Health
What is localized fat loss?
Localized fat loss is the idea that you can reduce body fat in a specific area of your body. Localized fat loss is also known as targeted fat loss and is such an exciting idea that it has been floating around the fitness world for several decades.
What evidence is there that localized fat loss is possible?
If you get very technical, there is some circumstantial evidence that localized fat loss is possible (and we're ignoring liposuction and other surgical options at this point). A big part of this circumstantial evidence is that we all have different shapes, but that shape is lost when we get heavy enough. If you lose some body fat, then your overall body shape will show (e.g. apple-shaped vs. pear-shaped). And this is often confused with localized fat loss (hey, all the fat I lost was in place xxxx!).
In addition, some old studies using a cream containing a fat loss ingredient (yohimbine, forskolin) that could be absorbed through the skin were able to observe fat loss in the areas where the cream was applied.
While we're still on the technical details, it's worth noting that training a specific muscle is associated with more regional fat loss than fat loss in other areas.
So technically, there is evidence of a difference in body fat distribution and weak evidence that you can selectively reduce fat preferentially in a specific area.
Can I integrate localized fat loss into my training program?
Even though we have shown that it is technically possible, the realistic answer is "no".
The fat loss creams mentioned above have not been available for a long time. And even the studies on liposuction (for localized fat reduction) have shown that there was a redistribution of body fat after the procedure and that body fat levels rebalanced.
Basically, this means that even if you somehow manage to lose fat in one area of the body, your body will compensate. This is the unavoidable reality.
Despite the previous sections, the answer is most likely 'no'. This is also due to the fact that in the studies with fat loss creams mentioned above, the studies ended at the same time as the use of the cream ended and there were no follow-up studies.
And what about the one study that showed that training a muscle means more localized fat loss? This study concluded that an additional 600 to 2100 micrograms of fat per 100 grams of adipose tissue were shed. In other words, this corresponds to an increase in local fat loss of 0.02%!
You can try to achieve localized fat loss, but the body will restore the balance of fat distribution.
Under what circumstances might I be able to achieve localized fat loss?
There is only one scenario in which a person can achieve selective and long-lasting fat loss in a specific area and this involves the loss of central excess weight.
There are a few varieties of body fat that include subcutaneous adipose tissue (the flabby fat that we notice most), retroperitoneal adipose tissue (on the lower back, important for physically supporting the kidneys and loss of this fat can cause damage to the uterus) and visceral adipose tissue (a hardened fatty tissue that is located in the abdomen and surrounds the organs). Other types of adipose tissue that are not considered aesthetically bad include adipose tissue in the brain, adipose tissue in the breast area and intramuscular adipose tissue.
All variants of body fat are regulated by different hormones and cytokines (signaling molecules that act like hormones) and therefore you may have one area that is larger than it should be relative to others:
- You may have more subcutaneous/flabby) fat relative to visceral (central) body fat. This will make you look soft but give you a relatively narrow waist.
- You may have much more visceral fat relative to subcutaneous fat, which can result in a very large and hard belly (alcohol consumption usually causes this).
- It may not be that the relative amount of flabby fat on your arms and thighs is different, as both are the same variety - subcutaneous fat.
- Cosmetic surgery can override the above three points because body fat is liposuctioned or burned with a laser.
Reduction of central body fat (which can usually be seen when a person with central obesity and a very unhealthy lifestyle changes their life for the better) without too much reduction of subcutaneous fat is something like localized fat loss and this can be maintained long after fat loss.
Summary
- Localized fat loss is the idea that you can prioritize fat loss in one area of the body, such as fat on the abdomen instead of fat on the thighs.
- Localized fat loss is a real phenomenon even without surgery, at least from a purely technical point of view, but in practical terms it is futile, as only minimal amounts of fat can be lost locally and the body is likely to compensate for this after some time.
- There are several different types of body fat, two of which are important for aesthetics and fat loss: subcutaneous (flabby and close to the skin) and visceral (hardened, central) fat.
