...INTENSITY...INSANITY...WATCH ME GROOW!!! - NaturalPursuit's Offseason Journey

[NaturalPursuit]

"Muscle growth can occur independent of an external load provided there are enough muscle fibers undergoing mechanotransduction."

I can't for the life of me understand the people that believe progressive overload just means moving a weight from point A to point B. Tension SHOULD ALWAYS BE A PRIORITY IF YOU'RE LOOKING TO MAXIMIZE SKELETAL MUSCLE HYPERTROPHY. Progressive overload means that you are adding more reps/weights/volume/etc over time and getting stronger. What that doesnt mean is just getting stronger by throwing weights around for the sake of it with no regard to contractions at all. Counts et al looked at the acute and chronic effects of "NO LOAD" resistance training and the lesson to be learned is a damn easy one...CONTRACT AND CREATE TENSION. In my mind, progressive overload and progressive tension ensures your body has no choice but to grow.


The acute and chronic effects of "NO LOAD" resistance training.

The purpose of the study was to remove the influence of an external load and determine if muscle growth can be elicited by maximally contracting through a full range of motion. In addition, the acute physiologic and perceptual responses to each stimulus were also investigated. Thirteen participants completed 18 sessions of unilateral elbow flexion exercise. Each arm was designated to either NO LOAD or HIGH LOAD condition (70% one repetition maximum). For the NO LOAD condition, participants repeatedly contracted as hard as they could through a full range of motion without the use of an external load. Our results show that anterior muscle thickness increased similarly from Pre to Post, with no differences between conditions for the 50% [Pre: 2.7 (0.8) vs. Post: 2.9 (0.7)], 60% [Pre: 2.9 (0.7) vs. Post: 3.1 (0.7)] or 70% [Pre: 3.2 (0.7) vs. Post: 3.5 (0.7)] sites. There was a significant condition×time interaction for one repetition maximum (p=0.017), with HIGH LOAD (+2.3kg) increasing more than the NO LOAD condition (+1kg). These results extend previous studies that have observed muscle growth across a range of external loads and muscle actions and suggest that muscle growth can occur independent of an external load provided there are enough muscle fibers undergoing mechanotransduction.

https://www.ncbi.nlm.nih.gov/pubmed/27329807

[NaturalPursuit]

L-TYROSINE

L-Tyrosine’s metabolic pathway actually begins with L-phenylalanine which then gets converted into L-tyrosine through phenylalanine hydroxylase (an enzyme.) It then gets converted into L-DOPA which is further decarboxylated into Dopamine. That then turns into noradrenaline before finally being converted to adrenaline. As you can assume given its catecholamine metabolic pathway, it will have significant impact on overall cognitive abilities, stress levels, and focus. Banderet et al looked at treating patients with tyrosine in an effort to reduce environmental stress as these acutely stressful situations can disrupt behavior, deplete brain norepinephrine, dopamine, and catecholaminergic neurotransmitters. This study used a double-blind, placebo-controlled crossover design utilizing 100 mg/kg of tyrosine after a 4.5 hour exposure to cold and hypoxia (again to see if supplementation would protect us from these stressful events.) What the researchers found was tyrosine significantly decreased symptoms, adverse moods, and performance impairments in subjects who exhibited average or greater responses to these environmental conditions. These results suggest that tyrosine should be evaluated in a variety of acutely stressful situations (1.) With that study showing us that tyrosine supplementation can aid in stressful environments, it should make more sense why its commonly found in our supplements. We as physique athletes are continuously running ourselves into the ground with resistance training and constant subjection to that type of stressful environment has the ability to lead to injury, over training, and/or unwanted central nervous system stress.

The next key point to touch on is tyrosine’s ability to help us as athletes from a cognitive functioning and performance standpoint. Neri and colleagues investigated the effects of tyrosine on cognitive performance during extended wakefulness. This particular study examine the effects of tyrosine during continuous nighttime work (which obviously involved sleep deprivation.) Subjects performed nine iterations of a battery of performance tasks and mood scales for approximately 13 h, beginning at 1930 and ending at 0820. They remained awake throughout the day on which the experiment began and were awake for more than 24 h by the end of testing. Six hours after the experiment began, one-half of the subjects received 150 mg.kg-1 tyrosine in a split dose while the other half received cornstarch placebo in a double-blind procedure. Tyrosine administration was associated with a significant amelioration of the usual performance decline on a psychomotor task and a significant reduction in lapse probability on a high-event- rate vigilance task. The improvements lasted on the order of 3 h. The results of this study also suggest that tyrosine is a relatively benign treatment at this dose. After further testing with other doses and timing of administration, tyrosine may prove useful in counteracting performance decrements during episodes of sustained work coupled with sleep loss (2.) With this information in mind, we need to remember context. If tyrosine has this ability to aid in counteracting cognitive performance decreases during sleep deprivation, does that also mean it will be even more effective when utilized when not sleep deprived? The answer is not as simple as just saying yes, but it is safe to say that with all of the other research from Hinz, Lenhert, Meeusen, Sved, etc on its ability to improve memory functioning, attention, and cognitive stress reduction, it certainly will be an aid (3, 4, 5, 6, 7, 8.)

In terms of practical application we’re looking at a dose of roughly 500mgs – 2g about 45 minutes before your resistance training (or even during periods of stress such as final examines, job interviews, presentations, etc.) Although that number is not set in stone, based on the literature available to us it is a good range to work within. As always start with the minimum effective dosage, takes notes on how it effects you personally, and adjust as needed. Hopefully you now have a better understanding of why tyrosine is in so many supplements.

References

Treatment with tyrosine, a neurotransmitter precursor, reduces environmental stress in humans. L. E. Banderet, H. R. Lieberman. Brain Res Bull. 1989 (https://www.ncbi.nlm.nih.gov/pubmed/2736402)

The effects of tyrosine on cognitive performance during extended wakefulness. D. F. Neri, D. Wiegmann, R. R. Stanny, S. A. Shappell, A. McCardie, D. L. McKay. Aviat Space Environ Med. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/7794222)

Treatment of attention deficit hyperactivity disorder with monoamine amino acid precursors and organic cation transporter assay interpretation. Hinz, M., Stein, A., Neff, R., Weinberg, R., & Uncini, T. (2011). Neuropsychiatric Disease and Treatment.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035600/)

Neurochemical and behavioral consequences of acute, uncontrollable stress: effects of dietary tyrosine. H. Lehnert, D. K. Reinstein, B. W. Strowbridge, R. J. Wurtman. Brain Res. 1984 (https://www.ncbi.nlm.nih.gov/pubmed/6204715)

Effects of coping behavior in different warning signal conditions on stress pathology in rats. J.M. Weiss. J Comp Physiol Psychol. 1971 (https://www.ncbi.nlm.nih.gov/pubmed/5166076)

The brain and fatigue: new opportunities for nutritional interventions? Romain Meeusen, Phil Watson, Jiri Dvorak. J Sports Sci. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16766505)

Tyrosine administration reduces blood pressure and enhances brain norepinephrine release in spontaneously hypertensive rats. Sved, A. F., Fernstrom, J. D., & Wurtman, R. J. (1979). Proceedings of the National Academy of Sciences of the United States of America.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC383857/)

Tyrosine reverses a cold-induced working memory deficit in humans. D. Shurtleff, J. R. Thomas, J. Schrot, K. Kowalski, R. Harford Pharmacol Biochem Behav. 1994 (https://www.ncbi.nlm.nih.gov/pubmed/8029265)

[NaturalPursuit]

One of the best molecules out there. Theres no reason everyone shouldnt be supplementing with CoQ10 in either the oxidized form (ubiquinone) or reduced form (ubiquinol.)

1. Ubiquinol supplementation enhances peak power production in trained athletes: a double-blind, placebo controlled study (https://jissn.biomedcentral.com/arti...550-2783-10-24)

2. Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals (https://www.ncbi.nlm.nih.gov/pubmed/18318910)

3. Safety assessment of coenzyme Q10 (CoQ10) (https://www.ncbi.nlm.nih.gov/pubmed/19096117)

4. Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2315638/)

[JohnMariettePT]

Your title seems fitting, I am sure I've commented before in here but god damn keep it up. Inspiring to say the least.

