Vitamin K is an essential vitamin that is one of the four fat-soluble vitamins. Vitamin K comes in different forms (vitamers) that are either phylloquinones (vitamin K1) or menaquinones (vitamin K2 which is abbreviated as MK-x.) The three forms of vitamin K that can be utilized by the body are vitamin K1 and dual forms of K2 (MK-4 and MK-7.) The health benefits of vitamin k seem endless and include regression of preformed arterial calcification, maintenance of bone density, and promotion of a healthy heart and vascular system. As with all of my articles, I do not feel making claims on a product or ingredient is good enough. Instead, we must dig into the research…and luckily for us. vitamin k has well over 400 studies that I have personally read over the years. The first one I wish to look at is from Knapen et al and looked at a three-year low-dose menaquinone-7 supplementation and how it helps decrease bone loss. The results were that MK-7 intake significantly improved vitamin K status and decreased the age-related decline in BMC and BMD at the lumbar spine and femoral neck, but not at the total hip. Bone strength was also favorably affected by MK-7. MK-7 significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the vertebrae. This lead to their conclusion that MK-7 supplements may help to prevent bone loss (1.)
But even more importantly that aiding in bone mineral density is its ability to fight atherosclerosis (as this is my main reason for recommending this vitamin to bodybuilders that are using potentially harsh supplements that can cause atherosclerosis over time.) Jennifer Ming has talked extensively on this topic stating that “numerous studies have demonstrated that people with higher intakes of vitamin K2 have a reduced risk for cardiovascular disease. Intrigued by this connection, Polish researchers from the Medical University at Lodz teamed up with researchers from Maastricht University in the Netherlands and Poland’s International Science and Health Foundation to determine if vitamin K2 supplementation could reduce the progression of existing atherosclerosis. The scientists evaluated the progression of atherosclerosis in a group of 42 patients with chronic kidney disease. These patients were ideal for this type of study because they are known to experience a rapid reduction in bone mineral density (a measure of bone strength) as a result of calcium losses from bone. They are also subject to equally excessive deposits of calcium in tissues where it doesn’t belong—particularly in the walls of major arteries. For the study, the subjects were divided into two groups. One group received vitamin K2 (90 mcg per day) plus vitamin D3 (400 IU per day). The second group received only vitamin D3 (400 IU per day). After nine months, it was already evident that the subjects taking the combination of vitamins K2 and D3 experienced a slower progression of the Common Carotid Intima Media Thickness, which is a good indicator of atherosclerosis, as well as a predictor of cardiovascular episodes and death. Specifically, the thickness of the carotid (major neck) arteries increased by 13.73% in the group taking vitamin D3, but in the group taking both vitamins, it only increased by 6.32%. Remember that the group of subjects in this study have a tendency for an increased carotid intima media thickness as a result of calcium losses from bone. In addition, subjects taking the combination of vitamins K2 and D3 showed a reduction in carotid artery calcification score in all patients except those with the highest scores at baseline. This indicates that calcium was staying in the bones, where it belongs, and out of the arteries. These results clearly indicated that vitamin K2 does indeed reduce the progression of atherosclerosis” (2, 3, 4.)
Vitamin K clearly has a place on everyone’s health supplement shelf and has more than enough literature and actual application to back that statement up. In terms of practical application, we need to look at a few different minimum effective dosages for the various forms of vitamin k. For phylloquinone (vitamin K1), the minimum effective dosage is 50mcgs. For short chain menaquinones (MK-4), the minimum effective dosage is 1500mcgs. For the longer chain menaquinones (MK-7, MK-8, and MK-9), the minimum effective dose is around 100-250mcgs. So be sure to purchase a vitamin k product that contains the effective forms of vitamin k and in the proper dosages.
