Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 7

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 14

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 21

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 28

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 35

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 42

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 49

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 56

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 63

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 70

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 77

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 84

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 91

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 98

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 105

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 112

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 119

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 126

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 133

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 140

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 147

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 154

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 161

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 168

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 175

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 182

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 189

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 196

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 203

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 210

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 217

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 223

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php on line 228

Deprecated: Function create_function() is deprecated in /var/www/wp-content/themes/Newspaper/functions.php on line 68

Warning: Cannot modify header information - headers already sent by (output started at /var/www/wp-content/themes/Newspaper/includes/widgets/td_page_builder_widgets.php:161) in /var/www/wp-includes/feed-rss2.php on line 8
pre workout supplements – Redcon1 Online Official https://redcon1online.com The Highest State of Readiness Wed, 16 Aug 2017 19:24:35 +0000 en-US hourly 1 https://wordpress.org/?v=6.5.2 Five Common Pre Workout Ingredients and Their Benefits https://redcon1online.com/pre-workout-ingredients-benefits/ Sun, 06 Aug 2017 04:00:54 +0000 https://redcon1online.com/?p=4384 The athletic world is strongly beholden to the use of sports supplements. Recent surveys have claimed that roughly 50% of gym goers utilize supplements, with 80-90% of these being male. Among the veritable sea of available items on today’s market, a few have managed to stand the test of time. One such supplement is the creatine-based preworkout. The usage of preworkouts has increased greatly since their introduction, and there’s no doubt that they are among the most popular products. Let’s take some time to explore the more common ingredients in such products and the benefits offered by each of them.

Creatine (a nitrogenous organic acid) is of course the base ingredient in such supplements. Its most important function in the human body is to enable the recycling of adenosine triphosphate (ATP) in muscle and brain tissue. ATP is a muscle cell’s primary source of energy, and is recycled by adenosine diphosphate (ADP) via the accumulation of a phosphate group molecule. Creatine has seen clinical use in treatment of individuals with muscular dystrophy, and has also been commonly utilized by the athletic community for decades. Roughly one half of the human body’s creatine is synthesized in the liver, with animal sources of protein (wild game, fish, lean red meat, etc.) providing the rest. The main benefits associated with a creatine-based preworkout are increased endurance and strength improvements. A dose of 5 grams per day is typically recommended for peak performance.

Another common ingredient is caffeine. Caffeine is a widely-used stimulant in products across the world, and has found a place in many workout supplements as well. 100-200 mg (or about the amount found in 1-2 cups of coffee) should be sufficient. The basis of caffeine’s use is its ability to block the action of the nucleoside adenosine on its receptor. This serves to block or delay the onset of drowsiness, which is typically prompted by adenosine. In practical terms, this means that its value in a preworkout is its propensity to discourage fatigue among athletes who choose to utilize it. Like all stimulants caffeine will somewhat depress the appetite, making it somewhat unhelpful for weightlifters engaging in a bulk phase.

L-arginine is an α-amino acid that, when used in preworkout, converts to nitric oxide upon metabolism. Products that contain this ingredient or are based on it are typically referred to as “vasoactive.” Nitric oxide serves to promote capillary and pulmonary dilation, allowing for faster and more efficient transport of oxygen to muscular tissues being used during training. This increased oxygen flow will result in better muscle contractions and higher production of ATP (created via certain enzymes through a process known as oxidative phosphorylation). Three grams is considered an effective dose. While it also serves other purposes and functions, its use among bodybuilders and similar athletes is by far its best documented.

The presence of a ph buffer such as taurine is also common. During a workout, skeletal muscles function at their best when the blood flowing to them is within a certain alkalytic ph range. A mitochondrial ph gradient exists across the inner membrane of cells, a fact that was demonstrated and proven in the 1960’s and 1970’s. Taurine’s role in the maintenance of this buffer is to stabilize it, keeping it safely within a ph range of 7.5-8.5. If a cell’s buffering capabilities are too low the gradient can potentially shift, ultimately disrupting ATP production in that cell. Simply put, taurine’s role (and that of other ph regulating substances) is to enable cells to produce ATP for energy. Taurine dosing is typically done at around one gram.

The amino acid tyrosine can also be found in many preworkouts. Its most common physiological role is to enable signal transduction in the brain. To this end it serves as a precursor to the organic chemical norepinephrine, which stimulates metabolism. Norepinephrine reserves are depleted as a result of prolonged intense training. 1-2 grams of tyrosine is sufficient to raise norepinephrine levels and enhance brain function.

At the end of the day it is the consumer’s responsibility to carefully analyze and select supplements that will best serve their personal needs. Many seek to enhance their endurance, strength, focus, and intensity at the gym. For these individuals a preworkout substance may hold great potential benefits. Having such a substance in your supplemental arsenal makes your goals more achievable, and allows your ambitions to rise higher. A good basic understanding of common supplement ingredients will greatly benefit such a person, helping them to select the product best suited for their interests and allowing them to pursue their goals with much more confidence.

Written by Trent Wozniak

]]>
Dallas McCarver- A Day in the Life https://redcon1online.com/dallas-mccarver-day-life/ Fri, 04 Aug 2017 20:53:32 +0000 https://redcon1online.com/?p=4445

On the new video out today from Redcon1, IFBB Pro Dallas McCarver takes us through his day. Before most people are even awake, Dallas headed his chiropractor to get adjusted by Dr. Nick Ruggiero. Dallas has had a little bit of shoulder impingement and is finding that Active Release Therapy (ART) to be helping quite a bit. Then Dallas heads over to the Stretch Zone in Boca Raton, Florida to get further loosened up. Watch as he gets twisted and pulled into submission. Then he heads back home for a Meal #1 and then onto chest training at Busy Body Fitness Center. Watch the 335lb freak jump out at your screen in each scene, you won’t want to miss it.