[NaturalPursuit]

An article I've written that is part of a series of health based supplements

HEALTH SUPPLEMENTS: Grape Seed Extract and Taurine

This next installment of health supplements that I feel deserve a bigger spot light involves grape seed extract and taurine. Thus far, we’ve covered basic multi-vitamins, fish oil, Vitamin C, and Vitamin D3. Now we are going to be getting away from most of the basics that everyone knows and moving deeper into seeing what the research has to offer us about some of the more popular health based supplements. This article will focus on grape seed extract and taurine. Grape Seed Extract (made of tannins and procyanidins) are metabolized into GTCs (green tea catechizes.) The list of benefits from grape seed extract goes on and on including:

•anti-estrogenic effects
•decreased blood pressure
•decreased heart rate
•increased blood flow
•decreased cholesterol

With grape seed extract, dosages per day range from 300-600mgs. If you have any hunger issues than taking it with a meal has the potential to increase satiety (1, 2, 3, 4, 5, 6.) Moving onto our next supplement we have taurine which typically isn't seen as a health supplement. Taurine is an organic acid which acts as a stablilizer within our bodies. Furthermore, this beta-amino acid is an amino group paired to a sulfonic group by two methylene groups in a chain with a tremendous amount of antioxidant effects. Those include:

•positive effects on the CNS
•positive effects within cardiac muscle
•increased renal protection
•increased hydration rates
•decreased cramping rates
•positive insulin regulation
•overall reduction in inflammation

With the literature we see taurine being dosed anywhere from as low as 500mgs to 5 grams per day. This is going to depend mainly on why you are using taurine. In general, I like to keep it as a rule of thumb to stick within the 3-5 gram range as there you will see ergogenic benefits along with the tremendous amount of beneficial health aspects that we already previous discussed (7, 8, 9, 10, 11, 12, 13, 14, 15.) Grape seed extract and taurine dont get their just due as aiding in health markers. I hope this article helped shed some light onto why I feel they have their place within a health based supplement program.



References

1. Effect of grape seed extract on blood pressure in subjects with the metabolic syndrome.
Brahmesh Sivaprakasapillai, Indika Edirisinghe, Jody Randolph, Francene Steinberg, Tissa Kappagoda. Metabolism. 2009 Dec; 58(12): 1743–1746. Published online 2009 Jul 15. doi: 10.1016/j.metabol.2009.05.030

2. The effect of grape seed extract on cardiovascular risk markers: a meta-analysis of randomized controlled trials. Harm H. H. Feringa, Dayne A. Laskey, Justine E. Dickson, Craig I. Coleman
J Am Diet Assoc. 2011 Aug; 111(8): 1173–1181. doi: 10.1016/j.jada.2011.05.015

3. Grape seed and red wine polyphenol extracts inhibit cellular cholesterol uptake, cell proliferation, and 5-lipoxygenase activity. Wayne R. Leifert, Mahinda Y. Abeywardena. Nutr Res. 2008 Dec; 28(12): 842–850. Published online 2008 Nov 8. doi: 10.1016/j.nutres.2008.09.001

4. Effects of grape seed extract in Type 2 diabetic subjects at high cardiovascular risk: a double blind randomized placebo controlled trial examining metabolic markers, vascular tone, inflammation, oxidative stress and insulin sensitivity. P. Kar, D. Laight, H. K. Rooprai, K. M. Shaw, M. Cummings. Diabet Med. 2009 May; 26(5): 526–531. doi: 10.1111/j.1464-5491.2009.02727.x

5. Effect of a standardized grape seed extract on low-density lipoprotein susceptibility to oxidation in heavy smokers. Giovanni B. Vigna, Fabrizio Costantini, Giancarlo Aldini, Marina Carini, Alberico Catapano, Fabio Schena, Arianna Tangerini, Rosanna Zanca, Egidio Bombardelli, Paolo Morazzoni, et al. Metabolism. 2003 Oct; 52(10): 1250–1257.

6. Specialty Supplements and Prostate Cancer Risk in the VITamins And Lifestyle (VITAL) Cohort. Theodore M. Brasky, Alan R. Kristal, Sandi L. Navarro, Johanna W. Lampe, Ruth E. Patterson, Ulrike Peters, Emily White. Nutr Cancer. Author manuscript; available in PMC 2012 May 1. Published in final edited form as: Nutr Cancer. 2011 May; 63(4): 573–582. doi: 10.1080/01635581.2011.553022

7. Effect of taurine supplementation on exercise capacity of patients with heart failure.
Mohamad Reza Beyranvand, Mahshid Kadkhodai Khalafi, Valiollah Dabidi Roshan, Sirrus Choobineh, Saeid Alipour Parsa, Mohammad Asadpour Piranfar. J Cardiol. 2011 May; 57(3): 333–337. Published online 2011 Feb 19. doi: 10.1016/j.jjcc.2011.01.007

8. The effect of acute taurine ingestion on endurance performance and metabolism in well-trained cyclists. Jane A. Rutherford, Lawrence L. Spriet, Trent Stellingwerff. Int J Sport Nutr Exerc Metab. 2010 Aug; 20(4): 322–329.

9. Effect of taurine supplementation on exercise capacity of patients with heart failure.
Mohamad Reza Beyranvand, Mahshid Kadkhodai Khalafi, Valiollah Dabidi Roshan, Sirrus Choobineh, Saeid Alipour Parsa, Mohammad Asadpour Piranfar. J Cardiol. 2011 May; 57(3): 333–337. Published online 2011 Feb 19. doi: 10.1016/j.jjcc.2011.01.007

10. Two weeks taurine supplementation reverses endothelial dysfunction in young male type 1 diabetics. Michael A. Moloney, Rowan G. Casey, David H. O'Donnell, Patricia Fitzgerald, Chris Thompson, David J. Bouchier-Hayes. Diab Vasc Dis Res. 2010 Oct; 7(4): 300–310. Published online 2010 Jul 28. doi: 10.1177/1479164110375971

11. The taurine transporter gene and its role in renal development. X. Han, A. M. Budreau, R. W. Chesney. Amino Acids. 2000; 19(3-4): 499–507.

12. Localization of the membrane defect in transepithelial transport of taurine by parallel studies in vivo and in vitro in hypertaurinuric mice. R W Chesney, C R Scriver, F Mohyuddin
J Clin Invest. 1976 Jan; 57(1): 183–193.

13. Adaptive regulation of taurine transport in two continuous renal epithelial cell lines.
D. P. Jones, L. A. Miller, R. W. Chesney. Kidney Int. 1990 Aug; 38(2): 219–226.

14. Perinatal Taurine Alters Arterial Pressure Control and Renal Function in Adult Offspring
Sanya Roysommuti, Wichaporn Lerdweeraphon, Pisamai Malila, Dusit Jirakulsomchok, J. Michael Wyss. Adv Exp Med Biol. Author manuscript; available in PMC 2010 Jan 1.
Published in final edited form as: Adv Exp Med Biol. 2009; 643: 145–156.

15. Perinatal taurine depletion increases susceptibility to adult sugar-induced hypertension in rats
Sanya Roysommuti, Atchariya Suwanich, Dusit Jirakulsomchok, J. Michael Wyss
Adv Exp Med Biol. Author manuscript; available in PMC 2010 Jan 1. Published in final edited form as: Adv Exp Med Biol. 2009; 643: 123–133. doi: 10.1007/978-0-387-75681-3_13

[NaturalPursuit]

Your title seems fitting, I am sure I've commented before in here but god damn keep it up. Inspiring to say the least.

Thanks brother! Sorry I havent had time to post up my workouts...things are changing almost daily at this point in prep

[NaturalPursuit]

Full article on Curcumin supplementation coming soon...

