Maximizing Muscle Hypertrophy with New Research (aka How to Lift and Eat)

Updation

Sorry for the delays here as I have been swamped and the last two days it feels like I got hit by a truck. Ugh.  So after lots of sleep I am back on track now.

Jodie and I had a blast in S. Padre Island kiteboarding and I will have an update soon.  I am working on TONS of great content coming up here.  As always, drop me a line on what YOU want to see.

Maximize Muscle Growth

Very cool new study today on what may be the best combination of lifting and eating for performance.  I am a huge geek and spend hours per week (literally) combing the literature to see if there are any new research gems that will help guide on how to increase muscle size and strength to make you a freaky athlete!    I am happy to report I found an AMAZING study.  Don’t worry, as I will break it down into terms even the most novice can understand and those who have been around for a bit will probably pick up some new things too.  Here we go!

We know that connective tissue (collagen) is a key component in strength since it is literally holding everything together (along with a specialized form called fascia).

Strong Connective Tissue + Bigger Muscle = Crazy Strength

A Tangent on “Jammed Joints = Muscular Weakness“

This is not a new thought, but it is rarely talked about and there has been really a big hole in the literature regarding any direct data to support this idea.  It makes sense that just like if you have a buggered up joint, it will start to decrease strength (”shut down”) the muscles around it.

I can say that first hand this is true when I messed up my ankle in a snowboarding incident about 5 years ago to this very day.   It swelled up to the size of a large softball, I had a walking cast, crutches, the whole 9 yards (hardcore all the way—haha).  I could not even MOVE my ankle, let alone generate any strength.   My body had shut every thing down there and increased fluid to the ankle (massive swelling) to further immobilize the ankle.

Now this is an extreme example, but it happens to a lesser degree with a joint that does not have optimal mobility (called the arthrokinetic reflex and taught in Z Health).

So we know the nervous system has a MASSIVE influence on strength.  It would only make sense that if we thought our connective tissue was not up to the task, our smart brains would limit our strength.

While we don’t have direct data on that point yet, we are getting closer and this study below holds some HUGE keys to muscle growth for you!

Contraction intensity and feeding affect collagen and myofibrillar protein synthesis rates differently in human skeletal muscle

This study looked at any changes to

1) connective tissue (collagen synthesis rates) and

2) muscle protein synthesis rates (FSR) which tells us how much protein is being added to muscles.

More protein added to muscles = bigger muscles (hypertrophy)

The great part is they looked a feeding them also to see if it helped out.  As you know, I highly recommend some protein around the time of your lifting session.

(from wikipedia)

Intramuscular total collagen protein synthesis rate (more connective tissue)

The heavy black is a direct quote from the study and the blue is my translation

“There was a clear effect of prior exercise on  skeletal muscle collagen FSR whether studied in the fasted or fed state (p<0.05)”

Even if you lift in a fasted state (no food before), there is still an increase in connective tissue formation.  Lifting BY ITSELF ALONE is highly anabolic for connective tissue.

“These changes in collagen FSR were unaffected by contractile intensity (p>0.10). Feeding did not increase  resting nor post exercise collagen protein synthesis rate and nor was the post exercise temporal response different compared with fasting”

It did not matter if you lifted a lighter load or heavier load, as there was still an increase in connective tissue.  This effect was NOT changed by eating.

Myofibrillar protein synthesis rate (bigger muscles)

“Fasting myofibrillar protein FSR was influenced by the contraction intensity of a prior exercise bout (interaction: p<0.05,).   Myofibrillar FSR was 303 0.08±0.01 %?hr-1 at rest and LL contractions was not sufficient to enhance the myofibrillar FSR  level significantly above that level (early: 0.11±0.01 and late: 0.09±0.02%hr-1; NS).

In contrast, HL contractions resulted in a delayed improvement (late: 0.14±0.02 %?hr-1, 2.0±0.4 fold, p<0.05).”

Lifting heavier (70% of max) was better than a very light load (16% of max) for bigger muscles.

Oral feeding elevated myofibrillar protein FSR at rest 2.3±0.3 fold up to 0.18±0.03 %?hr-1 (p<0.05,) and this elevated level was maintained at all post exercise time points irrespective of prior contraction intensity.

WOW!  If you eat protein after training, you can maximize your gains by over 2Xs as much as skipping it.  Very cool and simple to do!

When food was provided, LL contractions kept the myofibrillar protein  FSR elevated above fasting conditions at the late time point (p<0.05). Similarly, HL  contractions tended to increase the myofibrillar FSR at the late time point (p<0.10).

You are still building muscle HOURS after you leave the gym!  Simulate and then recover

What Did We Learn Today

Today we learned

Have a protein shake (I like a whey protein isolate from Protein Factory) after training to more than DOUBLE your gains.

Connective tissue increases are primarily only from lifting, even at a light load

Muscle growth needs a higher load and food help a ton!

Stay Tuned

Come back tomorrow for some tips on how you directly use this information to maximize your muscle gains in the gym with some novel methods

The full abstract is below

Any questions/thoughts let me know in the comments!  I want to know if you think this is helpful or not.  What do you want to see?

Rock on

Mike T Nelson

PS

You can also easily retweet any of my articles now!  Just hit the “retweet” symbol on the top right of any post.  Go crazy and thanks in advance for your help in spreading the good word!   Information needs to be shared.

Contraction intensity and feeding affect collagen and myofibrillar protein synthesis rates differently in human skeletal muscle

Exercise stimulates muscle protein fractional synthesis rate (FSR) but the importance of contractile intensity and whether it interplays with feeding is not understood. This was investigated following two distinct resistance exercise (RE) contraction intensities using an intra-subject design in the fasted (n=10) and fed (n=10) states. RE consisted of ten sets of knee-extensions. One leg worked against light-load (LL) at 16% of 1-repetition maximum (1RM), the other leg against heavy-load (HL) at 70% 1RM, with intensities equalized for total lifted load. Males were infused with (13)C-leucine and vastus lateralis biopsies were obtained bi-laterally at rest as well as 1/2, 3, and 51/2 hr after RE. Western blots were run on muscle-lysates and phospho-specific antibodies used to detect phosphorylation status of targets involved in regulation of FSR. The intramuscular collagen FSR was evenly increased following LL- and HL-RE and was not affected by feeding. Myofibrillar FSR was unaffected by LL-RE, whereas HL-RE resulted in a delayed improvement (0.14+/-0.02%xhr(-1), p<0.05). Myofibrillar FSR was increased at rest by feeding (p<0.05) and remained elevated late in the post-exercise period when compared with the fasting condition. The Rp-s6k-4E-BP1- and the MAPk-pathways were activated by the HL intensity and were suggested to be responsible for regulating myofibrillar FSR in response to adequate contractile activity. Feeding predominantly affected Rp-s6k and eEF2 phosphorylations in correspondence with the observed changes in myofibrillar FSR, whereas 4E-BP1 remained to respond only to the heavy load contraction intensity. Thus, the study design allows us to conclude that the MAPk and mTOR dependent signaling responds to contractile activity, whereas elongation mainly was found to respond to feeding. Further, although functionally linked, the contractile and the supportive matrix structures upregulate their protein synthesis rate quite differently in response to feeding and contractile-activity and -intensity.

