четверг, 28 августа 2014 г.

Rethinking The Role Of Antioxydants in Sports

 by 

antioxydants
This week’s guest blog article comes by way of John Meadows and his Mountain Dog Diet website. The website is known as one of the best in the bodybuilding world, and it’s easy to see why. When you join for less then 10 measly dollars you get to see the EXACT diets he has used with many of his top men and women competitors.
They are detailed and not something most coaches for allow others to see. The website also is loaded with brilliant articles such as the one his colleagues Bill Willis wrote that we are featuring this month. There is a Q & A where people can ask John and his team questions and they get answered on the site, as well as detailed descriptions of his insane but eloquently planned workouts. There are over 50 workouts on the site now.
Do yourself a favor and check it out.

Six Reasons to Avoid Taking Antioxidant Supplements 

By Bill Willis, PhD
On paper, at least, antioxidant supplements seem like a great idea. It has been known for quite some time that intense exercise increases the production of potentially toxic reactive oxygen species (ROS), which have been linked to aging and most chronic diseases, one way or another. If balls out training increases the production of damaging oxygen radicals than it makes perfect sense to limit oxidation as much as possible, right? This should limit muscle damage and decrease soreness, allowing us to train harder and recover faster. This was precisely the school of thought in the all-too recent dark ages of training science, when high doses of vitamin C were the state of the art in periworkout supplementation. Sore after training? Not recovering fast enough? Too much oxidation, bro. Take more antioxidants! Full disclosure from a guy who researches ROS for a living: I, too drank the Kool-aid, taking a couple grams of vitamin C before/after training for a period in the late 90’s. Fortunately, like most who experimented with high dose antioxidant supplementation, I ultimately stopped taking them; they just didn’t seem help with recovery or muscle soreness.
Thankfully in the present day, we know better. Although ROS levels increase during exercise, this is a good thing. Critical even, to get the most out of your training. Any attempt to decrease exercise-induced ROS production with antioxidant supplements is not only useless in terms increasing strength, performance, and recovery, but may be worse than useless(1), possibly canceling out much of your hard work in the gym. Want to get bigger, faster, and stronger to your maximum potential? ROS can be your best friend. Antioxidant supplements, more like your worst enemy.
Here are 6 good reasons to avoid them:
#1 Reduced ability to deal with metabolic stress
One of the major benefits of exercise (outside of the fact that it makes you jacked) is increased health and lifespan, made possible by increased protection from oxidative stress. Most, if not all chronic diseases are driven by inflammation and oxidation, which go hand and hand. The better our ability to overcome this type of metabolic stress, the more resilient we are to stress and disease. It may seem somewhat contradictory then that oxidative stress incurred during exercise actually increases our capacity to deal with future oxidative stress. In fact, we are hard-wired for this response, provided that we don’t screw it up with untimely antioxidant supplementation.
How exercise increases our ability to cope with metabolic stress:
Under non-stress conditions a transcription factor called NRF2 is sequestered in the cytosol by another protein called Keap1. When ROS levels increase, such as during a high volume Mountain Dog workout, Keap1 is degraded, releasing NRF2, which then moves into the nucleus. After entering the nucleus, NRF2 binds to and activates genes that have a special sequence called an “Antioxidant Response Element” (ARE) in their promoter. Think of this in terms of a lock and key; hundreds of stress-response genes in our DNA have a type of ‘lock’ that is opened by the same ‘key’, NRF2. In this way, NRF2 causes global activation of the antioxidant stress-response program, increasing the production of proteins important for defending against inflammation, oxidation, and metabolic stress (2-4). You can see an overview of how this works in the figure below:
graphic
While the increase in ROS production that occurs during training is stressful in and of itself, it is also a potent activator of this ARE/NRF2 stress-response pathway, which increases our capacity to deal with metabolic stress. Taking antioxidant supplements around training time quenches the ROS signal that activates this pathway, preventing the ROS signal from turning on this metabolic stress response program. It’s like taking weight off the bar and still expecting to grow.
Here’s the thing, the consequences of short-circuiting this pathway with antioxidants are not limited to increased health and longevity down the road. This oxidative stress response system is also needed to repair damage incurred during heavy training. Reduced ability to cope with metabolic stress results in less efficient recovery, limiting training progress in the long run.
#2 Antioxidants reduce the ability of exercise to increase insulin sensitivity
The lower your insulin levels are, the leaner you will tend to be. There are two ways to keep insulin levels consistently low. One is to limit carbohydrate intake. The other is to increase insulin sensitivity so that less insulin is needed to get the job done. This is where working out comes in; consistent, hard training plays a huge role in increasing insulin sensitivity. The effect this has on conditioning can’t be understated. Increased insulin sensitivity has a way transcending the amount of calories you take in or even macros; the more insulin sensitive you are the leaner, more anabolic you will be. Optimal insulin sensitivity also ensures that extra calories are used build new muscle tissue, rather than stored as bodyfat.
