I fixed it!

The link to the article below got hosed up some how. It worked for a bit and then it did not, but it is fixed now.

Rock on
Mike T Nelson

Dysfunctional Exercise Cues at XL Athlete (aka How to Cue Exercise Correctly)

Mike T Nelson on Super Human Radio: Visual Aspect of Performance

Just a heads up that I was recently on Super Human Radio again discussing how your vision affects your performance

Learn some simple exercises to improve your athletic performance on the field and in the gym

• Should you look in the mirror in the gym?
• Neurologic reflexes to maximize strength
• Should you lift without your glasses?
• Can you really "see" results from all this stuff?
  

Vision is MUCH more than just the ability to see clearly! Learn more below

Super Human Radio Show - # 295 - The Visual Aspect Of Performance

Special thanks to Carl as he does a great show and makes doing an interview a fun experience.

Be sure to check the Super Human Radio home page

If you missed the first episode I did on proprioception "2 way muscle talk" check it out below.

Z Health, Proprioception, Neuroplasticity all on Super Human Radio

Any comments, let me know!
Rock on
Mike T Nelson

Performance Research for April : Fat Loss and Exercise part 2

More studies than you can shake a stick at! As always, see my notes below each one.

Bring it!

Effects of Exercise Training Intensity on Nocturnal Growth Hormone Secretion in Obese Adults with the Metabolic Syndrome.

Irving BA, Weltman JY, Patrie JT, Davis CK, Brock DW, Swift D, Barrett EJ, Gaesser GA, Weltman A. Departments of Human Services, Internal Medicine, Division of Endocrinology and Metabolism, Pediatrics, Division of Cardiovascular Medicine, Health Evaluation Sciences, General Clinical Research Center, Center for the Study of Complementary and Alternative Therapies, University of Virginia, Charlottesville, Virginia 22908.


Context: Abdominal adiposity is associated with reduced spontaneous growth hormone (GH) secretion and increased incidence of the metabolic syndrome, type 2 diabetes, and cardiovascular disease. Exercise training increases GH secretion, induces abdominal visceral fat (AVF) loss and has been shown to improve the cardiometabolic risk factor profile. However, little is known about the effects of endurance training intensity on spontaneous GH release in obese individuals.

Objective: To examine the effects of sixteen weeks of endurance training on spontaneous 12-h overnight GH secretion in adults with the metabolic syndrome. Design and Setting: This randomized, controlled exercise intervention was conducted at the University of Virginia. Participants: Thirty-four adults with the metabolic syndrome (mean+/-SEM: Age: 49.1+/-1.8 years) participated.

Intervention: Subjects were randomized to one of three groups for 16 weeks: no-exercise training (Control), low-intensity exercise training (LIET), or high-intensity training (HIET).

Main Outcome Measure: Change in nocturnal integrated GH area under the curve (AUC). Results: Both exercise training conditions augmented within-group nocturnal GH AUC pre- to post-training [LIET approximately upward arrow49%, p<0.05 r =" -0.34," p="0.051," n="34)," r =" 0.02," p="0.920," n="34)." style="font-weight: bold;">

CONCLUSION: Sixteen weeks of supervised exercise training in adults with the metabolic syndrome increases spontaneous nocturnal growth hormone secretion independent of exercise training intensity.

My Notes: 1) Don't get Metabolic Syndrome---it screws up all sorts of things, and add GH to the list 2) ANY exercise will start to push you back towards "health" 3) GH was better, although it did not change the fat levels. This does not mean it has no effect, it just did not have an effect under these conditions.

Effects of Exercise and Low-Fat Diet on Adipose Tissue Inflammation and Metabolic Complications in Obese Mice.

Vieira VJ, Valentine RJ, Wilund KR, Antao N, Baynard T, Woods JA. UNIVERSITY OF ILLINOIS.