- Different types of body fat are regulated by different hormones and therefore react differently to hormonal changes.
- The reduction of central fat after a change from a very unhealthy to a healthy lifestyle is probably the only selective fat loss that can take place in practice.
And now you know. Is it technically possible to lose fat locally? Sure.
Will it make a difference in practice? No.
So the bottom line seems to be that localized fat loss is, for the most part, a myth.
By Nia Shanks
Source: http://www.niashanks.com/spot-reduction/
I'm talking about taking non-steroidal anti-inflammatory drugs - you know, those painkillers that you can find in any pharmacy in copious quantities.
There are dozens of brands and active ingredients to choose from: Aspirin, ibuprofen, diclofenac, etc. And it's not hard to get your hands on these medications. Most can be purchased without a doctor's prescription and even without a pharmacist's admonishing words.
Non-steroidal anti-inflammatory drugs have become an integral part of the daily training program of many strength athletes. In most cases, they are used to alleviate the effects of delayed onset muscle soreness, which can sometimes last for several days after an intense training session.
On the surface, taking non-steroidal anti-inflammatory drugs to reduce delayed onset muscle soreness seems to make sense - just pop a few pills and your soreness miraculously disappears. No missed training sessions, no reduction in performance. What's the problem?
Well, let's look a little deeper. Although the exact mechanisms are not yet fully understood, delayed onset muscle soreness is believed to be the product of damage to muscle tissue.
The proposed model looks something like this: Forces associated with muscular contractions-especially eccentric actions-cause the formation of small microtears in the contractile elements and surface membrane (sarcolemma) of working muscle fibers.
These microtears allow an outflow of calcium from the muscles, disrupting the intracellular balance and causing further injury to the muscle fibers.
Different proteins then interact with the free nerve endings surrounding the damaged fibers, resulting in local pain and stiffness. These symptoms can be exacerbated by swelling within the muscle fibers, which exerts pressure on sensory receptors (pain receptors), thereby increasing the pain (6).
Non-steroidal anti-inflammatory drugs are believed to reduce pain primarily by inhibiting cyclooxygenases (COX), a family of enzymes that catalyze the conversion of arachidonic acid into pro-inflammatory prostanoids (5, 22).
Prostanoids have been shown to be responsible - at least in part - for the pain associated with delayed onset muscle soreness. Studies have shown that they promote inflammation and make pain receptors more sensitive, thereby increasing pain sensitivity (16).
By inhibiting the synthesis of prostanoids, non-steroidal anti-inflammatory drugs can significantly reduce the pain experienced after exercise, allowing you to train hard and heavy day in, day out. And this should lead to better gains in muscle mass and strength, right?
Maybe not.
The acute post-workout inflammatory process appears to play a role in muscular adaptations to resistance training. Prostanoids in particular have been shown to play a role in anabolic signaling. They are involved in the stimulatory pathways responsible for the execution of protein synthesis (13, 18).
Considering that non-steroidal anti-inflammatory drugs impair the production of prostanoids, it seems logical that these drugs could also have a negative effect on muscle development. In fact, early studies have shown that this is the case.
Studies conducted in rodents have consistently shown that non-steroidal anti-inflammatory drugs impair protein metabolism (13, 18, 21) and reduce muscle development in response to muscle overload (3, 21).
Devastating effects on muscle adaptations have been observed with the use of both selective and non-selective non-steroidal anti-inflammatory drugs, resulting in a reduction in hypertrophy of up to 50% (19). In other words, muscle growth was halved after administration of non-steroidal anti-inflammatory drugs!
Confusing results in humans
The studies with rats and mice seem very convincing. But what about humans? Well, an early human study seemed to confirm these results.
In 2002, a team of researchers led by Dr. Todd Trappe found that non-selective non-steroidal anti-inflammatory drugs taken after a session of supramaximal eccentric exercise reduced protein synthesis by 50 to 75%. This seemed to be the final nail in the coffin for non-steroidal anti-inflammatory drugs. All evidence pointed to these drugs interfering with muscle development.