Alex Kikel
MS, PES, CPT, Speed and Explosion Specialist Level II
Owner of www.theprepcoach.com
References
Increased power output from muscle carnosine was shown by one of the more popular studies from Baguet et al in rowing performance. Chronic oral β-alanine supplementation is shown to elevate muscle carnosine content and improve anaerobic exercise performance during some laboratory tests, mainly in the untrained. It remains to be determined whether carnosine loading can improve single competition-like events in elite athletes. The aims of the present study were to investigate if performance is related to the muscle carnosine content and if β-alanine supplementation improves performance in highly trained rowers. Eighteen Belgian elite rowers were supplemented for 7 wk with either placebo or β-alanine (5 g/day). Before and following supplementation, muscle carnosine content in soleus and gastrocnemius medialis was measured by proton magnetic resonance spectroscopy ((1)H-MRS) and the performance was evaluated in a 2,000-m ergometer test. At baseline, there was a strong positive correlation between 100-, 500-, 2,000-, and 6,000-m speed and muscle carnosine content. After β-alanine supplementation, the carnosine content increased by 45.3% in soleus and 28.2% in gastrocnemius. Following supplementation, the β-alanine group was 4.3 s faster than the placebo group, whereas before supplementation they were 0.3 s slower (P = 0.07). Muscle carnosine elevation was positively correlated to 2,000-m performance enhancement (P = 0.042 and r = 0.498). It can be concluded that the positive correlation between baseline muscle carnosine levels and rowing performance and the positive correlation between changes in muscle carnosine and performance improvement suggest that muscle carnosine is a new determinant of rowing performance (1.)
Hobson et al conducted a very important bit of literature on beta alanine supplementation and its direct effects on exercise performance in a meta analysis. They stated that “due to the well-defined role of β-alanine as a substrate of carnosine (a major contributor to H+ buffering during high-intensity exercise), β-alanine is fast becoming a popular ergogenic aid to sports performance. There have been several recent qualitative review articles published on the topic, and here we present a preliminary quantitative review of the literature through a meta-analysis. A comprehensive search of the literature was employed to identify all studies suitable for inclusion in the analysis; strict exclusion criteria were also applied. Fifteen published manuscripts were included in the analysis, which reported the results of 57 measures within 23 exercise tests, using 18 supplementation regimes and a total of 360 participants [174, β-alanine supplementation group (BA) and 186, placebo supplementation group (Pla)]. BA improved (P=0.002) the outcome of exercise measures to a greater extent than Pla [median effect size (IQR): BA 0.374 (0.140-0.747), Pla 0.108 (-0.019 to 0.487)]. Some of that effect might be explained by the improvement (P=0.013) in exercise capacity with BA compared to Pla; no improvement was seen for exercise performance (P=0.204). In line with the purported mechanisms for an ergogenic effect of β-alanine supplementation, exercise lasting 60-240 s was improved (P=0.001) in BA compared to Pla, as was exercise of >240 s (P=0.046). In contrast, there was no benefit of β-alanine on exercise lasting <60 s (P=0.312). The median effect of β-alanine supplementation is a 2.85% (-0.37 to 10.49%) improvement in the outcome of an exercise measure, when a median total of 179 g of β-alanine is supplemented” (2.)
Finally, we’ll conclude on its ability to reduce fatigue from the works of Hoffman et al. The purpose of this study was to examine the effect of 30 days of beta-alanine supplementation in collegiate football players on anaerobic performance measures. Subjects were randomly divided into a supplement (beta-alanine group [BA], 4.5 g x d(-1) of beta-alanine) or placebo (placebo group [P], 4.5 g x d(-1) of maltodextrin) group. Supplementation began 3 weeks before preseason football training camp and continued for an additional 9 days during camp. Performance measures included a 60-second Wingate anaerobic power test and 3 line drills (200-yd shuttle runs with a 2-minute rest between sprints) assessed on day 1 of training camp. Training logs recorded resistance training volumes, and subjects completed questionnaires on subjective feelings of soreness, fatigue, and practice intensity. No difference was seen in fatigue rate in the line drill, but a trend (P = .07) was observed for a lower fatigue rate for BA compared with P during the Wingate anaerobic power test. A significantly higher training volume was seen for BA in the bench press exercise, and a trend (P = .09) for a greater training volume was seen for all resistance exercise sessions. In addition, subjective feelings of fatigue were significantly lower for BA than P. In conclusion, despite a trend toward lower fatigue rates during 60 seconds of maximal exercise, 3 weeks of beta-alanine supplementation did not result in significant improvements in fatigue rates during high-intensity anaerobic exercise. However, higher training volumes and lower subjective feelings of fatigue in BA indicated that as duration of supplementation continued, the efficacy of beta-alanine supplementation in highly trained athletes became apparent (3.)