Adipose tissue inflammation causes metabolic disturbances including insulin resistance and hepatic steatosis. Exercise training (EX) may decrease adipose tissue inflammation thereby ameliorating such disturbances, even in the absence of fat loss. The purpose of this study was to 1) compare the effects of low-fat diet (LFD), EX, and their combination on inflammation, insulin resistance, and hepatic steatosis in high-fat diet-induced obese mice and, 2) determine the effect of intervention duration (i.e. 6 vs. 12 wks). C57BL/6 mice (n=109) fed a 45% fat diet (HFD) for 6 wks were randomly assigned to an EX (treadmill, 5d/wk; 6 or 12 wks; 40 min/d; 65-70%VO2max) or sedentary (SED) group. Mice remained on HFD or were placed on a 10% fat diet (LFD) for 6 or 12 wks.


Following interventions, fat pads were weighed and expressed relative to body weight; hepatic steatosis was assessed by total liver triglyceride; insulin resistance by HOMA-IR and Glucose AUC. Rt-PCR was used to determine adipose gene expression of MCP-1, F4/80, TNF-alpha, and leptin. By 12 wks, MCP-1, F4/80, and TNF-alpha mRNA were reduced by EX and LFD. Exercise (p=0.02), adiposity (p=0.03), and adipose F4/80 (p=0.02) predicted reductions in HOMA-IR (R(2)=.75; p<0.001); p="0.04)" style="font-weight: bold;">

CONCLUSION: There are unique metabolic consequences of a sedentary lifestyle and fat high diet that are most evident long-term, highlighting the importance of both Exercise training and low-fat diet in preventing obesity-related metabolic disturbances.

My notes: Ok, this one is starting to piss me off. Why was it the high fat? The TYPE of fat will have a radical effect on the results and the amount of carbohydrates in the diet may also alter the way fats are used; as Jeff Volek's lab have shown that saturated fats (which again are not all equal) in a LOW carbohydrate environment don't seem to alter lipid levels.

Enough with the rat/mice studies already! Why was this done in mice? I know they are easier to study than those pesky humans (trust me, I've done human studies and anyone who has can attest to that the "pain in the butt factor" is MUCH higher), but we need more HUMAN data on this type of stuff. The good part is that exercise once again helps! Get your hand out of the cheese doodles bag and off the couch!

Influence of sex on total and regional fat loss in overweight and obese men and women.

Kuk JL, Ross R. 1School of Kinesiology and Health Science, Faculty of Health Science, York University, Toronto, Ontario, Canada.


Objective:To determine the influence of sex on the association between reductions in body weight (BW) and waist circumference (WC) with reductions in total (TAT), subcutaneous (SAT) and visceral adipose tissue (VAT) in response to lifestyle-based interventions.Design: Changes in TAT, SAT and VAT were assessed using magnetic resonance imaging in 81 men and 72 women who had participated in various diet and/or exercise interventions at Queen's University, Ontario, Canada.

Results:Reductions in BW and WC were significantly (P<0.001)>0.05). Reductions in BW and WC were both independent predictors of VAT loss.

CONCLUSION: These observations suggest that for a given reduction in body weight or waist circumference, men lose more visceral adipose tissue and less subcutaneous than women; however, the total loss observed for a given reduction in body weight or waist circumference in men and women is not different.

My Notes: I know you were hoping that this study was about how much sex you have and weight loss, so sorry to disappoint you. It does show that even the AMOUNT of weight lost, men and women can loose it from different areas. Nothing earth shattering there.


Moderate Exercise Attenuates the Loss of Skeletal Muscle Mass That Occurs With Intentional Caloric Restriction-Induced Weight Loss in Older, Overweight to Obese Adults.

Chomentowski P, Dubé JJ, Amati F, Stefanovic-Racic M, Zhu S, Toledo FG, Goodpaster BH. Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh School of Medicine, N810 Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh, PA 15213. bgood@pitt.edu.


BACKGROUND: Aging is associated with a loss of muscle mass and increased body fat. The effects of diet-induced weight loss on muscle mass in older adults are not clear. Purpose This study examined the effects of diet-induced weight loss, alone and in combination with moderate aerobic exercise, on skeletal muscle mass in older adults. METHODS: Twenty-nine overweight to obese (body mass index = 31.8 +/- 3.3 kg/m(2)) older (67.2 +/- 4.2 years) men (n = 13) and women (n = 16) completed a 4-month intervention consisting of diet-induced weight loss alone (WL; n = 11) or with exercise (WL/EX; n = 18). The WL intervention consisted of a low-fat, 500-1,000 kcal/d caloric restriction. The WL/EX intervention included the WL intervention with the addition of aerobic exercise, moderate-intensity walking, three to five times per week for 35-45 minutes per session. Whole-body dual-energy x-ray absorptiometry, thigh computed tomography (CT), and percutaneous muscle biopsy were performed to assess changes in skeletal muscle mass at the whole-body, regional, and cellular level, respectively.


