GreenMachineX
Well-known member
Pretty sure the same way, 1 cap per 60 carbs.
EvoMuse Presents: Slintensity (writeup)
- Thread starter dsade
- Start date
Pretty sure the same way, 1 cap per 60 carbs.
kbayne
Legend
Go back to page one and you can read the write up on the benefits.
Dose a cap prior to carb meals.
rosemont83
Active member
I think I'm gonna try this..
Used recompadrol for my gda previously and this will be my first evomuse product..
Used recompadrol for my gda previously and this will be my first evomuse product..
dsade
NutraPlanet Fanatic
3 slices of large pizza is my border point between 1 cap and 2.
kbayne
Legend
dsade
NutraPlanet Fanatic
Tough call....using standard ALA I honestly wouldn't go over 300mg.
kbayne
Legend
Alright. Again thanks! Going to try 1 cap ALA with 1 cap Slintensity and see how it goes prior to meals.
Geoforce
Well-known member
Piggybacking off Matt the stuff is potent. I saved two caps for the most heinous of cheats.
sinewave3
Member
Please keep us posted on your thoughts.
I have been taking ALA and looking to try a new GDA with it. This new Slintensity looks killer!
kbayne
Legend
Will do
EMPIREMIND
Well-known member
Just dropped a review on slintensity in my minilog.
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GNO
Well-known member
GNO
Well-known member
Sure ... Kind of like the days when you plan on chicken & veggies, but then come home with a pizza?
GreenMachineX
Well-known member
BamBam0319
Well-known member
I will find myself pouring a second bowl of cereal and then realizing I didn't take a cap, so I pop it between bowls. Still seems to work the same!
GNO
Well-known member
Whole box at a time brah :hitwithrock:
BamBam0319
Well-known member
hsk
Active member
Nice grab!
abformulations
Legend
I need too!! Vaca in a 5 weeks 
The1WhoKnocks
New member
Curious as to what people think is the best replacement option while Slintensity is out of stock? I hate to turn away from Evomuse, but I can't afford to purchase a year's supply at once in the few times it's actually available, and when you need something, you need something.
kbayne
Legend
I'm not going to recommend another product in EvoMuse company section, and to be honest, not much else I would recommend that would replace it. You could do your own stack of a few certain ingredients though.
But I know I will be loading up on this when it is available. Got 4 bottles coming now but want to have plenty in the cupboard.
hsk
Active member
I know what you mean. I found a place that had some in stock and grabbed 6 to tide me over till the next run is out.
MidwestBeast
Legend
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For those who are sub'd to this thread -- Slintensity restock and pre-sale!
For those who are sub'd to this thread -- Slintensity restock and pre-sale!
bosskardo
Well-known member
Thanks for the heads up
Ape McGrapes
Well-known member
dsade
NutraPlanet Fanatic
Slintensity as a post workout recovery tool.
PGE2, EP4 and activation of muscle specific stem cells.
Inhibited by NSAIDS, and augmented by berberine, further evidence that Slintensity taken with a carb heavy post workout meal can enhance recovery and increase muscle growth.
Prostaglandin E2 is essential for efficacious skeletal muscle stem-cell function, augmenting regeneration and strength.
Ho ATV, et al. Proc Natl Acad Sci U S A. 2017.
Show full citation
Abstract
Skeletal muscles harbor quiescent muscle-specific stem cells (MuSCs) capable of tissue regeneration throughout life. Muscle injury precipitates a complex inflammatory response in which a multiplicity of cell types, cytokines, and growth factors participate. Here we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that directly targets MuSCs via the EP4 receptor, leading to MuSC expansion. An acute treatment with PGE2 suffices to robustly augment muscle regeneration by either endogenous or transplanted MuSCs. Loss of PGE2 signaling by specific genetic ablation of the EP4 receptor in MuSCs impairs regeneration, leading to decreased muscle force. Inhibition of PGE2 production through nonsteroidal anti-inflammatory drug (NSAID) administration just after injury similarly hinders regeneration and compromises muscle strength. Mechanistically, the PGE2 EP4 interaction causes MuSC expansion by triggering a cAMP/phosphoCREB pathway that activates the proliferation-inducing transcription factor, Nurr1 Our findings reveal that loss of PGE2 signaling to MuSCs during recovery from injury impedes muscle repair and strength. Through such gain- or loss-of-function experiments, we found that PGE2 signaling acts as a rheostat for muscle stem-cell function. Decreased PGE2 signaling due to NSAIDs or increased PGE2 due to exogenous delivery dictates MuSC function, which determines the outcome of regeneration. The markedly enhanced and accelerated repair of damaged muscles following intramuscular delivery of PGE2 suggests a previously unrecognized indication for this therapeutic agent.
PMID 28607093 [PubMed - as supplied by publisher]
PGE2, EP4 and activation of muscle specific stem cells.
Inhibited by NSAIDS, and augmented by berberine, further evidence that Slintensity taken with a carb heavy post workout meal can enhance recovery and increase muscle growth.
Prostaglandin E2 is essential for efficacious skeletal muscle stem-cell function, augmenting regeneration and strength.
Ho ATV, et al. Proc Natl Acad Sci U S A. 2017.