]]>
Exercise Your Demons https://redcon1online.com/exercise-your-demons/ Tue, 18 Jul 2017 18:05:47 +0000 https://redcon1online.com/?p=4247 You would be hard pressed to find a more polarizing binary than the relationship society has with bodybuilding’s less-than-secretive marinade, “the sauce.” Anabolic-androgenic steroids have been a topic of controversial relevancy since their international debut via a cosmonaut air drop of Turinabol to Russian athletes in 1962. The introduction of these novel compounds stirred a literal arms race that prompted the research and development of hundreds of functional hormone derivatives, which have been the plight of anti-doping agencies for decades. As of recent, advances in drug detection technology have revealed what most already knew… athletes of every discipline and caliber are juiced up like a bottle of Florida Orange. Progression, however, is an intuitive component of human biology. The constant compulsion to improve has been the greatest catalyst of this species’ development – best exemplified by the universal practice of competitive sports over its evolutionary course. 

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.

]]>
Amino Acids- The Essentials https://redcon1online.com/amino-acids-essentials/ Mon, 17 Jul 2017 21:56:51 +0000 https://redcon1online.com/?p=4257 Amino acids have long been a popular go-to in the fitness industry and rightfully so.  The reason is very simple; recovery. As fitness junkies, we know how important recovery can be. Let us dive into which amino acids are responsible for our muscle repair. We are talking particularly about EAAs, or “Essential Amino Acids”. There are a total of nine EAAs, and these aminos like to play hard-to-get. Essential Amino Acids are critical for us to consume, as these aminos cannot be naturally produced in the body; we must obtain them either from food, or a supplement. There are three EAAs that are especially sought after by those who are looking for better, faster results. They are the following: Leucine, Isoleucine, and Valine. This trio of important aminos plays a critical role in our recovery.

Recovering from a brutal workout relies heavily on proper nutrition and rest. Once those two factors have been accounted for, the cherry on top would be incorporating excellent supplements. A protein source, such as Isotope, and an amino product like Breach, or Breach Ballistic (Caffeinated) are excellent examples. These products would be most beneficial post-workout. After intense activity, this is when our body is most in need of nutrients. Breach is fantastic, as it incorporates the three EAAs I previously described as being the most valuable when it comes to recovery. Each has a unique job, and together they form the perfect package.

Leucine, Isoleucine and Valine play the biggest role of all aminos when it comes to muscle growth/recovery. They stimulate protein synthesis, regulate blood sugar levels, and even give a slight boost in energy. Leucine is the biggest player of the three in promoting protein synthesis. For this reason, you will find Breach packs a phenomenal 2:1:1 ratio of these aminos (2 parts Leucine, 1 part Isoleucine, and 1 part Valine). Think of your muscles as a “building” you are looking to construct. You have all of the materials to build your idea, now you just need someone to put it all together and oversee the project.  We can view these three EAAs as being the team for the job. They signal for the muscle to grow/repair, and help you maintain an anabolic environment throughout your body. Anabolic means “muscle building state”, whereas if we were to be lacking the described EAAs, we would more often than not find ourselves in a catabolic situation, or “muscle loss state”.  Being anabolic is ideal for not just men, but women too! Both can benefit from taking these EAAs. With Breach, you will get all of the benefits from these aminos, and, a little extra.

Muscle recovery is critical, but so is proper hydration. As an added bonus, Breach also contains coconut water powder and electrolytes to help you stay adequately hydrated. This makes it a perfect product for not just post workout, but all day long! Many successful bodybuilders and athletes drink amino acids throughout the day. This ensures a constant muscle building and properly hydrated state. This solves one of the biggest complaints in the fitness industry; muscle soreness.

I absolutely love being sore. That is my sign that I had a killer workout the day prior. For those of you that have tattoos, think of it like when you are in the process of getting inked. Yes, it hurts, but it is a “good” hurt! I feel that same way about muscle soreness post workout. Not everyone feels the same, and they need a solution to help ease their troubles. There really is no absolute, orthodox solution to being pain free after an all-out lift or sporting event (like a football game). This being said, if you are looking to help alleviate this in any way possible, an amino acid product like Breach will undoubtedly help. When we put our bodies through strenuous activity and put tension on our muscles for long periods of time, our muscle fibers will literally tear. For those of you new to the gym life, do not be alarmed. These are tiny breaks in the muscle tissue, nothing that is going to need medical attention. Over time, these rips in the muscle fiber fill back in with NEW muscle, and this is where we experience muscle gains, and more strength! Adding Lecuine, Isoleucine, and Valine into our diet in order to help facilitate this growth and repair is crucial. With the added hydration/electrolyte benefits, this also allows for optimal function within our muscular system. If you are still on the fence on incorporating aminos into your regiment, allow me to introduce a not-so-good hormone, Coritsol.

Cortisol is a stress hormone, and it can be very destructive to our body, particularly our muscles. This nasty hormone actually binds to receptors in our muscles, and can cause the dreaded catabolic environment to set in. Additionally, cortisol actually breaks down amino acids. To make matters worse, cortisol levels elevate during stress. This includes both mental and physical stress. Essentially, we are fighting an up-hill battle when we go to the gym when it comes to cortisol. With an EAA product like Breach, we can stop trying to walk “up” the “down” escalator and get back on track to providing our bodies with the proper environment needed for maximum recovery.

