My name is Nick and I am currently doing my PhD in physiology with an emphasis in muscle physiology. Welcome to my exercise science blog. Unlike a lot of fitness blogs out there, this one is unique because it is backed by true science. You will find only articles that have been peer reviewed and published in top tier science journals on this blog. For the fast easy read, just read the bold type. If you have any questions do not hesitate to ask me. I am at your disposition for any advice in exercise or just basic physiology. This is not a progress blog to benefit myself but rather to share some of my knowledge and expertise with you that I have gained over my years dedicating my career to exercise science. If I do not know the answer, I will do my best to search through the journals to find it for you. Although I am in biomedical research, I am not a licensed medical professional so please consult a physician before entering any exercise or nutrition program.
Questions?
“Yo, you gotta take your casein before bed so you stay anabolic. Steady flow of amino acids while I sleep.” How many times have you heard that? How many people have showed you a study validating it? Finally, one exists.
Introduction: It is hypothesized that ingesting protein before sleep could be beneficial to increase plasma amino acid availability, stimulate skeletal muscle protein synthesis and increase whole-body protein balance during sleep. Thus, this group took 16 recreationally active young men and after a single bout of resistance training gave them either casein protein or a placebo before bed. This is the first study to look at the effect of ingesting casein protein immediately before sleep and subsequently seeing how it effects protein synthesis and protein balance overnight.
Methods: All subjects received a standard meal the evening before the test and a standardized diet throughout the experimental day. Tracers were implemented in this study which allows for measurements of certain molecule in the blood. A tracer is a molecular that contains radioactive isotopes that can be measured by machines to see the overall flux of the molecule throughout the body. In this study, the researchers traced radioactive amino acids (it’s safe because they are stable isotopes, trust me)throughout the night following the exercise protocol. The protocol consisted of leg extensions and leg press and was performed three hours before bed.
Results: After ingestion of protein before sleep, the total essential amino acid concentrations in the plasma increased rapidly and stayed higher throughout the night as compared to the placebo group. For the tracer, the amount of protein available from the plasma-derived amino acids was 50% higher in the protein ingestion group at time 7.5hrs after sleep compared to the placebo. Finally, whole-body protein synthesis rates were higher in the protein group versus the placebo group.
Discussion: It is evident that the casein protein was in fact digested and absorbed normally throughout the night because the tracer used in this case came directly from the casein protein shake. Not only did they observe and increase in whole-body protein synthesis with the blood plasma samples, but the group also showed an increase in synthetic rate by taking muscle biopsies as well. Of course this could not be confirmed throughout the night but only before bed otherwise the person would not be able to sleep when the biopsy was being performed. Also, it is important to keep in mind that this is an acute (one-time) bout of resistance training and not chronic (long-term).
Conclusion:
Casein protein at bedtime is effectively digested and absorbed which would lead to an increase in available amino acids from blood plasma overnight
Casein protein at bedtime stimulates muscle protein synthesis rates which would increase overnight protein balance.
My input: This study highlights the practicality and necessity of using tracers. Without labeling the amino acid in the casein drink, it would be difficult to tell whether or not the amino acids in the plasma are coming from inside the body (endogenous) or what was ingested (exogenous). The authors clearly show in the figures that the rise in the amino acids come from the isotope labelled casein source that they provided. Now for the first time, you can all finally tell your friends it is a good idea to supplement with casein before bed because science suggested it.
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.
The title says it all. Who is better able to recover following resistance training? The results may surprise you (or even motivate you).
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.
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):
The 10-20-30 group improved performance by 6% in the 1500m and 4% in the 5-K run with no difference in the control group.
The 10-20-30 group increased their VO2max (maximal oxygen uptake) by 4% with no changes in the control group.
The 10-20-30 group lowered their total cholesterol and LDL cholesterol with no changes in the control group.
The 10-20-30 group’s systolic blood pressure was lower with no changes in the control group.
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.
