Studies continue to be published attesting to the value of beta alanine as an effective ergogenic aid for increasing both training and athletic performance. Beta alanine is an amino acid, and when combined with another amino acid, histidine, it forms the core of carnosine. The significance of carnosine is that it’s a potent antioxidant, and also acts as a primary intramuscular buffer. What this means is that carnosine helps lower elevated acid levels that accrue in muscle following intense exertion, including exercise. Increased acid interferes with the activity of enzymes involved in energy production, so lowering acid levels in muscle would increase athletic performance.
While carnosine is available in supplement form, it’s only marginally effective in boosting intramuscular carnosine levels. A ubiquitous enzyme called carnosinase breaks down most of the ingested carnosine into its constituent beta alanine and histidine forms. But research shows that using supplemental beta alanine at dose of 4 to 6 grams a day does boost intramuscular carnosine as much as 64%. Although hard-training athletes tend to have naturally higher muscle carnosine levels as a result of regular training, these levels still increase when they use supplemental beta alanine.
The typical effects of beta alanine (BA) supplementation is evident by the results of a new study. The study involved 18 high level rowers who used BA for 7 weeks at a dose of 5 grams a day. Other rowers ingested a placebo for the same amount of time. Before and after supplementation, muscle carnosine levels were measured, and performance was evaluated in a 2000 meter ergometer test. The baseline test showed a strong correlation between muscle carnosine levels in the rowers and speed at various distances. After the BA supplementation, carnosine content increased by 45.3% in the soleus muscle (slow-twitch) and 28.2% in the gastrocnemius muscle (fast-twitch). Performance testing also showed that the BA group was 4.3 seconds faster than the placebo group. Prior to BA, they were 0.3 seconds slower. Muscle carnosine levels was positively correlated to 2000 meter rowing performance. As such, carnosine was able to increase speed in these elite athletes. Strength wasn’t measured in the study, although prior studies suggest that BA usage may increase muscle endurance, along with the ability to boost training intensity levels due to less muscle fatigue. What it all points to is that unlike many other sports supplements, BA is the real deal.
Baguet A, et al. Important role of carnosine in rowing performance. J Appl Physiol 2010;in press.
To learn the scientific truth about various supplements, read my e-book, Natural Anabolics, available at jerrybrainum.com
Monday, February 7, 2011
Can you lift light and still make muscle gains?
A long-standing tenet in bodybuilding is that if you want to promote muscular hypertrophy, or muscle size gains, you need to train heavy, using lower reps. Conversely, training with lighter weights will “tone” muscles, but isn’t effective for promoting gains in muscular size and strength. Much of this is based on a physiological principle called the Muscle fiber recruitment hierarchy. This principle states that the body activates only as many muscle fibers as possible to produce movement, beginning with the slow-twitch, or type-1 muscle fibers. As these fibers fatigue (and fatigue is the key word here, as we shall see), other muscle fibers, namely types 2-a and 2-b, also known as fast-twitch muscle fibers, are brought into play. What activates these fast-twitch fibers are neuromuscular connections. Simply put, when enough resistance is placed on the muscle, a signal is sent to the cerebellum section of the brain requesting more neural input to the muscle fibers in order to recruit the type-2 fibers. For years, it was thought that to recruit the type 2B muscle fibers required a greater neural input, and the best way to do this was to increase the intensity level of the imposed stress on the fibers. The best way to do this was to lift heavy. Indeed, most exercise physiology textbooks say that the fast-twitch type-2 muscle fibers are the fibers most amenable to gains in muscle size and strength. Type-1 slow-twitch fibers are more related to endurance, and would be activated with lower intensity exercise, such as when doing endurance activity, or when using lighter weights for higher reps. Again, it was thought that the body won’t recruit the type-2 fibers unless it was necessary. But note that the type-2 fibers can also be brought into play when the type-1 fibers become fatigued, for whatever reason.
