EvoMuse CardioTryx

[dsade]

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!

 

[dsade]

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]

 

[dsade]

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

 

[dsade]

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]

 

[dsade]

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.

 

[dsade]

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. [email protected].
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

 

[domore]

How many total compounds in CardioTryx?

 

[dsade]

How many total compounds in CardioTryx?

Around 20. It's going to be a 6 capsule serving size, 5 days on 2 days off.

 

[fcbarca12]

I want like 4 of the bottles. Special deal?? Most excited supp I've been waiting for

 

[testosteronet]

Around 20. It's going to be a 6 capsule serving size, 5 days on 2 days off.

20 compounds, wow!

 

[fcbarca12]

Eta?

 

[dsade]

Eta?

Ingredients are ordered and I will find out today if any of the new concentrations have a significant lead time.

 

[megadeth]

Cardiotryx + Ketoforce + TTA + COP + HIIT= CAN'T FRIGGEN WAIT!!!!

 

[xhrr]

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.

 

[MidwestBeast]

Absolutely can't wait for this one.

 

[burpees]

Womp womp

 

[domore]

Womp womp

Soon my friend. Mid-October.

 

[burpees]

Still mid October ?

 

[dsade]

Still mid October ?

Still right on schedule!

 

[3clipseGT]

Definitely interested in this being that i am in the military and we run atleast 3x a week. So ill be picking some up once its out!

 

[domore]

Definitely interested in this being that i am in the military and we run atleast 3x a week. So ill be picking some up once its out!

It's right around the corner. We would love to hear your feedback, especially in a military context!

 

[dsade]

 

[xhrr]

What a tease

 

[dsade]

What a tease

You been talking to my wife?

 

[dsade]

These two studies go together...do we want to play the "How"? game?

J Appl Physiol (1985). 2010 Dec;109(6):1653-61. doi: 10.1152/japplphysiol.00598.2010. Epub 2010 Sep 16.
Endurance training-induced accumulation of muscle triglycerides is coupled to upregulation of stearoyl-CoA desaturase 1.
Dobrzyn P, Pyrkowska A, Jazurek M, Szymanski K, Langfort J, Dobrzyn A.
Source

Laboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology, 3 Pasteur St., 02-093 Warsaw, Poland. [email protected]
Abstract

Stearoyl-CoA desaturase (SCD), a rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids, has recently been shown to be a critical control point in regulation of liver and skeletal muscle metabolism. Herein, we demonstrate that endurance training significantly increases both SCD1 mRNA and protein levels in the soleus muscle, whereas it does not affect SCD1 expression in the EDL muscle and liver. Desaturation index (18:1Δ9/18:0 ratio), an indirect indicator of SCD1 activity, was also significantly higher (3.6-fold) in soleus of trained rats compared with untrained animals. Consistent with greater SCD1 expression/activity, the contents of free fatty acids, diacylglycerol, and triglyceride were elevated in soleus of trained rats. However, training did not affect lipid concentration in EDL and liver. Additionally, endurance training activated the AMP-activated protein kinase pathway as well as increased peroxisome proliferator-activated receptor (PPAR)-δ and PPARα gene expression and activity in soleus and liver. Increased lipid accumulation in soleus was coupled with elevated protein levels of fatty acid synthase, mRNA levels of diacylglycerol acyltransferase and glycerol-3-phosphate transferase, as well as increased levels of proteins involved in fatty acid transport (fatty acid translocase/CD36, fatty acid transport protein 1). Interestingly, sterol regulatory element-binding protein (SREBP)-1c expression and SREBP-1 protein levels were not affected by exercise training. Together, the obtained data suggest that SCD1 upregulation plays an important role in adaptation of oxidative muscle to endurance training.

PMID:
20847127
[PubMed - indexed for MEDLINE]

PLoS One. 2012;7(3):e33815. doi: 10.1371/journal.pone.0033815. Epub 2012 Mar 27.
An ethanol extract of Artemisia iwayomogi activates PPARδ leading to activation of fatty acid oxidation in skeletal muscle.
Cho SY, Jeong HW, Sohn JH, Seo DB, Kim WG, Lee SJ.
Source

Health Science Research Institute, Research and Development Center, AmorePacific Corporation, Bora-dong, Giheung-gu, Yongin-si, Korea.
Abstract

Although Artemisia iwayomogi (AI) has been shown to improve the lipid metabolism, its mode of action is poorly understood. In this study, a 95% ethanol extract of AI (95EEAI) was identified as a potent ligand of peroxisome proliferator-activated receptorδ (PPARδ) using ligand binding analysis and cell-based reporter assay. In cultured primary human skeletal muscle cells, treatment of 95EEAI increased expression of two important PPARδ-regulated genes, carnitine palmitoyl-transferase-1 (CPT1) and pyruvate dehydrogenase kinase isozyme 4 (PDK4), and several genes acting in lipid efflux and energy expenditure. Furthermore, 95EEAI stimulated fatty acid oxidation in a PPARδ-dependent manner. High-fat diet-induced obese mice model further indicated that administration of 95EEAI attenuated diet-induced obesity through the activation of fatty acid oxidation in skeletal muscle. These results suggest that a 95% ethanol extract of AI may have a role as a new functional food material for the prevention and/or treatment of hyperlipidermia and obesity.