It was only recently discovered that exercise-induced increases in insulin sensitivity are driven by increased ROS production (5), and totally suppressed by antioxidant supplements. In a study in 2009 by Ristow et al, the effects of supplementation with vitamin C (500mg twice/day) and vitamin E (400IU/day) on changes in insulin sensitivity caused by exercise were investigated in both beginners and those with prior training experience. All subjects participated in a 5 day/week training program for 4 weeks consisting of both cardio and weight training. As expected, insulin sensitivity increased over the course of the training program in both beginners and those with more training experience. This also correlated with a large increase in the expression of a number of signaling proteins that promote insulin sensitivity. Importantly, those who took antioxidant supplements during this 4-week training period showed no increases in insulin sensitivity; the antioxidants completely eliminated this response. Keep in mind this happened at ‘normal’ supplement doses used every day, and the effect also occurred in both beginners and experienced subjects, ruling out any type of ‘beginner-effect’.
#3 Antioxidant supplements limit endurance and mitochondrial biogenesis
As the cellular powerplants that provide ATP to fuel intense muscular contractions and even life itself, mitochondria are pretty important. The more mitochondria we have, the greater our capacity to oxidize fuels for energy. As a result, endurance is largely a function of how many mitochondria we have, and how well they work.
It has been known for some-time that antioxidant supplements have subtle performance-suppressing effect on endurance exercise events. One study noted that giving greyhounds 1g of vitamin C before racing significantly slowed racing time relative to dogs that did not receive antioxidants (6). Another study in the 70’s noted that vitamin E supplementation (400IU/day for 6wks) reduced endurance performance in swimmers (7).
How, exactly, antioxidants may limit endurance came to light more recently, in a study by Gomez-Cabrera et al (8). The effects of antioxidant supplementation on endurance performance were evaluated in 14 men age 27-36 during an 8 week endurance training program. 5 of these men received a 1000mg daily dose of vitamin C, while the rest received a placebo. The investigators found that vitamin C significantly suppressed endurance capacity, which was linked to a reduction in proteins that activate mitochondrial biogenesis. The ROS dependence of mitochondrial biogenesis induced by endurance training was later confirmed in a study by Kang et al, where antioxidants severely limited mitochondrial biogenesis in response to exercise (9).
I can hear it now: Endurance performance?!? *Before I lose you here, the fact that antioxidants reduce mitochondrial biogenesis is not only a concern for cardio-bunnies. Two additional studies noted decreased performance with ubiquinone-10 supplementation (a fat-soluble antioxidant) in humans after a high-intensity training program (10, 11). In this case, both aerobic, and anaerobic performance were affected. As with endurance training, resistance training also activates mitochondrial biogenesis (12). This is not a coincidence, as most proteins are synthesized in the proximity of mitochondria (13). The more mitochondria we have, and the better they work, the better the cellular infrastructure for cranking out new proteins to GROW.
Take-home: Oxidative stress during exercise sends signals that increase mitochondrial number and efficiency to support the energy demands of exercise. Avoid antioxidant supplements to maximize mitochondrial adaptations to training. This is important for both endurance and (indirectly) strength and size.
#4 You might grow less?
In addition to limiting the indirect effects of mitochondria on muscle growth, a recent animal study suggests that antioxidant supplements may play a more active role in limiting muscle growth (14). In this study in rats, a ‘synergist ablation’ overload model was used, where the gastroc and soleus muscles on the right hindlimb were surgically removed, overloading and activating growth in the plantaris muscle. The opposite, left hindlimb of rats in this study did not receive the procedure, which served as an experimental control. Rats in this study were then treated with vitamin C at 500mg/kg orally once/day or a placebo for 14 days. Although both the placebo and vitamin C treated rats experienced some new growth in the plantaris muscle, the vitamin C group experienced around 11% less muscle growth! This also correlated with reduced protein synthesis and increased protein breakdown.
Importantly, the results of this particular study need to be interpreted with a great degree of caution. Rats received a daily dose of 500 mg/kg vitamin C, which is equivalent to around 50g vitamin C in a 100 kg man. This is a HUGE amount of vitamin C, not to mention that fact that vitamin C in doses this high could actually increase ROS production. The synergist ablation model used for muscle overload in this study also is very much a ‘sledge-hammer’ approach that can’t easily be extrapolated to weight training in humans. Taken alone, I wouldn’t make much of this study; the dose of vitamin C was too high and the model too out there, at least relative to weight training in humans. This study is consistent with the larger picture, however, that antioxidant supplements can throw a metabolic wrench in the cell signaling machinery that drives the adaptive response to exercise. Along those lines, it was also recently shown that ROS function as important signaling molecules for muscle hypertrophy in vitro, where it was found that IGF-1 induced hypertrophy of myotubes in culture is suppressed by antioxidants (15).
Taken together, the current body of research teaches us a very important lesson when it comes to ROS signaling and muscle growth; the acute increase in ROS induced by training is an intrinsic part of the exercise stimulus that turns on the switch for muscle growth/adaptation.
#5: Antioxidant supplements could delay recovery.