It is clear that beta alanine is a supplement that is beyond beneficial for any athletic endeavor! In these studies, we see a wide array of dosages from 2 grams all the way up to 5 grams. It has been concluded that 3.2 grams of beta alanine is the accepted clinical dosage. If your taking a pre workout that has LESS than that clinical amount then you’re pretty much wasting your money as you will not reap the full benefits. Luckily, supplements like Total War from RedCon1 provide the full 3.2 gram clinical dosage of beta alanine along with other great ergogenic aids like citrulline malate, agmatine sulfate, and a number of others ALL having the correct clinical dosage.
Alex Kikel
MS, PES, CPT, Speed and Explosion Specialist Level II
Owner of www.theprepcoach.com
References
Admiration. Fear. Disgust. Such terms often accompany an egregiously muscular physique. For better, or for worse, the general public remains enamored at the sight of a sidewalk cracking specimen despite any moral or aesthetic reservations they may carry. The need to even reference “morals” only exists due to the persistent demonizing of steroid use commonly associated with bodybuilders. More often than not the sheep of society will discredit a well-developed physique as nothing more than fictitious mass inflated by chronic drug abuse. These rampant displays of ignorance are a significant contributing factor for the sport’s inability to garner societal acceptance and financial interest from more conventional corporate contributors. A near-sighted perspective when considering that their absence places an inhibition on further athletic advancement beyond its current limitations. The policy in and of itself is contradictory to the very heart of competition. Competitors – true competitors, not mere participants – aspire to reach new tiers of human physical performance and despite many wasted pennies at the wishing-well, the viability of X-Men style genetic mutations is beginning to look bleak. If mainstream audiences continue to expect furthering degrees of superhuman abilities then they must come to understand the need for a superhuman physiology.
It is hardly news worthy to comment that PEDs(Performance Enhancing Drugs) exist at the upper echelon of nearly every competitive activity known. Yet, the populace is dumbfounded upon discovering that their favorite athletic icon has been dabbling in “extracurricular” supplementation between batting practice. Bodybuilding’s double-edged sword is its lack of subtlety regarding the more illicit elements that accompany it. Bombastic displays of freakish mass do little to quell steroid accusations, which, in truth, are usually correct. Consequently, bodybuilding is self-defeating by nature and continually fails to infiltrate sports programming networks or any significant level of mainstream exposure. Although Kai Greene has seen some success outside of wearing posing trunks, his reach is still quite limited when compared to the charismatic career of Arnold, who’s classic lines were befitting of Hollywood.
Despite the bastardization that stems from its use, steroids are more often than not referred to with a positive connotation in present day culture. Simply attach “on steroids” to the end of a noun and it instantly resonates a complimentary tone. Although the concept of needle-based drug usage will remain taboo around the dinner table, the popularity of PEDs within the fitness industry is higher than Snoop Dogg could ever hope to be. Ever since the Archduke of Anadrol, Bostin Loyd, expunged the extreme nature of bodybuilding culture, online forums have essentially transitioned into a pissing contest of Tren and Superdrol. This poses a quandary of a question: take the plunger and get country big or stand around in an extra schmedium tank top while wearing your D.A.R.E. sticker from middle school? Fortunately you do not need to compromise your childhood ethics in order to obtain a God-bod. For all their physically potentiating prowess, the novelty of risqué ‘roid usage wears faster than vital health markers.