Recovery is the key to success. It does not matter what walk of life you come from. Whether you are an athlete, a bodybuilder, cyclist, runner, weekend warrior, etc, any and everyone can benefit from essential amino acids. There is not a single person who is maintaining an active lifestyle that would not like to see better, faster, and overall, more efficient results. When thinking about recovering and optimizing your bodies’ potential, there are three things you must be aware of at all times; proper nutrition, sleep, and supplementation. After nailing your diet and making sure you get sufficient rest, the last component is finding the right supplements. When it comes to recovery and growth, adding an amino product like Breach would be the perfect addition to your daily routine. Lift on my friends!

-Garrett Skurnit

]]>
Sulforaphane to Inhibit Myostatin? 3 https://redcon1online.com/sulforaphane-inhibit-myostatin-3/ Sat, 24 Jun 2017 16:29:22 +0000 https://redcon1online.com/?p=4055 In closing, lets bring in its ability to act as a significant anti-inflammatory and anti-cancer agent. I would like to look at three pieces of literature. The first is on the inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: a novel basis for antileukemia activity of histone deacetylase inhibitors by Bali et al. The second is on  histone deacetylase inhibitors: signalling towards p21cip1/waf1 from Matthias Ocker. The third and final is entitled “A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase” from Myzak et al. The hydroxamic acid (HAA) analogue pan-histone deacetylase (HDAC) inhibitors (HDIs) LAQ824 and LBH589 have been shown to induce acetylation and inhibit the ATP binding and chaperone function of heat shock protein (HSP) 90. This promotes the polyubiquitylation and degradation of the pro-growth and pro-survival client proteins Bcr-Abl, mutant FLT-3, c-Raf, and AKT in human leukemia cells. HDAC6 is a member of the class IIB HDACs. It is predominantly cytosolic, microtubule-associated alpha-tubulin deacetylase that is also known to promote aggresome inclusion of the misfolded polyubiquitylated proteins. Here we demonstrate that in the Bcr-abl oncogene expressing human leukemia K562 cells, HDAC6 can be co-immunoprecipitated with HSP90, and the knock-down of HDAC6 by its siRNA induced the acetylation of HSP90 and alpha-tubulin. Depletion of HDAC6 levels also inhibited the binding of HSP90 to ATP, reduced the chaperone association of HSP90 with its client proteins, e.g. Bcr-Abl, and induced polyubiquitylation and partial depletion of Bcr-Abl. Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf. Collectively, these findings indicate that HDAC6 is also an HSP90 deacetylase. Targeted inhibition of HDAC6 leads to acetylation of HSP90 and disruption of its chaperone function, resulting in polyubiquitylation and depletion of pro-growth and pro-survival HSP90 client proteins including Bcr-Abl. Depletion of HDAC6 sensitized human leukemia cells to HAA-HDIs and proteasome inhibitors (9.) Chromatin-modifying enzymes such as histone deacetylases (HDAC) facilitate a closed chromatin structure and hence transcriptional repression. HDAC are commonly affected in human cancer diseases. Thus, inhibition of HDAC represents a novel therapeutic approach. Several studies have shown that HDAC inhibitors strongly activate the expression of the cyclin-dependent kinase inhibitor p21(cip1/waf1) through (i) enhanced histone acetylation around the p21(cip1/waf1) promoter and (ii) the Sp1 sites on the p21(cip1/waf1) promoter releasing the repressor HDAC1 from its binding. p21(cip1/waf1) expression is regulated in a p53-dependent and p53-independent manner. The decision if p21(cip1/waf1) up-regulation results in cell cycle arrest or apoptosis, decides about the therapeutic efficacy of an anti-cancer treatment with HDAC inhibitors (10.) Sulforaphane (SFN), a compound found at high levels in broccoli and broccoli sprouts, is a potent inducer of phase 2 detoxification enzymes and inhibits tumorigenesis in animal models. SFN also has a marked effect on cell cycle checkpoint controls and cell survival and/or apoptosis in various cancer cells, through mechanisms that are poorly understood. We tested the hypothesis that SFN acts as an inhibitor of histone deacetylase (HDAC). In human embryonic kidney 293 cells, SFN dose-dependently increased the activity of a beta-catenin-responsive reporter (TOPflash), without altering beta-catenin or HDAC protein levels. Cytoplasmic and nuclear extracts from these cells had diminished HDAC activity, and both global and localized histone acetylation was increased, compared with untreated controls. Studies with SFN and with media from SFN-treated cells indicated that the parent compound was not responsible for the inhibition of HDAC, and this was confirmed using an inhibitor of glutathione S-transferase, which blocked the first step in the metabolism of SFN, via the mercapturic acid pathway. Whereas SFN and its glutathione conjugate (SFN-GSH) had little or no effect, the two major metabolites SFN-cysteine and SFN-N-acetylcysteine were effective HDAC inhibitors in vitro. Finally, several of these findings were recapitulated in HCT116 human colorectal cancer cells: SFN dose-dependently increased TOPflash reporter activity and inhibited HDAC activity, there was an increase in acetylated histones and in p21(Cip1/Waf1), and chromatin immunoprecipitation assays revealed an increase in acetylated histones bound to the P21 promoter. Collectively, these findings suggest that SFN may be effective as a tumor-suppressing agent and as a chemotherapeutic agent, alone or in combination with other HDAC inhibitors currently undergoing clinical trials (11.)