RESULTS: Mixed analysis of variance demonstrated that both groups had similar decreases in bodyweight (WL, -9.2% +/- 1.0%; WL/EX, -9.1% +/- 1.0%) and whole-body fat mass (WL, -16.5%, WL/EX, -20.7%). However, whole-body fat-free mass decreased significantly (p < .05) in WL (-4.3% +/- 1.2%) but not in WL/EX (-1.1% +/- 1.0%). Thigh muscle cross-sectional area by CT decreased in both groups (WL, -5.2% +/- 1.1%; WL/EX, -3.0% +/- 1.0%) and was not statistically different between groups. Type I muscle fiber area decreased in WL (-19.2% +/- 7.9%, p = .01) but remained unchanged in WL/EX (3.4% +/- 7.5%). Similar patterns were observed in type II fibers (WL, -16.6% +/- 4.0%; WL/EX, -0.2% +/- 6.5%).


CONCLUSION: Diet-induced weight loss significantly decreased muscle mass in older adults. However, the addition of moderate aerobic exercise to intentional weight loss attenuated the loss of muscle mass.


My Notes: When you are on a "diet" to drop some fat, don't just cut your calories and hop on the treadmill till you puke. You need to do something to tell your body to keep the muscle you have, as that is what keeps your metabolic rate in tact long term. This study provides data showing that even moderate aerobic exercise (think "cardio") was better than nothing. Although it was not studied here, I would bet that strength training would be even better at keeping muscle in this study (and there are data to support that notion).


Effect of dietary adherence with or without exercise on weight loss: a mechanistic approach to a global problem.

Del Corral P, Chandler-Laney PC, Casazza K, Gower BA, Hunter GR. Department of Nutrition Science, Clinical Nutrition Research Unit; Department of Human Studies, University of Alabama at Birmingham.


Context: Weight loss using low calorie diets produce variable results, presumably due to a wide range of energy deficits and low dietary adherence. Objective: To quantify the relationship between dietary adherence, weight loss and severity of caloric restriction. Design and Setting: Participants were randomized to diet-only, diet-endurance-training, or diet-resistance-training until (60-539 days) BMI <25 n="141)" r=" -" r=" -0.349" r="0.364," r=" -0.387," style="font-weight: bold;">

CONCLUSION: Dietary adherence is strongly associated with rates of weight loss and adversely affected by the severity of caloric restriction. Weight loss programs should consider moderate caloric restriction relative to estimates of energy requirements, rather than generic low calorie diets.

My Notes: Um, yeah. The best "diet" (hate that word) in the world makes no difference if you do NOT follow it!

Rock on
Mike T Nelson

Dysfunctional Exercise Cues at XL Athlete (aka How to Cue Exercise Correctly)

I recently wrote an article about applying neurology to exercise cues. The full article is at

XL Athlete Dysfunctional Exercise Cues By Mike T Nelson

Special thanks to Cal Dietz for publishing in and editing my typos by Jonathon Janz, MS, CSCS, USAW

Below is the start of the article

If most agree that training full body
exercises (dead lifts, bench press, KB Swing,
etc) is better than isolating body parts for
the purpose of training athletes, why do
most coaches still cue athletes via body
parts (squeeze those lats, etc)?
For those that don't want to read any further,
here is the crazy thought:
Cue them by the movement you want them to
do and/or do an exercise to allow better
execution.
Ok, you can stop reading now. If you want
more details, down the rabbit hole we go!

Head over to XL Athlete and read the full article (click below) and put any discussion points/ experience/ comments in general here on my blog and I will reply to them.

XL Athlete Dysfunctional Exercise Cues By Mike T Nelson

There are tons and tons of great things on the XL Athlete site, so be sure to check out their main page below

XL Athlete
Rock on
Mike T Nelson

Mobility vs Stability, Primitive Patterns, Z Health and More!