Satire aside, there are notable anabolic alternatives presently available on the market. DHEA based prohormones have seen a surge in popularity since DASCA all but razed grey-area designers entirely. Traditionally, DHEA compounds have been overlooked due to being far less cost effective than their more readily active counterparts. Supplement industry innovator, Redcon1, however, has released a well-rounded line of these prohormones that afford the modern iron monger supraphysiological gains without supraphysiological side-effects. By introducing an ingenious Liposomal delivery system into its formulation, Redcon1’s SOMAL products are capable of achieving a standard of bioavailability nearing one-hundred percent. This exceptionally high conversion rate into the target compound allows users to experience the benefits of exogenous hormone usage without compromising the monthly food budget. Those who desire sheer mass and aggression would be wise to sample the tantalizing taste of SOMAL-4’s final form, Testosterone. As the predominant male hormone, no other compound shares its muscle potentiating effects. Alternatively, individuals who prefer less dramatic, leaner mass gains should reference SOMAL-1. Although a structural derivative of Testosterone, the introduction of 1-Testosterone via SOMAL-1 does not raise estradiol or impart a sudden spike in weight gain to the degree that Testosterone does. Rather, it exhibits a high binding affinity for androgen receptors that grant it superior strength enhancing properties, which makes its use advantageous in both bulking and cutting applications.
Rest assured, these two-stepping precursors meet all legal compliances despite their renowned effects on strength and mass acquisition. Lunge your way over to Redcon1.com, or download the app, to learn how SOMAL-1 and SOMAL-4 will allow you to reach your highest state of readiness.
]]>Sulforaphane’s ability to do everything we just discussed should make you want to start eating your broccoli as well as possibly supplementing with a good sulforaphane product (which is very few and fair between.) In terms of an applicable dosage, it seems that right around the 30mg per day mark is proven in literature to be beneficial (with some even dosing it up to double based on their body weight being higher.) Sulforaphane’s benefits are endless and is a must have health AND ergogenic aid supplement for any serious competitor (or at least it is in my eyes.)
References
In close relation is a study on sleep deprivation and how it reduces circulating androgens in healthy men. “The acute effect of sleep deprivation on the pituitary-testis axis was evaluated in 13 healthy men. To study such association, the circulating levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), Androstenedione (A), Testosterone (T), Dihydro-testosterone (DHT) and Estradiol (E2) were measured along with Cortisol (C) before and after sleep deprivation. Morning (8:00 AM) venous blood samples were obtained prior and after a continuous restless period of 24 hr and the values were analyzed by the paired Student’s t test. There was a significant and parallel decrease of each androgen and E2 but not of FSH, L.H. PRL, or C, associated with the acute sleep deprivation” (3.) The issues that we are seeing tie directly into cortisol. The issue that arises is that coristol usually pulsates in pattern (meaning its higher in the morning and lower at night) BUT when sleep is deprived, it essentially disrupts this pattern and there by increases serum cortisol levels. Leproult shows this very well in a study from 1997. Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess (4.)
References
I also knew I couldn’t do it alone. And that’s OK to admit. Find yourself a good coach.
What is a good coach/mentor to you?
To me, a good coach makes time to listen and communicate. I know I can expect a response in a reasonable time. (No waiting anxiously for weeks for a reply. A good coach is one who won’t allow you failure. It’s THEIR opinion you come to respect. As much as you want it for you, you want it for them,and if you drop the ball, you feel like you let two people down. Their excitement is your excitement. Their motivation is your motivation. Every day, I want to not only make myself proud, but also make my coach proud. I push harder knowing she is there,pushing me. And I know as bad as I want it,she may be the only other person that wants it more for me than I do….
The quote below is a long-time favorite:
“Life’s best coaches are those who believe in you and your potential, sometimes even before you do.”
Remember this when you look for someone who is going to be in charge of changing your lifestyle.
Disclaimer: There are as many good coaches as there are bad ones, so make sure you DO YOUR RESEARCH on the best fit for you. My perfect fit is Team Bombshell with Mama Bombshell, Shannon Dey, and my personal coach, Gennifer Strobo. You have to do what’s right for you, and sometimes that requires trial and error. Do not be afraid to say what you want. You pay an expert to help you so before you go and spend hard-earned money makesure you are willing to also invest your energy and time, and sweat. (Lots of sweat.) At the end of the day, YOU are still the one that must follow instructions. No one can make you get out of bed, food prep, or go to the gym. But a good coach sure can make you feel accountable! No matter how you do it – self-motivation or hiring help, DO IT FOR YOU!
