1kg (2.2lbs) of skeletal muscle contains approximately 650g of intracellular water. Representing normally around 40% of body weight, skeletal muscle in the whole body contains 80 grams of amino acids in the intracellular pool. The amino acids glutamine, glutamic acid, and alanine contribute approximately 80% to this pool.
Bergström et al 1974
“It is not who I am underneath, but what I do that defines me.”
Hope you’re having a great weekend!
Nick (ntb86)
“I never blame failure. There are too many complicated situations in life, but I am absolutely merciless toward lack of effort.”
- F. Scott Fitzgerald
I read three articles this week solely for the purpose of posting on here but it turned out I didn’t like any of them. So I apologize for not giving you all a new article. Instead, I suggest checking out this week’s ACSM sports medicine brief written by my doctoral adviser on how much exercise is necessary to improve insulin resistance.
Hope you have a great weekend!
Nick (@ntb86)
Introduction: Researchers sought out to see whether men or women have higher rates of protein synthesis during the early (1-5) and late (24-48) hour recovery periods. In addition to the resistance training, they also gave a dose of whey protein (25g) that is expected to induce maximal muscle protein synthesis. A secondary aim of this study was to see if the large amount of testosterone released by men post-exercise (10 to 15 times higher in men than women) would have an additive effect on muscle protein synthesis that women would not be able to obtain.
Methods: Eight men and eight women who were participating in regular physical activity took part in this study. The bout of exercise was an intense bout with 5 sets of 10 reps at 90% of a persons 10 rep maximum on the leg press as well as 3 sets of 12 reps of leg extensions/leg curls supersets. Upon finishing this workout, subjects were given 25g of whey protein.
Results: Starting rates of protein synthesis were similar between men and women. After exercise, protein synthesis increased in men and women at 1-3 hours and remained elevated at 26-28 hours after with no difference between the sexes.Testosterone was approximately 45 times greater in men than women fifteen minutes after exercise but did not have an effect on muscle protein synthesis more than that of women.
Discussion/Conclusion: This study shows that there are similar rates of muscle protein synthesis as well as anabolic cellular signaling events between men and women following resistance training plus a 25g dose of whey protein in the earl and late phases of post-exercise recovery. Even though men had a far greater increase in testosterone than women post-exercise, it was not enough to increase protein synthesis more than women. Therefore, the anabolic effect of resistance exercise clearly is working through some other mechanism other than spikes in testosterone levels.
My input: So, men do not have it easier when it comes to weight training anabolic responses. Both sexes are primed equally for muscle recovery. The fact that they looked at testosterone comparisons really added to the quality of this study. It is important to note that the authors are referring to muscle protein synthesis during a recovery phase and not muscle protein synthesis in a long-term muscle building sense. However, recovery is the first step to adding muscle.
West et al J Appl Physiol. 2012 Jun;112(11):1805-13
Have a 5K coming up or a race in a track meet? Would you like to improve your time in the event (wow, it sounds like I’m trying to sell something)? Well, a group from Denmark just published a paper with an interesting endurance training method to help you reach your new time goal. This one is for the runners and I assure you I’m not selling anything but exercise.
Introduction: It is known that people who are already trained need to intensify their training protocols to continue to improve. Training at maximal or near maximal intensities creates the muscular adaptations necessary for these improvements. A popular method to do this is introducing 30 second sprint intervals into your training coupled with a short recovery period. Normally, this is repeated 4-5 times. However, it is uncertain whether training using just 10 second near maximal sprints has the same effect as the 30 second intervals. In addition, it is unclear whether training at this high of an intensity can affect the health profile of people who are previously trained. Therefore, the 10-20-30 training concept is introduced and tested to see whether or not it can lead to endurance performance, increases in cardiovascular fitness, as well as health.
Methods: Eighteen moderately trained individuals (12 males and 6 females) were divided into 2 groups, the 10-20-30 group or a control group. For a period of 7-weeks, the 10-20-30 group trained with this method whereas the control group continued with their normal weekly training sessions (2-4 times per week, 27km and 137min total). The 10-20-30 training concept consists of 3-4 x 5 min running interspersed with 2 min of rest. During the 5 min running period, a person would run 1 min of an interval divided into 30, 20, and 10 seconds at an intensity related to <30%, <60%, and >90-100% of maximal intensity. They performed this 3 times per week with a volume of 14 km per week. To test differences in the training methods, the groups performed a 1500m race, a 5-K run, and a running test to exhaustion.
