Q and A Time: How Much Protein Do You Need to Build Muscle?  Is Whey Protein the Best?  Is Glutamine Good?

I have been looking to get some stuff from Protein Factory per your recommendation for post workout and I was wondering if you could point me in the right direction. A lot of the stuff just confuses me past the regular whey, casein, isolate, concentrate, hydrolysate… So that would be a big help. And is it worth getting the glutamine and creatine dropped in with it?

Just curious, you know more about this one than i do so any info is appreciated!

Dustin Schlichting BS, ATC, CSCS, USAW

Answer:

Hi there Dustin!  Thanks for the comment, and yes, it can get VERY confusing and few people want to sit down and read tons o’ research on new types or protein.  Ok, I do, and I will put my hand down now.  Add to the confusion is very supplement company telling you that their gold micro filtered subfractioned protein from organic goats that live up in the Himalaya is the most anabolic thing you can buy for $90 a bottle since it will add 27 pounds of muscle in 6 weeks!  Ok, so we all know that is bogus!  There is ZERO literature to support it.

Back to the Future: Got Protein?

Protein is good.  Get some first before you go bananas trying to figure out which is best.  Cover the basics first.  Protein has been a key thing for strength trainers for decades.  Make sure you actually LIKE it as the best protein on the planet if it tastes like you are drinking week old cottage cheese gone bad will not do you any good.  You have to consume it first before it can have any effect.

Once you get that down, there are some great proteins that work well, taste good and won’t break your bank.

Got Protein, Now What?  Do I Need Whey Protein?

For post training my favorite is some type of whey protein.  Whey protein has tons of benefits for building muscle and my favorite is CFM Whey as it is high quality and tastes good. If you add enough carbs and sweetner, the Hydrolyzed 1400 is good and does not have any lactose either.  With athletes over the years, I’ve found it to be the most non allergenic of almost all proteins too (rice protein would be high on that list too).  On its own, Hyrdolyzed 1400 (and Hydrolyzed 520 is worse) tastes like crap and mixes just as bad. I get it with vanilla and sucrolose and it is fine, but most don’t care for it.  A hydrolyzed (or hyrdo) protein is one that is broken into very small pieces.  The smaller the number, the more hydrolysis, thus the smaller the pieces (measured in daltons).  The theory goes that the smaller the proteins, the faster it is absorbed and should spike protein synthesis (building muscle processes) higher.   Not sure I am completely sold that yet, but the protein seems to work well; esp if you have allergies.

A slightly cheaper whey protein is Isochill and tastes pretty good too. I have used the TriFX whey and it is good also with a slightly bitter taste if you get it plain with no flavor or sweetner.  Can’t say I notice any huge difference or have found any lit. to show a massive difference to all the different types of whey.   Buy a good high quality one (such as the ones listed above) and add about 20-40 grams around your training time and you are set.

Total Amount of Protein?

Total protein should be around 1 gram per pound of body weight.  Yes I know there is not one piece of literature that comes up with that EXACT amount, but it is pretty close and I like easy math.  Currently i weigh about 215 lbs, so I shoot for about 215 grams of protein per day.   If I get 200 or 240 grams I don’t worry about it.  6 meals a day with about 30-40 grams works great.  No, your kidneys will NOT explode and fly across the room with that amount if you are healthy.   If you want some more benefits of protein, see this newsletter from Dr. John Berardi here JB answers “Is there a limit to protein?”

I love the Precision Nutrition system and use it all the time!

Protein Factory (Click below to order)

Creatine?

You can add creatine to it directly, but I just add it on its own and I buy my creatine from Protein Factory also.  5 gm per day is about all you need. Don’t waste your money on other forms of creatine; just go wtih creatine monohydrate.  Hundreds of studies to show it is safe and effective.  I have personally been using creatine monohydrate since my graduate work at Michigan Tech in about 1995, back when I was in college the first go round – ha!  You can take some time off from it, which is a good idea with any supplement, but taking a small amount on most training days should be just fine.

Glutamine, Don’t Believe the Hype?

Glutamine is worthless. There, I said it.  Most of the studies done to show its “anti catabolic” properties were done initially on burn patients, who break down muscle at an incredibly rate; not a rate seen by even the most hard training athlete. I have not seen one study yet that shows glutamine to help your average gym rat.  If you find one in trained athletes, please post it below as I would seriously like to read it.  Heck, if it works I will report on it here.

Evil Doers of the Gut

You can make an argument that glutamine may help gut health, but I would go with a pro-biotic first then and maybe some special types of fiber (like FOS). Here is a tip, if you or your athletes you work with have been on an antibiotic in the past 1-2 years I would automatically have them use a probiotic.  While antibiotics have there place in medicine, they are like indescriminate killers and they wipe out tons of good and bad bacteria in your gut.  If your gut is left on its own, the bad guys can start to take over.   Kind of like the US in the Middle East.  We could wipe out a whole area, but it may be built up to more “evil doers”; so we would be better off seeding it with new buildings, security and returning it to the people that will take care of it and keep out the evil doers.

Protein Factory

Click on the link below to get all the great products from Protein Factory.  ff you use the links here I make a whole 4%, but every bit helps.  I lost count of how many supplement companies I have turned down offers from since I feel that clients hire me to provide the best to them, not sell them some supplement that I make 50% commission on and they pay for it.   I have not disrespect to anyone that works or sell other supplements, it is just a personal decision that I made only for myself.  If you find a company that you believe it and it helps your athletes, go for it.

Get Protein Here

This can be a confusing area, so drop me some comment love with your thoughts on this article and any questions you have.

Rock on
Mike N

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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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.”