The Phillips group is back at it again with another great muscle paper that just came out about hypertrophy (gaining muscle mass). It is not nutrition oriented this time, but instead discusses the amount of weight necessary to stimulate an increase in muscle size.
Introduction: It has been shown that under an acute exercise bout, using 30% of a person’s 1 rep max (1RM) to the point of muscle fatigue (failure) was equally as effective at stimulating muscle protein synthesis in the muscle fibers as that of loads lifted at 90% of 1RM (also lifted to failure). This was shown previously by this same group. Even more intriguing, they found the 30%-1RM condition resulted in a more prolonged muscle protein synthetic response with a greater rise in muscle protein synthesis than the 90% 1RM group 24 hours post-exercise. Furthermore, other than a relative training load (weight), another important variable for resistance training is volume or the amount of work performed. The Phillips group also showed before that 3 sets at 70% of 1RM to failure led to greater and a more prolonged muscle protein synthetic rate in the fibers as compared to a single set condition. However, as I stated, these are all under short-term conditions. Thus, this new study wishes to see if these hold true under long-term conditions.
Methods: Eighteen healthy young men underwent 10 weeks of one leg knee extension resistance training where each leg was randomly assigned to one of the three training conditions: 1 set performed to voluntary failure at 80% of 1RM (80%-1), 3 sets performed to the point of fatigue at 80% of 1RM (80%-3), or 3 sets performed to the point of fatigue at 30% of 1RM (30%-3).
Results: After 10 weeks of training, quadriceps muscle volume increased significantly in all groups and average type I and type II muscle fiber area increased with training (irrespective of training condition with no significant differences between groups). All three groups also increased their 1RM but it was increased greatest in the 80%-1 & 80%-3 groups. Total work that could be completed with 80% of the subect’s 1RM increased in all groups and the number of reps that could be performed with 80% of their current 1RM increased in all groups.
Discussion: The main outcome from this paper is that there was no difference in the magnitude of quadriceps muscle hypertrophy (determined by MRI and muscle fiber area) between legs trained at 30% or 80% of 1RM after 10 weeks of knee-extensor exercise. Furthermore, there was no statistical difference in the degree of hypertrophy between the 80%-1 and 80%-3 group even though the 3 set group gained a little more volume than the 1 set group. More interestingly, the 80%-3 and 30%-3 showed more than double the average hypertrophy of the 80%-1 condition. This adds to the mounting evidence that lifting lighter loads, so long as fatigue is induced, induces roughly equal hypertrophy gains. It is important to note that both type I and type II fibers increased equally between the heavy and light loads meaning that both fiber types were recruited during the training to an almost equal amount.
My input: I can’t preach it enough or put it in bold enough; fatigue, fatigue, fatigue. Train your muscles till failure. Don’t worry about the weight on the bar or saving yourself for that last all out set. Take every set to muscle failure, even beyond with partial repetitions and forced repetitions (if you have a spotter). I have written it in the past but it needs reemphasized; when training for hypertrophy, the muscle does not “know” the weight on the bar, all it knows is fatigue. Check your ego, men. Women too, who use 5 lb dumbbells and do unlimited numbers of reps (you know who you are), aren’t accomplishing anything. I think it is also important to mention that this study pushes for a volume principle whereas the two groups that completed 3 sets instead of 1 had more muscle volume after the 10 weeks than the group that did only 1 set till failure. The next plausible step is to see if there is in fact a threshold where doing more sets than 3 will lead to an even greater increase in muscle size (future PhD thesis for anyone that wants to take it). I would also like to see this study repeated with subjects that are weight trained to eliminate the possibility of a first-time adaptive response to training (another future PhD thesis for anyone that wants to take it). That could have been the reason why the 1 set to failure condition saw an increase in muscle hypertrophy due to the fact they have not weight trained in over a year. On the strength side, it also lends to credence to specificity of training in that the leg conditions that used 80% of their 1RM increased their strength more than the group that used only 30%. If you want to solely increase your strength, focus on using heavier weight, duh. More long-term studies are needed because a lot of questions can still be asked, but this is already off to a great start when looking at chronic resistance training responses in muscle.