Question on Mobility, Stability, Primitive Patterns, Z Health and more!

Came across your blog and found it interesting as I have also taken some Z courses. I love it, but think that there doesn't have to be a distinction between the nervous system and biomechanical approaches.

I think both are necessary and we all need a balance between mobility and stability. Not sure if you're familiar with Gray Cook, but he wrote an interesting article on this topic a while back on T-nation.

I recently purchased his Primitive Movements DVD and he discusses movement patterns along with some stability work, including some Power Plate exercises. In one of his newsletters, Eric (Dr. Cobb of Z Health) stated his doubt about the use of anything electric, but I think he is wrong on this one.

I've been doing Z Health since 2003 and seen great results with it. At the same time, it hasn't restored proper function by itself and I believe most people will need some form of manual therapy and stability work for optimal results.

Vibration platforms are a great tool for addressing reflex stabilization. Just a tool, but effective none the less.

Look forward to reading your articles. Always looking to learn from someone new.

Thanks
Brian Morgan

Answer
Thanks for the note Brian! One of the things I love about this blog is the ability to interact with some really smart people.

I don't really like the term "stability" I think a better term is "coordination" (stole that from Frankie Faires). Much of this I covered in this past post

Jammed Joints and Muscular Weakness--Stability and Mobility

Also see Aaron's Blog post here

Not a Stability Issue

I do believe you need mobility before stability, as I stated in my lumbar mobility post quite some time ago (I am sure I am not the first to say that). Kids has tons of mobility and then learn coordination (stability).

Lumbar Mobility in Italy

Lumbar movement and Z Health comment

Cool that you have been doing Z-Health for a long time. Have you worked with a Z Health trainer? If so, what level? Many times after a period of time, you will need your eyes/vestibular systems checked as they can be impeding any progress. Don't just take my word for it, see this comment from Dr. Jim below

Testimonial for Z Health and New Dragon Door Workshop: Z-Health

I am actually totally for hands on work, as long as it is NOT painful---see my ART / Z Health post below (I think I am going for a record number of links in a post)

Active Release Technique (ART), Z Health, Hands on Work (Massage, Guided Exercise)

For research, I think vibe platforms are cool (although they feel really weird), but if I was going to build a gym from scratch, at 10K a piece I would put them on the bottom of the list. I do think they can get lots of mechanoreceptor stim going and many times that will even get people out of pain.

I spent about an hour talking to the nice people at the power plate stand at ACSM last year. Very cool people and I expect to see more use of them for pain reduction coming soon. How long that effect will hold once you step off is debatable. I think some cool mobility work (when done with precision) can get you a similar effect and will last (hold) longer due to the enhanced motor learning--you are ACTIVELY moving your limbs so that brain on top of your head has to work harder than if you just lay their like a dead fish while someone pokes/prods at ya.

Thoughts/ comments from others? Post them in the comments!

Rock on and special thanks to Brian for letting me post this here
Mike T Nelson

Movement and Brain Health: Running exercise-induced up-regulation of hippocampal brain-derived neurotrophic factor

Running exercise-induced up-regulation of hippocampal brain-derived neurotrophic factor is CREB-dependent.

Chen MJ, Russo-Neustadt AA. Department of Biological Sciences, California State University, 5151 State University Dr., Los Angeles, California.

The past decade has witnessed burgeoning evidence that antidepressant medications and physical exercise increase the expression of hippocampal brain-derived neurotrophic factor (BDNF). This phenomenon has gained widespread appeal, because BDNF is one of the first macromolecules observed to play a central role not only in the treatment of mood disorders, but also in neuronal survival-, growth-, and plasticity-related signaling cascades. Thus, it has become critical to understand how BDNF synthesis is regulated. Much evidence exists that changes in BDNF expression result from the activation/phosphorylation of the transcription factor, cAMP-response-element binding protein (CREB) following the administration of antidepressant medications. Utilizing a mouse model genetically engineered with an inducible CREB repressor, our current study provides evidence that increases in BDNF expression and cellular survival signaling resulting from physical exercise are also dependent upon activation of this central transcription factor.