A more direct study from Xu et al looked at how TB500 accelerates overall rates of wound healing. A prokaryotic vector harboring two complete Tβ4 genes with a short linker was constructed and expressed in Escherichia coli. A pilot-scale fermentation (10 L) was performed to produce engineered bacteria and the Tβ4 dimer was purified by one-step hydrophobic interaction chromatography. The activities of the Tβ4 dimer to promote endothelial cell proliferation, migration, and sprouting were assessed by tetramethylbenzidine (methylthiazol tetrazolium), trans-well, scratch, and tube formation assays. The ability to accelerate dermal healing was assessed on rats. After fermentation, the Tβ4 dimer accounted for about 30% of all the bacteria proteins. The purity of the Tβ4 dimer reached 98% after hydrophobic interaction chromatography purification. An average of 562.4 mg/L Tβ4 dimer was acquired using a 10 L fermenter. In each assay, the dimeric Tβ4 exhibited enhanced activities compared with native Tβ4. Notably, the ability of the dimeric Tβ4 to promote cell migration was almost two times higher than that of Tβ4. The rate of dermal healing in the dimeric Tβ4-treated rats was approximately 1 day faster than with native Tβ4-treated rats. The dimeric Tβ4 exhibited enhanced activity on wound healing than native Tβ4, and the purification process was simple and cost-effective. This data could be of significant benefit for the high pain and morbidity associated with chronic wounds disease. A better strategy to develop Tβ4 as a treatment for other diseases caused by injuries such as heart attack, neurotrophic keratitis, and multiple sclerosis was also described (9.) Even further studies show its ability to further increase strength, endurance, and reduce inflammation. Sosne et al states within their abstract “Thymosin beta 4 (Tβ4) is a low molecular weight protein present in all cells except erythrocytes. Although Tβ4 is the major monomeric actin-sequestering peptide in cells and can depolymerize F-actin, evidence is mounting to support the idea that it has multiple, seemingly diverse, cellular functions. In cornea, as in other tissues, Tβ4 promotes cell migration and wound healing, has anti-inflammatory properties, and suppresses apoptosis. In this review we discuss the current state of knowledge regarding the effects of Tβ4 in maintaining the healthy, functional cornea. The clinical implications of the use of Tβ4 as a wound healing and anti-inflammatory agent are discussed.” Read more about TB500’s role in inflammation and other beneficial properties below in the reference section (10.)
In conclusion, these two peptides have a tremendous ability to help up-regulate healing rates (however their long term effectiveness and side effects have yet to be determined.) In terms of practical application, many literature and anecdotal evidence reports show that dosing BPC-157 at 1-10mcgs per kg of body weight daily and TB500 at 2mgs twice per week to be a very effective starting point. Your optimal dosage will completely be dependent on how well or how poorly you metabolize these compounds so some trial and error will be required. BPC-157 is systemic where as TB500 should be applied as close to the injured area as possible. Now go out, read more literature on these two amazing peptides, and make an informed decision for yourself as to whether or not this is something that can benefit your athletic and recovery endeavors.
References
Although that is the only credible study I can attribute positive results on those fronts, we can play “connect the dots” with some other pieces of literature such as the ones done on TUDCA supplementation in correlation to glucose metabolism. A study done in 2006 (5) linked endoplasmic reticulum stress to obesity, insulin resistance, and diabetes. They state” here, we provide evidence that this mechanistic link can be exploited for therapeutic purposes with orally active chemical chaperones. 4-Phenyl butyric acid and taurine-conjugated ursodeoxycholic acid alleviated ER stress in cells and whole animals. Treatment of obese and diabetic mice with these compounds resulted in normalization of hyperglycemia, restoration of systemic insulin sensitivity, resolution of fatty liver disease, and enhancement of insulin action in liver, muscle, and adipose tissues. Our results demonstrate that chemical chaperones enhance the adaptive capacity of the ER and act as potent antidiabetic modalities with potential application in the treatment of type 2 diabetes.” Another study along similar lines of endoplasmic reticulum stress and its correlation to insulin resistance looked at glucose-induced beta cell dysfunction in vivo in rats which showed a link between oxidative stress and endoplasmic reticulum stress. Healthy Wistar rats were infused i.v. with glucose for 48 h to achieve 20 mmol/l hyperglycaemia with or without the co-infusion of the superoxide dismutase mimetic tempol (TPO), or the chemical chaperones 4-phenylbutyrate (PBA) or tauroursodeoxycholic acid (TUDCA). This was followed by assessment of beta cell function and measurement of ER stress markers and superoxide in islets. Glucose infusion for 48 h increased mitochondrial superoxide and ER stress markers and impaired beta cell function. Co-infusion of TPO, which we previously found to reduce mitochondrial superoxide and prevent glucose-induced beta cell dysfunction, reduced ER stress markers. Similar to findings with TPO, co-infusion of PBA, which decreases mitochondrial superoxide, prevented glucose-induced beta cell dysfunction in isolated islets. TUDCA was also effective. Also similar to findings with TPO, PBA prevented beta cell dysfunction during hyperglycaemic clamps in vivo and after hyperglycaemia (15 mmol/l) for 96 h. Here, we causally implicate ER stress in hyperglycaemia-induced beta cell dysfunction in vivo. We show that: (1) there is a positive feedback cycle between oxidative stress and ER stress in glucose-induced beta cell dysfunction, which involves mitochondrial superoxide; and (2) this cycle can be interrupted by superoxide dismutase mimetics as well as chemical chaperones, which are of potential interest to preserve beta cell function in type 2 diabetes (6.)
