The Adventures of Judo Josh
- 03-28-2011, 01:37 PM
The Adventures of Judo Josh
This is not going to be a typical log. It wil not be updated often except with notes on dietary, training and supplement changes. Basically I love to experiment and try new things out. One of my favorite quotes is :
Life is an experiment. The more experiments you make the better you become - Ralph Waldo Emerson
- 03-28-2011, 01:42 PM
yeah brother lets do this!!BJJ = life
- 03-28-2011, 01:57 PM
03-28-2011, 01:59 PM
03-28-2011, 02:00 PM
I am taking the week to deload and get some rest. During this time I am going to figure out what I am going to do for the next 12 weeks. The overall goal and focus is going to be fat loss. Currently I am at 188lbs and want to reach 170lbs with as little strength loss as possible.
Sometime today I am going to post up why i believe in fasted training for weight loss and how I plan on furthering that fat loss with supplementation. Then later on in the week I will put up my training and my diet.
As always I am appreciative of feedback. Let me know what you guys think. If I am wrong or off base about something then please correct me and explain how and why I am wrong.
03-28-2011, 02:08 PM
I am going to take a second to highlight what i just posted...
So please don't hesitate to join in and offer your input. Everything is open for discussion.
03-28-2011, 02:13 PM
03-28-2011, 02:44 PM
03-28-2011, 05:43 PM
I have always been a fan of fasted training. What first introduced me to this was a couple post by Mulletsolider on the topic of fasted training along with anabolic pump and the possible fat loss benfits.
I tried this and had great results with it but wanted to figure out more of why it worked and see if I could duplicate it with another cheaper product and in comes Berberine.*
One of the reason why Anabolic Pump was successful for weightloss when combined with fasted training was Anbolic Pumps ability to activate AMPk.
So again, the reason Anabolic Pump was successful for weight loss when combined with fasted training was because it activated AMPk.Anabolic Pump is often conceptualized as merely a supplement of glucose homeostasis. While that's true in part, its true identity is one of energy metabolism as a whole; specifically, modulating energy expenditure and transfer in both fat and muscle cells, via the modulation of energy storage and production mechanisms.
During a long bout of exercise (i.e., an hour long resistance training session) your body's energy homeostasis mechanisms need to take on a more oxidative (the B-oxidation of fatty acids) as opposed to glycolytic (GLUT4 translocation and glucose storage) role. This is due in part to the inability of the body to produce the fuel (glucose) for anabolic processes at the rates needed for anaerobic exercise. In response, your body has in place several mechanisms which prevent the accumulation and synthesis of triglycerides and lipids, and release them into the bloodstream to be oxidized.*
These lipolytic processes actually contribute to the majority of energy transaction in a bout of anaerobic exercise - the oxidation of fatty acids and plasma triglycerides, primarily, provide the energy for resistance training.
The reason I mention all this is Anabolic Pump's fascinating ability to regulate one of the vanguards of oxidative and glycolytic energy consumption - AMPk. AMPk works as an essential gate-keeper of energy production, reacting to extracellular fluctuations of various downstream energy messengers (AMP:ATP ratio included). Its activation is responsible for various roles, including all of the above mentioned.
Using such a product in conjunction with fasted cardio simply utilizes energy which would have been stored anyway. The mere presence of AMPk ensures that the liberated fatty acids and triglycerides will be oxidized as it plays a primary role in not only lipolysis, but the inhibition of lipid, triglyceride, and cholesterol synthesis.*
In terms of blood glucose, you should have circulating plasma levels which are enough to stave off hypoglycaemia, even with the use of Anabolic Pump. As carbohydrates have not been ingested, the presence of Insulin (the main inducer of hypoglycemia) is not necessarily present. Anabolic Pump works through Insulin-reactive, though not dependent, pathways of energy metabolism. The lipolytic role is also enough to provide ample energy.
Now, how does AMPk help with fat loss?
So what does have to do with Berberine?The role of AMPK, both in energy regulation and fat loss, should be highlighted more often. In particular, AMPK activation (either due to insulin sensitizers, insulin-independent glucose-disposal agents, PPAR-gamma activators, adipokines such as leptin and adiponectin, stress, or exercise), has short term and long(er) term effects. Short-term, AMPK activation stimulates cells to switch from active ATP consumption (synthesis of fatty acids and glycerol) to active ATP production (oxidation of fatty acids and glucose). Longer-term, AMPK activation impacts protein and insulin syntheses, gene expression, and appetite regulation. These longer-term effects not only have significance for metabolic processes in muscle cells and adipose tissue, but also in liver, heart, and pancreatic cells. The fat loss effects can be traced to the impact of AMPK activation on insulin metabolism and oxidation of fatty acids. In particular, by stimulating the translocation the GLUT-1 and GLUT-4 proteins, AMPK activation enhances glucose uptake, leading to enhanced glycolysis and elevated ATP production. Furthermore, by inhibiting the action of the enzyme, hormone sensitive lipase (HSL), AMPK activation ensures that the HSL-induced rate of release of fatty acids from triglycerides (that would normally induce higher ATP levels due to oxidized fatty acids) does not exceed the rate of fatty acid oxidation. This serves to hinder fat accumulation. Along these lines, the impact of AMPK activation on peroxisome proliferator-activated receptor gamma (PPAR-gamma), a receptor with primarily adipocyte domicile and activity, leads to increased insulin sensitivity and fatty-acid oxidation in hepatic and skeletal muscle cells. This occurs mainly via the action of the adipokine, adiponectin, that triggers glucose uptake and fatty acid oxidation in skeletal muscle cells, while promoting fatty acid oxidation and inhibiting gluconeogenesis in hepatic cells. In summary, AMPK activation can produce beneficial effects on fat loss via some of the mechanisms addressed earlier.*
Berberine Increases Glucose Uptake Independent of Insulin and also activates AMPk
Berberine stimulates glucose transport through a mechanism distinct from insulin.