What is the rate limiting step to muscle growth and increased athletic performance?

Is there something we can do to accelerate the process?

Here are my thoughts

Here I yack about

Tissue Turnover

• Is this a limiting factor?

• If so, how do we do it?

• Protein Intakes: High vs Low

• Protein Building (Protein Synthesis) and Protein Degradation (”Catabolic”)

• Increased Training Volume

• German Volume Training (GVT) meet Escalating Density Training (EDT)

Let me know your thoughts on this! I love comments, so let me have ‘em

Rock on
Mike T Nelson

Nutrition Chat : Cholesterol, Protein, Muscle Growth and More!

Here I talk about the latest research on how to maximize muscle growth through nutrition based on a phone chat I had with Dr. Lonnie Lowery.

You probably know Dr. Lowery from his writings at TMuscle.com (may not be uber work friendly and also Iron Radio.  I encourage you to check out both.

Here we go!

Here I yap about

• Cholesterol -  Is it that Evil?

• mTOR – What the heck is that?  Why do I give a crap?

• Calories Are King!

• How Much Protein?

• Diabetics and Carbs

• Metabolic Flexibility

Let me know what you think and what questions you have!  Post away in the comments!

Rock on
Mike T Nelson

3 Tips for Muscle Hypertrophy (Bigger Muscles): Research Review for November 2009

Jack Leon[between 1910 and 1915]

Just a few very cool studies this month and see my comments on how you can apply these for increased athletic performance on the field and in the gym!  Let’s roll

Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise

Despite the widespread consumption of nonsteroidal anti-inflammatory drugs (NSAIDs), the influence of these drugs on muscle satellite cells is not fully understood. The aim of the present study was to investigate the effect of a local NSAID infusion on satellite cells after unaccustomed eccentric exercise in vivo in human skeletal muscle. Eight young healthy males performed 200 maximal eccentric contractions with each leg. An NSAID was infused via a microdialysis catheter into the vastus lateralis muscle of one leg (NSAID leg) before, during, and for 4.5 h after exercise, with the other leg working as a control (unblocked leg). Muscle biopsies were collected before and 8 days after exercise. Changes in satellite cells and inflammatory cell numbers were investigated by immunohistochemistry. Satellite cells were identified using antibodies against neural cell adhesion molecule and Pax7. The number of Pax7+ cells per myofiber was increased by 96% on day 8 after exercise in the unblocked leg (0.14 ± 0.04, mean ± SE) compared with the prevalue (0.07 ± 0.02, P < 0.05), whereas the number of Pax7+ cells was unchanged in the leg muscles exposed to the NSAID (0.07 ± 0.01). The number of inflammatory cells (CD68+ or CD16+ cells) was not significantly increased in either of the legs 8 days after exercise and was unaffected by the NSAID. The main finding in the present study was that the NSAID infusion for 7.5 h during the exercise day suppressed the exercise-induced increase in the number of satellite cells 8 days after exercise. These results suggest that NSAIDs negatively affect satellite cell activity after unaccustomed eccentric exercise.

My thoughts

Very interesting study, but I am not convinced that NSAIDs are actually bad for muscle growth.  The data about 2-3 years ago, said that they were bad for muscle hypertrophy; but newer data is not pointing that way.     The eagle observer would notice that this study showed a negative effect on satellite cells, which would say that it is bad for muscle growth.  The downside is that muscle growth was not measured in this study.  Muscle can get bigger by various mechanisms, and while satellite cells is one way, it is not the only way.  Satellite cells are the little guys that hang out at the end of the muscle fibers and work to repair them from damage.   So for now I would not automatically reach for NSAIDs if you have muscle soreness, but if you have to, it is probably not affecting growth too much.  If people are interested, drop a note in the comments and I will do a blog post just on this.

Working around the clock: circadian rhythms and skeletal muscle

The study of the circadian molecular clock in skeletal muscle is in the very early stages. Initial research has demonstrated the presence of the molecular clock in skeletal muscle and that skeletal muscle of a clock-compromised mouse, Clock mutant, exhibits significant disruption in normal expression of many genes required for adult muscle structure and metabolism. In light of the growing association between the molecular clock, metabolism, and metabolic disease, it will also be important to understand the contribution of circadian factors to normal metabolism, metabolic responses to muscle training, and contribution of the molecular clock in muscle-to-muscle disease (e.g., insulin resistance). Consistent with the potential for the skeletal muscle molecular clock modulating skeletal muscle physiology, there are findings in the literature that there is significant time-of-day effects for strength and metabolism. Additionally, there is some recent evidence that temporal specificity is important for optimizing training for muscular performance. While these studies do not prove that the molecular clock in skeletal muscle is important, they are suggestive of a circadian contribution to skeletal muscle function. The application of well-established models of skeletal muscle research in function and metabolism with available genetic models of molecular clock disruption will allow for more mechanistic understanding of potential relationships.

My thoughts

Very cool study and the first I have seen in this area.  The age old question of what is the perfect time to lift has been around for a long time.   From what I have seen, there does not seem to be a perfect time.  The perfect time is when you can get to the gym and seems to be highly individual.  First priority is to get there, lift the weights and then later worry about finding the best time.  If I could set up my perfect schedule it would be to lift at 3pm in the afternoon.   Keep in mind that if you have a contest, say a powerlifting meet that start at 9am, you may want to do some lifts at that time in practice just to see how your body reacts.

For now, get to the gym first.

Translational signaling responses preceding resistance training-mediated myofiber hypertrophy in young and old humans

While skeletal muscle protein accretion during resistance training (RT)-mediated myofiber hypertrophy is thought to result from upregulated translation initiation signaling, this concept is based on responses to a single bout of unaccustomed resistance exercise (RE) with no measure of hypertrophy across RT. Further, aging appears to affect acute responses to RE, but whether age differences in responsiveness persist during RT leading to impaired RT adaptation is unclear. We therefore tested whether muscle protein fractional synthesis rate (FSR) and Akt/mammalian target of rapamycin (mTOR) signaling in response to unaccustomed RE differed in old vs. young adults, and whether age differences in acute responsiveness were associated with differences in muscle hypertrophy after 16 wk of RT. Fifteen old and 21 young adult subjects completed the 16-wk study. The phosphorylation states of Akt, S6K1, ribosomal protein S6 (RPS6), eukaryotic initiation factor 4E (eIF4E) binding protein (4EBP1), eIF4E, and eIF4G were all elevated (23–199%) 24 h after a bout of unaccustomed RE. A concomitant 62% increase in FSR was found in a subset (6 old, 8 young). Age x time interaction was found only for RPS6 phosphorylation (+335% in old subjects only), while there was an interaction trend (P = 0.084) for FSR (+96% in young subjects only). After 16 wk of RT, gains in muscle mass, type II myofiber size, and voluntary strength were similar in young and old subjects. In conclusion, at the level of translational signaling, we found no evidence of impaired responsiveness among older adults, and for the first time, we show that changes in translational signaling after unaccustomed RE were associated with substantial muscle protein accretion (hypertrophy) during continued RT.