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

  1. Protein oxidation and aging. E. R. Stadtman. Science. 1992 (https://www.ncbi.nlm.nih.gov/pubmed/1355616)
  2. Sulforaphane Activates Heat Shock Response and Enhances Proteasome Activity through Up-regulation of Hsp27. Nanqin Gan, Yu-Chieh Wu, Mathilde Brunet, Carmen Garrido, Fung-Lung Chung, Chengkai Dai, Lixin Mi. J Biol Chem. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20833711)
  3. Role of increased expression of the proteasome in the protective effects of sulforaphane against hydrogen peroxide-mediated cytotoxicity in murine neuroblastoma cells. Mi-Kyoung Kwak, Jeong-Min Cho, Bo Huang, Soona Shin, Thomas W. Kensler. Free Radic Biol Med. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17664144)
  4. Sulforaphane induced adipolysis via hormone sensitive lipase activation, regulated by AMPK signaling pathway. Ju-Hee Lee, Myung-Hee Moon, Jae-Kyo Jeong, Yang-Gyu Park, You-Jin Lee, Jae-Won Seol, Sang-Youel Park. Biochem Biophys Res Commun. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22982310)
  5. Identification and role of the basal phosphorylation site on hormone-sensitive lipase. A. J. Garton, S. J. Yeaman. Eur J Biochem. 1990 (https://www.ncbi.nlm.nih.gov/pubmed/2165906)
  6. 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside-induced AMP-activated protein kinase phosphorylation inhibits basal and insulin-stimulated glucose uptake, lipid synthesis, and fatty acid oxidation in isolated rat adipocytes. Mandeep Pinky Gaidhu, Sergiu Fediuc, Rolando Bacis Ceddia. J Biol Chem. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16816404)
  7. Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells. Huitao Fan, Rui Zhang, Dawit Tesfaye, Ernst Tholen, Christian Looft, Michael Hölker, Karl Schellander, Mehmet Ulas Cinar. Epigenetics. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/23092945)
  8. Sulforaphane attenuates hepatic fibrosis via NF-E2-related factor 2-mediated inhibition of transforming growth factor-β/Smad signaling. Chang Joo Oh, Joon-Young Kim, Ae-Kyung Min, Keun-Gyu Park, Robert A. Harris, Han-Jong Kim, In-Kyu Lee. Free Radic Biol Med. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22155056)
  9. Inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: a novel basis for antileukemia activity of histone deacetylase inhibitors. Purva Bali, Michael Pranpat, James Bradner, Maria Balasis, Warren Fiskus, Fei Guo, Kathy Rocha, Sandhya Kumaraswamy, Sandhya Boyapalle, Peter Atadja, et al. J Biol Chem. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/15937340)
  10. Histone deacetylase inhibitors: signalling towards p21cip1/waf1. Matthias Ocker, Regine Schneider-Stock. Int J Biochem Cell Biol. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17412634)
  11. A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. Melinda C. Myzak, P. Andrew Karplus, Fung-Lung Chung, Roderick H. Dashwood. Cancer Res. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15313918)
]]>
Why You Might Not Be Growing Part 3 https://redcon1online.com/growing-part-3/ Thu, 22 Jun 2017 04:00:07 +0000 https://redcon1online.com/?p=3997 If thats not enough, theres even more literature done on sleep disturbances and their correlation with decreased morning awakening salivary cortisol. “Morning and evening salivary cortisol levels were correlated with sleep parameters in 14 patients with primary insomnia and 15 healthy controls. Salivary cortisol was sampled immediately after awakening (T1), 15 min later (T2), and immediately before going to bed (T3) for 1 week at home. In parallel with this, subjects estimated parameters of sleep in a daily sleep log. Patients and controls were all non-smokers who did not differ regarding morning awakening time or bedtime. Cortisol after awakening was significantly decreased in primary insomnia. Salivary cortisol at the time of awakening correlated negatively with the subjective estimation of sleep quality, i.e. a low salivary cortisol level directly after awakening correlated with a higher frequency of nightly awakenings (r = -0.50), a diminished sleep quality (r = -0.34) and a decreased feeling of recovery after awakening (r = -0.35; all p < 0.05). Furthermore, awakening cortisol was negatively correlated with the Pittsburgh Sleep Quality Index (r = -0.43) and with a questionnaire on sleep-related cognitions with the subscales rumination in bed (r = -0.56 ) and focusing on sleep-related thoughts (r = -0.46; all p < 0.05)” (5.)

So far, we see sleep deprivation interrupting normal circadian rhythms that interrupt and cause a cascading effect with normal hormone functioning. Now onto one final hormone thats released during sleep that everyone is highly concerned with…growth hormone. Growth hormone has its biggest spike  with is roughly half of our daily growth hormone amount. If this process is interuppted, could this be another big reason why you’re not growing? Plasma growth hormone (GH), insulin, cortisol, and glucose were measured during sleep on 38 nights in eight young adults in a study from Takahashi et al (6.) Blood was drawn from an indwelling catheter at 30-min intervals; EEG and electrooculogram were recorded throughout the night. In seven subjects, a plasma GH peak (13-72 mmug/ml) lasting 1.5-3.5 hr appeared with the onset of deep sleep. Smaller GH peaks (6-14 mmug/ml) occasionally appeared during subsequent deep sleep phases. Peak GH secretion was delayed if the onset of sleep was delayed. Subjects who were awakened for 2-3 hr and allowed to return to sleep exhibited another peak of GH secretion (14-46 mmug/ml). Peak GH secretion was not correlated with changes in plasma glucose, insulin, and cortisol. The effects of 6-CNS-active drugs on sleep-related GH secretion were investigated. Imipramine (50 mg) completely abolished GH peaks in two of four subjects, whereas chlorpromazine (30 mg), phenobarbital (97 mg), diphenylhydantoin (90 mg), chlordiazepoxide (20 mg), and isocarboxazid (30 mg) did not inhibit GH peaks. Altered hypothalamic activity associated with initiation of sleep results in a major peak of growth hormone secretion unrelated to hypoglycemia or changes in cortisol and insulin secretion. Now, although that is disrupted, we know that our bodies are very good at compensating, and it seems overall 24 hour growth hormone levels are compensated for (7.) But the issue is, is this disruption causing a bigger issue? Could this change if it is chronic sleep deprivation? Would our bodies still compensate? I cannot answer that with certainty.