PMID:
22479450
[PubMed - indexed for MEDLINE]
PMCID:
PMC3313949

 

[Geoforce]

No one out sciences our label!

 

[xhrr]

You been talking to my wife?

She said I had to tighten up first with some CardioTryx and HIIT :/ feels bruh

 

[vasu]

Will this be coming out next week (mid-October) hopefully please pretty please?

Slightly related, I do fasted state cardio for an hour every morning, and I'm on a keto diet. It's pretty hard for me to stay down at 50-60% VO2 max for "optimal fat burn," as my heart rate wants to go higher. Is it a bad idea to go above that range if i'm not carbing up, and want to burn as much fat as possible during that hour? Would I just burn more ketones, or would I start eating up muscle?

Anything in CardioTryx that would help ?

 

[xhrr]

Will this be coming out next week (mid-October) hopefully please pretty please?

Slightly related, I do fasted state cardio for an hour every morning, and I'm on a keto diet. It's pretty hard for me to stay down at 50-60% VO2 max for "optimal fat burn," as my heart rate wants to go higher. Is it a bad idea to go above that range if i'm not carbing up, and want to burn as much fat as possible during that hour? Would I just burn more ketones, or would I start eating up muscle?

Anything in CardioTryx that would help ?

you should stop worrying about staying in fat burning/V02 ranges and do sprints or HIIT

 

[dsade]

Will this be coming out next week (mid-October) hopefully please pretty please?

Slightly related, I do fasted state cardio for an hour every morning, and I'm on a keto diet. It's pretty hard for me to stay down at 50-60% VO2 max for "optimal fat burn," as my heart rate wants to go higher. Is it a bad idea to go above that range if i'm not carbing up, and want to burn as much fat as possible during that hour? Would I just burn more ketones, or would I start eating up muscle?

Anything in CardioTryx that would help ?

This'll probably hit around the 24th, but yeah don't stress about the mythical fat burning zone. Go balls out with intervals.

 

[testosteronet]

This'll probably hit around the 24th, but yeah don't stress about the mythical fat burning zone. Go balls out with intervals.

I can 't wait to see what fills that white on the label. This will go great with my Sleephoria.

 

[vasu]

This'll probably hit around the 24th, but yeah don't stress about the mythical fat burning zone. Go balls out with intervals.

I wish I could do HIIT, but some old knee and foot injuries prevent this

 

[xhrr]

I wish I could do HIIT, but some old knee and foot injuries prevent this

Have access to a rower?

 

[vasu]

Have access to a rower?

Nope, but I was thinking about getting one in the future. All I have at home is an elliptical

 

[dsade]

Right on schedule!

 

[burpees]

<img src="http://anabolicminds.com/forum/attachment.php?attachmentid=89951"/> Right on schedule!

Since it's coming out on my birthday can u tell me where to purchase it before the public

 

[fcbarca12]

Is the 24th when it hits nutraplanet/predator nutrition?

 

[dsade]

Should hit Nutra by the 24th, and Predator a week later

 

[zb126]

How would this work with abliderate ammo on a low to no carb diet? I just picked up ammo from NP and was thinking about logging it but had my eye on this for a while.

 

[dsade]

How would this work with abliderate ammo on a low to no carb diet? I just picked up ammo from NP and was thinking about logging it but had my eye on this for a while.

How much and what type of Cardio are you planning? What are your goals?

 

[zb126]

How much and what type of Cardio are you planning? What are your goals?

I've been doing interval training, probably would continue with that and do a longer run on the weekends. Been doing full body circuit training, and intervals / cardio after. Goal is to recomp, and cut bodyfat particularly around the midsection.

 

[dsade]

I've been doing interval training, probably would continue with that and do a longer run on the weekends. Been doing full body circuit training, and intervals / cardio after. Goal is to recomp, and cut bodyfat particularly around the midsection.

Sounds like this would be perfect for you.

 

[zb126]

Sounds like this would be perfect for you.

forgot to specify how much -- usually around 25-30 minutes of 1:30 on 1:00 walking. Is that enough? I figured ammo would be a good addition for cortisol but wasn't sure if thats enough cardio for cardiotryx

 

[dsade]

forgot to specify how much -- usually around 25-30 minutes of 1:30 on 1:00 walking. Is that enough? I figured ammo would be a good addition for cortisol but wasn't sure if thats enough cardio for cardiotryx

If you are going balls out for your 1:30 (that was assumed since any other interval would be a waste) then that will be plenty.

 

[zb126]

If you are going balls out for your 1:30 (that was assumed since any other interval would be a waste) then that will be plenty.

Well I do skip for the first thirty seconds... hahaha

 

[dsade]

Well I do skip for the first thirty seconds... hahaha

As long as you keep repeating "Cinderella dressed in Yellow" then you are still hardcore.

 

[burpees]

Update ?

 

[dsade]

Scheduled for release around the 28th or 29th.

 

[phantom]

Will prob b doing an ammo cardiotryx stack. Will this still have that rhodiola extract u mentioned?