My thoughts

There is more and more research coming out on hypertrophy in older folks.  My good buddy Carl Lanore likes to say “muscle is metabolic currency, so go to the gym and make a deposit today,’ and I totally agree.   It appears that muscle size is harder to come by as we age; but how much harder is still not clear.  Early studies showed that it was difficult, but recent data like the one above show that maybe there is not much difference.  Again, this is a 16 week study (which is pretty good for most studies) and note that they used NOVEL exercises.  I think this is a key point.  You need to give the body a REASON to adapt.  It also showed that strength increased, so the old people in the study were not all show and no go!

What 3 Tips Did We Learn Today?

1. NSAIDs may not be as bad for muscle hypertrophy as we once thought

2. Timing may become a bigger issue in the future, but for now get to the gym first

3. If hypertrophy is your goal, you need to “surprise” the muscles.  Now don’t go all crazy with the Weirder “confusion” principle, as plain old overload (doing more work over time) is a very powerful stimulus as the work load is novel.  I am a big fan of adding volume since it allows you to manage fatigue (Charles Staley’s ears are burning) and keep doing perfect reps.

Any questions/thoughts, let me have it in the comments

Rock on

Mike T Nelson

PS

You will have to come back here on Monday as you will have to see what I am posting.  The feedback on it so far has been crazy (both good and bad crazy),  Stay tuned!

Hold on to your shorts, as tons o-studies headed your way soon. I was able to cut out some time and blast through a bunch, so you have been warned!

As always, any and all comments are welcome!

Protein supplementation before and after exercise does not further augment skeletal muscle hypertrophy after resistance training in elderly men.

Verdijk LB, Jonkers RA, Gleeson BG, Beelen M, Meijer K, Savelberg HH, Wodzig WK, Dendale P, van Loon LJ. Department of Human Movement Sciences, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands. lex.verdijk@bw.unimaas.nl

BACKGROUND: Considerable discrepancy exists in the literature on the proposed benefits of protein supplementation on the adaptive response of skeletal muscle to resistance-type exercise training in the elderly.

OBJECTIVE: The objective was to assess the benefits of timed protein supplementation on the increase in muscle mass and strength during prolonged resistance-type exercise training in healthy elderly men who habitually consume adequate amounts of dietary protein.

DESIGN: Healthy elderly men (n = 26) aged 72 +/- 2 y were randomly assigned to a progressive, 12-wk resistance-type exercise training program with (protein group) or without (placebo group) protein provided before and immediately after each exercise session (3 sessions/wk, 20 g protein/session). One-repetition maximum (1RM) tests were performed regularly to ensure a progressive workload during the intervention. Muscle hypertrophy was assessed at the whole-body (dual-energy X-ray absorptiometry), limb (computed tomography), and muscle fiber (biopsy) level.

RESULTS: The 1RM strength increased approximately 25-35% in both groups (P

CONCLUSION: Timed protein supplementation immediately before and after exercise does not further augment the increase in skeletal muscle mass and strength after prolonged resistance-type exercise training in healthy elderly men who habitually consume adequate amounts of dietary protein.

My Notes: I will be presenting some more data next week showing a difference between elderly people and younger people in response to protein. Keep in mind that this was done in older people, and from what we know currently, the response in younger (less than about 70 years old) is NOT the same as this study. My recommendation is the same–add some protein before and after your strength training sessions.

I am behind on some cool research, so I have jammed a bunch into one long post. Be sure to look towards the end for a new study on protein and carb timing while in a FED state (translation-more applicable to the standard athlete since most are not fasting).

Here we go!
Vps34 is activated following high resistance contraction.

Mackenzie MG, Hamilton DL, Murray JT, Taylor PM, Baar K.

University of Dundee. Following resistance exercise in the fasted state, both protein synthesis and degradation in skeletal muscle are increased. The addition of essential amino acids potentiates the synthetic response suggesting that an amino acid sensor, which is involved in both synthesis and degradation, may be activated by resistance exercise. One such candidate protein is the class 3 phosphatidylinositol 3OH -kinase (PI3K) Vps34. To determine whether mammalian Vps34 (mVps34) is modulated by high resistance contractions, mVps34 and S6K1 (an index of mTORC1) activity were measured in the distal hindlimb muscles of rats 0.5, 3, 6, and 18 hours after acute unilateral high resistance contractions with the contralateral muscles serving as a control.

In the lengthening tibialis anterior (TA) muscle, S6K1 (0.5h=366.3+/-112.08%, 3h=124.7+/-15.96%, and 6h=129.2+/-0%) and mVps34 (3h=68.8+/-15.1% and 6h=36.0+/-8.79%) activity both increased, whereas in the shortening soleus and plantaris (PLN) muscles the increase was significantly lower (PLN S6K1 0.5h=33.1+/-2.29% and 3h=47.0+/-6.65%; mVps34 3h=24.5+/-7.92%). HPLC analysis of the TA demonstrated a 25% increase in intramuscular leucine concentration in rats 1.5 hours after exercise. A similar level of leucine added to C2C12 cells in vitro increased mVps34 activity 3.2-fold.

Conclusion: These data suggest that, following high resistance contractions, mammalian Vps34 activity is stimulated by an influx of essential amino acids such as leucine and this may prolong mTORC1 signalling and contribute to muscle hypertrophy.

My notes: More data that protein around training time is a good thing!

Voluntary Wheel Running Initially Increases Adrenal Sensitivity to Adrenocorticotrophic Hormone, which is Attenuated with Long-term Training.

Campbell JE, Rakhshani N, Fediuc S, Bruni S, Riddell MC.

York University. Although exercise is a common and potent activator of the hypothalamic-pituitary adrenal (HPA) axis, the effects of exercise on the acute stress response are not well understood. Here, we investigated the effects of short (2wk)- and long-term (8wk) voluntary wheel running on adrenal sensitivity to ACTH stimulation and the acute stress response to restraint in male rats. Diurnal glucocorticoid (GC) patterns were measured on days 7 (all groups) and 35 (8 wk groups). Rats were subjected to 20 minutes of restraint stress on either week 1 or on week 7 of treatment to assess HPA activation. One week later, exogenous ACTH (75 ng/kg) was administered to assess adrenal sensitivity to ACTH. Following this, adrenals were collected and analyzed for key proteins involved in corticosterone (CORT) synthesis.

By the end of week one, exercising (E) animals had a 2-fold higher peak diurnal CORT levels compared with sedentary (S) animals (p

Concluison: These results show that volitional wheel running initially causes hyperactivation of the hypothalamic-pituitary adrenal -axis, due to enhanced adrenal sensitivity to ACTH, but that these alterations in hypothalamic-pituitary adrenal activity are completely restored by 8 weeks of training.

My notes: Very cool study that shows ACUTE (short lived) effects may not (and normally do not) hang around when viewed over a longer time frame.
Also note, this was VOLUNTARY wheel running and the results may be different if they force the little buggers to run on the wheel. Higher stress = even higher cortisol.