Sleep deprivation is also correlated to possible decline in thyroid hormone output, insulin sensitivity, and overall cognitive output (8, 9, 10.) The literature in this article makes it very clear that sleep deprivation very well COULD be why you’re not growing. So next time you hit a sticking point, remember to assess EVERY variable (looking at sleep first.) Once proper sleep patterns are assessed and corrected, you can move on to the next variable which could be holding back your progress.

References

  1. Acute partial sleep deprivation increases food intake in healthy men. Laurent Brondel, Michael A. Romer, Pauline M. Nougues, Peio Touyarou, Damien Davenne. Am J Clin Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20357041)
  2. Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men. Leproult, R., & Van Cauter, E. (2011). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445839/)
  3. Sleep deprivation reduces circulating androgens in healthy men. V. Cortés-Gallegos, G. Castañeda, R. Alonso, I. Sojo, A. Carranco, C. Cervantes, A. Parra. Arch Androl. 1983 (https://www.ncbi.nlm.nih.gov/pubmed/6405703)
  4. Sleep loss results in an elevation of cortisol levels the next evening. R. Leproult, G. Copinschi, O. Buxton, E. Van Cauter. Sleep. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9415946)
  5. Sleep disturbances are correlated with decreased morning awakening salivary cortisol. Jutta Backhaus, Klaus Junghanns, Fritz Hohagen. Psychoneuroendocrinology. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15219642)
  6. Growth hormone secretion during sleep. Y. Takahashi, D. M. Kipnis, W. H. Daughaday. J Clin Invest. 1968 (https://www.ncbi.nlm.nih.gov/pubmed/5675428)
  7. Effect of sleep deprivation on overall 24 h growth-hormone secretion. G. Brandenberger, C. Gronfier, F. Chapotot, C. Simon, F. Piquard. Lancet. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11052586)
  8. Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Anja Bosy-Westphal, Silvia Hinrichs, Kamila Jauch-Chara, Britta Hitze, Wiebke Later, Britta Wilms, Uta Settler, Achim Peters, Dieter Kiosz, Manfred James Muller. Obes Facts. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/20054188)
  9. Optimism and self-esteem are related to sleep. Results from a large community-based sample. Sakari Lemola, Katri Räikkönen, Veronica Gomez, Mathias Allemand. Int J Behav Med. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23055029)
  10. Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Kristen L. Knutson. Best Pract Res Clin Endocrinol Metab. (https://www.ncbi.nlm.nih.gov/pubmed/21112022)
]]>
Why You Might Not Be Growing Part 2 https://redcon1online.com/not-growing-2/ Wed, 21 Jun 2017 04:00:58 +0000 https://redcon1online.com/?p=3995 Participants completed the visual analog scales for global vigor and global affect at 2-hour intervals each day. Comparisons between conditions were performed using 2-sided nonparametric Wilcoxon tests with a significance level of .05. The 10 healthy men had a mean (SD) age of 24.3 (4.3) years and a mean (SD) body mass index of 23.5 (2.4) (calculated as weight in kilograms divided by height in meters squared). Total (SD) sleep time decreased from 8 hours 55 minutes (35 min) to 4 hours 48 minutes (6 min) with sleep restriction (P = .002). Relative to the rested condition, during each restricted night, participants lost a total (SD) of 2 hours 45 minutes (29 min) of stage-2 sleep (P = .002) and 1 hour 3 minutes (18 min) of REM sleep (P = .002) and gained 9 minutes (8 min) of sleep in stages 3 + 4 (P = .01). During waking hours common to both conditions (8 AM-10 PM), testosterone levels were lower after sleep restriction than in the rested condition (16.5 [2.8] nmol/L vs 18.4 [3.8] nmol/L; P = .049). The effect of restricted sleep was especially apparent between 2 PM and 10 PM (15.5 [3.1] nmol/L vs 17.9 [4.0] nmol/L; P = .02). Daytime cortisol profiles were similar under both conditions. Daily sleep restriction was associated with a progressive decrease in mean (SD) vigor scores from 28 (5) after the first night to 19 (7) after the seventh night (P = .002).  Shown are mean values. In the rested condition, bedtimes were from 10 PM to 8 AM. Values for partial sleep restriction were taken after 1 week of restriction, for which bedtimes were from 12:30 AM to 5:30 AM. On average over the 68 time points, the SD of testosterone levels at each time point was 5.01 nmol/L (range, 2.98-7.53 nmol/L) in the rested condition and 4.26 nmol/L (range, 2.82-6.92 nmol/L) in the restricted condition. On average over the 68 time points, the SD of cortisol levels at each time point was 67.1 nmol/L (range, 15.2-142.7 nmol/L) in the rested condition and 54.0 nmol/L (range, 7.7-162.3 nmol/L) in the restricted condition (2.)

