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.
Weight training and some form of aerobic in the same session. Does it hurt or help?
Introduction: Exercise scientists use the term concurrent exercise when referring to resistance training and aerobic exercise being performed in the same session. These two modes of exercise are different in regards to skeletal muscle profiles and therefore may not be compatible with one another on the cellular level. This is noted as an “interference effect” between the different signals occurring in the muscle. The purpose of this study was to see the effects of a short bout of aerobic exercise on the molecular responses that are supposed to control exercise-specific muscle adaptations to resistance exercise.
Methods: The subjects (9 men) underwent one-legged aerobic exercise in the morning followed by four sets of resistance exercise six hours later. One leg received both aerobic and resistance exercise while the other volunteer’s leg served as a control and only received resistance exercise. Standardized meals were given the day before and the day of to each person and muscle biopsies were taken.
Results: The leg that underwent both aerobic and resistance exercise decreased in muscle glycogen more than the leg that just did resistance (makes sense). A well-known marker of mitochondrial biogenesis was higher in the leg that underwent both training modes. Another marker or muscle size regulation (myostatin) was significantly lower in both the resistance trained leg and in the leg that underwent both modes. Finally, a marker of protein synthesis was higher in the leg that underwent aerobic plus resistance training than the other leg.
Discussion/conclusion: From this study, the authors conclude that concurrent exercise may in fact enhance the skeletal muscle anabolic environment although it is important to note that these differences between legs were modest. An interesting finding is that the well-known marker of mitochondrial biogenesis which is usually increased from endurance training also increased from the resistance trained leg as well. Myostatin inhibits muscle hypertrophy and the finding that both legs decreased myostatin levels shows that both training modes could be effective at increasing muscle mass (although both legs did resistance and this very well may be the main reason for that). In conclusion, the authors state that both exercise types can be scheduled on the same day without compromising important molecular signals in the muscle.
My input: I’ve written about this previously on my blog. This study has similar results to the other in that they conclude resistance training after aerobic training may in fact enhance muscle machinery and subsequently help with performance. Although, the two studies are truly hard to compare due to the fact that this current one waited 7 hours later to do the resistance training, while the previous one I wrote about hit the weights immediately after. A great strength of this study was using one leg for aerobic and resistance exercise and using the person’s other leg as the control that just received resistance exercise. As far as a doing weights after cardio on the same day in the gym, there seems to be no immediate inference effect but this can not yet be extrapolated to more long-term sessions.
“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).
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.
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.
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.
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.”
“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]
Here is what a gene microarray looks like. In this image, there are 824 genes that were scanned during resistance exercise; in this case, bicep curls. The red are higher levels of mRNA and the green are lower levels. It’s amazing, although sometimes quite messy in this case, what we can now do in science.
What this group found is that resistance training blunts genes involved in immune responses by minimizing expression of genes involved in the recruitment of immune cells while simultaneously upregulating genes responsible for inflammation.
In addition, resistance training blunted genes involved in glucose metabolism, mitochondrial structure, and oxidative phosphorylation. This makes sense due to the specificity of the training. Resistance training would not require the upregulation of genes involved in these processes because it is not an endurance type activity. For this reason, I always recommend trying to separate sessions in the gym of weight training and cardio as much as possible because they clearly upregulate and downregulate different genes. It may be detrimental to the specific adaptive training response if both are done around a similar period, but this is yet to be shown to my knowledge. Some studies were published on this but I would still say it’s just merely a working hypothesis for now.
Lift then run or run then lift? It’s a common question that is always asked in the sense of weight loss purposes. However, what about in the context of benefiting endurance athletes? Don’t let the title scare you away from reading because this is a really good study.
Introduction: A lot of people are worried that doing lifting and running together could impair the signaling events and subsequently, the skeletal muscle adaptive events that occur after training. That is to say, if you lift first, the signals that are released in your body could interact with and decrease important signals necessary for becoming a better runner. Therefore, the aim of this present study was to see if resistance training can alter molecular signaling events in response to endurance exercise in human skeletal muscle.
Methods: 10 subjects, male and female, were randomized into either a group that just cycled or a group that cycled and then performed resistance training on a leg press. After approximately 2-4 weeks, the same person then underwent the exercise test that they did not do the first time. Cycling was at 65% VO2max for 60 minutes and the leg press was 70-80% of 1 rep max. Muscle biopsies were taken before, 1 hour after, and 3 hours after training.
Results: There was an enhanced expression of genes involved in the signaling cascade of mitochondrial biogenesis as well those responsible for oxidative (endurance) metabolism when resistance training was performed after endurance training. There were more genes upregulated for protein synthesis as well.
Conclusion:Doing resistance training after endurance training helps increase the benefits of the endurance training on the molecular level which can lead to increases in performance for runners and cyclists.