Age-related differences in dose response of muscle protein synthesis to resistance exercise in young and old men.

Kumar V, Selby A, Rankin D, Patel R, Atherton P, Hildebrandt W, Williams J, Smith K, Seynnes O, Hiscock N, Rennie MJ.

University of Nottingham, School of Graduate Entry Medicine and Health, Derby, DE22 3DT. We investigated how myofibrillar protein synthesis and muscle anabolic signalling were affected by resistance exercise at 20-90% of 1 repetition maximum (1 RM) in two groups of 25 each, postabsorptive, healthy, young (24+/-6 y) and old (70+/-5 y) men with identical body mass indices (24+/-2 kg.m(-2)). We hypothesized that, in response to exercise, anabolic signalling molecule phosphorylation and MPS would be modified in a dose-dependant fashion, but to a lesser extent in older men. Vastus lateralis muscle was sampled before, immediately after, and 1, 2 and 4 h post-exercise. MPS was measured by incorporation of [1,2-(13)C]leucine (gas chromatography-combustion-mass spectrometry using plasma [1,2-(13)C]alpha-ketoisocaparoate as surrogate precursor); the phosphorylation of p70 ribosomal S6 kinase (p70s6K) and eukaryotic initiation factor 4E binding protein 1(4EBP1) was measured using Western analysis with anti-phosphoantibodies.

In each group, there was a sigmoidal dose-response relationship between MPS at 1-2 h post-exercise and exercise intensity, which was blunted (P

Conclusion: The results suggest that in the postabsorptive state (i) muscle protein synthesis is dose-dependant on intensity rising to a plateau at 60-90% 1 repetition maximum; (ii) older men show anabolic resistance of signalling and muscle protein synthesis to resistance exercise.

My Notes: There are more and more data to suggest that the response of older adults to the same amount of protein is different. I talked about this briefly in a recent newsletter (sign up on the upper right of this blog) and this is another study helping that argument along.

Nutritional consideration in the aging athlete.

Tarnopolsky MA.

Department of Pediatrics, Faculty of Health Science, McMaster University, Hamilton, Ontario, Canada. tarnopol@mcmaster.ca OBJECTIVE:: To evaluate the evidence for dietary recommendations in older adult athletes. DESIGN:: Interpretive review of the literature.

RESULTS:: Regarding resistance training, a protein intake of slightly more than 0.8 g/kg/d is
required to optimize gains in muscle strength.

The early provision of protein and carbohydrate following a weight training session can enhance resultant strength and fat-free mass gains. Supplementation with creatine monohydrate (approximately 5 g/d) can potentiate some of the gains in strength and fat free mass attained through resistance exercise training. Regarding endurance exercise training, there are no studies evaluating carbohydrate loading, during-event, or postexercise carbohydrate/nutritional replacement in older adults.

CONCLUSIONS::
The amount and timing of dietary protein is important to maximize strength and gains in fat-free mass during resistance exercise training. Creatine monohydrate supplementation can potentiate some of these gains during the first 4 to 6 months of training.

Older adults should consume adequate carbohydrates during endurance training (6-8 g/kg/d) and may benefit from the provision of carbohydrate and protein in the early recovery phase following endurance exercise to maximize glycogen re-synthesis for a subsequent exercise bout.

There is no scientific reason to assume that older athletes will respond differently to the pre- and during-race fluid and carbohydrate replacement strategies suggested for younger athletes.

My Notes: Note that the last few lines in the conclusion take about ENDURANCE training not strength training! Creatine is good—word!

Coingestion of carbohydrate and protein hydrolysate stimulates muscle protein synthesis during exercise in young men, with no further increase during subsequent overnight recovery.

Beelen M, Tieland M, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, Koopman R, van Loon LJ.

Department of Movement Sciences, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands. milou.beelen@bw.unimaas.nl We investigated the effect of carbohydrate and protein hydrolysate ingestion on whole-body and muscle protein synthesis during a combined endurance and resistance exercise session and subsequent overnight recovery. Twenty healthy men were studied in the evening after consuming a standardized diet throughout the day. Subjects participated in a 2-h exercise session during which beverages containing both carbohydrate (0.15 g x kg(-1) x h(-1)) and a protein hydrolysate (0.15 g x kg(-1) x h(-1)) (C+P, n = 10) or water only (W, n = 10) were ingested. Participants consumed 2 additional beverages during early recovery and remained overnight at the hospital.

Continuous i.v. infusions with L-[ring-(13)C(6)]-phenylalanine and L-[ring-(2)H(2)]-tyrosine were applied and blood and muscle samples were collected to assess whole-body and muscle protein synthesis rates. During exercise, whole-body and muscle protein synthesis rates increased by 29 and 48% with protein and carbohydrate coingestion (P

Conclusion: We conclude that, even in a fed state, protein and carbohydrate supplementation stimulates muscle protein synthesis during exercise. Ingestion of protein with carbohydrate during and immediately after exercise improves whole-body protein synthesis but does not further augment muscle protein synthesis rates during 9 h of subsequent overnight recovery.

My Notes: Most studies of this type are done on fasting subjects, so it is cool to see more work done on subjects in a fed (they ate recently) state as this is more applicable to most athletes.

Morphological Hypertrophic Muscle Adaptations (aka, Mechanisms Behind “I Wanna Get Hyoooge!!”)

Pop your head into just about any gym in America, and observe the male population (especially the younger ones) train. While the training methods are interesting in themselves, the common battle cry of the young Arnold wannabes is usually the same “I Wanna Get Hyoooge.” In an effort to explore the mechanisms behind the scenes in the body to help out these “bros” it is time to board the magical muscle mystery tour. Tour stops include a drive by of the nervous system, muscle fiber types, and how muscles adapt to exercise to get bigger and badder (as in a Michael Jackson “bad” is now good way).

Before we dive in head first into this, we need to do a short little anatomy tour. They say a picture is worth a thousand words, so check out figure below.

This time around I will spare you all the details on the exact names of each, but notice how a single fiber at the end goes into another group of fibers and then THAT group goes into another group until we are all the way up to the muscle itself. Muscle fibers can be broadly defined as type2 fast twitch or type 1 slow twitch (8). Fast twitch (type 2) fibers can produce more force, but they don’t last as long (26). Think of an NFL lineman. He can produce a ton of force to knock you into next week, but it is unlikely he will be chasing your around the block or very far at all. Type 2 (slow twitch) muscle fibers are like the slower cousin to the type 2, think energizer bunny. They can’t produce as much force, but they keep going and going and going and going………..

Remember that the nervous system is the head cheese, numero uno, el presidente, the commander in charge that controls all muscle movements. The nervous system also controls which fibers are type 1 or 2! Buller et al. (9) in 1960, carefully did the ole “switcheroo” on cats and switched nerves and a type 2 muscle fiber with a new type 1 NERVE now took on the properties of a type 1 muscle fiber! Think of this as “what the commander says goes.”
Another key point is that “living systems are build up through use and atrophy (get smaller) with disuse.” So when you are in the gym blasting away, you are actually making your muscle SMALLER! Yikes! The good part is that your body responds by BUILDING up those damaged fibers during the recovery period (33). So next time you do a similar exercise, the body has “new and improved” muscle tissue to better handle the damage. Pretty sweet!