“The last three or four reps is what makes the muscle grow. This area of pain divides the champion from someone else who is not a champion. That’s what most people lack, having the guts to go on and just say they’ll go through the pain no matter what happens.”
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.
Whey protein or leucine post-workout to increase muscle protein synthesis (MPS)? The Phillips group just published an article trying to answer this question.
Introduction: You all are probably aware that ingesting amino acids stimulates an increase in muscle protein synthesis even without resistance training. Leucine has been toted to best stimulate MPS by activating components of a signalling cascade known as mTOR. There is still controversy though as to whether or not leucine can enhance MPS following leucine infusion or by simply adding more of it to a post-workout protein drink. This group previously reported the the optimal dose of protein post-workout to stimulate MPS was 20g and that anything below this is not sufficient and anything above this number (40g) does not increase MPS further. Therefore, the aim of this study was to see if taking a “sub-optimal” dose of whey (6.25g with approximately 0.75g of leucine) protein and supplementing it with leucine or a mixture of essential amino acids without leucine would have an effect on MPS at rest and after acute resistance training. This will be compared to a dose of whey (25g with approximately 3.0g of leucine) which is sufficient to induce maximal stimulation of MPS after resistance exercise.
Methods: Twenty-four adult males were randomized to one of three groups that either ingested a whey protein drink, a leucine drink, or an essential amino acid drink. Prior to ingestion, the volunteers completed an acute bout of unilateral resistance exercise (knee extensions). Muscle biopsies were taken at the time of ingestion and at time points 1 hour, 3 hours, and 5 hours post-exercise.
Results: After whey protein ingestion, blood leucine, branch-chain amino acids, essential amino acids, and total amino acids were all highest as compared to the groups that ingested leucine or EAA (without leucine). Blood leucine was only higher initially after ingesting the leucine drink but stayed elevated longer by ingesting whey. Rates of MPS remained increased for 3-5 hours at exercise recovery above those volunteers who did not ingest anything, versus the groups who ingested leucine or the EAA drink.
Discussion: A dose of whey protein that has been previously shown to be less than maximally effective to stimulate MPS after resistance exercise, when supplemented with leucine, resulted in an early (1-3 hour post-exercise recovery) increase in rates of MPS equal to that of ingesting 25g of whey. Also, the same was found by supplementing a low dose of whey with essential amino acids void of leucine. However, MPS was sustained longer (3-5 hours post-exercise) only with the group that ingested whey protein. These differences occurred despite the fact that blood amino acid levels returned to baseline after 3-5 hours but MPS still continued. Therefore, the authors state that peak activation of MPS does not appear to be driven by increasing leucine in the blood and that amino acid transport across the sarcolemma (plasma membrance of the muscle cell) and intracellular amino acid availability may be important in the regulation of MPS.
Conclusion: Leucine stimulates MPS post-exercise equal to that of whey protein, despite only containing 45% of the total EAA content of the whey. However, similar increases in MPS were observed in the EAA ingestion group that did not contain leucine. Thus, the authors speculate that in young healthy individuals, the leucine content provided by approximately 6.25g (approximately 0.75g of leucine) of whey protein seems adequate to maximally stimulate MPS if sufficient amounts if the other EAA are provided (approximately 8.5g EAA). Also, the whey protein ingestion group was the only group that sustained MPS 3-5 hours post-exercise.
My input/practicality: What if I were to tell you I can make a 1lb bag of whey protein last me 3 months? Well I can, and I do, and I’ve been doing it for years. I only use a half scoop of whey protein post-exercise. Never a full scoop. Never a “heaping” scoop. Why do you even think they use the word heaping? It’s all about the dolla dolla bill y’all. This study shows that only 6.25g of whey is necessary to maximally stimulate protein synthesis as long as it contains approximately 750mg of leucine and 8.5g of the other 8 essential amino acids (which are histidine, isoleucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine). Make sure you check on the labels of your favorite whey protein because it usually lists the amount of leucine and the other essential amino acids on it. One scoop of whey is usually on average around 20g of protein so if you use a half scoop like me it is around 10g (still a little over from what this study suggests). Supplement companies are going to hate this study (like they read them anyways) as well as me for posting this but you’ll love it/me for saving you money.