The fact that antioxidant supplementation could delay recovery was discovered pretty much by accident. We have known for some time that intense exercise generates increases ROS production and hard training is a well-known cause of delayed onset muscle soreness. Putting two and two together, it was once believed that most, if not all muscle soreness was caused by oxidative damage. This also suggested that by limiting oxidative stress, antioxidant supplements might reduce muscle damage, eliminating muscle soreness and promoting faster recovery. One research group set out to test just this hypothesis: 20 active males participated in downhill running, an exercise model well known to cause high levels of muscle soreness (16). Vitamin C supplementation at 1g/day not only failed to reduce soreness, but also delayed recovery relative to subjects that took a placebo. Although downhill running decreased muscle strength in both groups during the recovery period, the vitamin C group recovered much slower. Strength levels in the placebo group were reduced only up-to 4 days post-exercise, while strength levels in the vitamin C group were still significantly impaired at day 7 and 14, failing to return to baseline by the end of the study (16).
What is going on here?
The type of forces involved with downhill running are very damaging to muscle tissue. The immune system, by sending in special cells called macrophages and neutrophils, plays a big role in cleaning up this damage (17). These phagocytic cells use ROS as a tool to take up, digest, and clear out damaged tissue. A good analogy here is a house-fire. Assuming the firefighters were able to get the fire out before it completely burned to the ground, all damaged sections and debris need to be cleaned up/cleared out before construction workers can be called in with new materials to rebuild. The same holds true for muscle tissue, more or less. Immune cells infiltrate into the injured tissue to clear the area of damaged, oxidized, and degraded proteins, paving the way for later increased protein synthesis, rebuilding and recovery. This suggests that ROS produced during exercise may also be critical to muscle regeneration. Although very intense, heavy training increases ROS levels, this is precisely what is needed for optimal recovery.
Take-home: Avoid pre-or post workout antioxidant supplements like the plague to ensure prompt recovery from the most damaging workouts.
#6 You are shooting the messenger
The fact that antioxidants have a negative effect on so many aspects of the positive, adaptive response to exercise suggests that something much bigger, more fundamental, is going on here. Study-after study has demonstrated that the health-promoting effects of exercise are driven ROS production, which, as explained above, strengthens the natural antioxidant defense machinery, protects from metabolic stress, and may even promote increased lifespan (18-31). ROS are important signaling molecules for a number of different cell signaling pathways, particularly those associated with stress-response, and we are stress-response machines. From the primordial soup through the caveman days to the present day, surviving is stressful business. From the cellular level up, we are designed to sense, respond to, and mount the appropriate response to stress. This causes us to adapt, becoming better able to overcome future stresses and ensuring our survival. What doesn’t kill us truly does makes us stronger. In this way, the stress of weight training is the same as any other: ROS are key messengers for sensing, responding, and adapting to this stress. By taking antioxidant supplements in and around training, we are killing the messenger.
But wait, aren’t antioxidants good for me?
Where does all this leave us when it comes to antioxidants in general? When should we take them, how should we take them, or should be take them at all? I’ve picked on vitamin C a lot today, so some clarification is needed here. Most animals, fish, and reptiles can synthesize vitamin C in their kidneys or liver, but us humans lost the ability some time ago (32-34). It is therefore essential that we obtain vitamin C from our diets. Among other things, it is needed for collagen synthesis and good health, in general (35). Moreover, not getting enough vitamin C leads to a disease called scurvy (36), so maintenance of plasma and tissue levels essential to avoid a deficiency. The same goes for other antioxidants.
Practical recommendations:
It goes without saying that you should avoid taking any type of supplemental antioxidants in, or around training time. Bulk suppression of cellular ROS levels with high doses of single-antioxidant supplements around training time is like shooting the messenger that delivers the signal to adapt and grow. *This includes multivitamins, most of which are loaded with antioxidants. Secondly, it is best to get most of your antioxidants from whole-food sources. A medium orange might have 100mg of vitamin C, far less than the typical vitamin C pill. Now that we are on the subject, what about antioxidants in whole-food? Should you skip those blueberries in your pre-workout oatmeal? Probably not; antioxidants in whole-food tend to be better ‘packaged’ for assimilation in a way that is less likely to disrupt endogenous ROS signaling. Although I wouldn’t recommend a bushel of blueberries pre-training, ½ cup in your pre-workout oatmeal is probably not an issue, taking into account digestion/assimilation times. It should also be noted that the health benefits of consuming lots of antioxidant rich fruits and vegetables is well established, so be sure to include lots of these in your diet.
To summarize:
  • Try to get most, if not all if your antioxidants from whole-food sources.
  • Single-dose antioxidant supplements may be worse than useless, possibly having a number of detrimental effects on your gains. If you are taking a multivitamin, do not take it within a few hours pre- or post- training
  • There is no evidence out there to suggest that food-sourced antioxidants have anything but positive effects. They absorbed more slowly, and packaged for optimal assimilation and health benefits.
Until next time,
Bill