"One study from Khajehdeh et al looked at how oral supplementation of turmeric decreases proteinuria, hematuria, and systolic blood pressure in patients suffering from relapsing or refractory lupus nephritis. In this randomized and placebo-controlled study, a total of 24 patients with relapsing or refractory biopsy-proven lupus nephritis, who were randomized in 2 groups (trial [n = 12] and control [n = 12] groups) were included in this study. With each meal, each patient in the trial group received 1 capsule for 3 months, which contained 500 mg turmeric, of which 22.1 mg was the active ingredient curcumin (3 capsules daily). The control group received 3 capsules (1 with each meal) for the same period, which contained starch and were identical in color and size to capsules given to patients in the trial group. Data were analyzed using Statistical Package for the Social Sciences software version 15.0. A significant decrease in proteinuria was found when comparing pre- (954.2 ± 836.6) and 1, 2, and 3 months supplementation values (448.8 ± 633.5, 235.9 ± 290.1, and 260.9 ± 106.2, respectively) in the trial group. Also, systolic blood pressure and hematuria were found to decrease significantly when pre- and post-turmeric supplementation values were compared in the trial group. However, placebo capsules did not exert any statistically significant effect on measured variables in the control group over 3 months of the study. No adverse effect related to turmeric supplementation was observed during the trial. They concluded that short-term turmeric supplementation can decrease proteinuria, hematuria, and systolic blood pressure in patients suffering from relapsing or refractory lupus nephritis and can be used as an adjuvant safe therapy for such patients (6.)"


References
1. Pharmacodynamic and pharmacokinetic study of oral Curcuma extract in patients with colorectal cancer. R. A. Sharma, H. R. McLelland, K. A. Hill, C. R. Ireson, S. A. Euden, M. M. Manson, M. Pirmohamed, L. J. Marnett, A. J. Gescher, W. P. Steward. Clin Cancer Res. 2001 (https://www.ncbi.nlm.nih.gov/pubmed/11448902)
2. Dose escalation of a curcuminoid formulation. Christopher D Lao, Mack T Ruffin, IV, Daniel Normolle, Dennis D Heath, Sandra I Murray, Joanne M Bailey, Martha E Boggs, James Crowell, Cheryl L Rock, Dean E Brenner. BMC Complement Altern Med. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16545122)
3. Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers. G. Shoba, D. Joy, T. Joseph, M. Majeed, R. Rajendran, P. S. Srinivas. Planta Med. 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9619120)
4. Insulin resistance associated to obesity: the link TNF-alpha. Iria Nieto-Vazquez, Sonia Fernández-Veledo, David K. Krämer, Rocio Vila-Bedmar, Lucia Garcia-Guerra, Margarita Lorenzo. Arch Physiol Biochem. 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18629684)
5. The expression of tumor necrosis factor in human adipose tissue. Regulation by obesity, weight loss, and relationship to lipoprotein lipase. Kern, P. A., Saghizadeh, M., Ong, J. M., Bosch, R. J., Deem, R., & Simsolo, R. B. (1995). Journal of Clinical Investigation (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC295809/)
6. Oral supplementation of turmeric decreases proteinuria, hematuria, and systolic blood pressure in patients suffering from relapsing or refractory lupus nephritis: a randomized and placebo-controlled study. Parviz Khajehdehi, Batol Zanjaninejad, Elham Aflaki, Mohamadali Nazarinia, Fariborz Azad, Leila Malekmakan, Gholam-Reza Dehghanzadeh. J Ren Nutr. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/21742514)
7. Screening of potential cancer preventing chemicals as aromatase inhibitors in an in vitro assay.
E. L. White, L. J. Ross, V. E. Steele, G. J. Kelloff, D. L. Hill. Anticancer Res. 1999 (https://www.ncbi.nlm.nih.gov/pmc/art...y/?tool=pubmed)
8. Reference profile correlation reveals estrogen-like trancriptional activity of Curcumin.
Beatrice E. Bachmeier, Valentina Mirisola, Francesco Romeo, Luca Generoso, Alessia Esposito, Raffaella Dell'eva, Fabiola Blengio, Peter H. Killian, Adriana Albini, Ulrich Pfeffer. Cell Physiol Biochem. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20798532)
9. Effects of dietary curcumin on glutathione S-transferase and malondialdehyde-DNA adducts in rat liver and colon mucosa: relationship with drug levels. R. A. Sharma, C. R. Ireson, R. D. Verschoyle, K. A. Hill, M. L. Williams, C. Leuratti, M. M. Manson, L. J. Marnett, W. P. Steward, A. Gescher. Clin Cancer Res. 2001 (https://www.ncbi.nlm.nih.gov/pubmed/11350917)

[NaturalPursuit]

Some nitrates are pretty cool when you look at some of their effects. Overall they definitely have their place but its not the end all be all like some people make them out to be



The effect of six days of dietary nitrate supplementation on performance in trained CrossFit athletes

Background
While it is well established that dietary nitrate reduces the metabolic cost of exercise, recent evidence suggests this effect is maintained 24 h following the final nitrate dose when plasma nitrite levels have returned to baseline. In addition, acute dietary nitrate was recently reported to enhance peak power production. Our purpose was to examine whether chronic dietary nitrate supplementation enhanced peak power 24 h following the final dose and if this impacted performance in a heavily power-dependent sport.

Methods
In a double-blind, randomized, crossover design, maximal aerobic capacity, body composition, strength, maximal power (30 s Wingate), endurance (2 km rowing time trial), and CrossFit performance (Grace protocol) were assessed before and after six days of supplementation with nitrate (NO) (8 mmol·potassium nitrate·d−1) or a non-caloric placebo (PL). A 10-day washout period divided treatment conditions. Paired t-tests were utilized to assess changes over time and to compare changes between treatments.

Results
Peak Wingate power increased significantly over time with NO (889.17 ± 179.69 W to 948.08 ± 186.80 W; p = 0.01) but not PL (898.08 ± 183.24 W to 905.00 ± 157.23 W; p = 0.75). However, CrossFit performance was unchanged, and there were no changes in any other performance parameters.

Conclusion
Consuming dietary nitrate in the potassium nitrate salt form improved peak power during a Wingate test, but did not improve elements of strength or endurance in male CrossFit athletes.

http://jissn.biomedcentral.com/artic...970-016-0150-y

[NaturalPursuit]

Role of myokines in exercise and metabolism

During the past 20 yr, it has been well documented that exercise has a profound effect on the immune system. With the discovery that exercise provokes an increase in a number of cytokines, a possible link between skeletal muscle contractile activity and immune changes was established. For most of the last century, researchers sought a link between muscle contraction and humoral changes in the form of an "exercise factor," which could mediate some of the exercise-induced metabolic changes in other organs such as the liver and the adipose tissue. We suggest that cytokines and other peptides that are produced, expressed, and released by muscle fibers and exert either paracrine or endocrine effects should be classified as "myokines." Since the discovery of interleukin (IL)-6 release from contracting skeletal muscle, evidence has accumulated that supports an effect of IL-6 on metabolism. We suggested that muscle-derived IL-6 fulfils the criteria of an exercise factor and that such classes of cytokines should be named "myokines." Interestingly, recent research demonstrates that skeletal muscles can produce and express cytokines belonging to distinctly different families. Thus skeletal muscle has the capacity to express several myokines. To date the list includes IL-6, IL-8, and IL-15, and contractile activity plays a role in regulating the expression of these cytokines in skeletal muscle. The present review focuses on muscle-derived cytokines, their regulation by exercise, and their possible roles in metabolism and skeletal muscle function and it discusses which cytokines should be classified as true myokines.

https://www.ncbi.nlm.nih.gov/pubmed/17347387

[NaturalPursuit]

MILK THISTLE

Milk thistle is actually an herb that contains a couple ingredients. These ingredients all together are referred to as silymarins. This supplement is commonly known to be a liver aid, but possess much more than simply aid to the liver. We are going to cover its main benefits in the following paragraphs.