Berberine exerts a hypoglycemic effect, but the mechanism remains unknown. In the present study, the effect of berberine on glucose uptake was characterized in 3T3-L1 adipocytes. It was revealed that berberine stimulated glucose uptake in 3T3-L1 adipocytes in a dose- and time-dependent manner with the maximal effect at 12 hours. Glucose uptake was increased by berberine in 3T3-L1 preadipocytes as well. Berberine-stimulated glucose uptake was additive to that of insulin in 3T3-L1 adipocytes, even at the maximal effective concentrations of both components. Unlike insulin, the effect of berberine on glucose uptake was insensitive to wortmannin, an inhibitor of phosphatidylinositol 3-kinase, and SB203580, an inhibitor of p38 mitogen-activated protein kinase. Berberine activated extracellular signal-regulated kinase (ERK) 1/2, but PD98059, an ERK kinase inhibitor, only decreased berberine-stimulated glucose uptake by 32%. Berberine did not induce Ser473 phosphorylation of Akt nor enhance insulin-induced phosphorylation of Akt. Meanwhile, the expression and cellular localization of glucose transporter 4 (GLUT4) were not altered by berberine. Berberine did not increase GLUT1 gene expression. However, genistein, a tyrosine kinase inhibitor, completely blocked berberine-stimulated glucose uptake in 3T3-L1 adipocytes and preadipocytes, suggesting that berberine may induce glucose transport via increasing GLUT1 activity. In addition, berberine increased adenosine monophosphate-activated protein kinase and acetyl-coenzyme A carboxylase phosphorylation. These findings suggest that berberine increases glucose uptake through a mechanism distinct from insulin, and activated adenosine monophosphate-activated protein kinase seems to be involved in the metabolic effect of berberine.”Berberine, a Natural Plant Product, Activates AMP-Activated Protein Kinase With Beneficial Metabolic Effects in Diabetic and Insulin-Resistant States*
Yun S. Lee1,2, Woo S. Kim1,2, Kang H. Kim1,2, Myung J. Yoon1, Hye J. Cho1, Yun Shen3,4, Ji-Ming Ye3, Chul H. Lee5, Won K. Oh5, Chul T. Kim5, Cordula Hohnen-Behrens3, Alison Gosby3, Edward W. Kraegen3, David E. James3, and Jae B. Kim1,2*
Berberine has been shown to have antidiabetic properties, although its mode of action is not known. Here, we have investigated the metabolic effects of berberine in two animal models of insulin resistance and in insulin-responsive cell lines. Berberine reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in db/db mice. Similarly, berberine reduced body weight and plasma triglycerides and improved insulin action in high-fat?fed Wistar rats. Berberine downregulated the expression of genes involved in lipogenesis and upregulated those involved in energy expenditure in adipose tissue and muscle. Berberine treatment resulted in increased AMP-activated protein kinase (AMPK) activity in 3T3-L1 adipocytes and L6 myotubes, increased GLUT4 translocation in L6 cells in a phosphatidylinositol 3' kinase?independent manner, and reduced lipid accumulation in 3T3-L1 adipocytes. These findings suggest that berberine displays beneficial effects in the treatment of diabetes and obesity at least in part via stimulation of AMPK activity.*
Obesity poses a serious health risk contributing to the increased prevalence of a host of other diseases including type 2 diabetes, hyperlipidemia, hypercholesterolemia, and hypertension (1,2). Peripheral insulin resistance, which is often associated with obesity, is one of the earliest detectable defects identified in individuals at risk of type 2 diabetes. For this reason, pharmacologic agents that overcome insulin resistance, so-called insulin-sensitizing agents, have received considerable attention. In recent years, several major insulin-sensitizing agents have been developed, including the thiazolidinediones (TZDs) (3) and metformin (4). Both of these agents are thought to have beneficial effects, at least in part, by activating the stress-activated kinase AMP-activated protein kinase (AMPK) (5,6). AMPK is activated under a variety of conditions that signify cellular stress, usually in response to a change in the intracellular ATP-to-AMP ratio. Active AMPK orchestrates a variety of metabolic processes, most of which lead to reduced energy storage and increased energy production. TZDs and metformin are thought to activate AMPK via discrete mechanisms; TZDs stimulate the proliferation of small adipocytes that secrete adipokines such as adiponectin, which have been shown to stimulate AMPK activity in muscle and liver cells (7). Conversely, it appears that metformin activates AMPK directly via an ill-defined mechanism (8). These studies emphasize the potential utility of targeting the AMPK pathway in the treatment of type 2 diabetes and obesity.*