The transcription and expression of hippocampal BDNF, as well as the activation of Akt, a key survival signaling molecule, were measured following acute exercise, and also following short-term treatment with the norepinephrine reuptake inhibitor, reboxetine. We found that both interventions led to a marked increase in hippocampal BDNF mRNA, BDNF protein, and Akt phosphorylation (as well as CREB phosphorylation) in wild-type mice. As expected, activation of the CREB repressor in mutant mice sharply decreased CREB phosphorylation. In addition, all measures noted above remained at baseline levels when mutant mice exercised or received reboxetine. Increases in BDNF and phospho-Akt were also prevented when mutant mice received a combination of exercise and antidepressant treatment.


CONCLUSION: The results are discussed in the context of what is currently known about brain-derived neurotrophic factor signaling.

My Notes: While this is a mechanistic study, once again science is starting to unwind the mysteries of brain function and movement. It is pretty clear that movement (running in this case, but exercise in general) affects brain function too! Another positive for mobility work and exercise in general.

Related posts

Movement and Brain Deterioration? New Study

More Brain Science and BAHG

Stroke of Insight

Neuroscience Research Updates for October

Neuroplasticity and Human Athletic Performance

Rock on!
Mike T Nelson

Performance Research for April : Fat Loss and Exercise part 1

Two-fer and Twitter!
It is a 2 for 1 Friday! I was up at 4:20am today to head for the lab for some more testing in the Energy Drink study, so I am feeling a bit brain dead between Exercise Physiology labs while trying to stay away from the coffee as long as I can; so I figured it would be a great time to kick out some new studies for ya. Yes, I do read studies to relax. Scary I know.

Twitter
If you are interested in what I am doing, you can follow me at Twitter. I will have random updates and even new studies I am reading weeks before they show up here (and some never make it that far) and other tips. Feel free to hit me up there with anything you want to see also!

Click the link below and then hit the "follow" button below my mug shot.

http://twitter.com/MikeTNelson

On to the studies on Fat Loss and Exercise

Influences of a dietary supplement in combination with an exercise and diet regimen on adipocytokines and adiposity in women who are overweight.

Fragala MS, Kraemer WJ, Volek JS, Maresh CM, Puglisi MJ, Vingren JL, Ho JY, Hatfield DL, Spiering BA, Forsythe CE, Thomas GA, Quann EE, Anderson JM, Hesslink RL Jr. Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT, 06269, USA.


The influence of a proprietary blend of modified cellulose and cetylated fatty acids (Trisynextrade mark, Imagenetix, Inc., San Diego, CA 92127, USA) on adipocytokine and regional body composition responses to a weight loss program was examined.

Twenty-two women (Supplement group (S) (n = 11): age = 36.8 +/- 7.2 years; weight = 87.1 +/- 6.2 kg; % body fat = 43.4 +/- 4.1; Placebo group (P) (n = 11): age = 38.3 +/- 6.8 years; weight = 86.9 +/- 4.7 kg; % body fat = 44.3 +/- 2.0) completed an 8-week placebo-controlled, double-blind study consisting of a caloric restricted diet and cardiovascular exercise.

Body composition and serum insulin, leptin, and adiponectin were assessed at pre-, mid-, and post-intervention.

From pre- to post-intervention, significant decreases (P < class="blsp-spelling-error" id="SPELLING_ERROR_31">leptin (S: 28.3 +/- 3.5-16.2 +/- 2.6 ng ml(-1); P: 29.4 +/- 3.2-19.9 +/- 1.1 ng ml(-1)) (P < class="blsp-spelling-error" id="SPELLING_ERROR_34">mU l(-1); P: 7.7 +/- 0.9-5.1 +/- 0.3 mU l(-1)).

Serum adiponectin increased (P < class="blsp-spelling-error" id="SPELLING_ERROR_37">microg ml(-1): 12.6 +/- 2.0-21.8 +/- 3.1 microg ml(-1)) (P < style="font-weight: bold;">

CONCLUSION: Supplementation with a proprietary blend of modified cellulose and cetylated fatty acids during an 8-week weight loss program exhibited favorable effects on adipocytokines and regional body composition.