Bodybuilders had larger muscles because of a selective hypertrophy of type 2B fast-twitch muscle fibers, and they achieved this through lifting heavy weights. But in recent years, this notion has come into question. As I reported in an Ironman magazine article a while ago, muscle biopsies of champion bodybuilders showed that they had a preponderance of type 2A fast-twitch muscle fibers, rather than the expected type 2B fibers. Type 2A fibers are considered an intermediate fiber, having characteristics of both type 1 and type 2 fibers. What this pointed to was that the typical bodybuilding workout of doing higher reps, averaging 8-12 per set, would likely produce better muscle gains compared to doing lower reps with heavier weight.While many powerlifters and Olympic weightlifters undeniably are strong, many don’t show the level of muscle hypertrophy that you would expect considering their chronic heavy lifting training routines, which usually involve heavy weights and low reps.
Occlusion training, which involves training with an impediment to blood flow, such as wearing an inflatable cuff while training, has been shown in several studies to produce significant gains in muscle size despite using light weights. Various reasons are offered to explain this effect, but the main mechanism seems to be an increase in localized fatigue products produced in the muscle as a result of the impeded blood flow. This increased fatigue, in turn, is interpreted by the brain as a call to recruit the type-2 muscle fibers, which result in the muscle gains apparent following this type of exercise. I also reported on another study, in which subjects lifted light weights, but under high tension, meaning that they did the exercises slower than normal, and forcefully contracted the trained muscles during every rep. Again, despite using weights only equivalent to 20% of one rep-maximum, which is very light, the subjects made gains in muscle size comparable to that achieved through lifting far heavier weights. The deciding factor here was again the level of local muscle fatigue produced in the trained muscle, which not only fully activated the type-2 fibers, but also promoted a greater release of anabolic hormones, such as growth hormone and IGF-1, which are stimulated by locallly produced muscle fatigue factors, such as increased lactic acid in the muscle.
In the latest study, 15 men, average age, 21, all of whom had at least 6 months of training experience, and had trained at least three times a week 6 months prior to the start of the study, did 4 sets of one-legged extensions using differing training protocols. These protocols were as follows:
1) 90% of one-rep maximum weight to failure (heavy weight)
2) 30% of one-rep maximum matched in reps and load to #1
3) 30% of one-rep maximum done to failure (light)
The scientists conducting the study calculated various rates of protein synthesis in the trained muscle, measuring both contractile protein synthesis and connective tissue or structural muscle protein synthesis. Increased muscle protein synthesis is directly related to increased gains in muscle size and strength, particularly the contractile proteins. The study results showed that the light weight to failure style (#3) was more effective at increasing muscle protein synthesis compared to #1, or high load, heavy weight. The light training to failure produced a level of muscle protein synthesis that was similar to that of the heavy load 4 hours after exercise, but it was sustained for 24 hours after training only in the light weight to failure training. The study authors suggest that the increased volume of training produced by the lighter weight to failure study resulted in more muscle fatigue, and more positively affected the amplitude of the muscle synthesis process. Only the #3 style of training produced sustained increases in the muscle protein synthesis rate of all proteins found in muscle: contractile, connective tissue, and mitochondrial. This means in simple terms that this style of training may be capable of increasing muscle size, strength, and even endurance simultaneously. The total number of completed reps was 94 in group #3; 19 in #1; and 62 in #2. The greater number of reps in #3 appeared to promote a greater activity of several muscle protein synthesis signaling factors. Group#3 also showed higher indicators of signaling factors for stimulation of muscle satellite cell activity, which is important for promoting muscle size and strength gains.
The authors suggest this information could be useful for prescribing exercise for those who are injured or too old to lift heavy weights.They point out that people over age 70 show an anabolic resistance to weight-training, meaning that they don’t show any significant increases in muscle protein synthesis following weight-training. This resistance,however, can be overcome by increasing the volume of exercise in the aged. This jives with the findings of this new study, which suggests that lifting lighter, but doing reps to muscle failure, is capable of fully turning on the muscle protein synthesis machinery of the body. The key is to induce enough fatigue in the muscle to kick-start the muscle protein synthesis reactions. And according to this study, it can be done by using lighter weights that feature higher reps to failure (reps in the
Learn the truth about various anabolic supplements in my e-book, Natural Anabolics, available at jerrybrainum.com.