Reference List

1. Gomez-Cabrera MC, Ristow M, Vina J. Antioxidant supplements in exercise: worse than useless? Am J Physiol Endocrinol Metab 2012;302:E476-E477.
2. van Muiswinkel FL, Kuiperij HB. The Nrf2-ARE Signalling pathway: promising drug target to combat oxidative stress in neurodegenerative disorders. Curr Drug Targets CNS Neurol Disord 2005;4:267-81.
3. Shih AY, Imbeault S, Barakauskas V, Erb H, Jiang L, Li P, et al. Induction of the Nrf2-driven antioxidant response confers neuroprotection during mitochondrial stress in vivo. J Biol Chem 2005;280:22925-36.
4. Kotlo KU, Yehiely F, Efimova E, Harasty H, Hesabi B, Shchors K, et al. Nrf2 is an inhibitor of the Fas pathway as identified by Achilles’ Heel Method, a new function-based approach to gene identification in human cells. Oncogene 2003;22:797-806.
5. Ristow M, Zarse K, Oberbach A, Kloting N, Birringer M, Kiehntopf M, et al. Antioxidants prevent health-promoting effects of physical exercise in humans. Proc Natl Acad Sci U S A 2009;106:8665-70.
6. Marshall RJ, Scott KC, Hill RC, Lewis DD, Sundstrom D, Jones GL, et al. Supplemental vitamin C appears to slow racing greyhounds. J Nutr 2002;132:1616S-21S.
7. Sharman IM, Down MG, Sen RN. The effects of vitamin E and training on physiological function and athletic performance in adolescent swimmers. Br J Nutr 1971;26:265-76.
8. Gomez-Cabrera MC, Domenech E, Romagnoli M, Arduini A, Borras C, Pallardo FV, et al. Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance. Am J Clin Nutr 2008;87:142-9.
9. Kang C, O’Moore KM, Dickman JR, Ji LL. Exercise activation of muscle peroxisome proliferator-activated receptor-gamma coactivator-1alpha signaling is redox sensitive. Free Radic Biol Med 2009;47:1394-400.
10. Malm C, Svensson M, Ekblom B, Sjodin B. Effects of ubiquinone-10 supplementation and high intensity training on physical performance in humans. Acta Physiol Scand 1997;161:379-84.
11. Malm C, Svensson M, Sjoberg B, Ekblom B, Sjodin B. Supplementation with ubiquinone-10 causes cellular damage during intense exercise. Acta Physiol Scand 1996;157:511-2.
12. Balakrishnan VS, Rao M, Menon V, Gordon PL, Pilichowska M, Castaneda F, et al. Resistance training increases muscle mitochondrial biogenesis in patients with chronic kidney disease. Clin J Am Soc Nephrol 2010;5:996-1002.
13. Margeot A, Garcia M, Wang W, Tetaud E, di Rago JP, Jacq C. Why are many mRNAs translated to the vicinity of mitochondria: a role in protein complex assembly? Gene 2005;354:64-71.
14. Makanae Y, Kawada S, Sasaki K, Nakazato K, Ishii N. Vitamin C administration attenuates overload-induced skeletal muscle hypertrophy in rats. Acta Physiol (Oxf) 2013;208:57-65.
15. Handayaningsih AE, Iguchi G, Fukuoka H, Nishizawa H, Takahashi M, Yamamoto M, et al. Reactive oxygen species play an essential role in IGF-I signaling and IGF-I-induced myocyte hypertrophy in C2C12 myocytes. Endocrinology 2011;152:912-21.
16. Close GL, Ashton T, Cable T, Doran D, Holloway C, McArdle F, et al. Ascorbic acid supplementation does not attenuate post-exercise muscle soreness following muscle-damaging exercise but may delay the recovery process. Br J Nutr 2006;95:976-81.
17. Leeuwenburgh C, Heinecke JW. Oxidative stress and antioxidants in exercise. Curr Med Chem 2001;8:829-38.
18. Crawford DR, Davies KJ. Adaptive response and oxidative stress. Environ Health Perspect 1994;102 Suppl 10:25-8.
19. Davies KJ. Intracellular proteolytic systems may function as secondary antioxidant defenses: an hypothesis. J Free Radic Biol Med 1986;2:155-73.
20. Kim JD, McCarter RJ, Yu BP. Influence of age, exercise, and dietary restriction on oxidative stress in rats. Aging (Milano ) 1996;8:123-9.
21. Marzatico F, Pansarasa O, Bertorelli L, Somenzini L, Della VG. Blood free radical antioxidant enzymes and lipid peroxides following long-distance and lactacidemic performances in highly trained aerobic and sprint athletes. J Sports Med Phys Fitness 1997;37:235-9.
22. Balakrishnan SD, Anuradha CV. Exercise, depletion of antioxidants and antioxidant manipulation. Cell Biochem Funct 1998;16:269-75.
23. Ji LL, Gomez-Cabrera MC, Vina J. Exercise and hormesis: activation of cellular antioxidant signaling pathway. Ann N Y Acad Sci 2006;1067:425-35.
24. Powers SK, Lennon SL. Analysis of cellular responses to free radicals: focus on exercise and skeletal muscle. Proc Nutr Soc 1999;58:1025-33.
25. Niess AM, Dickhuth HH, Northoff H, Fehrenbach E. Free radicals and oxidative stress in exercise–immunological aspects. Exerc Immunol Rev 1999;5:22-56.
26. Hollander J, Fiebig R, Gore M, Ookawara T, Ohno H, Ji LL. Superoxide dismutase gene expression is activated by a single bout of exercise in rat skeletal muscle. Pflugers Arch 2001;442:426-34.
27. Higuchi M, Cartier LJ, Chen M, Holloszy JO. Superoxide dismutase and catalase in skeletal muscle: adaptive response to exercise. J Gerontol 1985;40:281-6.
28. Gomez-Cabrera MC, Domenech E, Vina J. Moderate exercise is an antioxidant: upregulation of antioxidant genes by training. Free Radic Biol Med 2008;44:126-31.
29. Quintanilha AT. Effects of physical exercise and/or vitamin E on tissue oxidative metabolism. Biochem Soc Trans 1984;12:403-4.
30. Vincent HK, Powers SK, Demirel HA, Coombes JS, Naito H. Exercise training protects against contraction-induced lipid peroxidation in the diaphragm. Eur J Appl Physiol Occup Physiol 1999;79:268-73.
31. Boveris A, Navarro A. Systemic and mitochondrial adaptive responses to moderate exercise in rodents. Free Radic Biol Med 2008;44:224-9.
32. Benzie IF. Evolution of antioxidant defence mechanisms. Eur J Nutr 2000;39:53-61.
33. Benzie IF. Evolution of dietary antioxidants. Comp Biochem Physiol A Mol Integr Physiol 2003;136:113-26.
34. Frei B, England L, Ames BN. Ascorbate is an outstanding antioxidant in human blood plasma. Proc Natl Acad Sci U S A 1989;86:6377-81.
35. Benzie IF. Vitamin C: prospective functional markers for defining optimal nutritional status. Proc Nutr Soc 1999;58:469-76.
36. Doll S, Ricou B. Severe vitamin C deficiency in a critically ill adult: a case report. Eur J Clin Nutr 2013;67:881-2.


