments indicated that acute exposure of LCR muscle to (-)-epicatechin incubation was not sufficient to increase mitochondrial respiration. The results suggest that increases in skeletal muscle capillarity and mitochondrial biogenesis are associated with 30 days of (-)-epicatechin treatment and sustained for 15 days following cessation of treatment. Clinically, the use of this natural compound may have potential application in populations that experience muscle fatigue and are unable to perform endurance exercise.

    PMID:
    23252598
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC3715875
    [Available on 2014/6/1]
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    For those that want to take that last study and continue on....

    Free Radic Biol Med. 2009 Nov 15;47(10):1394-400. doi: 10.1016/j.freeradbiomed.2009.08.007. Epub 2009 Aug 14.
    Exercise activation of muscle peroxisome proliferator-activated receptor-gamma coactivator-1alpha signaling is redox sensitive.
    Kang C, O'Moore KM, Dickman JR, Ji LL.
    Source

    The Biodynamics Laboratory, Department of Kinesiology, University of Wisconsin at Madison, Madison, WI 53706, USA.
    Abstract

    The peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha)-activated signal transduction pathway has previously been shown to stimulate mitochondrial biogenesis in skeletal muscle in response to endurance exercise. In vitro data indicate that PGC-1alpha signaling may be sensitive to reactive oxygen species (ROS) but its role in vivo is not clear. The objectives of this study were (1) to investigate whether the PGC-1alpha pathway could be activated by a single bout of anaerobic exercise in rats, wherein a major portion of ROS was generated via the cytosolic xanthine oxidase (XO), and (2) to examine whether allopurinol (ALP), a specific XO inhibitor, would attenuate PGC-1alpha expression and signaling owing to decreased ROS generation. Female Sprague-Dawley rats were randomly divided into three groups: (1) subjected to sprinting on a treadmill at 35 m/min, 15% grade, for 3 min followed by 3 min slow running at 15 m/min, 0% grade, repeated until exhaustion (88 +/- 4 min; Exer; N= 9); (2) subjected to the same exercise protocol (88 +/- 4 min) but injected with two doses of ALP (0.4 mmol/kg, ip) 24 and 1 h before the experiment (Exer+ ALP; N= 9); and (3) rested control (C; N= 9). Exercise increased XO activity and ROS generation in the Exer rat vastus lateralis muscle (P< 0.05), whereas the Exer+ ALP group displayed only 7% XO activity and similar ROS level compared with the C group. PGC-1alpha protein content showed a 5.6-fold increase (P< 0.01) in Exer vs C, along with a 200% (P< 0.01) increase in both nuclear respiratory factor (NRF)-1 and mitochondrial transcription factor A (Tfam) content. ALP treatment decreased PGC-1alpha, NRF-1, and Tfam levels by 45, 19, and 20% (P< 0.05), respectively. Exercise doubled the content of the phosphorylated cAMP-responsive element-binding protein in the Exer group (P< 0.01) and tripled phosphorylated p38 mitogen-activated protein kinase (P< 0.01), whereas these effects were reduced by 60 and 30% (P< 0.01, P< 0.05), respectively, in Exer+ ALP rats. Nuclear factor-kappaB binding and phospho-IkappaB content were also increased in Exer rats (P< 0.01) and these increases were abolished by ALP treatment. The data indicate that contraction-activated PGC-1alpha signaling pathways in skeletal muscle are redox sensitive and that nonmitochondrial ROS play an important role in stimulating mitochondrial biogenesis.
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    And farther, though you will have to click and read:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020130/

    Cardiovasc Res. 2011 Feb 1;89(2):426-35. doi: 10.1093/cvr/cvq296. Epub 2010 Sep 16.
    Baicalin increases VEGF expression and angiogenesis by activating the ERR{alpha}/PGC-1{alpha} pathway.
    Zhang K, Lu J, Mori T, Smith-Powell L, Synold TW, Chen S, Wen W.
    Source

    Department of Molecular Medicine, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA.
    Abstract
    AIMS:

    Baicalin is the major component found in Scutellaria baicalensis root, a widely used herb in traditional Chinese medicine. Although it has been used for thousands of years to treat stroke, the mechanisms of action of S. baicalensis have not been clearly elucidated. In this report, we studied the modulation of angiogenesis as one possible mechanism by investigating the effects of these agents on expression of vascular endothelial growth factor (VEGF), a critical factor for angiogenesis.
    METHODS AND RESULTS:

    The effects of baicalin and an extract of S. baicalensis on VEGF expression were tested in several cell lines. Both agents induced VEGF expression in all cells without increasing expression of hypoxia-inducible factor-1α (HIF-1α). The expression of reporter genes was also activated under the control of the VEGF promoter containing either a functional or a defective HIF response element (HRE). Only minimal effects were observed on reporter activation under the HRE promoter. Instead, both agents significantly induced oestrogen-related receptor (ERRα) expression as well as the activity of reporter genes under the control of ERRα-binding element. Their ability to induce VEGF expression was suppressed once ERRα expression was knocked down by siRNA or ERRα-binding sites were deleted in the VEGF promoter. We also found that both agents stimulated cell migration and vessel sprout formation from the aorta.
    CONCLUSION:

    Our results implicate baicalin and S. baicalensis in angiogenesis by inducing VEGF expression through the activation of the ERRα pathway. These data may facilitate a better understanding of the potential health benefits of these agents in the treatment of cardiovascular diseases.

    PMID:
    20851810
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC3020130
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    J Int Soc Sports Nutr. 2013 Apr 15;10(1):21. doi: 10.1186/1550-2783-10-21.
    Effect of HX108-CS supplementation on exercise capacity and lactate accumulation after high-intensity exercise.
    Oh SL, Chang H, Kim HJ, Kim YA, Kim DS, Ho SH, Kim SH, Song W.
    Source

    Health and Exercise Science Laboratory, Institute of Sports Science, Seoul National University, 599 Gwanang-no, Gwanak-gu, Seoul, 151-742, Korea. songw3@snu.ac.kr.
    Abstract
    BACKGROUND:

    In the present study, we determined the effects of HX108-CS (mixed extract of Schisandra chinensis and Chaenomeles sinensis) supplementation on lactate accumulation and endurance capacity. Furthermore, we examined CK (creatine kinase), LDH (lactate dehydrogenase) activity to determine whether the HX108-CS affected markers of skeletal muscle injury in vivo and in vitro.
    METHODS:

    Exercise capacity was measured by an exhaustive swimming test using ICR mice divided into four groups; one group received distilled water (DW) (Control group, n = 10), and the other groups received three different dosages of HX108-CS (10, 50 and 100 mg/kg, n = 10 per group) solution in water orally. Then, for the time-dependent measurements of blood lactate, CK, and LDH, Sprague-Dawley rats were divided into two groups; one received DW (Control group, n = 10), and the other group received HX108-CS (100 mg/kg, n = 10) solution in the same way as mice. Before the exercise test, the animals were given either DW or HX108-CS for 2 weeks. High-intensity treadmill exercise was performed for 30 minutes. Blood samples were collected and analyzed during and after exercise. For the in vitro experiment, C2C12 cells were treated with HX108-CS to examine its effect on lactate production, CK, and LDH activity.
    RESULTS:

    Blood lactate concentration was significantly lowered immediately after treadmill exercise in HX108-CS group; however, there were no significant differences in activities of CK and LDH between HX108-CS and control during treadmill exercise and recovery phase. Furthermore, treatment with 100 mg/kg of HX108-CS led to a significant increase in the time to exhaustion in swimming test, and concurrently blood lactate concentration was significantly decreased in 50 and 100 mg/kg treated group. Moreover, our results of in vitro experiment showed that HX108-CS suppressed lactate production, CK, and LDH activity in a dose-dependent manner.
    CONCLUSIONS:

    These results suggest that supplementation with HX108-CS may enhance exercise capacity by lowering lactate accumulation. This may in part be related to an amelioration of skeletal muscle injury.

    PMID:
    23587302
    [PubMed]
    PMCID:
    PMC3659049
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    How many total compounds in CardioTryx?
    EvoMuse
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    Quote Originally Posted by domore View Post
    How many total compounds in CardioTryx?
    Around 20. It's going to be a 6 capsule serving size, 5 days on 2 days off.
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    I want like 4 of the bottles. Special deal?? Most excited supp I've been waiting for
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    Quote Originally Posted by dsade View Post
    Around 20. It's going to be a 6 capsule serving size, 5 days on 2 days off.
    20 compounds, wow!
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    Eta?
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    Quote Originally Posted by fcbarca12 View Post
    Eta?
    Ingredients are ordered and I will find out today if any of the new concentrations have a significant lead time.
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    Cardiotryx + Ketoforce + TTA + COP + HIIT= CAN'T FRIGGEN WAIT!!!!
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    A lot of very cool science and ingredients so far which look great on paper. I haven't really divulged into the ingredients past what has been posted but what do the pharmocokinetics of these compounds look like? Half life? Bioavailabilty? etc.
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    Absolutely can't wait for this one.
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    Womp womp
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    Quote Originally Posted by burpees View Post
    Womp womp
    Soon my friend. Mid-October.
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    Still mid October ?
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    Quote Originally Posted by burpees View Post
    Still mid October ?
    Still right on schedule!
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