Bodybuilders had larger muscles because of a selective hypertrophy of type 2B fast-twitch muscle fibers, and they achieved this through lifting heavy weights. But in recent years, this notion has come into question. As I reported in an Ironman magazine article a while ago, muscle biopsies of champion bodybuilders showed that they had a preponderance of type 2A fast-twitch muscle fibers, rather than the expected type 2B fibers. Type 2A fibers are considered an intermediate fiber, having characteristics of both type 1 and type 2 fibers. What this pointed to was that the typical bodybuilding workout of doing higher reps, averaging 8-12 per set, would likely produce better muscle gains compared to doing lower reps with heavier weight.While many powerlifters and Olympic weightlifters undeniably are strong, many don’t show the level of muscle hypertrophy that you would expect considering their chronic heavy lifting training routines, which usually involve heavy weights and low reps.
Occlusion training, which involves training with an impediment to blood flow, such as wearing an inflatable cuff while training, has been shown in several studies to produce significant gains in muscle size despite using light weights. Various reasons are offered to explain this effect, but the main mechanism seems to be an increase in localized fatigue products produced in the muscle as a result of the impeded blood flow. This increased fatigue, in turn, is interpreted by the brain as a call to recruit the type-2 muscle fibers, which result in the muscle gains apparent following this type of exercise. I also reported on another study, in which subjects lifted light weights, but under high tension, meaning that they did the exercises slower than normal, and forcefully contracted the trained muscles during every rep. Again, despite using weights only equivalent to 20% of one rep-maximum, which is very light, the subjects made gains in muscle size comparable to that achieved through lifting far heavier weights. The deciding factor here was again the level of local muscle fatigue produced in the trained muscle, which not only fully activated the type-2 fibers, but also promoted a greater release of anabolic hormones, such as growth hormone and IGF-1, which are stimulated by locallly produced muscle fatigue factors, such as increased lactic acid in the muscle.
In the latest study, 15 men, average age, 21, all of whom had at least 6 months of training experience, and had trained at least three times a week 6 months prior to the start of the study, did 4 sets of one-legged extensions using differing training protocols. These protocols were as follows:
1) 90% of one-rep maximum weight to failure (heavy weight)
2) 30% of one-rep maximum matched in reps and load to #1
3) 30% of one-rep maximum done to failure (light)
The scientists conducting the study calculated various rates of protein synthesis in the trained muscle, measuring both contractile protein synthesis and connective tissue or structural muscle protein synthesis. Increased muscle protein synthesis is directly related to increased gains in muscle size and strength, particularly the contractile proteins. The study results showed that the light weight to failure style (#3) was more effective at increasing muscle protein synthesis compared to #1, or high load, heavy weight. The light training to failure produced a level of muscle protein synthesis that was similar to that of the heavy load 4 hours after exercise, but it was sustained for 24 hours after training only in the light weight to failure training. The study authors suggest that the increased volume of training produced by the lighter weight to failure study resulted in more muscle fatigue, and more positively affected the amplitude of the muscle synthesis process. Only the #3 style of training produced sustained increases in the muscle protein synthesis rate of all proteins found in muscle: contractile, connective tissue, and mitochondrial. This means in simple terms that this style of training may be capable of increasing muscle size, strength, and even endurance simultaneously. The total number of completed reps was 94 in group #3; 19 in #1; and 62 in #2. The greater number of reps in #3 appeared to promote a greater activity of several muscle protein synthesis signaling factors. Group#3 also showed higher indicators of signaling factors for stimulation of muscle satellite cell activity, which is important for promoting muscle size and strength gains.