The use of natural products for the treatment of metabolic diseases has not been explored in depth despite the fact that a number of modern oral hypoglycemic agents such as metformin are derivatives of natural plant products (9,10). Although several traditional medicines have been reported to have antidiabetic effects (10), the molecular targets of such compounds have not been revealed, and a careful analysis of their mode of action in animal models has not been undertaken. In the present study, we have focused on berberine because this natural product has been reported in the Chinese literature and several recent studies (11?14) to have beneficial effects in human type 2 diabetes, although its mechanism of action is not known. Here, we show that in vivo administration of berberine has insulin sensitizing as well as weight- and lipid-lowering properties in both db/db mice and in high-fat?fed rats. Strikingly, berberine acutely stimulated AMPK activity in both myotubes and adipocytes in vitro, contributing to enhanced GLUT4 translocation in myotubes and reduced lipid mass in adipocytes. Based on these studies, we propose that berberine may have a major application as a new treatment for obesity and/or insulin resistance in humans.”Berberine is a plant alkaloid used in traditional Chinese medicine and has been reported to have antihyperglycemic activity in NIDDM patients. However, the molecular basis for this action is yet to be elucidated. Here we investigate the effects and signaling pathways of berberine on L6 rat skeletal muscles. Our study demonstrates that berberine stimulates glucose uptake in a time- and dose-dependent manner. Intriguingly, berberine-stimulated glucose uptake does not vary as insulin concentration increases, and could not be blocked by the PI 3-kinase inhibitor wortmannin. Berberine only weakly stimulates the phosphorylation of Akt/PKB, a key molecule in the insulin signaling pathway, but strongly promotes the phosphorylation of AMPK and p38 MAPK. The effects of berberine are not a result of pro-oxidant action, but a consequence of an increased cellular AMP:ATP ratio. Moreover, berberine-stimulated glucose uptake is inhibited by the AMPK inhibitor Compound C and the p38 MAPK inhibitor SB202190. Inhibition of AMPK reduces p38 MAPK phosphorylation, suggesting that AMPK lies upstream of p38 MAPK. These results suggest that berberine circumvents insulin signaling pathways and stimulates glucose uptake through the AMP-AMPK-p38 MAPK pathway, which may account for the antihyperglycemic effects of this drug.So the plan is fasted training combined with barberine should help with my fat loss goal.Berberine has been shown to have antidiabetic properties, although its mode of action is not known. Here, we have investigated the metabolic effects of berberine in two animal models of insulin resistance and in insulin-responsive cell lines. Berberine reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in db/db mice. Similarly, berberine reduced body weight and plasma triglycerides and improved insulin action in high-fat-fed Wistar rats. Berberine downregulated the expression of genes involved in lipogenesis and upregulated those involved in energy expenditure in adipose tissue and muscle. Berberine treatment resulted in increased AMP-activated protein kinase (AMPK) activity in 3T3-L1 adipocytes and L6 myotubes, increased GLUT4 translocation in L6 cells in a phosphatidylinositol 3' kinase-independent manner, and reduced lipid accumulation in 3T3-L1 adipocytes. These findings suggest that berberine displays beneficial effects in the treatment of diabetes and obesity at least in part via stimulation of AMPK activity.
03-28-2011, 05:52 PM
Either way I still want to continue you my plan of fasted training + barberine and see what kind of results I get.
As for my references on fasted training..
Exercise in the fasted state facilitates fibre type-specific intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans.
De Bock K, Richter EA, Russell AP, Eijnde BO, Derave W, Ramaekers M, Koninckx E, Léger B, Verhaeghe J, Hespel P.
Exercise Physiology and Biomechanics Laboratory, Faculty of Kinesiology and Rehabilitation Sciences, K.U.Leuven, Tervuursevest 101, B-3001 Leuven (Heverlee), Belgium.