Read more: http://www.strengthsensei.com/rethinking-the-role-of-antioxydants-in-sports/#ixzz3Bl54ribV

среда, 27 августа 2014 г.

Фэн-Фу

Точка Фэн-Фу и омоложение организма. 
Методика заключается в следующем: прикладывать кубик льда 2,5 х 2,5 см к затылку непосредственно к точке Фэн-фу (ее очень просто найти: ямка, где голова соединяется с шеей).
Делать регулярно, с перерывами в 2-3 дня утром натощак и вечером перед сном. Сначала может показаться, что холодит очень сильно, но буквально через 30-40 секунд идет прилив тепла. Когда кубик полностью растает, растереть затылок полотенцем. В первые дни может возникнуть чувство эйфории за счет выброса эндорфинов в кровь.
Что это дает?
* Улучшается сон.
* Всегда отличное настроение.
* Повышается общий жизненный тонус.
* Лучше работает желудочно-кишечный тракт.
* Вы забудете про простуды, лед можно прикладывать и при температуре.
* Снимает головную, зубную, суставные боли.
Специально для фанатиков- Лед обычный НЕ СУХОЙ!))




Рабиндранат Тагор

Мы познаём человека не потому, что он знает, а по тому, чему он радуется.
© Рабиндранат Тагор

ЛЕГЕНДА

У индейцев Южной Америки имеется такой миф: он рассказывает о том времени, когда на Земле из представителей homo sapience обитали лишь женщины. Впрочем, тогда они тоже были не совсем того, в смысле homo, и тем более в смысле sapience, поскольку размножались вегетативным способом, вступая в интимную связь с грибами, которые в те далекие мифологические времена были тоже не совсем растениями, а, скорее, своеобразными растительными, но мыслящими фаллосами. Все было хорошо, пока одни грибы не вздумали проникать в женщин противоестественным путем, принуждая их к употреблению себя в пищу. От этого женщины стали рожать невиданных прежде антропоидных существ, имеющих морфологические признаки родства с псилобициновыми грибами. Так появились мужчины. Они переняли у грибов все основные функции, включая охоту на крупный рогатый скот.Очень правдоподобный миф...

© А.В.Шаповалов, Известный российский этномиколог, директор Новосибирского краеведческого музея

illustration by Apollonia Saintclair - La trouvaille (There you are!...)
Lat.: Phallus impudicus - Fr.: Satyre puant



вторник, 26 августа 2014 г.

Avoid Pain Relievers During Training



From Charles Poliquin Live

Avoid pain killers and non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen during training because they damage the gut and hinder absorption of nutrients, delaying recovery. NSAIDs have also been shown to impair healing of tendons and blunt muscle hypertrophy response.

A recent study published in the journal Medicine and Science in Sports and Exercise tested what happens in the gastrointestinal tract during intense exercise after taking ibuprofen. Researchers measured a biomarker called IFABP, which when elevated, indicates damage to intestinal cells and is a marker of extended inflammation. IFABP was tested in trained cyclists at rest with ibuprofen, and after intense cycling with and without ibuprofen. A dose of 400 mg of ibuprofen was taken about 12 hours before exercise and another 400 mg was taken an hour before exercise.

Results showed significant damage to the cells in the intestines after exercise with ibuprofen. Markers of damage following the cycling trial with ibuprofen was almost double that following the cycling trial without the drug (875 vs. 474 pg/mL). In addition, following exercise with ibuprofen, other markers indicated that the barrier of the gut was injured, essentially causing leaky gut.