I could continue on and on about the benefits of TUDCA! Heck, we didn’t even cover the fact that bile acids have the ability to induce energy expenditure by promoting intracellular thyroid hormone activation (7.) But, I do feel I’ve presented enough pertinent information to prove TUDCA has its place in everyone’s supplement regimen given the fact that it is a potent health and ergogenic aid that is more than affordable. In terms of practical application, there have been studies done showing improvements of liver regenesis rates at a dosage as low as 10mgs and other studies showing benefits for muscle tissue insulin sensitivity and for the treatment of liver disease as high as almost 2000mgs. In actual application I personally recommend my clients (that are competitive athletes) to supplement with 250mgs of TUDCA per day year round. Then, during periods of high stress such as a contest prep or anytime you’re truly pushing your “supplements”, upwards of 1000mgs per day. You will obviously need to get bloodwork done to see where your liver enzyme levels are and how they change at what specific dosage to know for sure (once again, thank you biological inter-individuality!) I have also included four more studies linked below in the reference section for your academic pleasure (8, 9, 10, 11.) Please read more and make the decision for yourself if TUDCA is something that could be beneficial in your everyday supplement stack.
References
HMB acts within the body very similarly to leucine meaning that they both inhibit muscle protein breakdown as well as increasing muscle protein synthesis. Maintenance of skeletal muscle mass is contingent upon the dynamic equilibrium (fasted losses-fed gains) in protein turnover. Of all nutrients, the single amino acid leucine (Leu) possesses the most marked anabolic characteristics in acting as a trigger element for the initiation of protein synthesis. While the mechanisms by which Leu is ‘sensed’ have been the subject of great scrutiny, as a branched-chain amino acid, Leu can be catabolized within muscle, thus posing the possibility that metabolites of Leu could be involved in mediating the anabolic effect(s) of Leu. Our objective was to measure muscle protein anabolism in response to Leu and its metabolite HMB. Using [1,2-(13)C2]Leu and [(2)H5]phenylalanine tracers, and GC-MS/GC-C-IRMS we studied the effect of HMB or Leu alone on MPS (by tracer incorporation into myofibrils), and for HMB we also measured muscle proteolysis (by arteriovenous (A-V) dilution). Orally consumed 3.42 g free-acid (FA-HMB) HMB (providing 2.42 g of pure HMB) exhibited rapid bioavailability in plasma and muscle and, similarly to 3.42 g Leu, stimulated muscle protein synthesis (MPS; HMB +70% vs. Leu +110%). While HMB and Leu both increased anabolic signalling (mechanistic target of rapamycin; mTOR), this was more pronounced with Leu (i.e. p70S6K1 signalling 90 min vs. 30 min for HMB). HMB consumption also attenuated muscle protein breakdown (MPB; -57%) in an insulin-independent manner. We conclude that exogenous HMB induces acute muscle anabolism (increased MPS and reduced MPB) albeit perhaps via distinct, and/or additional mechanism(s) to Leu (2.)
References