But something interesting happened. Follow-up studies conducted in humans were unable to reproduce the initial results in humans. Studies involving both young and older subjects taking selective and non-selective COX inhibitors showed no differences in protein synthesis (4, 11, 15).
If these results aren't confusing enough, consider some recent studies that examined the long-term effects of nonsteroidal anti-inflammatory drug use on muscle growth in humans. None of these studies were able to find any negative effects on muscle hypertrophy (8, 14, 20).
In fact, one of these studies even showed that non-steroidal anti-inflammatory drugs increased muscle hypertrophy by about 50% (20). Yes, you heard right - the group taking painkillers significantly increased their muscle gains!
What are the explanations for these contradictions?
If you look at the research, it seems that non-steroidal anti-inflammatory drugs are highly catabolic in small rodents, but not in humans. You might even suspect that regular use might have performance-enhancing effects. Considering the studies mentioned, this seems logical, right?
Not so fast. A whole range of factors need to be considered before any relevant conclusions can be drawn on the subject.
First of all, these protein synthesis studies, interesting as they may be, need to be considered in the right context. Acute studies of anabolic processes in humans do not necessarily correlate with long-term hypertrophy.
Just because protein synthesis or signaling factors are increased after exercise does not necessarily mean that this will result in greater gains in muscle mass over a period of weeks or months (1).
Another potential problem with the current state of studies is that all studies to date have been conducted with untrained subjects. You don't have to be a rocket scientist to realize that adaptations differ between people with no training experience and people who regularly train with weights. Would the results have been different in a group of serious strength athletes? Quite possibly.
In addition, two of the three studies that examined hypertrophy were conducted with older subjects. In fact, the age of the subjects in the study that observed significant hypertrophy benefits with the use of non-steroidal anti-inflammatory drugs was between 60 and 85 years.
The problem here is that older people - and especially older people who do not exercise regularly - are susceptible to subthreshold inflammation. In contrast to acute post-workout inflammatory processes, chronic inflammation has devastating effects on muscle development, impairing anabolism and accelerating muscle protein breakdown (17).
It is therefore quite possible - if not likely - that non-steroidal anti-inflammatory drugs may have helped to reduce underlying inflammation in these subjects, thereby promoting the positive effects on muscle growth. This is irrelevant for healthy, young exercisers, as subliminal inflammation is not an issue for these people.
The satellite connection
If you're serious about strength training, the biggest dilemma with using non-steroidal anti-inflammatory drugs is their potential negative impact on satellite cells.
Simply put, satellite cells are muscle stem cells located next to the muscle fibers. These non-specialized cells remain dormant until they are needed for muscle repair or regeneration, as is the case after resistance training.
One of the most important roles of satellite cells is their ability to increase the number of nuclei in the muscle, which are responsible for the production of proteins needed for muscle growth.
During normal daily activities, the number of nuclei in the muscles is sufficient to remodel the muscle tissue. This is no longer the case when you perform intensive training with weights.
Heavy training substantially increases the need for protein synthesis. This is where satellite cells come into play. Muscle contractions activate satellite cells, which then divide, form (become more specialized) and fuse with the working muscle fibers, donating their nuclei so that the muscle can produce more protein to support continued growth.
The current theory is that without a consistent available supply of satellite cells, muscle hypertrophy will eventually stall (1).
But what does all this have to do with non-steroidal anti-inflammatory drugs?
Well, recall that non-steroidal anti-inflammatory drugs exert their effects by blocking the synthesis of various prostanoids. However, prostanoids are known to stimulate the division, formation and fusion of satellite cells (2).
And (drum roll please) studies conducted with both animals and humans have repeatedly observed a significant reduction in satellite cell activity when non-steroidal anti-inflammatory drugs were administered in response to muscle damage (2, 3, 9, 10).
This raises the possibility that non-steroidal anti-inflammatory drugs, although they may not affect hypertrophy in the short term, could have devastating effects on long-term muscle growth.