My input: Six muscle biopsies total for each subject is rare (must have a pretty tolerant ethical committee). For that alone, this paper is very novel because of the different time points of the biopsies. A huge flaw/assumption in this study is that the researchers state that in real life, every one runs and the lifts. Clearly, this is not true. Due to this rational, they did not have a third group that did resistance exercise first then the cycling to see if weight lifters can benefit for endurance training after lifting. It is bothersome that they went through all this effort and could have had an even more powerful paper by recruiting 5 more subjects for a group doing resistance training first. I’m also wondering why they chose 65% of VO2max as the intensity for the cycling because this was not even enough to induce lactate accumulation in the plasma. Other than that, the study was one of the most well-designed I’ve read in a while and the amount of data they collected is substantial in comparison to other groups that perform exercise and muscle biopsies. If you want more on it don’t hesitate to ask. A+
This post stems from a question about whether or not there is a significant hormonal rise during leg training that is enough to elicit increased size in other muscles of the body.
With all things aside, the answer to this question is, yes.There are significant increases in testosterone in exercises such as Olympic lifts, deadlifts, and jump squats (lifts that use a relatively large amount of muscle mass).It’s even suggested that one should perform exercise with large muscles first before smaller muscles with the thought of the surge in testosterone from the large muscle groups increasing the hypertrophy effect on the smaller muscle groups.Below is a table from a review that shows various methods of training and whether or not they show significant increases in testosterone.
Now for some testosterone physiology (and I’ll keep this short & simple, I promise).Testosterone works by binding to intracellular androgen receptors that translocate to the nucleus of the cell eliciting a complex which transcribes specific genes.When you perform large muscle mass lifts, your body will subsequently release testosterone which will mainly be bound to sex-hormone binding globulin (44-66% of free testosterone).The amount of testosterone that is biologically active is in a free form.Unfortunately, (for those wanting to put on muscle), only 0.2-2% of testosterone is in the free form.Specifically in the muscle, testosterone increases the amount of androgen receptors in the muscle, stimulates protein synthesis, inhibits protein breakdown, promotes satellite cell (stem cells of muscle) replication and activation, and increases IGF-1 (insulin-like growth factor-1).
With this said and the plethora of articles that support it, I would like to change your mind on this entire idea of large increases in hormones being the main reason for increases in hypertrophy. Where is the fun in believing one method and never doing any inquiry of your own?My interest from this came a few years ago when I read some studies that castrated mice still possess the ability to increase their muscle size.I now want to direct you to some recent studies that can argue the point of an intrinsic process for muscle hypertrophy not due to increases in growth hormone or testosterone.
The two intrinsic local processes in the muscle are sarcomerogenesis and remodeling which both prime the muscle for protein accretion and subsequently, hypertrophy.These are both mechanical steps, if you will, in allowing the muscle cell to become plastic and respond to the stress placed on it by resistance training.Think of it as an entire system of sensors beginning at the membrane of the cell in which these sensors respond by releasing complex signals into an array of converging pathways with one end goal, growth.The following diagram is the proposed pathway working through the protein p70s6k (which scientists are now saying is a better predictor of hypertrophy because this protein increases significantly after training and outlasts the period of growth hormone release):
To conclude, sure there is a large rise in hormones following training that includes large muscle mass.However, studies are starting to emerge that show that testosterone, GH, and IGF-1 may not be the entire mechanism necessary to induce hypertrophy.Hope this answered your question.
So you’re sore and you want to know what is going on in your muscle. Why? Don’t you just love being sore?
Introduction: Changes in muscle function after exercise training as well as the infamous DOMS (delayed onset muscle soreness) are collectively referred to as exercise-induced muscle damage (EIMD). These changes can be brought upon my enzymes, inflammatory markers, and/or glycogen stores inside of the muscle, which in turn will alter your time to fatigue and eventually your ability to perform the next time you exercise. One of the most damaging training methods is eccentric training, or as we know the negative portion of a rep. Therefore, this study induced eccentric exercise to discover changes in muscle metabolism.
Hypothesis: EIMD alters the muscle metabolic response to dynamic exercise and thus contributes to reduced exercise tolerance in humans.
Results: There were changes in all markers of muscle damage following eccentric exercise. Muscle pH levels were lower, and the concentration of inorganic phosphate (measured by 31P-MRS) increased as well as the ratio of inorganic phosphate to phosphocreatine. Time to exhaustion and peak work rates were decreased following eccentric exercise.
Conclusion: This study is the first of its kind to use MRI techniques to evaluate changes in muscle metabolism following an EMID protocol. This finding of a decrease in time to exhaustion is not linked towards a lower muscle pH or lower levels of phosphocreatine, but researchers believe it is due to higher levels of circulating inorganic phosphates. Increases in intracellular [Pi] can inhibit force production via direct action on cross-bridge formation or on other sites in the excitation contraction pathway and may play a key role in the development of muscle fatigue.
My input: So you’re probably thinking, so what? We know that we are sore after exercise and we know that we cannot have optimal performances the next time because of this soreness. I say to you, correct, but I also say to you that this is novel because of this being linked to circulating levels of this inorganic phosphate even during rest before exercise was initiated. Therefore, those that think it is solely due to a decreased pH that causes soreness and a decreased performance may be slightly mistrued.
Practicality: I just wanted to note that the training protocol used here to induce muscle damage was that of German Volume Training. That is 10 sets of 10 reps, which in this case, 10 sets of 10 reps for the squat. Thus, those that are training high volume in the gym should give themselves >48 hours rest before training that body group again because this was the time-frame used in between testing for the subjects.