The authors suggest this information could be useful for prescribing exercise for those who are injured or too old to lift heavy weights.They point out that people over age 70 show an anabolic resistance to weight-training, meaning that they don’t show any significant increases in muscle protein synthesis following weight-training. This resistance,however, can be overcome by increasing the volume of exercise in the aged. This jives with the findings of this new study, which suggests that lifting lighter, but doing reps to muscle failure, is capable of fully turning on the muscle protein synthesis machinery of the body. The key is to induce enough fatigue in the muscle to kick-start the muscle protein synthesis reactions. And according to this study, it can be done by using lighter weights that feature higher reps to failure (reps in the
study averaged 34 reps per set in the light weight to failure sessions). I believe that a key element of these findings is that even in the light weight group, each set was done to muscular failure, no matter how many reps that took. Just lifting light weights and not training to failure won’t do diddly squat in promoting muscle gains, since it won’t activate the muscle protein synthesis signaling factors that play a central role in producing muscle gains.
Creatine: once more falsely accused
It amazes me how often creatine is blamed for various athletic problems. These problems range from dehydration to severe muscle cramps. This is true despite the fact that numerous, well-controlled studies have shown that creatine is safe and is not the cause of these problems. The creatine hysteria peaked back in 1997, when three collegiate wrestlers who were otherwise healthy, abruptly died within a two month time frame. The actual cause of death of the wrestlers turned out to be severe dehydration and kidney failure. In an effort to make weight, the wrestlers had severely restricted their fluid intake, while also exercising vigorously in a hot environment and wearing heavy rubber exercise apparel. Several self-styled experts quickly accused creatine usage as the primary culprit behind the young wrestlers premature demise. But it turned out that there was no evidence that any of the dead wrestlers had used creatine. If anything, they likely avoided creatine shortly before their tragic deaths, because creatine is known to promote a certain level of water retention. And the wrestlers were doing everything they could to lose water.
In the latest incident, 19 high school football players from McMinnville High School in Oregon were afflicted with compartment syndrome, to the extent that most of them had to be hospitalized. Compartment syndrome is a swelling of the connective tissue or fascia that surrounds muscles. If the swelling becomes severe, it can choke off blood vessels, nerves, and destroy muscle tissue. One characteristic of this syndrome, besides pain, is an elevation of creatine kinase (CK), an enzyme found in muscle that functions to add a phosphate group to creatine, allowing the creatine to be stored in muscle. Whenever muscle is damaged, including heart muscle, CK is released into the blood. Normal levels of CK range form 200 to 2,000. The level found in the Oregon football players averaged 40,000. Since compartment syndrome is a relatively rare event in sports, the fact that 19 players on the same time all came down with it at the same time suggested that something was amiss. A finger had to be pointed somewhere, and creatine appeared to be a prominent suspect.
In fact, the players had engaged in a so-called “immersion camp,” that involved intensive pre-conditioning activity in the heat. None of the players had conditioned themselves to do high intensity exercise, much less in a hot environment. They started to complain about excessive swelling in their triceps after doing a series of push-ups and chair dips in a 30-second alternating series of reps over 20 minutes in a hot, humid wrestling room where temperatures averaged 115 to 120 degrees. If the athletes didn’t complete their rep goal, they had to start over again. In addition, they were not permitted to drink any water during the workout. All this is a classic scenario for the onset of rhabdomyolysis, or rapid destruction of muscle tissue. Rhabdo,as it’s often called, is linked to dehydration and unaccustomed exercise in a hot environment. One the primary signs of rhabdo is an extremely high release of CK into the blood. If not rapidly treated, release of a muscle iron pigment called myoglobin can jam up the kidneys, resulting in total kidney failure. There are several case studies on record of bodybuilders who suffered from rhabdo, often from trying a new intense style of training while dehydrated and in hot conditions.