Muscle Growth Time
Skeletal muscle is a very dynamic tissue capable of adapting to the stress placed on it. The process of exercise-induced adaptation in skeletal muscle involves a multitude of signaling mechanisms all the way down to the genetic level, ultimately putting together strings of amino acids to form new proteins in the form of more muscle tissue (10). Whooo ha, and the gym “bros” rejoice!

As mentioned, muscle growth is commonly referred to as “hypertrophy” (34) or more accurately as an increase in muscle fiber SIZE. How does this happen? While a complete answer to that question is beyond this short article, what do you think are some key processes? “TESTOSTERONE!” Good guess and there is a fair amount of data to support this (16, 17, 29, 30), there is also data (although less) to show that in castrated (denutted—youch!!!) animals (yeah I know it was not done in humans but do you want to volunteer for those studies?) are still able to increase muscle size despite having testosterone levels at very low levels (22, 24). “NUTRITION!” Yes, there is no denying that nutrition especially extra calories and protein are needed for muscle hypertrophy (11, 13, 19) but even in caloric restriction muscles can still get bigger (12). “INSULIN!” While insulin is the most anabolic (building) hormone in the body, it is not required either (7). (Side note, I am using the term “anabolic” in the physiologic sense where it is taking small things and making bigger things with them. This can be proteins into new muscle or fatty acids into new fat storage around your waist. And yes, too much insulin can make you a fat bastard). So the muscle building process is a complicated one.

How Do These Genes Look
Further down the hole, we have a whole slew of molecular signaling guys, some newly discovered like Mighty that can dramatically influence muscle growth. Mighty is a downstream metabolite of myostatin. Most have probably heard of myostatin now or seen the huge picture of the Belgium Bull.

Belgian Blue Bulls (say that fast three times in a row) have a mutation in the myostatin gene that produces a truncated, ineffective form of the protein (20), so in English there is almost no myostatin hanging around. The absence of myostatin allows unchecked muscle growth and interferes with fat deposition; the result is a lean, “double-muscled” bull. Yikes! Remember that LESS myostatin = MORE muscle.

The new kid on the block now is Mighty. Mighty is expressed in a variety of different tissues but appears to be specifically regulated by myostatin in skeletal muscle. Overexpression of Mighty in certain cells (ok, C2C12 cells if you really want to know) results in enhanced and accelerated differentiation and hypertrophy of myotubes (this is good for muscle growth, trust me) and leads to increased and earlier expression of MyoD and insulin like growth factor II (IGF-II) (both are good for muscle growth) (23).

Enough Biochem Yacking already
So I spared you from a detailed talk on Interleukin-4 (IL-4) and interleukin-13 (IL-13) that are involved in getting hyoooge (27), so be thankful! Watch out—Geek alert! Serrano et al. (28) recently showed a role for IL-6 in hypertrophic muscle growth and provide mechanistic evidence for the contribution of satellite cells to this process, in our fury friends the mouse.

So back to our irregularly scheduled program. So far we know 1) nutrition is key-calories and protein are needed to build muscle 2) we need a stimulus—weight training works well here (31) 3) certain hormonal and biochemical changes need to take place—from hormonal changes down to even the molecular level.
Shut Up Already and Tell Me HOW to Get Hyoooooooooge!
During short term studies of less than 10 weeks, it was shown that type 2 fibers hypertrophy (get bigger) much faster from training than their slow cousins the Energizer bunny type 1 fibers (1). MacDougall et al.(21) however investigated a longer time period of 5–6 months of heavy resistance training (weight lifting) in seven males and demonstrated a significant cross sectional increase in type 2 AND type 1 fibers; so long term it appears that BOTH fiber types can increase in size. Take home message, use a wide variety of reps.

Damage Plan
The goal of some dedicated Arnold wannabes is to destroy tissue! No pain no gain! Go hard or go home! Is there any research to support this method if we can get hyoooooooooge? There is actually some evidence to support this notion. Goldspink about 30 years ago proposed that if you literally tear the muscle fiber in half (these would be very small tears of course), that this may promote splitting of the muscle fibers once the body goes to work repairing those fibers; thus resulting in more fibers over time. More fibers= more siz
e. The fancy word associated with increasing muscle fiber NUMBER is hyperplasia. The downside is that this phenomena is highly debatable with virtually the studies being conducted on animals (primarily cats and birds), so how it applies to humans is not currently known (2-6, 15, 18, 32).

We know that eccentric (lowering a heavy weight) can scramble the muscle fibers (induce lots of damage) and it appears that fiber disruption induced by habitual weightlifting exercise is essentially repaired after 5 days of inactivity in trained men (14) and oxidative stress indices changed significantly with most peaking at 48 hours (25).

What does any of this mean?
Although data is somewhat limited on the “destroy tissue” approach in relation to hypertrophy there is enough to support the idea for muscle hypertrophy, but keep in mind that your recovery time may be longer with this approach. Your muscles get bigger OUTSIDE the gym when they are repairing!

Conclusion
Thus ends our very brief ride on the magically, muscle mystery tour! I hoped you have enjoyed the tour and kept your hands inside the bus at all times. We got to spend some time in the land of the nervous system, fiber types, stimulus for adaptation (aka weight training), and the adaptation process itself. The take away is that muscle hypertrophy is a complicated process and our best bet in the quest for huge-dom is 1) excellent nutrition with a surplus of calories and proteins and 2) consistent weight training with adequate time for recovery; especially if eccentric movements are used to induce muscle damage.
Time to get to the gym!

Mike T. Nelson has a BA in Natural Science, a MS in Mechanical Engineering (Biomechanics) and is currently a PhD student in Kinesiology (Exercise Physiology) at the University of Minnesota. His research interests are on the effects of energy drinks on metabolic health and the nervous system.

References
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27. Prokopchuk O, Y Liu, L Wang, K Wirth, D Schmidtbleicher, JM Steinacker. Skeletal muscle IL-4, IL-4Ralpha, IL-13 and IL-13Ralpha1 expression and response to strength training. Exerc Immunol Rev. . 2007; 13:67-75.
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29. Singh R, JN Artaza, WE Taylor, NF Gonzalez-Cadavid, S Bhasin. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology. . 2003; 144(11):5081-8.
30. Sinha-Hikim I, SM Roth, MI Lee, S Bhasin. Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men. Am J Physiol Endocrinol Metab. . 2003; 285(1):E197-205.
31. Spiering BA, WJ Kraemer, JM Anderson, et al. Resistance exercise biology : manipulation of resistance exercise programme variables determines the responses of cellular and molecular signalling pathways. Sports Med. . 2008; 38(7):527-40.
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33. Wernig A. Regeneration capacity of skeletal muscle. Ther Umsch. . 2003; 60(7):383-9.
34. Wilmore JH, DL Costill. Physiology of Sport and Exercise, Fourth Edition. Human Kinetics Publishers; 2007. p. 574.