Researchers believe that when you combine intense physical activity with NSAIDs, damage to the intestines is increased as a result of redistribution of blood flow from the gut to the muscles, skin, heart, and lungs. This harms the lining of the gut, which could put you at risk for greater susceptibility to toxins because the gut lining is more permeable and not as protective. It will also inhibit absorption of nutrients, and long-term NSAID use could lead to serious damage to the gut and chronic inflammation.

There is other bad news about NSAID use with exercise: It has been associated with increased risk of cardiovascular adverse events and been shown to get in the way of long-term tendon and muscle repair. NSAIDs reduce the regeneration of satellite cells, which are the cells that rebuild connective tissue that joins muscle with bone.

NSAIDs also impair the muscle hypertrophy response by 50 to 75 percent in animals. In addition, we know they suppress protein synthesis following a single bout of exercise, possibly blunting muscle development in humans as well.

Reference :
Wijck, K., Lenaerts, K., et al. Aggravation of Exercise-Induced Intestinal Injury by Ibuprofen in Athletes. Medicine and Science in Sports and Exercise. 2012. Published Ahead of Print.

пятница, 22 августа 2014 г.

30 Seconds to Leanness

 


Share onFacebook Sprinters
Every time you turn around, there's a new diet plan based on a hormone. While there's some merit to all this madness, most of the plans fail to completely understand their respective physiological underpinnings. The body isn't a simple, linear, straightforward machine – it's complex and redundant at almost every turn.
This article will reveal some new research on the hormone leptin to provide some simple actions for you to take to help you get leaner. Just because the physiology is messy doesn't mean your actions need to be complicated!
First, here's a short crash course on this important hormone.

Leptin 101

Leptin was discovered by Ingalls and friends in the early 1950's (Ingalls, AM, et al 1950). Fast forward to the early 90's when it was "rediscovered", and many were predicting it would be the biggest weight loss breakthrough ever.
It's a hormone that is released primarily by fat cells (adipocytes) and works to regulate appetite, body fat mass, and basal metabolic rate.
Until just a few years ago, researchers thought that fat cells sat on their collective butts all day and were only a storage place for unsightly body fat.
We know now that those pesky fat cells are very metabolically active, releasing and receiving a myriad of messenger hormones, one of which is leptin.

How Does Leptin Work?

Sprinting for Leanness
Leptin travels up to the brain where it acts on receptors in the hypothalamus toinhibit appetite.
More leptin in your brain = less food intake.
This is great news for anyone looking to get leaner, since more leptin means you'll be less likely to prowl your kitchen at 3 AM in search of leftover birthday cake. Leptin is your body's way of putting the brakes on fat gain by decreasing appetite.
The chronic level of leptin you have is also a rough measure of the amount of fat you have on your body. Many things can affect leptin as shown in the table below:

Factors promoting leptin secretion

• Excess energy stored as fat (obesity)
• Overfeeding
• Glucose
• Insulin
• Glucocorticoids
• Estrogens
• Inflammatory cytokines, including tumor necrosis factor and Interleukin-6 (acute effect)

Factors inhibiting leptin secretion

• Low energy states with decreased fat stores (leanness)
• Fasting
• Catecholamines and adrenergic agonists
• Thyroid hormones
• Androgens
• Peroxisome proliferator–activated receptor-agonists
• Inflammatory cytokines, including tumor necrosis factor (prolonged effect)

Leptin Super Mouse to the Rescue!

Researchers lead by Zhang,Y in the mid-1990s did a series of mouse experiments to show that mice with messed up leptin (ob/ob mouse) became fat little fury bastards (Zhang, Y et al. 1994).
Their metabolic rate was lower, they didn't move as much, and they ate tons of mouse chow.
The catch was that this mouse ob/ob (think double obese) .
To make the mouse lean, they injected it with leptin, and voila – a thin mouse again!
The researchers all joined hands, sang Kumbaya, and went out for tasty adult beverages while taking turns patting each other on the back for single-handedly solving the obesity problems. We just need to inject humans with leptin and poof, thin humans, and more visually appealing shopping experiences at Walmart.
The problem was it didn't work.
Researchers measured blood levels of leptin in obese humans and found that leptin levels were !
That wasn't supposed to happen. Leptin levels were expected to be low since the humans were fat. As leptin increases, it signals that the body has enough fat, so we would expect low leptin levels in obese populations.
As you recall, when injected with leptin (thus increasing the level), the mice in the studies got thinner.
But these obese humans already had high levels of leptin. Injecting more leptin was like pissing in the ocean to try to raise the water level.

Leptin 201: The Receptor

It appeared that the receptor for leptin is out of joint. The receptor isn't telling the brain that leptin is high. Tons of leptin, but the silly brain can't tell since the receptor is as broke as Terrell Owens.

Why it Matters

Sprinting
We already know that sprint training is a great way to burn fat, but it may have another benefit.
A study done by Guerra et al. in 2011 looked at sprints as a leptin signaling mimetic.
Unlike most research, this study used a group of T Nation style humans who were pretty lean (about 15% body fat) and young (23 years old). They split them into two groups: a fasting group, and a glucose group where they ingested 75 grams of glucose one hour before sprints.
Both groups did one Wingate bike sprint for only 30 seconds.
If you're not familiar with this set up, in short, it's hop on a bike set to a high workload (10% of body weight used here) and pedal like a rabid grizzly bear is chasing you.