The effects were compared of exercise in the fasted state and exercise with a high rate of carbohydrate intake on intramyocellular triglyceride (IMTG) and glycogen content of human muscle. Using a randomized crossover study design, nine young healthy volunteers participated in two experimental sessions with an interval of 3 weeks. In each session subjects performed 2 h of constant-load bicycle exercise (approximately 75% ), followed by 4 h of controlled recovery. On one occasion they exercised after an overnight fast (F), and on the other (CHO) they received carbohydrates before ( approximately 150 g) and during (1 g (kg bw)(-1) h(-1)) exercise. In both conditions, subjects ingested 5 g carbohydrates per kg body weight during recovery. Fibre type-specific relative IMTG content was determined by Oil red O staining in needle biopsies from m. vastus lateralis before, immediately after and 4 h after exercise. During F but not during CHO, the exercise bout decreased IMTG content in type I fibres from 18 +/- 2% to 6 +/- 2% (P = 0.007) area lipid staining. Conversely, during recovery, IMTG in type I fibres decreased from 15 +/- 2% to 10 +/- 2% in CHO, but did not change in F. Neither exercise nor recovery changed IMTG in type IIa fibres in any experimental condition. Exercise-induced net glycogen breakdown was similar in F and CHO. However, compared with CHO (11.0 +/- 7.8 mmol kg(-1) h(-1)), mean rate of postexercise muscle glycogen resynthesis was 3-fold greater in F (32.9 +/- 2.7 mmol kg(-1) h(-1), P = 0.01). Furthermore, oral glucose loading during recovery increased plasma insulin markedly more in F (+46.80 microU ml(-1)) than in CHO (+14.63 microU ml(-1), P = 0.02). We conclude that IMTG breakdown during prolonged submaximal exercise in the fasted state takes place predominantly in type I fibres and that this breakdown is prevented in the CHO-fed state. Furthermore, facilitated glucose-induced insulin secretion may contribute to enhanced muscle glycogen resynthesis following exercise in the fasted state.The fact that there is new research saying there is no difference in fat loss between fasted training and regular training is interesting. I feel I have always experienced a better body compostion when training fasted compared to when i was training mid-day. Although, there could have been many factors that could be contributed to the results.Intramyocellular lipids form an important substrate source during moderate intensity exercise in endurance-trained males in a fasted state.
van Loon LJ, Koopman R, Stegen JH, Wagenmakers AJ, Keizer HA, Saris WH.
Nutrition Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. firstname.lastname@example.org
Both stable isotope methodology and fluorescence microscopy were applied to define the use of intramuscular triglyceride (IMTG) stores as a substrate source during exercise on a whole-body as well as on a fibre type-specific intramyocellular level in trained male cyclists. Following an overnight fast, eight subjects were studied at rest, during 120 min of moderate intensity exercise (60 % maximal oxygen uptake capacity (VO2,max)) and 120 min of post-exercise recovery. Continuous infusions of [U-13C]palmitate and [6,6-2H2]glucose were administered at rest and during subsequent exercise to quantify whole-body plasma free fatty acid (FFA) and glucose oxidation rates and the contribution of other fat sources (sum of muscle- plus lipoprotein-derived TG) and muscle glycogen to total energy expenditure. Fibre type-specific intramyocellular lipid content was determined in muscle biopsy samples collected before, immediately after and 2 h after exercise. At rest, fat oxidation provided 66 +/- 5 % of total energy expenditure, with FFA and other fat sources contributing 48 +/- 6 and 17 +/- 3 %, respectively. FFA oxidation rates increased during exercise, and correlated well with the change in plasma FFA concentrations. Both the use of other fat sources and muscle glycogen declined with the duration of exercise, whereas plasma glucose production and utilisation increased (P < 0.001). On average, FFA, other fat sources, plasma glucose and muscle glycogen contributed 28 +/- 3, 15 +/- 2, 12 +/- 1 and 45 +/- 4 % to total energy expenditure during exercise, respectively. Fluorescence microscopy revealed a 62 +/- 7 % net decline in muscle lipid content following exercise in the type I fibres only, with no subsequent change during recovery. We conclude that IMTG stores form an important substrate source during moderate intensity exercise in endurance-trained male athletes following an overnight fast, with the oxidation rate of muscle- plus lipoprotein-derived TG being decreased with the duration of exercise.
PMID: 14514877 [PubMed - indexed for MEDLINE]
I see science as something that is always changing. What is thought to be true one day can easily be disproven another day. This is why it really baffles my mind when members of the forum get so crazy over what a study says or doesn't say. While yes a study could help reason if a product will work for you or have a desired effect on you, it isn't 100% conclusive. Meaning it doesn't always work the way it is soupposed to. The human body is an insanely complicated thing and we are still discovering new things about ourselves every day. This is the main reason why I like to try new things out. To say "thats not going to work" or to say "this will DEFINETELY work" based off studies is ludacris. One has to try it out and see if the desired results are obtained in order to say if it worked or not for them.
The way I see it at least
Anyway please if you have that information I would like to give it a read
03-28-2011, 05:56 PM
Also to note on barberine it shows to have anti-inflammatory activity along with potential antiproliferative effect on cancer cells.
Laboratory studies of berberine used alone and in combination with 1,3-bis(2-chloroethyl)-1-nitrosourea to treat malignant brain tumors.
Zhang RX, Dougherty DV, Rosenblum ML.
Department of Neurosurgery, Second Affiliated Hospital, Hebei Medical College, Shijiazhuang.