So I am a few months behind on research updates, but have no fear as more good stuff is coming. For June some great studies on pre and post protein and carbohydrate beverages, NSAIDs (like Advil) and their effects on muscle growth, and some molecular mechanisms in action.

Be sure to check out my previous post HERE on protein synthesis (adding muscle) and what you can do to maximize it based on bleeding edge research.

If all this crazy research makes your head spin back like a Pez dispenser and just want to get the plan and get started today, check out Jimmy Smith’s Physique Formula.

Let’s get to it

Differential effects of resistance and endurance exercise in the fed state on signaling molecule phosphorylation and protein synthesis in human muscle.

Wilkinson SB, Phillips SM, Atherton PJ, Patel R, Yarasheski KE, Tarnopolsky MA, Rennie MJ. McMaster University.

Resistance (RE) and endurance (EE) exercise stimulate mixed skeletal muscle protein synthesis. The phenotypes induced by RE (myofibrillar protein accretion) and EE (mitochondrial expansion) training must result from differential stimulation of myofibrillar and mitochondrial protein synthesis. We measured the synthetic rates of myofibrillar and mitochondrial proteins and the activation of signaling proteins (Akt-mTOR-p70S6K) at rest and after an acute bout of RE or EE in the untrained state and after 10 wk of RE or EE training in young healthy men. While untrained, RE stimulated both myofibrillar and mitochondrial protein synthesis, 67% and 69% (P

Conclusion: Chronic resistance exercise (wt training) or endurance exercise training modifies the protein synthetic response of functional protein fractions, with a shift toward exercise phenotype-specific responses, without an obvious explanatory change in the phosphorylation of regulatory signaling pathway proteins.

My notes: sounds like the SAID principle in action! The body is adapting specifically to the stimulus (exercise)

Essential amino acid and carbohydrate ingestion prior to resistance exercise does not enhance post-exercise muscle protein synthesis.

Fujita S, Dreyer HC, Drummond MJ, Glynn EL, Volpi E, Rasmussen BB.University of Tokyo. Ingestion of an essential amino acid-carbohydrate (EAA+CHO) solution following resistance exercise enhances muscle protein synthesis during post-exercise recovery. It is unclear whether EAA+CHO ingestion prior to resistance exercise can improve direct measures of post-exercise muscle protein synthesis (FSR; fractional synthetic rate). We hypothesized that EAA+CHO ingestion prior to a bout of resistance exercise would prevent the exercise-induced decrease in muscle FSR and would result in an enhanced rate of muscle FSR during post-exercise recovery. We studied 22 young healthy subjects before, during, and for 2 hr following a bout of high-intensity leg resistance exercise. The Fasting control group (N=11) did not ingest nutrients and the EAA+CHO group (N=11) ingested a solution of EAA+CHO 1 hr prior to beginning the exercise bout. Stable isotopic methods were used in combination with muscle biopsies to determine FSR. Immunoblotting procedures were utilized to assess cell signaling proteins associated with the regulation of FSR. We found that muscle FSR increased in the EAA+CHO group immediately following EAA+CHO ingestion (P0.05). Eukaryotic elongation factor 2 phosphorylation was reduced in both groups at 2 hr post-exercise (EAA+CHO: 39+/-7%; Fasting: 47+/-9%; P

Conclusion: We conclude that essential amino acids and carbs (EAA+CHO) ingestion prior to resistance exercise does not enhance post-exercise fractional synthesis rate (FSR–Fractional Synthetic Rate–aka rate of adding protein to muscles) as compared to exercise without nutrients.

My note–while this interesting, I would not dump your protein carb drink before lifting just yet. Based on info from Dave Barr (source, AI and personal conversation) moving it to 15 minutes before training may be more ideal. Stay tuned!

Gene expression profiling in human skeletal muscle during recovery from eccentric exercise.

Mahoney DJ, Safdar A, Parise G, Melov S, Fu M, MacNeil L, Kaczor J, Payne ET, Tarnopolsky MA. Department of Medical Sciences, McMaster University Medical Center, 1200 Main Street W., Hamilton, Ontario, Canada. We used cDNA microarrays to screen for differentially expressed genes during recovery from exercise-induced muscle damage in humans. Male subjects (n = 4) performed 300 maximal eccentric contractions, and skeletal muscle biopsy samples were analyzed at 3 h and 48 h after exercise. In total, 113 genes increased 3 h postexercise, and 34 decreased. At 48 h postexercise, 59 genes increased and 29 decreased. On the basis of these data, we chose 19 gene changes and conducted secondary analyses using real-time RT-PCR from muscle biopsy samples taken from 11 additional subjects who performed an identical bout of exercise.
Real-time RT-PCR analyses confirmed that exercise-induced muscle damage led to a rapid (3 h) increase in sterol response element binding protein 2 (SREBP-2), followed by a delayed (48 h) increase in the SREBP-2 gene targets Acyl CoA:cholesterol acyltransferase (ACAT)-2 and insulin-induced gene 1 (insig-1). The expression of the IL-1 receptor, a known regulator of SREBP-2, was also elevated after exercise. Taken together, these expression changes suggest a transcriptional program for increasing cholesterol and lipid synthesis and/or modification. Additionally, damaging exercise induced the expression of protein kinase H11, capping protein Z alpha (capZalpha), and modulatory calcineurin-interacting protein 1 (MCIP1), as well as cardiac ankryin repeat protein 1 (CARP1), DNAJB2, c-myc, and junD, each of which are likely involved in skeletal muscle growth, remodeling, and stress management.

Conclusion: In summary, using DNA microarrays and RT-PCR, we have identified novel genes that respond to skeletal muscle damage, which, given the known biological functions, are likely involved in recovery from and/or adaptation to damaging exercise.

My notes: I wonder why all this muscle physiology stuff is so elusive, to quote the authors “In total, 113 genes increased 3 h postexercise, and 34 decreased.” That is a lot of stuff going on! Still wondering if you need to damage the muscle for it to increase in size?

Post exercise carbohydrate-protein supplementation: phosphorylation of muscle proteins i
nvolved in glycogen synthesis and protein translation.

Ivy JL, Ding Z, Hwang H, Cialdella-Kam LC, Morrison PJ.Exercise Physiology and Metabolism Laboratory, Department of Kinesiology and Health Education, The University of Texas, Austin, Texas 78712-0360, USA. johnivy@mail.utexas.edu The enzymes Akt, mTOR, p70(S6K), rpS6, GSK3, and glycogen synthase interact in the control of protein and/or glycogen synthesis in skeletal muscle, and each has been found to respond to exercise and nutrient supplementation. In the present study, we tested the hypothesis that nutrient supplementation post exercise, in the form of a carbohydrate-protein (CHO-PRO) supplement, would alter the phosphorylation state of these enzymes in a manner that should increase muscle protein and glycogen synthesis above that produced by exercise alone. After a 45 min cycling session followed by sprints and again 15 min later, the subjects (n = ingested 400 ml of a CHO-PRO drink (7.8% dextrose and 1.8% protein-electrolyte) or a placebo drink, as assigned using a randomized, counter-balanced design with repeated measures. Biopsies of the vastus lateralis were taken before exercise and at 45 min of recovery.
At 45 min after supplementation, CHO-PRO treatment yielded greater phosphorylation of Akt (65%), mTOR (86%), rpS6 (85-fold), and GSK3alpha/beta (57%) than pre-exercise levels (p

Conclusion: These results suggest that a post exercise carb and protein (CHO-PRO) supplement alters the phosporylation levels of the enzymes tested in a manner that should accelerate muscle glycogen synthesis and protein initiation during recovery from cycling exercise.