As a liver aid, milk thistle works by enhancing cellular protein synthesis. This action essentially means it has the ability to increase the rate of protein synthesis within liver cells. Even further more, it may even be able to cause injured liver cells to begin repairing themselves. It induces your liver cells to synthesize more glutathione, which is a major anti-oxidant that improves overall liver functioning (1, 2, 3.) Its abundantly clear that milk thistle has its place in terms of liver health, but as I previous mentioned, the list of its other benefits goes on and on. There was one study from Murata and colleagues that looked into its relationship with Alzheimer’s disease. As this supplement is very well known for its ability to reduce the accumulation of cholesterol and fats within the body, the researchers hypothesized that had some correlation to positive effects on the health of the brain. The researchers gave half of their testing population (mice) the supplement while the others did not receive them. These mice were all genetically modified to synthesize plaques as this is the most common way researchers study Alzheimer’s disease. At the end of the study, they found that the mice that consumed milk thistle reduced the formation of the blocks that these plaques were composed of which lead to the inhibition of the entire process of forming these plaques. They had also taken photos of the mice’s brain tissue and found the tissue from those that did not supplement with milk thistle had essentially more plaques when compared to the group that had supplemented with it (4.)

At this point, we know conclude that milk thistle aids in liver health and regeneration as well as aids in overall brain health. If that wasn't enough to make you want to start looking into milk thistle supplementation, this next one might. Milk thistle supplementation has aid in reducing insulin resistance. In fact, its been used to help type II diabetics managing their lifestyle. Looking at the National Institute of Health, there is an exceedingly high amount of literature showing that the anti-oxidants found within milk thistle have been able to decrease blood sugar levels in diabetic/insulin resistant patients. They found that these diabetic patients utilizing milk thistle over a four week timeframe, were able to improve their fasting blood glucose and insulin levels significantly (5.) Milk thistle has even been related to decreasing the risk for cancer. When you look at silymarin from a molecular standpoint, you’ll see roughly 50% of those molecules are classified as silybin. This is the main anti-oxidant that stimulates protein synthesis and actually alters the outermost layer of cells which keeps them from occurring any damage from free radicals, chemical, heavy metals, etc. Researcher Post-White even made a fairly bold statement in his study titled “Advances in the use of milk thistle (Silybum marianum).” His statement was ““There is strong preclinical evidence for silymarin’s hepatoprotective and anticarcinogenic effects, including inhibition of cancer cell growth in human prostate, skin, breast, and cervical cells” (6.) Even researchers at the University Magna Graecia Department of Experimental and Clinical Medicine say that silymarin acts as a cancer protector mainly because of its ability to block the entering and binding of toxins to our cell membranes and receptors (2.)

Currently, there is no standardized dosages to prescribe given the research we have available to us. It dose seem to point towards a 100-300mg dosage per day to be the range in which it may potentially act properly. There have even been pieces of literature to show hepatic protection at dosages as low as 20mgs per day. All in all, milk thistle is a health supplement I would recommend to anyone trying to optimize their health and longevity. In general its a very affordable supplement that can pay off massively long term.


References

1. Biochemical effects of the flavonolignane silibinin on RNA, protein and DNA synthesis in rat livers. J. Sonnenbichler, I. Zetl. Prog Clin Biol Res. 1986 (https://www.ncbi.nlm.nih.gov/pubmed/2424029)

2. Milk thistle in liver diseases: past, present, future. Ludovico Abenavoli, Raffaele Capasso, Natasa Milic, Francesco Capasso. Phytother Res. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20564545)

3. Free radicals in tissue damage in liver diseases and therapeutic approach. J. Fehér, I. Láng, G. Deák, A. Cornides, K. Nékám, P. Gergely. Tokai J Exp Clin Med. 1986 (https://www.ncbi.nlm.nih.gov/pubmed/3452238)

4. Silymarin attenuated the amyloid β plaque burden and improved behavioral abnormalities in an Alzheimer's disease mouse model. Nakaba Murata, Kazuma Murakami, Yusuke Ozawa, Noriaki Kino****a, Kazuhiro Irie, Takuji Shirasawa, Takahiko Shimizu. Biosci Biotechnol Biochem. 2010; 74(11): 2299–2306. Published online 2010 (https://www.ncbi.nlm.nih.gov/pubmed/21071836)

5. The efficacy of Silybum marianum (L.) Gaertn. (silymarin) in the treatment of type II diabetes: a randomized, double-blind, placebo-controlled, clinical trial. H. Fallah Huseini, B. Larijani, R. Heshmat, H. Fakhrzadeh, B. Radjabipour, T. Toliat, Mohsin Raza. Phytother Res. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/17072885)

6. Advances in the use of milk thistle (Silybum marianum). Janice Post-White, Elena J. Ladas, Kara M. Kelly. Integr Cancer Ther. 2007 (https://www.ncbi.nlm.nih.gov/pubmed/17548789)

[NaturalPursuit]

The anabolic response to a meal containing different amounts of protein is not limited by the maximal stimulation of protein synthesis in healthy young adults

We have determined whole body protein kinetics, i.e., protein synthesis (PS), breakdown (PB), and net balance (NB) in human subjects in the fasted state and following ingestion of ~40 g [moderate protein (MP)], which has been reported to maximize the protein synthetic response or ~70 g [higher protein (HP)] protein, more representative of the amount of protein in the dinner of an average American diet. Twenty-three healthy young adults who had performed prior resistance exercise (X-MP or X-HP) or time-matched resting (R-MP or R-HP) were studied during a primed continuous infusion of l-[(2)H5]phenylalanine and l-[(2)H2]tyrosine. Subjects were randomly assigned into an exercise (X, n = 12) or resting (R, n = 11) group, and each group was studied at the two levels of dietary protein intake in random order. PS, PB, and NB were expressed as increases above the basal, fasting values (mg·kg lean body mass(-1)·min(-1)). Exercise did not significantly affect protein kinetics and blood chemistry. Feeding resulted in positive NB at both levels of protein intake: NB was greater in response to the meal containing HP vs. MP (P < 0.00001). The greater NB with HP was achieved primarily through a greater reduction in PB and to a lesser extent stimulation of protein synthesis (for all, P < 0.0001). HP resulted in greater plasma essential amino acid responses (P < 0.01) vs. MP, with no differences in insulin and glucose responses. In conclusion, whole body net protein balance improves with greater protein intake above that previously suggested to maximally stimulating muscle protein synthesis because of a simultaneous reduction in protein breakdown.

https://www.ncbi.nlm.nih.gov/pubmed/26530155

[NaturalPursuit]

High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine

We determined the effect of coingestion of caffeine (Caff) with carbohydrate (CHO) on rates of muscle glycogen resynthesis during recovery from exhaustive exercise in seven trained subjects who completed two experimental trials in a randomized, double-blind crossover design. The evening before an experiment subjects performed intermittent exhaustive cycling and then consumed a low-CHO meal. The next morning subjects rode until volitional fatigue. On completion of this ride subjects consumed either CHO [4 g/kg body mass (BM)] or the same amount of CHO + Caff (8 mg/kg BM) during 4 h of passive recovery. Muscle biopsies and blood samples were taken at regular intervals throughout recovery. Muscle glycogen levels were similar at exhaustion [ approximately 75 mmol/kg dry wt (dw)] and increased by a similar amount ( approximately 80%) after 1 h of recovery (133 +/- 37.8 vs. 149 +/- 48 mmol/kg dw for CHO and Caff, respectively). After 4 h of recovery Caff resulted in higher glycogen accumulation (313 +/- 69 vs. 234 +/- 50 mmol/kg dw, P < 0.001). Accordingly, the overall rate of resynthesis for the 4-h recovery period was 66% higher in Caff compared with CHO (57.7 +/- 18.5 vs. 38.0 +/- 7.7 mmol x kg dw(-1) x h(-1), P < 0.05). After 1 h of recovery plasma Caff levels had increased to 31 +/- 11 microM (P < 0.001) and at the end of the recovery reached 77 +/- 11 microM (P < 0.001) with Caff. Phosphorylation of CaMK(Thr286) was similar after exercise and after 1 h of recovery, but after 4 h CaMK(Thr286) phosphorylation was higher in Caff than CHO (P < 0.05). Phosphorylation of AMP-activated protein kinase (AMPK)(Thr172) and Akt(Ser473) was similar for both treatments at all time points. We provide the first evidence that in trained subjects coingestion of large amounts of Caff (8 mg/kg BM) with CHO has an additive effect on rates of postexercise muscle glycogen accumulation compared with consumption of CHO alone.