Results (after 7 weeks):
Discussion: After a 7-week period, the 10-20-30 training method, lead to an increase in VO2max of 4% and decreased times on the 1500m by 21 seconds and on the 5-K by 48 seconds. In regards to health, this training concept also decreased LDL cholesterol as well as resting systolic blood pressure. This all occurred even though the volume of training reduced by 54%. One explanation for this by the authors is that high cardiac stress (the max effort 10 second sprints) coupled with a reduction in training volume is sufficient enough to increase VO2max because the group that did the 10-20-30 spent approximately 40% of training time spent above 90% of maximal heart rate whereas the control group spent 0% of training at this level. For health parameters, the authors also state that the 5 mmHg decrease in systolic blood pressure is of clinically significant because a decrease such as this can reduce the risk of cardiovascular death by 10-15%.
Practicality: If you were wondering approximate running speeds in case you want to try this out on the treadmill, the 10 second intervals were at speeds >20 km/h, the 20 second intervals were between 10-14 km/h, and the 30 second intervals were <10 km/h. For those still having trouble understanding the 10-20-30 principle I will give an example: You would run a warm-up of 5 min at a very low intensity, following this you would begin the 5 minutes interval which is divided into 10-20-30 seconds for each minute. You run <10 km/h for 30 seconds then right away increase the speed to 10-14 km/h for 20 seconds then again immediately increase the speed to >20 km/h (or as fast as you can run for 10 seconds). After repeating this another 4 (to make 5 minutes) times you would then have a recovery period of 2 min at a low intensity before repeating the 5 minute intervals 2 or 3 more times. For those who have tight time schedules, this is practical because all of these improvements with this technique can be accomplished in just 30 minutes. The authors also state that 10-20-30 is also applicable for anyone who is sedentary up to elite running levels.
Gunnarsson and Bangsbo J Appl Physiol. 2012 May 3
Taking ice baths post-exercise seems to be the most popular method of reducing delayed onset muscle soreness for novice and elite athletes. This method, known scientifically as cryotherapy, is growing to be more popular than traditional ones such as massage, stretching, or taking non-steroidal anti-inflammatory drugs (NSAIDs). The most popular forms of cryotherapy are cycling 1 min in ice water (5 degrees Celsius) followed by 1 minute out for a total of three times or a longer duration of 15 minutes at 15 degrees Celsius. Now that you have the background, I’ve went out and found an enormous extensive review on the subject to make clear whether or not this technique is useful or useless at combating muscle soreness and aiding recovery.
The scientific claims: You know that you treat sprains, strains, or any swelling in the body with ice. The mechanisms for why cryotherapy works are similar; reduce pain, swelling, and inflammation. There is also vasoconstriction (decreasing the diameter of the blood vessel) which stimulates blood flow and nutrient and waste transfer as well as decrease in nerve transmission speed, which could alter the threshold of pain receptors.
The studies used: The review included 17 small trials (published from 1998-2009) of 366 participants. No restrictions were placed on age (16-29), gender female, or type of level of exercise. Also, no restrictions were placed on duration or frequency of immersions or depth of immersion. The studies were all of small sample size (20 participants or less) except for one that used 54.
The exercises used: All exercise used were designed to produce delayed onset muscle soreness (DOMS) under laboratory controlled conditions. Repetitions for resistance exercise ranged from 50-100 of eccentric or alternative concentric and eccentric contractions. The other studies used running or cycling in single bout efforts (for the bike) or steady state efforts. Few actually included team sport exercise (basketball and soccer).
The cryotherapy used: The most common for the studies was 10-15 degrees Celsius with an average immersion of 12.6 minutes. This was employed in almost all of the studies immediately after exercise. The different methods of cold-water immersion were compared to nothing/rest (the most common), cold-water immersion vs. contrast immersion (switching between hot and cold), cold-water immersion vs. warm water, and cold-water immersion vs. active recovery.
Enough with the technicalities. Let’s go to the results.
Cold-water immersion vs. nothing: In terms of muscle soreness, there is no significant difference immediately between the two conditions but at 24, 49, 72, 96 hours later the cold-immersion group reported a significantly lower amount of muscle soreness than the group that just rested. This effect seems to be more prevalent after running based exercises than resistance exercises but the authors not that due to the various types of exercises that were performed between all the studies, plus the sample sizes being small, it is difficult to find whether or not this is truly significant. There were no significant differences in strength, power, functional performance, swelling, or biomarkers of muscle damage.