My notes: cool info, but I would like to see this carried out in the future to any performance changes. This would say that it should help. I am sure that is in the pipeline and there is some data already out in that area

The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training.

Krentz JR, Quest B, Farthing JP, Quest DW, Chilibeck PD. High doses of ibuprofen have been shown to inhibit muscle protein synthesis after a bout of resistance exercise. We determined the effect of a moderate dose of ibuprofen (400 mg.d-1) consumed on a daily basis after resistance training on muscle hypertrophy and strength. Twelve males and 6 females (~24 years of age) trained their right and left biceps on alternate days (6 sets of 4-10 repetitions), 5 d.week-1, for 6 weeks.
In a counter-balanced, double-blind design, they were randomized to receive 400 mg.d-1 ibuprofen immediately after training their left or right arm, and a placebo after training the opposite arm the following day. Before- and after-training muscle thickness of both biceps was measured using ultrasound and 1 repetition maximum (1 RM) arm curl strength was determined on both arms.
Subjects rated their muscle soreness daily. There were time main effects for muscle thickness and strength (p

Conclusion: We conclude that a moderate dose of ibuprofen ingested after repeated resistance training sessions does not impair muscle hypertrophy or strength and does not affect ratings of muscle soreness.

My Notes: If you would have asked me even a few months ago, I would have said that the use of NSAIDs (like Advil) is not a good idea as it may limit muscle growth (hypertrophy). After talking to some at ACSM, looking at some newer litature, I am thinking it will probably be ok. It may even be beneficial after an acute injury to keep your movement quality better and limit pain, thus reducing the chance on longer term chronic pain ala the neuromatrix of pain. See the following posts on that below

Pain Perception and the Neuromatrix–Guest Blog by Katelin Bigelow

Pre-emptive Analgescis–what is he talking about now?

Cellular and molecular events controlling skeletal muscle mass in response to altered use.

Favier FB, Benoit H, Freyssenet D.Unité Physiologie et Physiopathologie de l’Exercice et Handicap, IFR143, Université Jean Monnet, 15 rue Ambroise Paré, 42023, Saint Etienne, cedex 2, France.
Gain or loss of skeletal muscle mass occurs in situations of altered use such as strength training, aging, denervation, or immobilization. This review examines our current understanding of the cellular and molecular events involved in the control of muscle mass under conditions of muscle use and disuse, with particular attention to the effects of resistance exercise/training. The DNA content, which is a critical determinant of protein synthesis by providing the amount of DNA necessary to sustain gene transcription, can be either increased (activation of satellite cells) or decreased (apoptosis) depending on muscle activity and ongoing physiological processes. In addition, several transcription factors are sensitive to functional demand and may control muscle-specific protein expression to promote or repress myofiber enlargement. The control of skeletal muscle mass is also markedly mediated by the regulation of transduction pathways that promote the synthesis and/or the degradation of proteins. Insulin-like growth factor-I plays a key role in this balance by activating the Akt/tuberous sclerosis complex 2/mammalian target of rapamycin pathway.

Conclusion: Stimulation of this pathway leads to the concomitant activation of initiation and elongation factors resulting in the elevation of protein translation and the downregulation of ubiquitin proteasome components through Forkhead-box O transcription factors.

My Notes: Good review (with lots of big words), but the take away is still the same–USE IT OR LOSE IT!

Rock on
Mike N

Hypertrophy with unilateral resistance exercise occurs without increases in endogenous anabolic hormone concentration.

Conclusion: “Unilateral training induced local muscle hypertrophy only in the exercised limb, which occurred in the absence of changes in systemic hormones that ostensibly play a role in muscle hypertrophy.”

My comments
Muscle hypertrophy (increasing muscle mass to get hyoooooooge) is a complicated process and although anabolic hormones do help, they are NOT required for muscle growth!

Cross-transfer effects of resistance training with blood flow restriction.

CONCLUSION: “The results indicate that low-intensity resistance training increases muscular size and strength when combined with resistance exercise with blood flow restriction for other muscle groups. It was suggested that any circulating factor(s) was involved in this remote effect of exercise on muscular size.”

My comments
Nothing like science to show different results from different studies! This one showing a systemic effect due to exercise (probably anabolic hormones but could be related to the nervous system). Previous studies have shown that there is a cross transfer from one limb to the next, so if I only do RIGHT bicep curls, my LEFT bicep will actually increase in strength to some degree

Growth hormone isoform responses to GABA ingestion at rest and after exercise.

CONCLUSIONS: “Our data indicate that ingested GABA elevates resting and postexercise irGH and ifGH concentrations. The extent to which irGH/ifGH secretion contributes to skeletal muscle hypertrophy is unknown, although augmenting the postexercise irGH/ifGH response may improve resistance training-induced muscular adaptations.”

My comments
I can see the supplement add now “GABBA increases GH!!!” While that may be true, this does NOT gaurantee any performance (increased muscle, decreased fat) changes. Yes the amount of GH (dose) does matter, but newer research is showing that how and when (pattern) of release is also very important.

Myocardial gene expression in heart failure patients treated with cardiac resynchronization therapy responders versus nonresponders.

CONCLUSIONS: “In HF patients with electromechanical cardiac dyssynchrony, functional improvement related to CRT is associated with favorable changes in established molecular markers of HF, including genes that regulate contractile function and pathologic hypertrophy.”

My comments
This study shows the amazing ability of the body to ADAPT! Despite what we throw at it, the body will almost ALWAYS ADAPT! This adaptation could be good or bad however. In this case with a better stimulus (CRT–cardiac resynchronization therapy–think of a fancy pacemaker for BOTH sides of the heart) the heart adapted in a POSITIVE fashion, all the way down to molecular markers. Amazing.

The salivary testosterone and cortisol response to three loading schemes.

Conclusion:” The similar T and C responses to the power and maximal strength schemes (of equal volume) support such a view and suggest that differences in load intensity, rest periods, and technique are secondary to volume. Because the acute hormonal responses to resistance exercise contribute to protein metabolism, then load volume may be the most important workout variable activating the endocrine system and stimulating muscle growth.”

My comments
See my above comments–ha! I wish more studies would measure hormonal changes AND performance changes. Most athletes only care about performance changes and you will not have the ability (most of us) to measure hormones anyway. Remember, hormones are only MESSENGERS!!!! Create the best stimulus first and then recover.