Conclusion on the use of non-steroidal anti-inflammatory drugs
Based on the research currently available, it seems clear that the occasional use of non-steroidal anti-inflammatory drugs will not derail your training efforts. However, it is too early to draw any firm conclusions about chronic use of these drugs.
Studies are limited and more research is needed - especially with well-trained strength athletes - to understand how these drugs affect muscle hypertrophy in the long term. Further information can be found in a recent review published in the Journal Sports Medicine(https://www.ncbi.nlm.nih.gov/pubmed/23013520).
In the meantime, it seems wise to avoid regular use of non-steroidal anti-inflammatory drugs for the treatment of muscle pain and/or performance enhancement. Apart from one isolated study that showed positive effects in older people, the effects of non-steroidal anti-inflammatory drugs on muscle adaptations to exercise will be neutral at best.
Furthermore, the data regarding satellite cells suggest that non-steroidal anti-inflammatory drugs may have a negative effect on long-term muscle gains. This is a particular concern for those with extensive training experience, as an inability to increase the number of nuclei in the muscles could be a limiting factor in maximizing muscle development.
And then there are the side effects. Continuous use of non-steroidal anti-inflammatory drugs has been associated with stomach problems in a large proportion of the population. Other potentially more dangerous consequences that are less common include bleeding stomach ulcers, cardiovascular complications and even liver and kidney failure. Not a good risk/benefit ratio, to say the least.
Interestingly, curcumin may be a safer alternative to non-steroidal anti-inflammatory drugs. Curcumin, which usually turns out to be free of side effects, has similar mechanisms of action to relieve pain. If you need a boost to exercise through a sore muscle, then this would be a better way to go.
As a final note, it should be mentioned that it is questionable whether non-steroidal anti-inflammatory drugs really help to reduce perceived pain and promote recovery of muscle function. The majority of studies seem to indicate that their use has no better therapeutic effect than a placebo (7).
It may well be that the primary pain-relieving benefits of these drugs are largely psychological. If this is indeed the case, the question arises as to whether non-steroidal anti-inflammatory drugs are worth the risk at all in light of all their potential negative effects.
References
- Adams, G, and Bamman, MM. Characterization and regulation of mechanical loading-induced compensatory muscle hypertrophy. Comprehensive Physiology 2829, 2012.
- Bondesen, BA, Mills, ST, Kegley, KM, and Pavlath, GK. The COX-2 pathway is essential during early stages of skeletal muscle regeneration. Am. J. Physiol. Cell Physiol. 287: 475-483, 2004.
- Bondesen, BA, Mills, ST, and Pavlath, GK. The COX-2 pathway regulates growth of atrophied muscle via multiple mechanisms. Am. J. Physiol., Cell Physiol. 290: 1651-1659, 2006.
- Burd, NA, Dickinson, JM, Lemoine, JK, Carroll, CC, Sullivan, BE, Haus, JM, Jemiolo, B, Trappe, SW, Hughes, GM, Sanders, CE,Jr, and Trappe, TA. Effect of a cyclooxygenase-2 inhibitor on postexercise muscle protein synthesis in humans. Am. J. Physiol. Endocrinol. Metab. 298: E354-61, 2010.
- Burian, M, and Geisslinger, G. COX-dependent mechanisms involved in the antinociceptive action of NSAIDs at central and peripheral sites. Pharmacol. Ther. 107: 139-154, 2005.
- Clarkson, PM, and Hubal, MJ. Exercise-induced muscle damage in humans. Am. J. Phys. Med. Rehabil. 81: 52-69, 2002.
- Connolly, DA, Sayers, SP, and McHugh, MP. Treatment and prevention of delayed onset muscle soreness. J. Strength Cond Res. 17: 197-208, 2003.
- Krentz, JR, Quest, B, Farthing, JP, Quest, DW, and Chilibeck, PD. The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training. Appl. Physiol. Nutr. Metab. 33: 470-475, 2008.