Cold-water immersion vs. contrast immersion: In terms of muscle soreness, there was no significant differences between the groups. Also, there was no significant differences in strength, power, functional performance (time to fatigue), swelling, range of movement, or biomarkers of muscle damage.
Cold-water immersion vs. warm-water immersion: There was significant lower levels of muscle soreness reported only for the cold-water immersion group at time-point 96 hours with no differences in strength, power, functional performance, swelling, or biomarkers of muscle damage.
Cold-water immersion vs. active recovery: There are no significant differences in reports of muscle soreness, strength, power, functional performance, swelling, or biomarkers of muscle damage.
Discussion/Conclusions: Cold-water immersion did significantly reduce muscle soreness at time points 24, 48, 72, and 96 hours post-exercise. However, it is important to note that these were all subjective reporting (self-reports) and the authors state it is hard to draw true conclusions from the data due to poor methodological quality. There were high risks of bias due to the fact that blinding was performed poorly as well as concealment of group assignments (only 1 study did this effectively). There were also large differences in the types of exercises used and subjects were a mix between trained and untrained. The effectiveness very well may rely on the specificity of the exercise performed as well as the athletic level of the individual.
My input: Did you know that in the 1920s, cyclists in the Tour de France would smoke during the race because they believed that smoking opened up the blood vessels and oxygen transport machinery of the lungs? Ridiculous, right? I’m not saying ice-baths are as crazy as this, but are they truly beneficial to aid recovery in the muscle? I’m not so sure. From the most basic laws of chemistry, we know that when something is heated up the molecules in it move faster and when something is cooled down the molecules in it slow down. If you are exposing your muscles to cold, all of the molecular processes will slow down. You need enzymes (which function effectively at specific temperatures) and proteins moving post-exercise to begin the repair process and signal inflammation, and if you’ve read my previous posts on muscle hypertrophy, you know inflammation is necessary. It is the same reasoning to avoid NSAIDs in hopes of reducing muscle soreness. For this reason, I’m always heading for the exact opposite after training, a hot shower. The reason I do this is not only to continue normal biochemical processes in the muscle but also to incorporate the activation of what are called heat shock proteins. Heat shock proteins are proteins in the body that respond to stress or elevated temperatures. They function as chaperones for other proteins by aiding them to conform to a certain shape and stabilize proteins that are not shaped properly. Basically, they can clean up the mess inside of the muscle cell and help with repair. This is another reason why I’m not on the ice-bath bandwagon. You might feel that it has helped you before in the past and it possibly could have helped, but I just want to let you know there is no scientific evidence supporting it. The studies are low quality studies. If you truly want a good study on this, take a group of at least 35 people, train their legs or their arms simultaneously with the same protocol and put one limb in the ice and one limb not in the ice or in warm water, take muscle biopsies, and see the differences between the conditions (Anyone want to take this on as a nice Master’s or PhD project? I’ll be glad to give advice for it). To my knowledge this has not been done and this would be the best way to see if cold-immersion truly helps. Although there was some evidence in a decrease in self-reported muscle soreness, I’m still not convinced and higher quality studies are necessary before I’ll be convinced.
Bleakley et al Cochrane Database Syst Rev. 2012 Feb 15;2:CD008262.
You’ve heard the debate before, you know you have. High intensity interval training (HIT) versus continued steady state running. Which is better? A new article has been published showing that when it comes to the two, they may in fact be more similar than we initially thought.
Introduction: When we talk about adaptations to endurance training, we’re talking about muscle mitochondria. These adaptations are thought to be turned on by increases in molecular responses from the onset of contraction (e.g. increases in the AMP/ATP ratio, calcium levels, reactive oxygen species, lactate, reduced glycogen availability, etc). All of these lead to activation of proteins called kinases which phosphorylate targets such as transcription factors or transcriptional coactivators. Okay, I know, too much science. It’s gross for you. Basically, what this means is that these signals increase markers responsible for allowing the mitochondria to adapt to the endurance training and subsequently, you become a better athlete. However, it is uncertain if there is an optimal exercise stimulus to create these adaptations. Therefore, the aim of this study was to see the whether or not the signals of these molecular responses after an acute bout of either HIT or continuous running increase greater for one mode of exercise or the other. The primary hypothesis is that HIT will increase these signals responsible for adaptation to a greater level than that of continuous running.
Methods: The study recruited 10 recreationally active males who underwent both the HIT and the continued running protocol. For those unfamiliar with HIT, the protocol was 3-min running at 90% of one’s maximal oxygen uptake followed by a recovery period of 3-min at 50% maximal oxygen uptake (this was repeated 6 times). The group in the continued running ran the entire time at 70% maximal oxygen uptake. Muscle biopsies were taken pre-exercise, post-exercise, and 3 hours after exercise.