My Notes: Interesting idea for a study, but while the results were statistically significant, dropping 1% of body fat over 8 weeks is not much. Even if you were 400 lbs that would only be 4 lbs. Again, statistically significant does not mean REAL world significant. Perhaps if you are a competitive bodybuilder in the single digits for body fat and you are looking to drop a few more pounds, than 1 lbs a week is great. These subjects were far from that group though.

Adiponectin is a "good guy" and we actually want higher levels of it, was shown here.

Speaking of it.......

Adipocytokine and ghrelin levels in relation to bone mineral density in physically active older women: longitudinal associations.

Jürimäe J, Kums T, Jürimäe T. Institute of Sport Pedagogy and Coaching Sciences Institute of Exercise Physiology and Physiotherapy, Centre of Behavioural and Health Sciences, University of Tartu, Tartu, Estonia. jaakj@ut.ee


PURPOSE: We investigated the relationship between the decrease in bone mineral mass (BMC) and bone mineral density (BMD) values with baseline adipocytokine and ghrelin concentrations in physically active postmenopausal women.

METHODS: Leptin, adiponectin, ghrelin, BMC, BMD and different body composition values were measured in 35 women (age: 69.7+/-6.0 years) before and after a 12-month prospective study period.

RESULTS: Significant (P<0.05) class="blsp-spelling-error" id="SPELLING_ERROR_58">FFM) (by 2.56%) and BMC (by 1.63%) and increases in adiponectin (by 14.8%) were seen in older females as a result of the study period. The independent variables that were associated with decreases in total BMC were baseline fat mass (FM) and adiponectin explaining 30.6% (R(2)x100) of the total variance. In another model, baseline FFM and leptin were the independent variables that explained 20.6% (P<0.05) class="blsp-spelling-error" id="SPELLING_ERROR_65">BMD value. The variables that were associated with decreases in femoral neck BMD were FM and leptin (R(2)=0.102; P<0.05), class="blsp-spelling-error" id="SPELLING_ERROR_68">adiponectin in the model with decreases in lumbar spine BMD as the dependent variable, and accounted for 13.1% (P<0.05) class="blsp-spelling-error" id="SPELLING_ERROR_70">BMD variance.

CONCLUSIONS: Initial adiponectin concentration together with specific body composition characteristics predicted loss in bone mineral mass and lumbar spine bone mineral density values, while initial leptin concentration together with specific body composition parameters determined the loss in total and femoral neck bone mineral density values in physically active older women.

My notes: Keep in mind that this is an ASSOCIATION study which means that "Hey, we saw this and this!" It does NOT mean that "This CAUSED that"

A classic example is if you observe a large fire and see tons of fire trucks there. You could INcorrectly assume that the huge number of fire trucks there CAUSED the fire (which would be untrue).

Having said all that, I am interested as we start to uncover how the body is all interconnected. It makes sense that if we have more muscle and muscle pulls on bone, great muscle mass means greater stress on the bones (from the shear weight and more likely the higher forces exerted on the bone).

Beyond that, there is some early data showing a correlation between bone and fat loss and this study provides a little more data in the area as it was looking at hormone level.

Supervised exercise versus non-supervised exercise for reducing weight in obese adults.

Nicolaï SP, Kruidenier LM, Leffers P, Hardeman R, Hidding A, Teijink JA. Department of Vascular Surgery, Atrium medical centre Parkstad Heerlen, The Netherlands j.a.kragten@wcnnet.nl.


AIM: The prevalence of obesity is rising. Because obesity is positively associated with many health related risks and negatively associated with life expectancy this is a threat to public health. Physical exercise is a well known method to lose fat mass. Due to shame of their appearance, bad general condition and social isolation, starting and continuing physical exercise tends to be problematic for obese adults. A supervised training program could be useful to overcome such negative factors. In this study we hypothesized that offering a supervised exercise program for obese adults would lead to greater benefits in body fat and total body mass reduction than a non-specific oral advice to increase their physical activity.