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

  1. Acute partial sleep deprivation increases food intake in healthy men. Laurent Brondel, Michael A. Romer, Pauline M. Nougues, Peio Touyarou, Damien Davenne. Am J Clin Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20357041)
  2. Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men. Leproult, R., & Van Cauter, E. (2011). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445839/)
  3. Sleep deprivation reduces circulating androgens in healthy men. V. Cortés-Gallegos, G. Castañeda, R. Alonso, I. Sojo, A. Carranco, C. Cervantes, A. Parra. Arch Androl. 1983 (https://www.ncbi.nlm.nih.gov/pubmed/6405703)
  4. Sleep loss results in an elevation of cortisol levels the next evening. R. Leproult, G. Copinschi, O. Buxton, E. Van Cauter. Sleep. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9415946)
  5. Sleep disturbances are correlated with decreased morning awakening salivary cortisol. Jutta Backhaus, Klaus Junghanns, Fritz Hohagen. Psychoneuroendocrinology. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15219642)
  6. Growth hormone secretion during sleep. Y. Takahashi, D. M. Kipnis, W. H. Daughaday. J Clin Invest. 1968 (https://www.ncbi.nlm.nih.gov/pubmed/5675428)
  7. Effect of sleep deprivation on overall 24 h growth-hormone secretion. G. Brandenberger, C. Gronfier, F. Chapotot, C. Simon, F. Piquard. Lancet. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11052586)
  8. Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Anja Bosy-Westphal, Silvia Hinrichs, Kamila Jauch-Chara, Britta Hitze, Wiebke Later, Britta Wilms, Uta Settler, Achim Peters, Dieter Kiosz, Manfred James Muller. Obes Facts. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/20054188)
  9. Optimism and self-esteem are related to sleep. Results from a large community-based sample. Sakari Lemola, Katri Räikkönen, Veronica Gomez, Mathias Allemand. Int J Behav Med. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23055029)
  10. Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Kristen L. Knutson. Best Pract Res Clin Endocrinol Metab. (https://www.ncbi.nlm.nih.gov/pubmed/21112022)
]]>
Why You Might Not Be Growing Part 1 https://redcon1online.com/not-growing-1/ Tue, 20 Jun 2017 14:30:45 +0000 https://redcon1online.com/?p=3993 You’re probably reading this and wondering why you may not be making the progress you want in the gym. Maybe you’re not loosing fat fast enough, maybe your not gaining muscle at the rate that you want, maybe its a combination of the two. Either way, these are the situations were people typically first start doing MORE. MORE cardio. MORE training. MORE of a caloric deficit, and if theres one thing I learned from my last contest prep, its that MORE ISNT ALWAYS BETTER. Simply put, better is better or quality over quantity. And one of the most overlooked variables in muscle growth or fat loss IS SLEEP. Sleep deprivation is linked with obesity and many health disorders, so its no wonder, IF YOUR NOT SLEEPING, YOU SIMPLY CANNOT PROGRESS. In fact, acute partial sleep deprivation increases plasma concentrations of ghrelin and decreases those of leptin. This was a study looked at by Brondel et al (1).

“The objective was to observe modifications in energy intake and physical activity after acute partial sleep deprivation in healthy men. Twelve men [age: 22 +/- 3 y; body mass index (in kg/m(2)): 22.30 +/- 1.83] completed a randomized 2-condition crossover study. During the first night of each 48-h session, subjects had either approximately 8 h (from midnight to 0800) or approximately 4 h (from 0200 to 0600) of sleep. All foods consumed subsequently (jam on buttered toast for breakfast, buffet for lunch, and a free menu for dinner) were eaten ad libitum. Physical activity was recorded by an actimeter. Feelings of hunger, perceived pleasantness of the foods, desire to eat some foods, and sensation of sleepiness were also evaluated. In comparison with the 8-h sleep session, subjects consumed 559 +/- 617 kcal (ie, 22%) more energy on the day after sleep restriction (P < 0.01), and preprandial hunger was higher before breakfast (P < 0.001) and dinner (P < 0.05). No change in the perceived pleasantness of the foods or in the desire to eat the foods was observed. Physical activity from 1215 to 2015 was higher after sleep restriction than after 8 h of sleep (P < 0.01), even though the sensation of sleepiness was more marked (P < 0.01). One night of reduced sleep subsequently increased food intake and, to a lesser extent, estimated physical activity-related energy expenditure in healthy men. These experimental results, if confirmed by long-term energy balance measurements, suggest that sleep restriction could be a factor that promotes obesity.” But this is just the beginning. Not only can it be very closely linked with obesity but its hormonal effects are astounding!

First, we should look at testosterone levels in a study from Leproult et al on the effects of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men. After 1 week of 8-hour bedtimes (from 11 PM to 7 AM) at home, the participants spent 11 days in the laboratory for 3 nights of 10-hour bedtimes (from 10 PM to 8 AM; rested condition) followed by 8 nights of 5-hour bedtimes (from 12:30 AM to 5:30 AM; sleep restriction). Sleep was recorded each night and visually scored in stages 1, 2, 3, 4, and rapid eye movement (REM). Blood sampling every 15 to 30 minutes for 24 hours was initiated after the second 10-hour night and after the seventh 5-hour night. Samples were assayed for total testosterone and cortisol using an immunochemiluminescent assay (Immulite, Los Angeles, California). (To convert serum testosterone to ng/dL, divide by 0.0347; to convert serum cortisol to μg/dL, divide by 27.588.)