https://www.ncbi.nlm.nih.gov/pubmed/18467543

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Part of an article I wrote on Light Weights Stimulating Hypertrophy

The first bit of literate comes from Mitchell et al where they looked at how resistance exercise load does not determine training-mediated hypertrophic gains in young men. They had eighteen men had their legs randomly assigned to two of three training conditions that differed in contraction intensity or contraction volume. Subjects trained each leg with their assigned regime for a period of 10 wk, 3 times/wk. They made pre- and posttraining measures of strength, muscle volume by magnetic resonance (MR) scans, as well as pre- and posttraining biopsies of the vastus lateralis, and a single postexercise (1 h) biopsy following the first bout of exercise, to measure signaling proteins. Training-induced increases in MR-measured muscle volume were significant, with no difference between groups. Isotonic maximal strength gains were not different between 80%-1 and 80%-3, but were greater than 30%-3, whereas training-induced isometric strength gains were significant but not different between conditions. Biopsies taken 1 h following the initial resistance exercise bout showed increased phosphorylation of p70S6K only in the 80%-1 and 80%-3 conditions. There was no correlation between phosphorylation of any signaling protein and hypertrophy. In accordance with our previous acute measurements of muscle protein synthetic rates a lower load lifted to failure resulted in similar hypertrophy as a heavy load lifted to failure (1.)

Based off of that study from Mitchell et al, we find that hypertrophy is more correlated to fatigue/failure than actual load. But obviously one study is not enough to draw an accurate conclusion so we will now continue on to work from Dr. Brad Schoenfeld et al. The first study measured the effects of low- vs. high-load resistance training on muscle strength and hypertrophy. The purpose of this study was to compare the effect of low- versus high-load resistance training on muscular adaptations in well-trained subjects. Eighteen young men experienced in RT were matched according to baseline strength and then randomly assigned to 1 of 2 experimental groups: a low-load RT routine where 25-35 repetitions were performed per set per exercise or a high-load RT routine where 8-12 repetitions were performed per set per exercise. During each session, subjects in both groups performed 3 sets of 7 different exercises representing all major muscles. Training was performed 3 times per week on nonconsecutive days, for a total of 8 weeks. Both HL and LL conditions produced significant increases in thickness of the elbow flexors, elbow extensors, and quadriceps femoris, with no significant differences noted between groups. Improvements in back squat strength were significantly greater for HL compared with LL, and there was a trend for greater increases in 1 repetition maximum (1RM) bench press. Upper body muscle endurance improved to a greater extent in LL compared with HL. These findings indicate that both HL and LL training to failure can elicit significant increases in muscle hypertrophy among well-trained young men; however, HL training is superior for maximizing strength adaptations (2.) Now we see a different side of the argument where, although light load training increased hypertrophy, heavy load training is favored for maximizing strength. This brings on onto our second study again from Schoenfeld et al that was a meta analysis of muscular adaptations in low- versus high-load resistance training. The purpose of this paper therefore was to conduct a meta-analysis of randomised controlled trials to compare the effects of low-load (≤60% 1 repetition maximum [RM]) versus high-load (≥65% 1 RM) training in enhancing post-exercise muscular adaptations. The strength analysis comprised 251 subjects and 32 effect sizes, nested within 20 treatment groups and 9 studies. The hypertrophy analysis comprised 191 subjects and 34 ESs, nested with 17 treatment groups and 8 studies. There was a trend for strength outcomes to be greater with high loads compared to low loads. The mean ES for low loads was 1.23 ± 0.43. The mean ES for high loads was 2.30 ± 0.43. There was a trend for hypertrophy outcomes to be greater with high loads compared to low loads (difference = 0.43 ± 0.24.) The mean ES for low loads was 0.39 ± 0.17 (CI: 0.05, 0.73). The mean ES for high loads was 0.82 ± 0.17. In conclusion, training with loads ≤50% 1 RM was found to promote substantial increases in muscle strength and hypertrophy in untrained individuals, but a trend was noted for superiority of heavy loading with respect to these outcome measures with null findings likely attributed to a relatively small number of studies on the topic (3.)


Reference List

1. Mitchell CJ, Churchward-Venne TA, West DD, Burd NA, Breen L, Baker SK and Phillips SM. Resistance exercise load does not determine training-mediated hypertrophic gains in young men. J Appl Physiol 113: 71-77, 2012. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404827/)

2. Schoenfeld BJ, Peterson MD, Ogborn D, Contreras B and Sonmez GT. Effects of Low- vs. High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men. J Strength Cond Res 29: 2954-2963, 2015. (https://www.ncbi.nlm.nih.gov/pubmed/25853914)

3. Schoenfeld BJ, Wilson JM, Lowery RP and Krieger JW. Muscular adaptations in low- versus high-load resistance training: A meta-analysis. Eur J Sport Sci 1-10, 2014. (https://www.ncbi.nlm.nih.gov/pubmed/25530577)

4. Burd NA, Mitchell CJ, Churchward-Venne TA and Phillips SM. Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Appl Physiol Nutr Metab 37: 551-554, 2012. (https://www.ncbi.nlm.nih.gov/pubmed/22533517)

5. Burd NA, West DW, Staples AW, Atherton PJ, Baker JM, Moore DR, Holwerda AM, Parise G, Rennie MJ, Baker SK and Phillips SM. Low-Load High Volume Resistance Exercise Stimulates Muscle Protein Synthesis More Than High-Load Low Volume Resistance Exercise in Young Men. PLoS ONE 5: e12033, 2010. (http://journals.plos.org/plosone/art...l.pone.0012033)

6. Brad J. Schoenfeld . The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res. 2010. (https://www.ncbi.nlm.nih.gov/pubmed/20847704)

7. Counts, Brittany R., et al. “The acute and chronic effects of “NO LOAD” resistance training.” Physiology & Behavior (2016.) (https://www.ncbi.nlm.nih.gov/pubmed/27329807)

8. Loenneke, J. P., Abe, T., Wilson, J. M., Ugrinowitsch, C., & Bemben, M. G. Blood Flow Restriction: How Does It Work? (2012). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3463864/)

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Greater Strength Gains after Training with Accentuated Eccentric than Traditional Isoinertial Loads in Already Strength-Trained Men

As training experience increases it becomes more challenging to induce further neuromuscular adaptation. Consequently, strength trainers seek alternative training methods in order to further increase strength and muscle mass. One method is to utilize accentuated eccentric loading, which applies a greater external load during the eccentric phase of the lift as compared to the concentric phase. Based upon this practice, the purpose of this study was to determine the effects of 10 weeks of accentuated eccentric loading vs. traditional isoinertial resistance training in strength-trained men. Young (22 ± 3 years, 177 ± 6 cm, 76 ± 10 kg, n = 28) strength-trained men (2.6 ± 2.2 years experience) were allocated to concentric-eccentric resistance training in the form of accentuated eccentric load (eccentric load = concentric load + 40%) or traditional resistance training, while the control group continued their normal unsupervised training program. Both intervention groups performed three sets of 6-RM (session 1) and three sets of 10-RM (session 2) bilateral leg press and unilateral knee extension exercises per week. Maximum force production was measured by unilateral isometric (110° knee angle) and isokinetic (concentric and eccentric 30°.s−1) knee extension tests, and work capacity was measured by a knee extension repetition-to-failure test. Muscle mass was assessed using panoramic ultrasonography and dual-energy x-ray absorptiometry. Surface electromyogram amplitude normalized to maximum M-wave and the twitch interpolation technique were used to examine maximal muscle activation. After training, maximum isometric torque increased significantly more in the accentuated eccentric load group than control (18 ± 10 vs. 1 ± 5%, p < 0.01), which was accompanied by an increase in voluntary activation (3.5 ± 5%, p < 0.05). Isokinetic eccentric torque increased significantly after accentuated eccentric load training only (10 ± 9%, p < 0.05), whereas concentric torque increased equally in both the accentuated eccentric load (10 ± 9%, p < 0.01) and traditional (9 ± 6%, p < 0.01) resistance training groups; however, the increase in the accentuated eccentric load group was significantly greater (p < 0.05) than control (1 ± 7%). Knee extension repetition-to-failure improved in the accentuated eccentric load group only (28%, p < 0.05). Similar increases in muscle mass occurred in both intervention groups. In summary, accentuated eccentric load training led to greater increases in maximum force production, work capacity and muscle activation, but not muscle hypertrophy, in strength-trained individuals.

http://journal.frontiersin.org/artic...016.00149/full

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Currently writing an article on Boswellia Serrata and should have it out within a week! Theres a TON of info out there and its a pretty intriguing compound!