Berberine was evaluated for antitumor activity against malignant brain tumors. In addition, studies on combination of berberine with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) were done. Several experimental approaches were used. In vitro studies were performed on a series of 6 human malignant brain tumor cell lines and rat 9L brain tumor cells (gliosarcoma) by using a colony forming efficiency (CFE) assay. 9L was also evaluated by a sister chromatid exchange (SCE) assay. In addition, in vivo treatment of intracerebral 9L solid brain tumors was analyzed by CFE assay. Berberine used alone at a dose of 150 micrograms/ml showed an average of 91% cell kill (1.08 log kill) for the 6 malignant brain tumor cell lines. On the average, BCNU alone at a dose of 23 microM gave a 43% cell kill (0.24 log kill). Treatment with a combination of berberine and BCNU at 23 microM showed additive effects with an average of 97% cell kill (1.55 log kill). The relative number of SCEs for 9L cells was increased 2.7 times over background following in vitro treatment with 150 micrograms/ml berberine. Following in vivo treatment of animals harboring solid 9L brain tumors with 10 mg/kg of berberine, an 80.9% cell kill (0.69 log kill) was noted. This activity is equivalent to treatment with 1/3 LD10 dose of BCNU (4.44 mg/kg). In vivo combination treatment with berberine and BCNU showed additive cytotoxicity. Using a BCNU-resistant 9L subline (9L-2), treatment with berberine in combination with BCNU also demonstrated additive cytotoxicity. In conclusion, our results indicate that berberine has potent antitumor activity against human and rat malignant brain tumors.So worst case if the barberine doesn't help with the fat loss there are still other general health benefits achieved by supplementing with it.The anti-inflammatory potential of berberine in vitro and in vivo.
Kuo CL, Chi CW, Liu TY.
Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan, ROC.
Berberine, an isoquinoline alkaloid, has a wide range of pharmacological effects, including anti-inflammation, yet the exact mechanism is unknown. Because cyclooxygenase-2 (COX-2) plays a key role in prostaglandins (PGs) synthesis, which is elevated in inflammation, we examined whether the anti-inflammatory mechanism of berberine is mediated through COX-2 regulation. In oral cancer cell line OC2 and KB cells, a 12 h berberine treatment (1, 10, and 100 microM) reduced prostaglandin E2 (PGE2) production dose-dependently with or without 12-O-tetradecanoylphorbol-13-acetate (TPA, 10 nM) induction. This berberine induced effect occurred rapidly (3 h) as a result of reduced COX-2 protein, but not enzyme activity. The electrophoretic mobility shift assay revealed that activator protein 1 (AP-1) binding was decreased in oral cancer cells treated with berberine for 2 h. Further analysis showed that berberine inhibited AP-1 binding directly. These anti-inflammatory effects paralleled to the in vivo results where berberine pretreatment of Wistar rat inhibited the production of exudates and PGE2 in carrageenan induced air pouch.
But with everything good comes a bad side..
With the potential fat loss effects from AMPk comes the idea that AMPk activation will lead to a decrease in protein synthesis.
What is speculated is that supplementing with leucine this problem can be circumvented. Can leucine's activation of mTOR override the AMPk suppression of mTOR??In a rat model, AMPk activation has been shown to suppress protein synthesis by down regulating another molecular target called the mammalian target of rapomyacin, or mTOR4 which is heavily involved in protein synthesis.
Although this hasn't been shown in humans to my knowledge, the general picture is that AMPk activation turns off energetically costly processes (such as protein synthesis) and turns on energy producing processes (such as glucose and fat oxidation).
So an AMPk inhibition of skeletal muscle protein synthesis would be consistent in humans. I'll note that years ago, Dan Duchaine commented how insulin sensitizers (of which metformin was one of the ones in use) caused muscle loss and I have to wonder if this isn't part of the mechanism.
Currently I supplement with XTEND intra-workout so hopefully this will help, maybe some extra leucine will help a little more. My concern currently is fat loss overall so I am not too concerned with this issue but for those looking to bulk this theory might not be the best route for growth.
03-28-2011, 05:59 PM
Oh I forgot to add in addition to the barberine I plan on starting to take Relora from NOW foods.
Relora is a prop blend of Magnolia and Phellodendron extract and is marketed by NOW food as a product to help reduce cortisol.
I plan on taking the Relora with all glucose uptake products. Increased glucose uptake combined with cortisol control might lead to increased glycogen storage and less muscle protein breakdown I think.
So this will also be thrown along in the mix of supplementsEffect of a proprietary Magnolia and Phellodendron extract on weight management: a pilot, double-blind, placebo-controlled clinical trial.
Garrison R, Chambliss WG.
Next Pharmaceuticals, Inc, Irvine, CA, USA.