METHODS: Thirty-four participants were randomised to a supervised exercise program group (N.=17) and a control group (N.=17). Fifteen candidates in the intervention group and 12 in the control group appeared for baseline measurements and bought an all inclusive sports pass to a health club for Euro 10, per month. The control group just received the oral advice to increase their physical activity at their convenience. The supervised exercise group received biweekly exercise sessions of 2 hours with an estimated energy expenditure of 2 500 kJ per hour. Both groups received no dietary advice. RESULTS: After 4 months the overall decrease in body mass in the intervention group was 8.0 kg (SD 6.2) and the decrease in body fat was 6.2 kg (SD 4.5). The control group lost 2.8 kg overall (SD 4.2) and the decrease in body fat was 1.7 kg (SD 3.1). Correction for differences between groups in gender and age by multiple linear regression analysis showed significantly greater loss of total body mass (P = 0.001) and fat mass (P =0.002) in the intervention group compared with the control group.


CONCLUSIONS: Stimulation of physical activity alone seems to result in a slight short term body mass and fat mass reduction in obese adults who are eager to lose weight. Supervised exercise under supervision of a qualified fitness instructor leads to a larger decrease.

My Notes: Part of me is sad that we even have to do studies like this, but they are good to have.

Once again it goes to show you that if you want RESULTS get a PROFESSIONAL to help you!

If you get in trouble, are you going to try to represent yourself in court--I sure hope not! Do you try to diagnose yourself when you have a serious health issue--again, I hope not. So why do you think you can design and even further FOLLOW your own nutrition and exercise plan? If you want serious results, you need to get professional help.

Rock on!
Mike T Nelson

Performance Research for April : Ergogenics and Exercise: Caffeine

Greetings! Just a quick update on a new study below.\

I will be having dinner with my good friend "The Movement Doctor" tonight, so I am super excited to learn lots of new stuff. Check out her website below

ESSENTIAL STRENGTH

on to the study

EFFECT OF PHYSIOLOGICAL LEVELS OF CAFFEINE ON Ca2+ HANDLING AND FATIGUE DEVELOPMENT IN XENOPUS ISOLATED SINGLE MYOFIBERS.

Rosser JI, Walsh B, Hogan MC. University of California - San Diego.


The purpose of the present study was to determine whether exposure to exogenous physiological concentrations of caffeine influence contractility, Ca(2+) handling, and fatigue development in isolated single Xenopus laevis skeletal muscle fibers. After isolation, two identical contractile periods (separated by 60 min rest) were conducted in each single myofiber (n=8) at 20 degrees C. During the first contractile period, four fibers were perfused with a non-caffeinated Ringer's solution, while the other four fibers were perfused with a caffeinated (70 microM) Ringer's solution.


The order was reversed for the second contractile period. The single myofibers were stimulated during each contractile period at increasing frequencies (0.16, 0.20, 0.25, 0.33, 0.50, and 1.0 tetanic contractions/second) with each stimulation frequency lasting 2 minutes until fatigue ensued, defined in this study as a fall in tension development to 66% of maximum. Tension development and free cytosolic [Ca(2+)] (fura-2 fluorescence spectroscopy) were simultaneously measured. There was no significant difference in the peak force generation, time to fatigue, cytosolic Ca(2+) levels, or relaxation times between the non-caffeinated and caffeinated trials.


CONCLUSION: These results demonstrate that physiological levels of caffeine have no significant effect on Xenopus single myofiber contractility, Ca(2+) handling, and fatigue development and suggest that that any ergogenic effects of physiological levels of caffeine on muscle performance during contractions of moderate-to-high intensity are likely related to factors extraneous to the muscle fiber.

My Notes: While readers of this blog will be quick to point out that this was a highly isolated study done in a dish, the cool part is that you can isolate some interesting things. Having said that, this is a very crude study and I am scratching my head at what was novel here? How is this new in 2009?

For those that are wondering, it is a type of frog; although classically many of the early experiments on the neuromuscular junction (NMJ) were done in a similar set up. Heck, I took a whole class where we did this and the crazy set up to the experiment may take you 2-3 hours BEFORE you measure anything.

The newer researcher shows that the main effect of caffeine is central nervous system related (CNS). I am still amazed at how much we don't know about the mechanisms of caffeine, even though it has been studied for quite some time.