- Mackey, AL, Kjaer, M, Dandanell, S, Mikkelsen, KH, Holm, L, Dossing, S, Kadi, F, Koskinen, SO, Jensen, CH, Schroder, HD, and Langberg, H. The influence of anti-inflammatory medication on exercise-induced myogenic precursor cell responses in humans. J. Appl. Physiol. 103: 425-431, 2007.
- Mikkelsen, UR, Langberg, H, Helmark, IC, Skovgaard, D, Andersen, LL, Kjaer, M, and Mackey, AL. Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise. J. Appl. Physiol. 107: 1600-1611, 2009.
- Mikkelsen, UR, Schjerling, P, Helmark, IC, Reitelseder, S, Holm, L, Skovgaard, D, Langberg, H, Kjaer, M, and Heinemeier, KM. Local NSAID infusion does not affect protein synthesis and gene expression in human muscle after eccentric exercise. Scand. J. Med. Sci. Sports 21: 630-644, 2011.
- Novak, ML, Billich, W, Smith, SM, Sukhija, KB, McLoughlin, TJ, Hornberger, TA, and Koh, TJ. COX-2 inhibitor reduces skeletal muscle hypertrophy in mice. Am. J. Physiol. Regul. Integr. Comp. Physiol. 296: R1132-9, 2009.
- Palmer, RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot. Essent. Fatty Acids 39: 95-104, 1990.
- Petersen, SG, Beyer, N, Hansen, M, Holm, L, Aagaard, P, Mackey, AL, and Kjaer, M. Nonsteroidal anti-inflammatory drug or glucosamine reduced pain and improved muscle strength with resistance training in a randomized controlled trial of knee osteoarthritis patients. Arch. Phys. Med. Rehabil. 92: 1185-1193, 2011.
- Petersen, SG, Miller, BF, Hansen, M, Kjaer, M, and Holm, L. Exercise and NSAIDs: effect on muscle protein synthesis in patients with knee osteoarthritis. Med. Sci. Sports Exerc. 43: 425-431, 2011.
- Prisk, V, and Huard, J. Muscle injuries and repair: the role of prostaglandins and inflammation. Histol. Histopathol. 18: 1243-1256, 2003.
- Rieu, I, Magne, H, Savary-Auzeloux, I, Averous, J, Bos, C, Peyron, MA, Combaret, L, and Dardevet, D. Reduction of low grade inflammation restores blunting of postprandial muscle anabolism and limits sarcopenia in old rats. J. Physiol. 587: 5483-5492, 2009.
- Rodemann, HP, and Goldberg, AL. Arachidonic acid, prostaglandin E2 and F2 alpha influence rates of protein turnover in skeletal and cardiac muscle. J. Biol. Chem. 257: 1632-1638, 1982.
- Soltow, QA, Betters, JL, Sellman, JE, Lira, VA, Long, JH, and Criswell, DS. Ibuprofen inhibits skeletal muscle hypertrophy in rats. Med. Sci. Sports Exerc. 38: 840-846, 2006.
- Trappe, TA, Carroll, CC, Dickinson, JM, LeMoine, JK, Haus, JM, Sullivan, BE, Lee, JD, Jemiolo, B, Weinheimer, EM, and Hollon, CJ. Influence of acetaminophen and ibuprofen on skeletal muscle adaptations to resistance exercise in older adults. Am. J. Physiol. Regul. Integr. Comp. Physiol. 300: R655-62, 2011.
- Vandenburgh, HH, Hatfaludy, S, Sohar, I, and Shansky, J. Stretch-induced prostaglandins and protein turnover in cultured skeletal muscle. Am. J. Physiol. 259: C232-40, 1990.
- Vane, JR, and Botting, RM. Anti-inflammatory drugs and their mechanism of action. Inflamm. Res. 47 Suppl 2: S78-87, 1998.
By Brad Schoenfeld, PhD | 11/13/12
Source: https://www.t-nation.com/training/do-pain-pills-impair-muscle-growth
Tip: Do not perform straight sentences
Do you want to activate your nervous system and stay strong from sentence to sentence? Then try this method.