OBJECTIVE: To determine the efficacy of a dietary supplement ingredient containing proprietary extracts of Magnolia officinalis and Phellodendron amurense in helping overweight, otherwise healthy, premenopausal female adults, who typically eat more in stressful situations manage their body weight. DESIGN: Randomized, double-blind, placebo-controlled clinical study. Setting Miami Research Associates, a clinical research organization consisting of 32 board-certified physicians, Miami, Fla. SUBJECTS: Healthy, overweight (BMI 25 to 34.9), premenopausal female adults, between the ages of 20 and 50 years, who typically eat more in response to stressful situations and scored above the national mean for women on self-reported anxiety. INTERVENTIONS: Two-hundred-fifty-mg capsules or identical placebo capsules 3 times a day for 6 weeks. MAIN OUTCOME MEASURES: Salivary cortisol levels, weight change, psychological measures of stress and anxiety. RESULTS: Twenty-eight subjects completed the study. Extracts of M officinalis and P amurense were well tolerated. There was a significant weight gain during the study for the placebo group (P < ,01), but no significant weight gain for the group receiving extracts of M officinalis and P amurense (P < .89). Paired t-tests comparing baseline to post-treatment weight showed an average gain of 1.5 kg in the placebo group and no change in the treatment group (P = .89). When groups were divided into gainers (ie, participants who gained at least 1 kg or more) and maintainers or losers, 75% of the control group were gainers versus 37% of the treatment group (P < .04). There was a nonsignificant trend for lowered average cortisol in the treatment group at the end of the study (group X time interaction, F = 1.1, P < .15). This difference was due to a treatment effect on evening cortisol. There was a marginally significant group X time interaction (P = .06), showing the treatment group tended to have lower levels of cortisol in the evening, whereas the control group tended to have higher levels of cortisol in the evening. Bedtime cortisol levels decreased in the treatment group and increased in the placebo group. Participants in both the treatment and placebo groups had improved scores on a number of psychological measures during the study. There was a correlation between perceived stress and weight change. CONCLUSION: The results of this pilot clinical study indicate that obese subjects who eat in response to stress may benefit from taking a dietary supplement ingredient containing proprietary extracts of M officinalis and P amurense. The mechanism of action appears to be through reduction of cortisol levels and possibly perceived stress, thereby helping participants maintain body weight. The sample size was small, however, and there was higher attrition in the control group than in the treatment group.”
03-28-2011, 07:04 PM
03-28-2011, 07:12 PM
I am in
How am I already behind in this log
03-28-2011, 07:17 PM
Does Cardio After an Overnight Fast Maximize Fat Loss?
Doctor Layne Norton's thoughts on the topic: New Research on Fasted Cardio
As far as research, it doesn't mean that it's true for everyone. Like I said before, there are always going to be anomalies that do not fit what should be.
I personally prefer to train fasted like you, but I HAVE done the unfasted training (i.e. when I was cycling and if I do 2-a-day training sessions), and I honestly don't notice a difference re fat loss or body composition with training fasted than unfasted.
03-28-2011, 07:43 PM
03-28-2011, 07:49 PM
03-28-2011, 07:54 PM
03-28-2011, 08:21 PM
I just picked up these 2 books and will be reading them before bed
Also will be listening to this CD
I feel asleep to the Delta CD and havent ever experienced sleep that deep before! I also used the Alpha CD during a soak in the tub with some Epsom salt and lavender oil and got so zoned out in a day dream i forgot where i was. I dont know if it is the CDs are THAT effective or I am just that susceptible to it.
Gonna start reading from the two books and listening to the CD as part of my nightly ritual, will probably be stealing you style and posting up quotes from them
I will definitely be giving those two links you posted a read. Interested to see their reasoning behind it. I am a fan of Layne Norton as I base a lot of by diet around things he has said.
03-28-2011, 09:29 PM
Ok I'm al caught up my head hurts tho, lol
03-28-2011, 10:11 PM
In for the ride, looks like I will learn a thing or two by the end of this
03-28-2011, 10:50 PM
Im in bud
E-Pharm Rep... PM me with any questions or concerns
03-29-2011, 08:32 AM
Gonna have to go to the bookstore and find a copy of bioligy for dummies.
Taste the rainbow.
03-29-2011, 09:27 AM
the delta CD's are cool, i bought my gf both of them. some of it gets really weird though so you gotta find the part you like to fall asleep to
BJJ = life
03-29-2011, 01:55 PM
So far everything is right on and as far as fasted training burning more fat, not so much. The only reason why it could have this effect is due to it typically being first thing in the morning and lifting weights that early will raise your metabolism longer then at night due to natural sleep patterns slowing it down a bit.
I do think that berberine in and of itself will help with fat loss for sure. Also not only leucine but L-Glutamine will increase protein synthesis. The other factor would be how severe, and over what period of time does the berberine slow the protein synthesis down? Could it be possible that the other anabolic effects of the berberine outweigh this when eating in order to gain weight. Obviously more protein will reach the muscle so is the synthesis actually blunted enough that the increased nutrient shuttling effect does not still over power the decrease in protein synthesis? Kind of like with Steady state low intensity cardio, it burns a slightly higher percent of calories from fat than does interval training but only slightly, however if you burn 300 cals from SS cardio and an extra 150 calories doing HIIT, that minimal percent higher fat burn during low intensity aerobics wont add up to how much fat was burned during the HIIT, nor the larger rise in metabolism brought on by the intense activity. So the big picture is actually more important than the individual pieces.
Live Hard, Laugh Hard, Love Hard and Heal Fast! - KLEEN
Olympus Labs Rep - check us out at Olympus-Labs.com
03-29-2011, 02:00 PM
I was going to mention the delta cd's and there use of classical as being a fallacy as well but i see that it has some type of Brain pulse added into the mix. Otherwise there is not truth to the addage that Classical music (specifically) increases inteligence or brain activity this theory was disproved and then broadened out to any type or style of music. So heavy metal stimulates your brain just as much, rap, folk, whatever your flavor is you will get the same benefit. It is simply the auditory stimulation and the feeling/stimulation you personally get from the music. Curious about the "pulse" thing mentioned and will have to look into that.