Mechanism of 5-lipoxygenase inhibition by acetyl-11-keto-beta-boswellic acid.

The formation of 5-lipoxygenase (EC 1.13.11.34) products from endogenous substrate by intact rat neutrophilic granulocytes and from exogenous arachidonic acid by rat granulocyte 105,000 x g supernatants and affinity chromatography-purified human leukocyte 5-lipoxygenase was inhibited by acetyl-11-keto-beta-boswellic acid (IC50 values of 1.5 microM, 8 microM, and 16 microM, respectively). With other pentacyclic triterpenes lacking the 11-keto function and/or the carboxyl function on ring A (e.g., amyrin and ursolic acid), no 5-lipoxygenase inhibition was observed. The presence of the noninhibitory pentacyclic triterpenes both in intact cells and in the cell-free system caused a concentration-dependent reversal of the 5-lipoxygenase inhibition by acetyl-11-keto-beta-boswellic acid, whereas the inhibitory actions of 5-lipoxygenase inhibitors from different chemical classes (MK-886, L-739,010, ZM-230,487, and nordihydroguaiaretic acid) were not modified. The inhibition by acetyl-11-keto-beta-boswellic acid and the antagonism by noninhibitory pentacyclic triterpenes were not due to nonspecific lipophilic interactions, because lipophilic four-ring compounds (cholesterol, cortisone, and testosterone) neither inhibited the activity of the 5-lipoxygenase nor antagonized the inhibitory action of acetyl-11-keto-beta-boswellic acid. Therefore, we conclude that acetyl-11-keto-beta-boswellic acid acts directly on the 5-lipoxygenase enzyme at a selective site for pentacyclic triterpenes that is different from the arachidonate substrate binding site.

https://www.ncbi.nlm.nih.gov/pubmed/7603462

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Fats suppressing hormone-sensitive lipase even when insulin levels are low

Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism

We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001). There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids. There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion.

https://www.ncbi.nlm.nih.gov/pubmed/...ubmed_RVDocSum

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One of many studies to help give you a better understanding how insulin response to meals. This study had two different meals.

Meal #1
21g Protein
125g Carbs
675 kcals

Meal #2
75g Protein
75g Carbs
675 kcals

The blood sugar response was much higher in meal #1 but the insulin response wasn't (and actually in meal #2, the insulin response was higher.)


Measures of postprandial wellness after single intake of two protein-carbohydrate meals

The general feeling of wellness after food consumption may play an important role in regulating food intake. This exploratory study aimed at identifying and evaluating measures of such postprandial wellness, tentatively defined as subjective appreciation of life after food intake. The study had a randomized cross-over, double blind design. Twenty-one healthy men with mean age of 33 + or - 14 years received two liquid breakfasts with either high protein/low carbohydrate (HP/LC) or low protein/high carbohydrate (LP/HC) ratio on separate days with a washout period of one week in between. Subjective reports on satiety and postprandial wellness (pleasantness, satisfaction, relaxation, sleepiness, physical energy and mental alertness) were established using visual analogue scales at regular time points after consumption of the breakfasts up to 240 min. Blood concentrations of CCK, ghrelin, glucose, and insulin were determined at the same time points. The HP/LC breakfast induced higher levels of satiety and specific parameters of postprandial wellness (satisfaction, pleasantness and the pleasantness of these feelings) than the LP/HC breakfast at 3 or 4h after consumption. The corresponding higher CCK and lower ghrelin concentrations at these time points supported these subject reported changes. These results indicate that meal composition influences some parameters of postprandial wellness in line with physiological responses. Further research is warranted to confirm the observed relationships. Also the relevance for food intake behaviour remains to be established.

https://www.ncbi.nlm.nih.gov/pubmed/20060863

[NaturalPursuit]

True lipolysis comes predominately from a caloric deficit. There are way too many biological differences to take into consideration to say "fasted cardio is more beneficial than fed for everyone." It completely depends on the person, their biological differences, their lifestyle factors, their extra-circular compound usage, etc.

Everything has a place within the right context


Effects of post-absorptive and postprandial exercise on 24 h fat oxidation

Objective
Fat oxidation during exercise depends on nutritional state, and exercise performed in the post-absorptive state oxidizes more fat than that performed in the postprandial state. However, the effects of exercise on energy metabolism continue during the post-exercise period, and the difference in fat oxidation during exercise may be compensated for during the post-exercise period. The present study compared the effects of an acute exercise bout in the post-absorptive or postprandial state on 24 h fat oxidation.

Methods
Twelve young male athletes stayed twice in a room-size metabolic chamber for 24 h indirect calorimetry in a randomized repeated-measure design. Before or after breakfast, i.e. in the post-absorptive or postprandial state, subjects exercised at 50% VO2 max for 60 min.

Results
During the 60 min of exercise, energy expenditure in the two exercise trials were equivalent, but exercise in the post-absorptive state was performed with lower RQ compared with that in the postprandial state (P<0.01). The time of exercise relative to breakfast did not affect 24 h energy expenditure (P>0.5). However, accumulated 24 h fat oxidation was higher (P<0.05) and that of carbohydrate oxidation was lower (P<0.05) when exercise was performed in the post-absorptive state.

Conclusions
Compared with exercise performed in the postprandial state, exercise performed in the post-absorptive state oxidized more fat and saved more carbohydrate in the body, without affecting 24 h energy expenditure.

http://www.metabolismjournal.com/art...461-1/abstract

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Another study that doesnt hold true for everyone


Appetite, energy intake and resting metabolic responses to 60 min treadmill running performed in a fasted versus a postprandial state

This study investigated the effect of fasted and postprandial exercise on appetite, energy intake and resting metabolic responses. Twelve healthy males (mean±SD: age 23±3 years, body mass index 22.9±2.1 kg m(-2), maximum oxygen uptake 57.5±9.7 mL kg(-1) min(-1)) performed three 10 h experimental trials (control, fasted exercise and postprandial exercise) in a Latin Square design. Trials commenced at 8 am after an overnight fast. Sixty min of treadmill running at ∼70% of maximum oxygen uptake was performed at 0-1 h in the fasted exercise trial and 4-5 h in the postprandial exercise trial. A standardised breakfast was provided at 1.5 h and ad libitum buffet meals at 5.5 and 9.5 h. Appetite ratings and resting expired air samples were collected throughout each trial. Postprandial exercise suppressed appetite to a greater extent than fasted exercise. Ad libitum energy intake was not different between trials, resulting in a negative energy balance in exercise trials relative to control after accounting for differences in energy expenditure (control: 9774±2694 kJ; fasted exercise: 6481±2318 kJ; postprandial exercise: 6017±3050 kJ). These findings suggest that 60 min treadmill running induces a negative daily energy balance relative to a sedentary day but is no more effective when performed before or after breakfast.