Results: Muscle glycogen decreased by 30% in both groups but there was no difference between HIT and continuous running (CONT). There were increases in all of the molecular markers of mitochondrial content (AMPK, p38MAPK, PGC-1a) in both HIT and CONT but again, no differences between the two modes.
Discussion/Conclusion: This is the first study to demonstrate that both HIT and continuous running induce comparable responses of molecular markers in muscle. The authors state that this could be due to both protocols being relatively intense since there is only a difference of 20% maximal oxygen uptake between the two groups. Another first-time discovery of this study was an increase in stress proteins in response to HIT training indicating a stress response on the body (although this was not significant).
My input: The main power of this study is that the even though the 2 groups performed different types of endurance training, the researchers matched the groups to perform the same intensity, duration, and work performed. Without doing that, it would have been very difficult for them to conclude that HIT and continuous running show similar molecular responses. It bothers me that the intervals were not the usual ones prescribed for exercise protocols in studies (4-6 times of 30 seconds all out cycling/sprinting). My only critique comes with the time. When matching for time, the HIT group exercised for 18 min of sprinting and 18 min of recovery plus a warm up and cool down period totaling 50 min. The continuous running group did 50 minutes without a warm up and cool down. If they took the biopsies after the sprints were finished and not after a cool down, they may have seen responses similar to what they hypothesized. It is also worth mentioning that this study is short-term and it is not yet known the responses to long-term endurance training of this variety. Other than that, this is the first study to show that following a short bout of endurance exercise, there are similar responses in the mitochondrial of muscle between both HIT and continuous running. It seems that for now, both are sufficient in making you a better athlete.
Bartlett et al J Appl Physiol. 2012 Apr;112(7):1135-43
“Bro, how can I put on some mass? I’m a hard-gainer.” ”I need some more muscle, I’m too skinny.” ”I’m lifting hard several times a week but I just can’t add any size”. Sound familiar? Luckily, a group published an excellent review in the NSCA journal a few weeks ago on exercise induced muscle damage and it’s association with muscle hypertrophy. Sparing you the molecular science as much as I can, I’ll highlight for you the key practical findings which support the recommendations that I give to people for training as well as incorporate in my own routines. An all muscle review. I’m drooling. Women can take away from this too because there is nothing sexier than a girl that can deadlift her own body weight. Right, men? Right.
When we talk about exercise induced muscle damage (EIMD) most scientific studies look at eccentric exercise. That is to say, the negative portions of the rep. For example, if you’re doing a bench press, it is the portion that you’re lowering the weight down. This eccentric portion has been shown to display the most damage to the muscle. Looking at meta-analyses on the topic, it is clear that eccentric exercise is superior to inducing gains in muscle mass rather than concentric and that optimal exercise-induced muscle growth is not attained unless eccentric muscle movements are performed.
So what is EIMD exactly? When we’re talking about skeletal muscle damage it is actually shearing of myofibrils (the smallest contractile units of the muscle). Subsequently, this causes damage to the membrane of the cells which disrupts the flow of calcium. When the tearing destroys the membrane and calcium levels are tampered with, you get a decrease in muscle force, swelling, and eventually the lovely friend DOMS (delayed onset muscle soreness).
“Bro, how can I get rid of the DOMS?”. One proposed way to attenuate this response is what is described as the repeated bout effect. Basically it is adaptation of the muscle to the next training session. The authors note that the arm muscles appear to be more predisposed to EIMD than the leg muscles when taking into account this effect. Repeating the same routine the next time around will not elicit the same response as the previous because the body has adapted. Thus, attenuating DOMS for the next session.
“Bro, how can I increase my satellite cells in my muscle? You know, the stem cells of muscle, brah.” Satellite cells donate their nuclei to existing muscle fibers, which aid in their ability to synthesize new contractile proteins. When the muscle grows the ratio of nuclear content to fiber mass stays the same. Therefore, to put on muscle long-term, it would be essential to add new nuclei to the muscle. Damaged fibers require new nuclei to repair. Therefore, satellite cells are necessary for muscle repair but it is still not entirely known how much of a role this has in hypertrophy. Although it is important to note that this process is regulated by an enzyme COX-2, deemed necessary to achieve maximal skeletal muscle hypertrophy in response to weight training. However, non-steroidal anti-inflammatory drugs (NSAIDs) such as Ibuprofen (Advil) or Acetaminophen (Tylenol) block COX-2, which in turn blunts the satellite cell response, which in turn blunts hypertrophy.