In truth, none of the football players said they had used creatine prior to the disease incident. So why was creatine wrongly accused? My guess is that because creatine can promote water retention, it was thought that this caused the rapid onset of compartment syndrome in the athletes. Also, the fact that the CK levels were extremely high in the players, also pointed to creatine, since CK works with creatine in muscle. But the flaw in these suggestions is that most of the water retained by creatine is intracellular, not extracellular. Extracellular water retention can cause the familiar bloating effect, but that doesn’t happen with creatine. If anything, the extra “internal” water retention promoted by creatine would serve to prevent heat related illness, including rhabdo and the compartment syndrome. Besides, none the football players used creatine anyway. But a convenient scapegoat was needed. The truth of the matter is that the players became ill because of stupid training practices, such as doing unaccustomed intense exercise that they weren’t used to, along with not consuming any fluids. So don’t blame creatine, blame the moron coaches who pushed the players into becoming seriously ill.
Find out the truth about creatine and other popular sports supplements in my e-book, Natural Anabolics, available at jerrybrainum.com.
In the latest incident, 19 high school football players from McMinnville High School in Oregon were afflicted with compartment syndrome, to the extent that most of them had to be hospitalized. Compartment syndrome is a swelling of the connective tissue or fascia that surrounds muscles. If the swelling becomes severe, it can choke off blood vessels, nerves, and destroy muscle tissue. One characteristic of this syndrome, besides pain, is an elevation of creatine kinase (CK), an enzyme found in muscle that functions to add a phosphate group to creatine, allowing the creatine to be stored in muscle. Whenever muscle is damaged, including heart muscle, CK is released into the blood. Normal levels of CK range form 200 to 2,000. The level found in the Oregon football players averaged 40,000. Since compartment syndrome is a relatively rare event in sports, the fact that 19 players on the same time all came down with it at the same time suggested that something was amiss. A finger had to be pointed somewhere, and creatine appeared to be a prominent suspect.
In fact, the players had engaged in a so-called “immersion camp,” that involved intensive pre-conditioning activity in the heat. None of the players had conditioned themselves to do high intensity exercise, much less in a hot environment. They started to complain about excessive swelling in their triceps after doing a series of push-ups and chair dips in a 30-second alternating series of reps over 20 minutes in a hot, humid wrestling room where temperatures averaged 115 to 120 degrees. If the athletes didn’t complete their rep goal, they had to start over again. In addition, they were not permitted to drink any water during the workout. All this is a classic scenario for the onset of rhabdomyolysis, or rapid destruction of muscle tissue. Rhabdo,as it’s often called, is linked to dehydration and unaccustomed exercise in a hot environment. One the primary signs of rhabdo is an extremely high release of CK into the blood. If not rapidly treated, release of a muscle iron pigment called myoglobin can jam up the kidneys, resulting in total kidney failure. There are several case studies on record of bodybuilders who suffered from rhabdo, often from trying a new intense style of training while dehydrated and in hot conditions.
In truth, none of the football players said they had used creatine prior to the disease incident. So why was creatine wrongly accused? My guess is that because creatine can promote water retention, it was thought that this caused the rapid onset of compartment syndrome in the athletes. Also, the fact that the CK levels were extremely high in the players, also pointed to creatine, since CK works with creatine in muscle. But the flaw in these suggestions is that most of the water retained by creatine is intracellular, not extracellular. Extracellular water retention can cause the familiar bloating effect, but that doesn’t happen with creatine. If anything, the extra “internal” water retention promoted by creatine would serve to prevent heat related illness, including rhabdo and the compartment syndrome. Besides, none the football players used creatine anyway. But a convenient scapegoat was needed. The truth of the matter is that the players became ill because of stupid training practices, such as doing unaccustomed intense exercise that they weren’t used to, along with not consuming any fluids. So don’t blame creatine, blame the moron coaches who pushed the players into becoming seriously ill.
Find out the truth about creatine and other popular sports supplements in my e-book, Natural Anabolics, available at jerrybrainum.com.
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