What They Found

Subjects had a series of muscle biopsies done over the course of the study and researchers found that  showed alterations in leptin signaling. The sprints were jacking up leptin that, in theory, should get the waddling Walmart shoppers to start dropping fat.
However, this was not seen in the group that ingested glucose before their sprint.
It appears insulin may interfere with the leptin signaling to some degree. To quote the researchers directly:
"Altogether, these results indicate that sprint exercise performed under fasting conditions elicits signaling events similar to those described in the rodent skeletal muscle after leptin injections, i.e. sprint exercise under fasting conditions acts as a leptin signaling mimetic in human muscle. However, ." (Guerra et al. 2011)
So it appears that fasted sprint training can pinch hit for leptin.

Do This! A Training Template

bike-sprint
Hop on a bike and work up to one maximum, all out, pedal-as-hard-as-you-can sprint for 30 seconds.
The tension should be relatively high, but the goal is to keep your pedaling at a fast pace for the entire 30 seconds. If you slowed to a snail pace 20 seconds in, go to a lighter workload.
Make sure this is done in a fasted condition, such as first thing in the morning.
Don't have a bike? While the study didn't look at running, it may elicit the same response as the pathways are very similar.
It sounds ridiculously simple, but my purely anecdotal experience with my athletes shows that this does seem to help speed fat loss.

Summary

hot-sprinter
• More leptin is associated with less food intake.
• Some may have a leptin receptor issue where it's not responding to the amount of leptin floating around. Unfortunately, science isn't at the point yet where we can easily tell who has a receptor issue, but the more overweight you are, the more prone you are to having broken leptin receptors.
• Doing just one sprint in a fasted state works to pinch hit for leptin, putting you on the road to leanness. However, non-fasted training does not have the same effect. So add some sprint training in, but it has to be done in a fasted state.
• Fasted sprints can be done any time on a fasting day (where you're not consuming any calories), or done before breakfast. This way it's unlikely to interfere with your normal training session.
While we don't have a long-term study to show how much this will help your body composition, it's simple to add in and there's some very strong data to show it will help.
Heck, it only takes literally 30 seconds to do the sprint. Try it out, and let me know what you find.
Questions or comments? Post them in the LiveSpill below.

Selected References

Everard, A., Lazarevic, V., Derrien, M., Girard, M., Muccioli, G. G., Neyrinck, A. M., Cani, P. D. (2011). Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice. Diabetes, 60(11), 2775-2786. doi:10.2337/db11-0227
Finocchietto PV, Holod S, Barreyro F, Peralta JG, Alippe Y, Giovambattista A, Carreras MC, Poderoso JJ. Defective leptin-AMP-dependent kinase pathway induces nitric oxide release and contributes to mitochondrial dysfunction and obesity in ob/ob mice. Antioxid Redox Signal. 2011 Nov 1;15(9):2395-406. Epub 2011 Jun 28.
Galgani, J. E., Greenway, F. L., Caglayan, S., Wong, M. L., Licinio, J., & Ravussin, E. (2010). Leptin replacement prevents weight loss-induced metabolic adaptation in congenital leptin-deficient patients. The Journal of Clinical Endocrinology and Metabolism, 95(2), 851-855. doi:10.1210/jc.2009-1739
Guerra, B., Olmedillas, H., Guadalupe-Grau, A., Ponce-Gonzalez, J. G., Morales-Alamo, D., Fuentes, T., . . . Calbet, J. A. (2011). Is sprint exercise a leptin signaling mimetic in human skeletal muscle? Journal of Applied Physiology (Bethesda, Md.: 1985), 111(3), 715-725. doi:10.1152/japplphysiol.00805.2010
Ho, J. N., Jang, J. Y., Yoon, H. G., Kim, Y., Kim, S., Jun, W., & Lee, J. (2012). Anti-obesity effect of a standardised ethanol extract from curcuma longa L. fermented with aspergillus oryzae in ob/ob mice and primary mouse adipocytes. Journal of the Science of Food and Agriculture, doi:10.1002/jsfa.5592; 10.1002/jsfa.5592
INGALLS, A. M., DICKIE, M. M., & SNELL, G. D. (1950). Obese, a new mutation in the house mouse. The Journal of Heredity, 41(12), 317-318.
Kelesidis, T., Kelesidis, I., Chou, S., & Mantzoros, C. S. (2010). Narrative review: The role of leptin in human physiology: Emerging clinical applications. Annals of Internal Medicine, 152(2), 93-100. doi:10.1059/0003-4819-152-2-201001190-00008
Kowalik, S., & Kedzierski, W. (2011). The effect of interval versus continuous exercise on plasma leptin and ghrelin concentration in young trotters. Polish Journal of Veterinary Sciences, 14(3), 373-378.
Plinta, R., Olszanecka-Glinianowicz, M., Drosdzol-Cop, A., Chudek, J., & Skrzypulec-Plinta, V. (2011). The effect of three-month pre-season preparatory period and short-term exercise on plasma leptin, adiponectin, visfatin and ghrelin levels in young female handball and basketball players. Journal of Endocrinological Investigation, doi:10.3275/8014
Wolsk, E., Mygind, H., Grondahl, T. S., Pedersen, B. K., & van Hall, G. (2011). The role of leptin in human lipid and glucose metabolism: The effects of acute recombinant human leptin infusion in young healthy males. The American Journal of Clinical Nutrition, 94(6), 1533-1544. doi:10.3945/ajcn.111.012260
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372(6505), 425-432. doi:10.1038/372425a0



среда, 20 августа 2014 г.