Effects of short-term hypocaloric diet on sympatho-vagal interaction assessed by spectral analysis of heart rate and blood pressure variability during stress tests in obese hypertensive patients.

Conclusion:” The LF/high frequency component (HF) ratio of the RR interval at rest on the regular-calorie diet was negatively correlated with the decrease in blood leptin concentration. These results suggest that the autonomic nervous function assessed by analysis of heart rate and blood pressure variability during stress tests may be improved by weight loss due to a short-term low-calorie diet in obese patients with hypertension.”

My comments
Show us again that the nervous system is running the show!

Effects of exercise on adipokines and the metabolic syndrome.

Conclusion: “Future studies are needed to investigate the cellular mechanisms by which exercise training affects inflammation and whether alterations in inflammation are one mechanism by which exercise improves components of the metabolic syndrome in at-risk individuals.”

My comments
Watch for inflammation to continue to play a huge role in exercise physiology and many other fields. Check out the guest blog by Dr. Lonnie Lowery HERE

Interleukin-6 markedly decreases skeletal muscle protein turnover and increases non-muscle amino acid utilization in healthy individuals.

Conclusion: “We demonstrated that IL-6 profoundly alters amino acid turnover. A substantial fall in plasma amino acids was observed with a concomitant 50% decrease in muscle protein turnover, however modest increase in net muscle degradation. We hypothesize that the profound reduction in muscle protein turnover and modest increase in net degradation is primarily caused by the reduced plasma amino acid availability and not directly mediated by IL-6.”

My comments

Most inflammatory compounds are probably not just “good” or “bad”. Some is probably needed for a response, but too much will be an issue. Some inflammation is probably needed for optimal muscle growth (hypertrophy) but too much will dampen the optimal response. So how much? Good question and I really have no idea yet!

Any comments, let me know. Hope you enjoyed this highly geeeked out look at
some brand new research!

Changes due to eccentric exercise?
Some more studies for you! We know that a great way to create a lot of Delayed Onset Muscle Soreness (DOMS) is by eccentric exercise. Again, I am not recommended that you go out of your way to create muscle damage, but it happens and is probably an important step in the hypertrophy (increase in muscle size) process. Now that does not mean that it is always painful, however. Pain is an interpretation in the brain! Below are some brand new studies to shed some light on what is really going on….

(NOTE–the hyperlinks below are all fixed now!)

Sensory and electromyographic mapping during delayed-onset muscle soreness

Authors: Hedayatpour,N.; Falla,D.; Arendt-Nielsen,L.; Farina,D.
Source: Med.Sci.Sports Exerc., 2008, 40, 2, 326-334

Conclusion: “Novel topographical mapping of both surface EMG (Electromyography) and PPT (Pressure-pain thresholds) of the quadriceps showed site-dependent effects of eccentric exercise, probably attributable to variations in the morphological and architectural characteristics of the muscle fibers. Greater manifestations of DOMS (Delayed Onset Muscle Soreness) in the distal region of the quadriceps may indicate a greater susceptibility of this region to further injury after eccentric exercise.”

Effects of neuromuscular electrical stimulation of the knee extensor muscles on muscle soreness and different serum parameters in young male athletes: preliminary data

Authors: Zorn,C.; Szekeres,T.; Keilani,M.; Fialka-Moser,V.; Crevenna,R.
Source: Br.J.Sports Med., 2007, 41, 12, 914-916

Conclusions: “Although the changes of blood parameters measured in the present work correspond to those reported in the literature on eccentric strength training, no delayed onset muscle pain could be detected. Further studies should be carried out, also investigating different stimulation protocols in non-trained healthy subjects and in patients with less muscle mass.”

Uniform and prolonged changes in blood oxidative stress after muscle-damaging exercise

Authors: Paschalis,V.; Nikolaidis,M.G.; Fatouros,I.G.; Giakas,G.; Koutedakis,Y.; Karatzaferi,C.; Kouretas,D.; Jamurtas,A.Z.
Source: In Vivo, 2007, 21, 5, 877-883

Conclusion: “We believe that muscle-damaging exercise should be viewed as a different challenge compared to non-muscle-damaging exercise with regard to its effects on blood oxidative stress.”

Adaptive changes in motor control of rhythmic movement after maximal eccentric actions

Authors: Bottas,R.; Nicol,C.; Komi,P.V.; Linnamo,V.
Source: J.Electromyogr.Kinesiol.

Conclusion: “The present results emphasize the capacity of the neuromuscular system to compensate for prolonged eccentric-induced contractile failure by optimizing antagonistic muscles coordination in a demanding rhythmic task. The underlying compensatory mechanisms could be related to increased sensitization of small diameter muscle nerve endings.”

Decreased blood oxidative stress after repeated muscle-damaging exercise

Authors: Nikolaidis,M.G.; Paschalis,V.; Giakas,G.; Fatouros,I.G.; Koutedakis,Y.; Kouretas,D.; Jamurtas,A.Z.
Source: Med.Sci.Sports Exerc., 2007, 39, 7, 1080-1089

Conclusion: “A repeated bout of lengthening contractions attenuated muscle damage and blood oxidative stress compared with the first bout.”

Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction

Authors: Crameri,R.M.; Aagaard,P.; Qvortrup,K.; Langberg,H.; Olesen,J.; Kjaer,M.
Source: J.Physiol., 2007, 583, Pt 1, 365-380

Conclusion: “The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extra cellular matrix in the phenomenon of delayed onset of muscle soreness.”

Changes in serum cytokines after repeated bouts of downhill running

Authors: Smith,L.L.; McKune,A.J.; Semple,S.J.; Sibanda,E.; Steel,H.; Anderson,R.
Source: Appl.Physiol.Nutr.Metab., 2007, 32, 2, 233-240

Conclusion: “The pro-inflammatory macrophage inflammatory factor-1beta (MIF-1beta) was 18% higher during the 12 h after RUN2. The overall cytokine profile suggests a slight reduction in systemic inflammation after RUN2.”

Quantifying delayed-onset muscle soreness: a comparison of unidimensional and multidimensional instrumentation

Authors: Cleather,D.J.; Guthrie,S.R.
Source: J.Sports Sci., 2007, 25, 8, 845-850

Conclusion: “So the findings may be of use to researchers and sports medicine professionals in their deliberations about which instrumentation to use in quantifying DOMS (Delayed Onset Muscle Soreness) and in distinguishing such pain from other, potentially more serious, musculoskeletal damage.”

Delayed onset muscle soreness does not alter O2 uptake kinetics during heavy-intensity cycling in humans

Authors: Schneider,D.A.; Berwick,J.P.; Sabapathy,S.; Minahan,C.L.
Source: Int.J.Sports Med., 2007, 28, 7, 550-556

Conclusion: “The change in blood lactate concentration from rest to end-exercise was significantly greater during exercise performed with DOMS (Delayed Onset Muscle Soreness). Eccentric exercise causing a moderate degree of DOMS (Delayed Onset Muscle Soreness) does not appear to impact upon the mechanisms mediating phase II or the slow component of O2 uptake kinetics.”