References

  1. Acute partial sleep deprivation increases food intake in healthy men. Laurent Brondel, Michael A. Romer, Pauline M. Nougues, Peio Touyarou, Damien Davenne. Am J Clin Nutr. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20357041)
  2. Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men. Leproult, R., & Van Cauter, E. (2011). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445839/)
  3. Sleep deprivation reduces circulating androgens in healthy men. V. Cortés-Gallegos, G. Castañeda, R. Alonso, I. Sojo, A. Carranco, C. Cervantes, A. Parra. Arch Androl. 1983 (https://www.ncbi.nlm.nih.gov/pubmed/6405703)
  4. Sleep loss results in an elevation of cortisol levels the next evening. R. Leproult, G. Copinschi, O. Buxton, E. Van Cauter. Sleep. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9415946)
  5. Sleep disturbances are correlated with decreased morning awakening salivary cortisol. Jutta Backhaus, Klaus Junghanns, Fritz Hohagen. Psychoneuroendocrinology. 2004 (https://www.ncbi.nlm.nih.gov/pubmed/15219642)
  6. Growth hormone secretion during sleep. Y. Takahashi, D. M. Kipnis, W. H. Daughaday. J Clin Invest. 1968 (https://www.ncbi.nlm.nih.gov/pubmed/5675428)
  7. Effect of sleep deprivation on overall 24 h growth-hormone secretion. G. Brandenberger, C. Gronfier, F. Chapotot, C. Simon, F. Piquard. Lancet. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11052586)
  8. Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Anja Bosy-Westphal, Silvia Hinrichs, Kamila Jauch-Chara, Britta Hitze, Wiebke Later, Britta Wilms, Uta Settler, Achim Peters, Dieter Kiosz, Manfred James Muller. Obes Facts. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/20054188)
  9. Optimism and self-esteem are related to sleep. Results from a large community-based sample. Sakari Lemola, Katri Räikkönen, Veronica Gomez, Mathias Allemand. Int J Behav Med. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23055029)
  10. Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Kristen L. Knutson. Best Pract Res Clin Endocrinol Metab. (https://www.ncbi.nlm.nih.gov/pubmed/21112022)
]]>
Coaches https://redcon1online.com/coaches/ Tue, 13 Jun 2017 17:34:14 +0000 https://redcon1online.com/?p=3980 Why do we ​decide to ​stop​? ​Wh​at makes us “end” only to sometime begin again?. ​My countless beginnings have always been about the gym. I can’t count how many times I’ve “started over.” What makes each time supposedly ​”​d​​ifferent​?”​ After a 22​-​month talk​ (with my 22-month toddler)​ I started over​ again​. Weights were heavier than I remember​. Each set was harder than the last. Why is this time any different​? ​Why ​i​s starting over now go​ing​ to be the difference between then and now​? Surprise – it’s not. Starting over is starting over. But the real difference this time is ​that I genuinely want it. I want the body I know is ​there, ​underneath it all. I want to be healthy​ and happy,​ and keep up with my daughter. I want ​to​ avoid the ​​diabetes I will ​certainly have if I stay where I am. I want ​this​ for my next baby​,​ s​imply s​o ​Pregnancy 2 is far happier and healthier than Pregnancy 1. And I want it for ​Faviana, who ​watches me work – I want her to grow up knowing it’s a​n incredible​ thing to ​truly ​t​​ake care of yourself and​ develop a​ love ​for ​fitness. Motivation is what starts you and drive is what​ propels​ you ​further​. Plain and simple, this time is the same​. Starting over, like all of the times ​before​. But the difference is…I ​finally WANT it.

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​ ​​​wait​ing 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​ da​y, 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 go​ing 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 be​st fit for you. ​My perfect fit is Team Bombshell with​ Mama Bombshell, Shannon De​y​, 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 make​sure 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!

-Wendy Capurso
@WendyLeeGovoni_Capurso
]]>
Protein Requirements for Bodybuilders- Part 2 https://redcon1online.com/protein-requirements-bodybuilders-part-2/ Wed, 24 May 2017 04:00:47 +0000 https://redcon1online.com/?p=3735 We must once again look to the works from Dr. Antonio (2) on the effects of a high protein diet on indices of health and body composition (a crossover trial in resistance-trained men.) The study was eight weeks of a high protein diet (>3 g/kg/day) coupled with a periodized heavy resistance training program has been shown to positively affect body composition with no deleterious effects on health. Using a randomized, crossover design, resistance-trained male subjects underwent a 16-week intervention (i.e., two 8-week periods) in which they consumed either their normal (i.e., habitual) or a higher protein diet (>3 g/kg/day). Thus, the purpose of this study was to ascertain if significantly increasing protein intake would affect clinical markers of health (i.e., lipids, kidney function, etc.) as well as performance and body composition in young males with extensive resistance training experience. Twelve healthy resistance-trained men volunteered for this study (mean ± SD: age 25.9 ± 3.7 years; height 178.0 ± 8.5 cm; years of resistance training experience 7.6 ± 3.6) with 11 subjects completing most of the assessments. In a randomized crossover trial, subjects were tested at baseline and after two 8-week treatment periods (i.e., habitual [normal] diet and high protein diet) for body composition, measures of health (i.e., blood lipids, comprehensive metabolic panel) and performance. Each subject maintained a food diary for the 16-week treatment period (i.e., 8 weeks on their normal or habitual diet and 8 weeks on a high protein diet). Each subject provided a food diary of two weekdays and one weekend day per week. In addition, subjects kept a diary of their training regimen that was used to calculate total work performed. During the normal and high protein phase of the treatment period, subjects consumed 2.6 ± 0.8 and 3.3 ± 0.8 g/kg/day of dietary protein, respectively. The mean protein intake over the 4-month period was 2.9 ± 0.9 g/kg/day. The high protein group consumed significantly more calories and protein (p < 0.05) than the normal protein group. There were no differences in dietary intake between the groups for any other measure. Moreover, there were no significant changes in body composition or markers of health in either group. There were no side effects (i.e., blood lipids, glucose, renal, kidney function etc.) regarding high protein consumption. In resistance-trained young men who do not significantly alter their training regimen, consuming a high protein diet (2.6 to 3.3 g/kg/day) over a 4-month period has no effect on blood lipids or markers of renal and hepatic function. Nor were there any changes in performance or body composition. This is the first crossover trial using resistance-trained subjects in which the elevation of protein intake to over four times the recommended dietary allowance has shown no harmful effects.