Show full citation
Abstract
Skeletal muscles harbor quiescent muscle-specific stem cells (MuSCs) capable of tissue regeneration throughout life. Muscle injury precipitates a complex inflammatory response in which a multiplicity of cell types, cytokines, and growth factors participate. Here we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that directly targets MuSCs via the EP4 receptor, leading to MuSC expansion. An acute treatment with PGE2 suffices to robustly augment muscle regeneration by either endogenous or transplanted MuSCs. Loss of PGE2 signaling by specific genetic ablation of the EP4 receptor in MuSCs impairs regeneration, leading to decreased muscle force. Inhibition of PGE2 production through nonsteroidal anti-inflammatory drug (NSAID) administration just after injury similarly hinders regeneration and compromises muscle strength. Mechanistically, the PGE2 EP4 interaction causes MuSC expansion by triggering a cAMP/phosphoCREB pathway that activates the proliferation-inducing transcription factor, Nurr1 Our findings reveal that loss of PGE2 signaling to MuSCs during recovery from injury impedes muscle repair and strength. Through such gain- or loss-of-function experiments, we found that PGE2 signaling acts as a rheostat for muscle stem-cell function. Decreased PGE2 signaling due to NSAIDs or increased PGE2 due to exogenous delivery dictates MuSC function, which determines the outcome of regeneration. The markedly enhanced and accelerated repair of damaged muscles following intramuscular delivery of PGE2 suggests a previously unrecognized indication for this therapeutic agent.
PMID 28607093 [PubMed - as supplied by publisher]
dsade
NutraPlanet Fanatic
Mol Biol Rep. 2014 May;41(5):3339-47. doi: 10.1007/s11033-014-3196-4. Epub 2014 Feb 1.
Berberine regulates the expression of E-prostanoid receptors in diabetic rats with nephropathy.
Tang LQ1, Liu S, Zhang ST, Zhu LN, Wang FL.
Author information
Abstract
Diabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients. Effective therapies to prevent the development of this disease and to improve advanced kidney injury are required. Berberine (BBR) has preventive effects on diabetes and its complications. This study is to investigate the effects of BBR on the expression of E-prostanoid receptors (EPs) in rats with high-fat diet and streptozotocin (STZ)-induced DN and underlying molecular mechanisms of BBR on DN rats. DN model was induced in male Sprague-Dawley rats with high-fat diet and low dose of STZ injection. BBR (50, 100, 200 mg/kg/d) were orally administered to rats after STZ injection and conducted for 8 weeks. The levels of interleukin-6 (IL-6) and prostaglandin E2 (PGE2) in renal cortex were measured by enzyme-linked immunosorbent assay. Expression of EPs receptors (EP1-EP4) were determined by western blotting. Remarkable renal damage, hyperglycemia and hyperlipidemia were observed in DN rats. BBR could restore renal functional parameters, suppress alterations in histological and ultrastructural changes in the kidney tissues, improve glucose and lipid metabolism disorders, and increase cAMP levels compared with those of DN model group (Wang et al. in Mol Biol Rep 40:2405-2418, 2013). The level of IL-6 and PGE2 were significantly increased in DN model group compared with normal group, BBR could apparently reduced the level of IL-6 and PGE2. Furthermore, the expression of EP1 and EP3 were both increased and EP4 was lessened in the DN model group compared with normal group, BBR could down-regulate total protein expression of EP1 and EP3 of renal cortex in DN rats and up-regulate the expression of EP4, and there is no significant difference on the expression of EP2 among all groups. These studies demonstrate, for the first time, that BBR exerts renoprotection in high-fat diet and STZ-induced DN rats by modulating the proteins expression of EPs in EP-G protein-cAMP signaling pathway.
Berberine regulates the expression of E-prostanoid receptors in diabetic rats with nephropathy.
Tang LQ1, Liu S, Zhang ST, Zhu LN, Wang FL.
Author information
Abstract
Diabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients. Effective therapies to prevent the development of this disease and to improve advanced kidney injury are required. Berberine (BBR) has preventive effects on diabetes and its complications. This study is to investigate the effects of BBR on the expression of E-prostanoid receptors (EPs) in rats with high-fat diet and streptozotocin (STZ)-induced DN and underlying molecular mechanisms of BBR on DN rats. DN model was induced in male Sprague-Dawley rats with high-fat diet and low dose of STZ injection. BBR (50, 100, 200 mg/kg/d) were orally administered to rats after STZ injection and conducted for 8 weeks. The levels of interleukin-6 (IL-6) and prostaglandin E2 (PGE2) in renal cortex were measured by enzyme-linked immunosorbent assay. Expression of EPs receptors (EP1-EP4) were determined by western blotting. Remarkable renal damage, hyperglycemia and hyperlipidemia were observed in DN rats. BBR could restore renal functional parameters, suppress alterations in histological and ultrastructural changes in the kidney tissues, improve glucose and lipid metabolism disorders, and increase cAMP levels compared with those of DN model group (Wang et al. in Mol Biol Rep 40:2405-2418, 2013). The level of IL-6 and PGE2 were significantly increased in DN model group compared with normal group, BBR could apparently reduced the level of IL-6 and PGE2. Furthermore, the expression of EP1 and EP3 were both increased and EP4 was lessened in the DN model group compared with normal group, BBR could down-regulate total protein expression of EP1 and EP3 of renal cortex in DN rats and up-regulate the expression of EP4, and there is no significant difference on the expression of EP2 among all groups. These studies demonstrate, for the first time, that BBR exerts renoprotection in high-fat diet and STZ-induced DN rats by modulating the proteins expression of EPs in EP-G protein-cAMP signaling pathway.