Serious strength athletes always talk about the endocrine system, the muscular system and the cardiovascular system, but they hardly ever talk about the neural system. This is a big mistake. Neuronal regeneration is often ignored.
How most strength athletes train
99 out of 100 exercisers perform multiple sets of a specific exercise in succession, also known as straight sets. For example, they will perform a set of bench presses, followed by another set of bench presses, followed by another set of bench presses. In between sets, they will "recover" while pretending to pull a loose thread out of their socks as they compile the playlist on their smartphone.
Scientific research tells us that these athletes could benefit from much better recovery if they performed a set for an antagonist muscle group between sets.
A better way: antagonistic training
Here's how it works: Perform a set of dumbbell bench presses, perform a set of barbell rows for the latissimus between sets, and then perform your next set of dumbbell bench presses (and continue this alternating exercise pattern for the desired number of sets). You will experience a smaller drop in strength from set to set compared to straight sets.
No one knows exactly why this is the case, but it certainly has something to do with the neurological system. This is the reason I started using the "A1" and "A2" designations in my training sessions - a method that has since been adopted by many trainers. Unfortunately, many coaches who use this system do not understand why they are using it, or if they do understand it, they rarely explain it to their athletes.
Other examples of useful antagonistic pairings of muscle groups would be:
- Bicep curls and tricep presses
- Leg extensions and leg curls
- Overhead presses and pull-ups
From Charles Poliquin | 07/23/16
Source: https://www.t-nation.com/training/tip-dont-do-straight-sets
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>> Why the big three basic exercises are not enough to build mass
The anterior cruciate ligament connects the femur to the tibia. It prevents the tibia from moving forward on the femur and also prevents internal rotation of the tibia. Tears in the anterior cruciate ligament do not heal on their own and must be repaired surgically. This surgery usually involves the removal of tendon tissue from the hamstrings or patellar tendon, so the athlete has to recover from two operations.
Boston surgeons Martha Murray and Lyle Micheli found in a study using pigs that inserting a sponge into the injured portion of the anterior cruciate ligament and flooding it with the patient's blood allowed the ligament to heal on its own. They tried this operation on a limited number of patients. The surgery was so successful that they received approval for more extensive human studies.
This surgery could reduce the time it takes to heal and recover from anterior cruciate ligament surgery from one year to six months.
(The Wall Street Journal, February 3, 2016)
Our tip: take curcumin every day
Curcumin is not only an excellent anti-inflammatory, it also has 7 other benefits. Find out more!
Curcumin is a powerful anti-inflammatory, but its other effects range from pain management to benefits that affect almost every organ system in the body.
Curcumin can:
- Reduce body fat
- Improve cardiovascular health
- Support healthy cholesterol levels
- Alleviate a decline in cognitive ability
- Act as an aromatase inhibitor (and thus increase testosterone levels)
- Reduce plaque levels in the arteries
- Lower the risk of diabetes
And like everything else that comes from a plant, it has antioxidant capabilities.
Can I just eat a lot of Indian food?
Curcumin is found in a spice called turmeric and Indians probably use more of this spice than anyone else in the world. Considering the seemingly endless health benefits of curcumin, one would probably assume that Indians must be one of the healthiest peoples on the planet. However, this is not the case. Unfortunately, the body does not absorb curcumin well. Simply eating a lot of curry powder, regardless of the amount of curcumin it provides, is not going to have any great health benefits.
To reap the benefits of curcumin, you need to consume it in combination with piperine, which can improve the absorption of curcumin by up to 2000%. There are several supplements on the market that contain exactly this combination. In this combination, curcumin is one of the few substances that, when taken, you will consciously notice that you feel better.
Source: https://www.t-nation.com/supplements/tip-take-curcumin-every-day
From TC Luoma | 01/01/16
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>>Whycurcumin is the next big superfood?
>>Curcumin for muscle growth