Live Hard, Laugh Hard, Love Hard and Heal Fast! - KLEEN
Olympus Labs Rep - check us out at Olympus-Labs.com
03-29-2011, 02:31 PM
03-29-2011, 02:51 PM
I know the information can be a little overwhelming at times. I get confused all the freaking time when trying to make sense of something. If at anytime I post something and it doesn't make sense or you don't understand it just let me know and I will try my best to try and interrupt it for you. Questioning is a good thing, it can cause me to go back and re-read something and then I may realize I misread or misinturpted some data or something.
In turn I will occisonally post up information myself and will ask you guys to give me your thoughts on it.
As for the biology book, google works wonders! I only had about 2-3 formal classes in bio at college. Mist of my information I get from online and when I don't understand something I just try and break it down into pieces and figure them out and hopefully the big picture will come together.
03-29-2011, 03:13 PM
I was completely shocked when I felt how powerful they were. I was a huge skeptic of it actually doing anything and thought it was a bunch of hoopla! But after it was suggested to me from a member here I figured hey I will give it a shot.
I didn't get the sounds one, the CD set I bought is classical symphony type music and the sounds are supposed to be in the background.
I want to try the Beta CD. I was thinking maybe hooking up the CD to my alarm clock and playing it while I get ready in the morning and see if it helps me be more productive in the morning and not drag my feet like I usually do in the morning. I have tried the Alpha and Delta CDs and they are awesome!
03-29-2011, 03:19 PM
I am not too sure on how they work exactly I never really looked too much into it. As I said to Anton I didn't even think that were going to work at all. Since using them I might be more interested to see exactly how they work.
The website for more information is http://www.neuroacoustic.com/
And here is a link for their articles on it http://www.neuroacoustic.com/articles.html
If you look around the site and find any info please share with us
03-29-2011, 03:33 PM
The reason I thought fasted training burned fat more was due to the lack of energy (food) available to the body which would switch your muscles from from glucose to triglycerides as its primary energy source. This would mean your body would be literately burning fat stores for its energy. The studies I posted above support this claim HOWEVER both studies were done on endurance athletes. In both of them I believe the individuals were cycling as there workout. Now the question I could have is would cycling be anaerobic or aerobic? And what effect would this have on fuel used? Would it even matter?
I still havent read the articles Rosie posted earlier but I plan on reading them on my next day off (thursday) and will be commenting on them then.
As for the Barberine, its isnt the barberine itself it is that barberine is said to activate AMPk. Its the AMPk that is believed to effect protein synthesis, to what extent I dont know. Furthermore I dont think there were any human studies that support this, only animal ones (not 100% sure though) Would Leucine help combat it? Don't know? The excerpt I posted on AMPk was from Lyle McDonald and he suggested to supplement with Leucine to combat the AMPk effect of protein synthesis.
Thanks for the advice of the glutamine! I didnt know glutamine had the same effect leucine had on protein synthesis. Do you think I would need more than what is in 4 scoops of Xtend? I have some bulk glut and might just toss a couple extra grams into my amino drink
03-29-2011, 06:52 PM
03-30-2011, 10:21 AM
Subbed of course, always love reading your logs
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03-30-2011, 10:37 AM
im personally on the fence about the whole glycogen usage. i eat paleo and eat complex carbs (potatoes) maybe once a week at most. i train BJJ and wrestling 6-7 days a week and im not feeling any lack of energy. last night we trained and rolled from 6:30 until 9 something and I was still ready to go afterwards. i havent had a complex carb in days. i feel like carbs besides vegetables arent really that important. i mean yes im not riding a bicycle for 80 miles but our training is super intense and burns up to 1000 cals an hour.
just yesterday i saw an Oxygen magazine at the gym and in there some doctor was recommending women to take 60-80 grams of carbs with their protein shake if they lifted weights for an hour. i feel like thats excessive, especially for a 120 lb woman. my girlfriend gains weight with that many carbs PWO and we got her at her best body composition with just vegetables for carbs. those carbs pwo jack the insulin too much which isnt good for fat loss which is what most of women that read Oxygen are concerned with. another "expert" in there suggested eating complex carbs with EVERY meal.
sure there are exceptions to the rule like Rosie who eats 400g of carbs a day and stays super ripped but for general population this glycogen refilling is overrated. i can get just as much of an insulin release from beef/eggs/fish if im bodybuilding without all the blood sugar issues.
BJJ = life
03-30-2011, 11:25 AM
A couple of things I'd like to add to the log:
1. The NSCA's journal is crap. Respected for some reason, but, just like their tests and stances, they're pretty much crap.
2. Beware on taking berberine for an extended period of time. It can mess with the bacteria in your gut and subsequent digestion. I would assume that probiotics would help, but I can't say for sure.
3. Substrate usage during exercise is dependent on the subject. Depending on your Respiratory Exchange Rate (RER), your substrate usage will vary.