“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 thatoptimal 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.
Eccentric portions of the rep are superior in inducing damage and increases in muscle mass. Always make sure you are slowly controlling the weight on the negative portion of the rep. Even try to add some negative only sets in your routines where someone helps you completely with the concentric and you slowly lower the weight for a count of 4-10 seconds.
The arm muscles are more predisposed to EIMD than the legs. Don’t be afraid to train your legs with high volume, a lot of sets and a lot of reps to induce growth. Even training them twice a week if you feel you really want to add size to them. They can handle the punishment since you walk on them daily.
NSAIDs blunt the response of the enzyme that initiates the signal to increase muscle size. Try to avoid Advil, Tylenol, etc even if you are very sore from a training session as much as you can.
Cell swelling may be responsible for an increase in muscle size. Always try to focus on getting a complete stretch of the muscle on every set as well. This is important because the greater the stretch, the more you can squeeze the muscle at the end of the movement. Also, focus on achieving a maximal pump to really stretch the fascia of the muscle even further.
Stimulate, don’t annihilate. A moderate amount of damage is needed for growth but more than this will not maximize the hypertrophic response.
Focus on controlling the weight first and the actual weight on the bar second.
Once again as I’ve said before, if possible, it may help to separate endurance activities and resistance activities.
Finally, consider changing your routine often due to the repeated bout effect to not allow your body to continually adapt to the same stimulus over and over again. This is even more important in people that are highly trained and want to keep accumulating muscle.
There you have it. All the best in your getting swole endeavors, brah [or girl]
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.”
How would you like to be in a study where they fatten you up for 2 months? Well, this group recruited volunteers just for that and have provided a significant advancement in what is known about adipose tissue structural changes during the first several weeks of weight gain.
Introduction: The purpose was to examine molecular changes in adipose tissue structure after 2 months of an overfeeding protocol.
Methods: Forty-four healthy males were recruited and told to increase their daily caloric consumption to excess of 760 kcal/day. To accomplish this, they added 100 grams of cheese, 20 grams of butter, and 40 grams of almonds to their usual diet. Fat biopsies were taken at 2 weeks and again at the end of the 2 months.
Results: MRI revealed a significant increase in abdominal tissue volume both for subcutaneous and visceral. No changes in mean adipocyte (fat cell) surface size or number. There was a significant increase in the density of capillary vessels. As you would expect, there was an increase in the number of genes related to fatty acid and lipid biosynthesis. There was also an upregulation in genes involved in formation of the extracellular matrix and angiogenesis (the creation of blood vessels).
Discussion/Conclusion: Although there was an increase in genes responsible for storing excess fat, there was not yet a significant increase in size or number of fat cells. Interestingly, there was an upregulation in capillary density and genes involved in creating more blood vessels to supply the adipocytes. This could also be a reason why the extracellular matrix was remodeled to create space during initial weight gain.
My input: There were also some other important molecular pathways that were downregulated in this study but for sake of boring you I decided to leave those out. I think the main important finding in this study is the disovery of genes involved in creating new blood vessels for the fat cells. It makes sense if you think about it, that an increase in adipose tissue would demand a larger supply of blood. Therefore, it is necessary to increase the amount of vessels perfusing the cells. This group did well in not only showing this in gene arrays but also in histological staining from the fat biopsies. Another article from a different group found similar results in that the adipose tissue of obese and insulin resistant subjects had larger vessels but fewer capillaries when compared to lean subjects. I would not be surprised to see pharmaceutical studies in the near future aiming at trying to reduce the amount of blood vessels as a way to amerilorate adiposity. After that, I would not be surprised if that is soon the next gimmick in supplement companies’ “fat burners”/thermogenic products.