Steroid Injections

Doctors sometimes recommend cortisone injections to patients experiencing joint inflammation and pain. These steroids, called corticosteroids or cortisone, do not alleviate pain directly. Instead, cortisone injections alleviate joint inflammation, including swelling, heat, and redness, which in turn alleviates joint pain.
The inflammation and resulting pain may be caused by:
  • Problems affecting the soft tissue surrounding the joint, such asbursitis and tendonitis
  • Conditions that originate inside the joint capsule, such as osteoarthritis, rheumatoid arthritis, or crystalloid diseases such as gout
A cortisone injection will not necessarily treat the underlying condition at the root of these symptoms. For example, osteoarthritis and rheumatoid arthritis can be treated, but not cured. Similarly, a cortisone injection can reduce or eliminate pain from a gout flare-up, but it will not reduce the likelihood of future gout flare-ups.

Why Get a Cortisone Injection?

In general, patients receive cortisone injections for one of two reasons: to treat the condition or to provide information for an accurate diagnosis.

    Temporary pain relief allows the patient to:
    • Treat an arthritic flare-up. For arthritic conditions such as a gout flare-up, a cortisone injection can relieve pain while the gout episode runs its course. The patient may also be prescribed oral medications and be advised to make dietary changes.
    • Participate in physical therapy. Pain relief from a cortisone injection gives the patient an opportunity to participate in physical therapy to improve the affected joint's biomechanics. Ideally, by the time the effects of the cortisone wear off, the joint is healthier so pain is tolerable or even eliminated.
    • Rest the joint. A painfully inflamed joint needs to rest to recover. For example, patients with an inflamed bursa may need to adequately rest the affected joint in addition to participating in physical therapy.
    • Postpone surgery. In moderate to severe cases of arthritis, a joint replacement or another surgical treatment may be recommended. For patients who want to postpone or avoid surgery, cortisone injections may allow them to live with less pain.
    Almost all types of arthritis are chronic, and a cortisone injection is just one part of a larger treatment plan.
    Cortisone injections for aiding diagnosis
    When the underlying cause of pain is uncertain, a doctor may recommend a cortisone shot to help narrow the list of possible diagnoses. This procedure is common in the hip and shoulder joints.
    For example, a doctor may recommend a cortisone injection for a patient with persistent, undiagnosed hip pain.
    • If the injection relieves the patient's hip pain, the pain probably originates in the hip
    • If the hip pain persists even after the injection, the doctor may consider problems affecting spine or the sacroiliac joint (where the spine and pelvis meet), both of which can cause referred hip pain.
    If a diagnosis is still uncertain following a diagnostic injection, the doctor may recommend an MRI or other detailed imaging study.
Of course, an injection meant to aid in diagnosis can be useful for treatment, and vice versa. However, a doctor and patient should take time to discuss the primary purpose of the cortisone injection before it is administered. During this conversation a doctor should let the patient know what part of the joint is being targeted, what are reasonable expectations regarding pain relief, and if follow-up treatment will involve medications, physical therapy, or lifestyle changes.

What is Cortisone?

Cortisone refers to a category of man-made steroids that mimic the effects of cortisol, a hormone that naturally occurs in the body. Both cortisone and cortisol are types of corticosteroids.
It is important to note that these types of steroids differ from anabolic steroids (e.g. testosterone) that are used to enhance athletic performance. Both types of steroids share similar chemical structures but play opposite roles in the body.

Not a Cure-All for All Types of Joint Problems

A patient usually receives a cortisone injection to help reduce pain-causing inflammation. Once this inflammation is reduced, the patient can participate in physical therapy (which plays a very important role in most situations). However, cortisone, like all medications, can have side effects.
Most notably, cortisone is known to break down tissues, such as articular cartilage in the joint.1,2 Cartilage is crucial to joint health, acting as a shock absorber and reducing friction between bones when a person moves. Therefore, most physicians will refuse to administer repeated cortisone injections into the same joint over a short period of time, simply because too much cortisone can cause more harm than good.
References
  1. Dragoo JL. Chondrotoxicity of commonly used single injection corticosteroids. Presented at the 2010 Annual Meeting of the American Orthopaedic Society for Sports Medicine. July 15-18. Providence, R.I. Cited by Orthopedics Today. Preservative noted as possible key to intra-articular injection corticosteroid chondrotoxicity. Helio Orthopedics. www.healio.com. Published September 2010. Accessed February 18, 2014.
  2. Papacrhistou G, Anagnostou S, Katsorhis T. The effect of intraarticular hydrocortisone injection on the articular cartilage of rabbits. Acta Orthop Scand Suppl. 1997 Oct;275:132-4. PubMed PMID: 9385288.