Dr. Jose Antonio’s research continues. This study (3) looked at the consumption of a high protein diet (>4 g/kg/d) in trained men and women who did not alter their exercise program. Thus, the purpose of this investigation was to determine if a high protein diet in conjunction with a periodized heavy resistance training program would affect indices of body composition, performance and health. Forty-eight healthy resistance-trained men and women completed this study (mean ± SD; Normal Protein group [NP n = 17, four female and 13 male]: 24.8 ± 6.9 yr; 174.0 ± 9.5 cm height; 74.7 ± 9.6 kg body weight; 2.4 ± 1.7 yr of training; High Protein group [HP n = 31, seven female and 24 male]: 22.9 ± 3.1 yr; 172.3 ± 7.7 cm; 74.3 ± 12.4 kg; 4.9 ± 4.1 yr of training). Moreover, all subjects participated in a split-routine, periodized heavy resistance-training program. Training and daily diet logs were kept by each subject. Subjects in the NP and HP groups were instructed to consume their baseline (~2 g/kg/d) and >3 g/kg/d of dietary protein, respectively. Subjects in the NP and HP groups consumed 2.3 and 3.4 g/kg/day of dietary protein during the treatment period. The NP group consumed significantly (p < 0.05) more protein during the treatment period compared to their baseline intake. The HP group consumed more (p < 0.05) total energy and protein during the treatment period compared to their baseline intake. Furthermore, the HP group consumed significantly more (p < 0.05) total calories and protein compared to the NP group. There were significant time by group (p ≤ 0.05) changes in body weight (change: +1.3 ± 1.3 kg NP, −0.1 ± 2.5 HP), fat mass (change: −0.3 ± 2.2 kg NP, −1.7 ± 2.3 HP), and % body fat (change: −0.7 ± 2.8 NP, −2.4 ± 2.9 HP). The NP group gained significantly more body weight than the HP group; however, the HP group experienced a greater decrease in fat mass and % body fat. There was a significant time effect for FFM; however, there was a non-significant time by group effect for FFM (change: +1.5 ± 1.8 NP, +1.5 ± 2.2 HP). Furthermore, a significant time effect (p ≤ 0.05) was seen in both groups vis a vis improvements in maximal strength (i.e., 1-RM squat and bench) vertical jump and pull-ups; however, there were no significant time by group effects (p ≥ 0.05) for all exercise performance measures. Additionally, there were no changes in any of the blood parameters (i.e., basic metabolic panel). They concluded by stating “consuming a high protein diet (3.4 g/kg/d) in conjunction with a heavy resistance-training program may confer benefits with regards to body composition. Furthermore, there is no evidence that consuming a high protein diet has any deleterious effects.”

References

  1. A High Protein Diet Has No Harmful Effects: A One-Year Crossover Study in Resistance-Trained Males. Jose AntonioAnya EllerbroekTobin SilverLeonel VargasArmando TamayoRichard Buehn, and Corey A. Peacock. Exercise and Sport Science Laboratory, Nova Southeastern University, Davie, FL, USA. 2016. (https://www.hindawi.com/journals/jnme/2016/9104792/)
  2. The effects of a high protein diet on indices of health and body composition – a crossover trial in resistance-trained men. Jose Antonio, Anya Ellerbroek, Tobin Silver, Leonel Vargas and Corey Peacock. Journal of the International Society of Sports Nutrition. 2016 (https://jissn.biomedcentral.com/articles/10.1186/s12970-016-0114-2)
  3. A high protein diet (3.4 g/kg/d) combined with a heavy resistance training program improves body composition in healthy trained men and women – a follow-up investigation. Jose Antonio, Anya Ellerbroek, Tobin Silver, Steve Orris, Max Scheiner, Adriana Gonzalez and Corey A Peacock. Journal of the International Society of Sports Nutrition. 2015 (https://jissn.biomedcentral.com/articles/10.1186/s12970-015-0100-0)
  4. International Society of Sports Nutrition position stand: protein and exercise. Bill Campbell, Richard B Kreider, Tim Ziegenfuss, Paul La Bounty, Mike Roberts, Darren Burke, Jamie Landis, Hector Lopez and Jose Antonio. Journal of the International Society of Sports Nutrition. 2007 (https://jissn.biomedcentral.com/articles/10.1186/1550-2783-4-8)
  5. Protein requirements and muscle mass/strength changes during intensive training in novice bodybuilders. P. W. Lemon, M. A. Tarnopolsky, J. D. MacDougall, S. A. Atkinson. J Appl Physiol (1985) (https://www.ncbi.nlm.nih.gov/pubmed/1400008)
  6. Protein requirements and muscle mass/strength changes during intensive training in novice bodybuilders. P. W. Lemon, M. A. Tarnopolsky, J. D. MacDougall, S. A. Atkinson. J Appl Physiol (1985) (https://www.ncbi.nlm.nih.gov/pubmed/1400008)
  7. Exercise-induced changes in protein metabolism. K. D. Tipton, R. R. Wolfe. Acta Physiol Scand. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9578384)
  8. Muscle protein synthesis in response to nutrition and exercise. P. J. Atherton, K. Smith. The Journal of Physiology. 2012 (http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2011.225003/abstract)
  9. Beyond the zone: protein needs of active individuals. P. W. Lemon. J Am Coll Nutr. 2000 (https://www.ncbi.nlm.nih.gov/pubmed/11023001)
  10. Meta-analysis of nitrogen balance studies for estimating protein requirements in healthy adults. William M. Rand, Peter L. Pellett, Vernon R. Young. Am J Clin Nutr. 2003 (https://www.ncbi.nlm.nih.gov/pubmed/12499330)
]]>