https://www.ncbi.nlm.nih.gov/pubmed/22366285

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Currently writing an article on "Is Fasted Cardio Beneficial for Everyone?"...spoiler alert...biological inter-individuality

1. Effects of post-absorptive and postprandial exercise on 24 h fat oxidation. Kenshiro Shimada, Yuki Yamamoto, Kaito Iwayama, Kazuteru Nakamura, Sachiko Yamaguchi, Masanobu Hibi, Yoshiharu Nabekura, Kumpei Tokuyama. Metabolism. 2013 (https://www.ncbi.nlm.nih.gov/pubmed/23313101)

2. Appetite, energy intake and resting metabolic responses to 60 min treadmill running performed in a fasted versus a postprandial state. Kevin Deighton, Jessica C. Zahra, David J. Stensel. Appetite. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22366285)

3. Body composition changes associated with fasted versus non-fasted aerobic exercise. Brad Jon Schoenfeld, Alan Albert Aragon, ****n D Wilborn, James W Krieger, Gul T Sonmez. J Int Soc Sports Nutr. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/25429252)

4. Training in the fasted state improves glucose tolerance during fat-rich diet. Karen Van Proeyen, Karolina Szlufcik, Henri Nielens, Koen Pelgrim, Louise Deldicque, Matthijs Hesselink, Paul P Van Veldhoven, Peter Hespel. J Physiol. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20837645)

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Hard worker, great friend, and one of those clients that follows my instructions to a T! Dominic is 12 weeks out and is going to be doing some DAMAGE!

[NaturalPursuit]

Great friend and client Nick is about to be in a GREAT position to push growth! We're pulling back on calories and adding in some cardio to resensitize, drop some fat, and make sure we're growing in the highest partitioning environment as possible



________________________________________

Mr. Consistency is the new name I'm giving my client. He handles all his own training and I simply do his nutrition and DAMN do I appreciate when a client gives me DAILY updates with as much detail as he does! Consistency over time is what changes physique

[NaturalPursuit]

A little look into how much lean tissue truly increases metabolism (roughly 6 kcals per pound.) But remember that with more lean tissue comes much more caloric expenditure in a variety of other ways.


Organ-tissue mass measurement allows modeling of REE and metabolically active tissue mass

Investigators have expressed interest in the associations between resting energy expenditure (REE) and body mass for over a century. Traditionally, descriptive models using regression analysis are applied, linking REE with metabolically active compartments such as body cell mass (BCM) and fat-free body mass (FFM). Recently developed whole body magnetic resonance imaging (MRI) and echocardiography methods now allow estimation of all major organs and tissue volumes in vivo. Because measured values are available for REE, BCM, and FFM content of individual organs and tissues, it should now be possible to develop energy expenditure-body composition estimation models based on MRI-measured organ-tissue volumes. Specifically, the present investigation tested the hypothesis that in vivo estimation of whole body REE, BCM, and FFM is possible using MRI- and echocardiography-derived organ volumes combined with previously reported organ-tissue metabolic rates and chemical composition. Thirteen subjects (5 females, 8 males) had REE, BCM, and FFM measured by indirect calorimetry, whole body 40K counting, and dual-energy X-ray absorptiometry, respectively. Models developed from estimated and measured variables were highly correlated, with no significant differences between those estimated and measured [e.g., calculated vs. measured REE: r = 0.92, P < 0. 001; (mean +/- SD) 6,962 +/- 1,455 and 7,045 +/- 1,450 kJ/day, respectively (P = not significant)]. Strong associations were observed between REE, individual or combined organ weights, BCM, and FFM that provide new insights into earlier observed metabolic phenomona. The present approach, the first to establish an energy expenditure-body composition link with a mechanistic model in vivo, has the potential to greatly expand our knowledge of energy expenditure-body size relationships in humans.

https://www.ncbi.nlm.nih.gov/pubmed/9688626

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Another article being written! This one's on gelatin and bodybuilding. Here's a little teaser on how gelatin (or more specifically hydroxyprolylglycine) can play a role in hypertrophy.

"First, lets look at a study from Kitakaze et al that observed the collagen derived dipeptide hydroxyprolyl-glycine and how it promotes C2C12 myoblast differentiation and myotube hypertrophy. They state: “The majority of studies on possible roles for collagen hydrolysates in human health have focused on their effects on bone and skin. Hydroxyprolyl-glycine (Hyp-Gly) was recently identified as a novel collagen hydrolysate-derived dipeptide in human blood. However, any possible health benefits of Hyp-Gly remain unclear. Here, we report the effects of Hyp-Gly on differentiation and hypertrophy of murine skeletal muscle C2C12 cells. Hyp-Gly increased the fusion index, the myotube size, and the expression of the myotube-specific myosin heavy chain (MyHC) and tropomyosin structural proteins. Hyp-Gly increased the phosphorylation of Akt, mTOR, and p70S6K in myoblasts, whereas the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibited their phosphorylation by Hyp-Gly. LY294002 and the mammalian target of rapamycin (mTOR) inhibitor rapamycin repressed the enhancing effects of Hyp-Gly on MyHC and tropomyosin expression. The peptide/histidine transporter 1 (PHT1) was highly expressed in both myoblasts and myotubes, and co-administration of histidine inhibited Hyp-Gly-induced phosphorylation of p70S6K in myoblasts and myotubes. These results indicate that Hyp-Gly can induce myogenic differentiation and myotube hypertrophy and suggest that Hyp-Gly promotes myogenic differentiation by activating the PI3K/Akt/mTOR signaling pathway, perhaps depending on PHT1 for entry into cells” (2.) Suggesting to a bodybuilder that hydroxyprolylglycine may actually increase hypertrophy might have them scratching their heads confused. If hydroxyprolylglycine can promote hypertrophy, obviously it seems like a simple decision to add it into your diet. But what if it does more? In fact and as previously stated, it does a tremendous amount more. Kimira et al saw it promoting differentiation of MC3T3-E1 osteoblastic cells. They found that cells treated with prolyl-hydroxyproline (Pro-Hyp) significantly upregulated gene expression of Runx2, Osterix, and Col1α1. These results indicate that Pro-Hyp promotes osteoblast differentiation. This demonstrates that Pro-Hyp has a positive effect on osteoblast differentiation with upregulation of Runx2, Osterix, and Collα1 gene expression (3.)"


References
    
1. Identification of food-derived collagen peptides in human blood after oral ingestion of gelatin hydrolysates. Iwai K, Hasegawa T, Taguchi Y, Morimatsu F, Sato K, Nakamura Y, Higashi A, Kido Y, Nakabo Y, Ohtsuki K. J Agric Food Chem. 2005 (https://www.ncbi.nlm.nih.gov/pubmed/16076145)

2. The collagen derived dipeptide hydroxyprolyl-glycine promotes C2C12 myoblast differentiation and myotube hypertrophy. Kitakaze T, Sakamoto T, Kitano T, Inoue N, Sugihara F, Harada N, Yamaji R. Biochem Biophys Res Commun. 2016 (https://www.ncbi.nlm.nih.gov/pubmed/27553280)

3. Collagen-derived dipeptide prolyl-hydroxyproline promotes differentiation of MC3T3-E1 osteoblastic cells. Yoshifumi Kimira, Kana Ogura, Yuri Taniuchi, Aya Kataoka, Naoki Inoue, Fumihito Sugihara, Sachie Nakatani, Jun Shimizu, Masahiro Wada, Hiroshi Mano. Biochem Biophys Res Commun. 2014 (https://www.ncbi.nlm.nih.gov/pubmed/25285626)

4. Chondroprotective effect of the bioactive peptide prolyl-hydroxyproline in mouse articular cartilage in vitro and in vivo. Nakatani S, Mano H, Sampei C, Shimizu J, Wada M. Osteoarthritis Cartilage. 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19615963)

5. Vitamin C–enriched gelatin supplementation before intermittent activity augments collagen synthesis. Gregory Shaw, Ann Lee-Barthel, Megan LR Ross, Bing Wang, Keith Baar. Am J Clin Nutr. 2017 (https://www.ncbi.nlm.nih.gov/pubmed/27852613)

[NaturalPursuit]

Just about 2 months of working together with Jay and his numbers are improving nicely! Slow and steady as we learn his body and what he needs to improve

Squat from 245 to 275

Bench from 200 to 205 (no spotter or could have gone another 10lbs)

Deadlift from 335 to 365

[NaturalPursuit]

Insulin is constantly misunderstood when its being discussed with blood sugar regulation. Insulin's main role in the body is inhibitory rather than excitatory. The paper below is a little old but many hypothesizes have been proven since.

https://www.ncbi.nlm.nih.gov/pubmed/10927996

https://academic.oup.com/bja/article...-in-health-and

[NaturalPursuit]

Here's a study looking at resistance training-induced changes in integrated myofibrillar protein synthesis and how they are related to hypertrophy only AFTER attenuation of muscle damage

Key points

1. Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown.