M.Ed. Ex Phys
03-30-2011, 02:34 PM
Same for the gentlemen above, who said the carbs were not needed for performance. Once the body is efficient at burning fats for energy you should not feel a dip in energy from lack of carbs if anything more sustainable energy can probably be achieved. Never saw a Lioness carb up after a kill. Moving 300+ lbs around at high speeds then wrestling the prey down would definitely be considered explosive activity. I am just now learning that beef causes a higher insulin release than many carbs adds to that assertion that the nutrients are still getting shuttled into the muscle for speedy recovery without starchy carbs.
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03-30-2011, 03:40 PM
BJJ = life
03-30-2011, 10:34 PM
Man, I am just going to have to promise myself I catch up on all this over the weekend, lots of good minds in this thread.
03-31-2011, 02:34 PM
- 5'10" 205 lbs.
- Join Date
- Jun 2007
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well, as far as fasted training helping with fat loss, I wasn't ever quite sure of that, but what I do know is that the studies that people refer to about protein + carbs postworkout being better for building muscle were actually done with fasted training. So that seems to make sense to me at the very least.
as far as the music goes, look at idosing.
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03-31-2011, 09:22 PM
As far as the links you posted, I am not a member of the NSCA and couldn't read that one and I am downloading the SHR episode now and will listen to it on my drive to and from work tomorrow. I did do a little more searching on it and found some postings of Layne Norton on another forum in regards to fasted training. In one of his postings he references this study
The bold part confuses me. The way I am reading it is the subjects were given a carb drink during the exercise regardless if they were fasted prior or not. Also would the fact that all of their diets were 65% carbs, 20% fat, & 15% protein effect the results at all? Your typical weightlifter would probably have a way different macro ratio and I am not sure how that would effect the results. For a low carb person wouldn't their body be more efficient at burning stored body fat for energy, so when put in a postion of needing energy the body would be able to turn to fat for fuel more efficiently than a person whose body is used to having carbs as their primary source of energy?1: J Appl Physiol. 2008 Apr;104(4):1045-55. Epub 2008 Feb 14.
Effect of training in the fasted state on metabolic responses during exercise with carbohydrate intake.
De Bock K, Derave W, Eijnde BO, Hesselink MK, Koninckx E, Rose AJ, Schrauwen P, Bonen A, Richter EA, Hespel P.
Research Center for Exercise and Health, F.A.B.E.R. - K.U.Leuven, Tervuursevest 101, B-3001 Leuven Heverlee, Belgium.
Skeletal muscle gene response to exercise depends on nutritional status during and after exercise, but it is unknown whether muscle adaptations to endurance training are affected by nutritional status during training sessions. Therefore, this study investigated the effect of an endurance training program (6 wk, 3 day/wk, 1-2 h, 75% of peak Vo(2)) in moderately active males. They trained in the fasted (F; n = 10) or carbohydrate-fed state (CHO; n = 10) while receiving a standardized diet [65 percent of total energy intake (En) from carbohydrates, 20%En fat, 15%En protein]. Before and after the training period, substrate use during a 2-h exercise bout was determined. During these experimental sessions, all subjects were in a fed condition and received extra carbohydrates (1 g.kg body wt(-1) .h(-1)). Peak Vo(2) (+7%), succinate dehydrogenase activity, GLUT4, and hexokinase II content were similarly increased between F and CHO. Fatty acid binding protein (FABPm) content increased significantly in F (P = 0.007). Intramyocellular triglyceride content (IMCL) remained unchanged in both groups. After training, pre-exercise glycogen content was higher in CHO (545 +/- 19 mmol/kg dry wt; P = 0.02), but not in F (434 +/- 32 mmol/kg dry wt; P = 0.23). For a given initial glycogen content, F blunted exercise-induced glycogen breakdown when compared with CHO (P = 0.04). Neither IMCL breakdown (P = 0.23) nor fat oxidation rates during exercise were altered by training. Thus short-term training elicits similar adaptations in peak Vo(2) whether carried out in the fasted or carbohydrate-fed state. Although there was a decrease in exercise-induced glycogen breakdown and an increase in proteins involved in fat handling after fasting training, fat oxidation during exercise with carbohydrate intake was not changed.
I also found this quote by LayneSo if his concern is that the fasted state workout would suppress protein synthesis wouldn't supplementing with a BCAA mix either before, during, or both counteract that?"Our lab has shown an overnight fast will depress protein synthesis and that exercise will depress protein synthesis further from baseline."
I think I will use this to start branching into my next plan which is my intra-workout nutrition.
Previously I have always used Xtend during all training sessions. I love xtend and believe that while I am in a calorie deficit the extra aminos taken during and immediately after my workouts help me retain muscle and it prevents catabolism. I have noticed a lot of peoples fear with fasted workout is the body will start to break down muscle for its glucose needs. I think by taking in the aminos you prevent this from happening..
But here raises a couple more questions:
Does taking in aminos then provide fuel for your workout and prevent the fat loss? If so to what extent?
If the aminos are being used strictly for energy during a workout then is its function no different than say Gatorade?
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