“Bro, what about my hormones so I can get SWOLE?”. When we talk about natural hormonal signaling involved in muscle growth we’re talking about insulin-like growth factor 1 (IGF-1). One form of this growth factor is primarily responsible for compensatory hypertrophy. A target of this factor has been shown to be greater in eccentric contractions than isometric but this is still not certain. In addition, IGF-1 has been shown to increase rates of protein synthesis.
“Bro, what about the sick pump?” There is a novel theory by which EIMD may induce hypertrophy by increasing the intracellular water content. Cell swelling = getting SWOLE (in a scientific meaning). This is due to pressure against the cell membrane which leads to reinforcement of the structure. There are specific sensors that respond to the stretch in the membrane.
“Bro, I just annihilated my arms, I won’t be able to shampoo my hair for a week.” So far there is no true direct cause and effect relationship established between EIMD and hypertrophy. There does however exist a threshold beyond which more damage does not elicit a greater effect on hypertrophy. The great 8 time Mr. Olympia Lee Haney is known best for saying, “stimulate, don’t annihilate.”
“Bro, what about lifting heavy ass weight?” In the plethora of studies looking at hypertrophy-oriented routines, they all use submaximal intensities of 65%-85% of a person’s one-rep max and that similar anabolic responses are found for programs that are >90%.
“Bro, what about running and lifting? I don’t want to get small.” Finally, this review touches upon a “switch” whereby signaling can be shuttled from a catabolic endurance gene activation and an anabolic resistance dominant state and is specific to the type of training you are performing. Muscle damage is not sufficient enough to override the endurance switch once it is activated.
Taking all the text in bold, I will now finally outline for you the practical messages from this review that I suggest and deploy in my own training to maximize muscle growth. Let’s got from the lab to the gym.
A few questions ago someone asked me how to find creditable journal articles. Write this name down, Steven N. Blair. One of the number one, if not the #1 person, for exercise interventions and large popluation studies in fitness. His group just published a new article that I will highlight for you below.
Introduction: How fit someone is as well as how fat someone is are both strong predictors of cardiovascular disease (CVD) risk factors and mortality. Some studies suggest that being fit can attenuate the harmful effects of being fat. That is to say, you can be overweight but as long as you are fit, it helps eliminate risk factors of CVD. However, this group points out that there is a continuous change between being fit or fat, which could skew the results. Therefore, the purpose of this study was to examine the independent and combined associations of changes in fitness and fatness within the development of risk factors of CVD; hypertension, metabolic syndrome, and hypercholesterolemia.
Results: After a 6 year follow-up, participants (all 3,148 of them) who maintained or improved fitness had 26% and 28% lower risk of hypertension, 42% and 52% lower risk of metabolic syndrome, and 26% and 30% lower risk of hypercholesterolemia compared with those who last fitness. On the other hand, those who increased in percent body fat, had 27%, 71%, and 48% higher risk of hypertension, metabolic syndrome, and hypercholesterolemia. Interestingly, every 1-MET improvement in fitness between the beginning of the study and the follow-up was associated with a 7%, 22%, and 12% lower risk of subsequent incidence of hypertension, metabolic syndrome, and hypercholesterolemia. On the fat side, every unit increase in BMI or percent body fat was associated with increases in higher risks of these CVD risk factors. Similar results were found when looking at just waist circumference. Finally, both losing fitness regardless of fatness and gaining fatness regardless of fitness change were associated with a higher risk of developing metabolic syndrome.
Discussion/Conclusion: Maintaining a certain level of fitness or improving on that level seems to alleviate, although not completely terminate, some of the negative effects of fat gain. In addition, losing body fat can reduce CVD risk factors associated with a loss in fitness. It is important to note that both, separately, are important risk factors in the development of CVD.
My input: Keep in mind when reading these results that they are correlations and that does not give us a cause-effect relationship. Other than that, I’m going to let Dr. Blair give you his final input this time (I urge you to please click this link) on this topic because he says it so much better than I could:
“My recommendation is to focus on good health habits, no matter what number you see on the scale. Give fruits, vegetables and whole grains a major place in your daily diet. Be moderate about fat and alcohol. Don’t smoke. Work on managing stress. Perhaps most important, get out
of your chair and start moving for at least 30 minutes every day.”
Lee et al J Am Coll Cardiol. 2012 Feb 14;59(7):665-72.