2. We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post-RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3.

3. Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3.
When muscle damage was the highest, so was the integrated MyoPS (at T1), but neither were related to hypertrophy; however, integrated MyoPS at T2 and T3 were correlated with hypertrophy.

4. We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.


http://onlinelibrary.wiley.com/doi/1...B71DF69.f02t04

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Part 1 of 2 on Light Weights Stimulating Hypertrophy article I wrote.

"If you were to simply read this title, many would shrug it off and say that you either CAN or you CANNOT grow from light weight (low load) training. It seems everyone is stuck in one end of the spectrum when it comes to this topic that no one connects the dots and discusses hypertrophy as a whole. For that reason, I wanted to cover this topic a little more in depth to help shed some light on this matter. Before we begin I must attribute credit to Dr. Stuart Phillips who has discussed this matter extensively and has taught me a great deal. I must also credit the researchers that all of these upcoming studies will be coming from. Those being Burd, Mitchell, and Schoenfeld as their work is what allows us to correlate anecdotal evidence in order to find the truth. We must begin with first looking at the research presented from these researchers before answering the question of “does light weight training stimulate hypertrophy?”

The first bit of literate comes from Mitchell et al where they looked at how resistance exercise load does not determine training-mediated hypertrophic gains in young men. They had eighteen men had their legs randomly assigned to two of three training conditions that differed in contraction intensity or contraction volume. Subjects trained each leg with their assigned regime for a period of 10 wk, 3 times/wk. They made pre- and posttraining measures of strength, muscle volume by magnetic resonance (MR) scans, as well as pre- and posttraining biopsies of the vastus lateralis, and a single postexercise (1 h) biopsy following the first bout of exercise, to measure signaling proteins. Training-induced increases in MR-measured muscle volume were significant, with no difference between groups. Isotonic maximal strength gains were not different between 80%-1 and 80%-3, but were greater than 30%-3, whereas training-induced isometric strength gains were significant but not different between conditions. Biopsies taken 1 h following the initial resistance exercise bout showed increased phosphorylation of p70S6K only in the 80%-1 and 80%-3 conditions. There was no correlation between phosphorylation of any signaling protein and hypertrophy. In accordance with our previous acute measurements of muscle protein synthetic rates a lower load lifted to failure resulted in similar hypertrophy as a heavy load lifted to failure (1.)

Based off of that study from Mitchell et al, we find that hypertrophy is more correlated to fatigue/failure than actual load. But obviously one study is not enough to draw an accurate conclusion so we will now continue on to work from Dr. Brad Schoenfeld et al. The first study measured the effects of low- vs. high-load resistance training on muscle strength and hypertrophy. The purpose of this study was to compare the effect of low- versus high-load resistance training on muscular adaptations in well-trained subjects. Eighteen young men experienced in RT were matched according to baseline strength and then randomly assigned to 1 of 2 experimental groups: a low-load RT routine where 25-35 repetitions were performed per set per exercise or a high-load RT routine where 8-12 repetitions were performed per set per exercise. During each session, subjects in both groups performed 3 sets of 7 different exercises representing all major muscles. Training was performed 3 times per week on nonconsecutive days, for a total of 8 weeks. Both HL and LL conditions produced significant increases in thickness of the elbow flexors, elbow extensors, and quadriceps femoris, with no significant differences noted between groups. Improvements in back squat strength were significantly greater for HL compared with LL, and there was a trend for greater increases in 1 repetition maximum (1RM) bench press. Upper body muscle endurance improved to a greater extent in LL compared with HL. These findings indicate that both HL and LL training to failure can elicit significant increases in muscle hypertrophy among well-trained young men; however, HL training is superior for maximizing strength adaptations (2.) Now we see a different side of the argument where, although light load training increased hypertrophy, heavy load training is favored for maximizing strength. This brings on onto our second study again from Schoenfeld et al that was a meta analysis of muscular adaptations in low- versus high-load resistance training. The purpose of this paper therefore was to conduct a meta-analysis of randomised controlled trials to compare the effects of low-load (≤60% 1 repetition maximum [RM]) versus high-load (≥65% 1 RM) training in enhancing post-exercise muscular adaptations. The strength analysis comprised 251 subjects and 32 effect sizes, nested within 20 treatment groups and 9 studies. The hypertrophy analysis comprised 191 subjects and 34 ESs, nested with 17 treatment groups and 8 studies. There was a trend for strength outcomes to be greater with high loads compared to low loads. The mean ES for low loads was 1.23 ± 0.43. The mean ES for high loads was 2.30 ± 0.43. There was a trend for hypertrophy outcomes to be greater with high loads compared to low loads (difference = 0.43 ± 0.24.) The mean ES for low loads was 0.39 ± 0.17 (CI: 0.05, 0.73). The mean ES for high loads was 0.82 ± 0.17. In conclusion, training with loads ≤50% 1 RM was found to promote substantial increases in muscle strength and hypertrophy in untrained individuals, but a trend was noted for superiority of heavy loading with respect to these outcome measures with null findings likely attributed to a relatively small number of studies on the topic (3.)"

Reference List

1. Mitchell CJ, Churchward-Venne TA, West DD, Burd NA, Breen L, Baker SK and Phillips SM. Resistance exercise load does not determine training-mediated hypertrophic gains in young men. J Appl Physiol 113: 71-77, 2012. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404827/)

2. Schoenfeld BJ, Peterson MD, Ogborn D, Contreras B and Sonmez GT. Effects of Low- vs. High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men. J Strength Cond Res 29: 2954-2963, 2015. (https://www.ncbi.nlm.nih.gov/pubmed/25853914)

3. Schoenfeld BJ, Wilson JM, Lowery RP and Krieger JW. Muscular adaptations in low- versus high-load resistance training: A meta-analysis. Eur J Sport Sci 1-10, 2014. (https://www.ncbi.nlm.nih.gov/pubmed/25530577)

4. Burd NA, Mitchell CJ, Churchward-Venne TA and Phillips SM. Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Appl Physiol Nutr Metab 37: 551-554, 2012. (https://www.ncbi.nlm.nih.gov/pubmed/22533517)

5. Burd NA, West DW, Staples AW, Atherton PJ, Baker JM, Moore DR, Holwerda AM, Parise G, Rennie MJ, Baker SK and Phillips SM. Low-Load High Volume Resistance Exercise Stimulates Muscle Protein Synthesis More Than High-Load Low Volume Resistance Exercise in Young Men. PLoS ONE 5: e12033, 2010. (http://journals.plos.org/plosone/art...l.pone.0012033)

6. Brad J. Schoenfeld . The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res. 2010. (https://www.ncbi.nlm.nih.gov/pubmed/20847704)

7. Counts, Brittany R., et al. “The acute and chronic effects of “NO LOAD” resistance training.” Physiology & Behavior (2016.) (https://www.ncbi.nlm.nih.gov/pubmed/27329807)

8. Loenneke, J. P., Abe, T., Wilson, J. M., Ugrinowitsch, C., & Bemben, M. G. Blood Flow Restriction: How Does It Work? (2012). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3463864/)

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