Bustin' Broscience: Leucine (BCAAs) stimulate insulin

Bustin' Broscience: Leucine and insulin
I am going to start some short research articles here called "Bustin Broscience" Most of these will be short using newer research and while they will be far from a complete literature review I want to promote some good discussion and attempt to whittle away at some of the misinformation out there.

While I find anecdotal information interesting, it can be affected by so many things that on the evidence chain I would have it at the bottom. There is a reason we have placebo controlled trials/experiments and blinded subjects and researchers.

Thanks to Joel for the image on the right. Can anyone alter it to put a big red line through it?

If you are looking for much more depth, I would highly recommend Alan Aragon's Research Review. It is only 10 clams a month and I make zero money from recommending it, but he does his homework on all of the topics he covers each month.

Click below for more information

Alan Aragon's Research Review

Bustin' Broscience
What the heck is broscience? Here is the definition from the Urban Dictionary. Not sure where the term started and Alan Aragon was the first I read who had used it.

Broscience is the predominant brand of reasoning in bodybuilding circles where the anecdotal reports of jacked dudes are considered more credible than scientific research.

Broscience in action: "Bro, you gotta slam 40-60 grams of waxy maize plus 20 grams of BCAA within 7 seconds of finishing your last set of squat rack curls. Otherwise, you'll go straight catabolic."

Broscience says "Leucine stimulates insulin"

Is this one about to busted?

Leucine
I am predicting some interesting data on the use of the amino acid leucine coming soon. We know that acutely it stimulates the mTOR receptor which is one of the keys to protein synthesis (build more muscle). Long term data, however, is not as plentiful (although I hear there are several cool studies being conducted now.)

Insulin
While a whole review of the actions of insulin would be volumes, the very very short take away is that insulin is one of the key anabolic hormones in the body. I am using the strict definition of anabolic from the term anaolism.

a·nab·o·lism (-nb-lzm)
n.
The phase of metabolism in which simple substances are synthesized into the complex materials of living tissue.

It is just the fancy term for putting stuff together in the body. Most bodybuilders use this term to exclusively talk about taking amino acids and stuffing them into muscle proteins (which I am all for of course since that will make larger muscles), but it can also apply to taking free fatty acids (FFAs) from the blood and putting them in fat (adipose) tissue.

So insulin is the main anabolic hormone and the basic theory is that more insulin will increase the process of stuffing more fats into adipose tissue.

Do you get get fat by using leucine?

Here is an interesting study where they added leucine to the drinking water of our fury little friends. Let's see if there is an effects on fatness (obesity) and insulin?

Leucine Supplementation of Drinking Water Does Not Alter Susceptibility to Diet-Induced Obesity in Mice,

They stated, "Branched-chain amino acids (BCAA), Leu, and the signaling pathways they regulate have been reported to either improve or worsen adiposity and insulin sensitivity."

They added leucine or BCAAs to the rat's water and fed them lots of food and measured metabolic rate and insulin tolerance.

They found that, "Compared with control, supplementation did not affect body weight, food intake, oxygen consumption, locomotor activity, body composition, insulin tolerance, or total cholesterol."

While this study is limited and done in rats, that is strike one

What else?

Here is another study

Leucine, when ingested with glucose, synergistically stimulates insulin secretion and lowers blood glucose

The goal of this study was to determine whether leucine stimulates insulin and/or glucagon secretion and whether, when it is ingested with glucose, it modifies the glucose, insulin, or glucagon response.

They used 13 human subjects, which is good as we are not rats; but those little fury guys are much easier to do highly controlled studies on though. The arrived fasted and got some leucine and 25 g of glucose wile they measured serum leucine, glucose, insulin, glucagon, and α-amino nitrogen concentrations over a 2.5-hour period after ingestion of the test meal. The amount of leucine provided was equivalent to that present in a high-protein meal, that is, that approximately present in a 350-g steak.

Leucine concentrations
Leucine did appear in the blood and acutally REDUCED the 2.5-hour glucose area response by 50%. Leucine, when ingested ALONE, increased the serum insulin area response modestly but glucagon (the antangonist to insulin) also changed.

Think of glucagon as one of the "anti-insulin" hormones and leucine actually increased glucagon!

Shut up and get to the point
2 fold on this study

1) Leucine at a dose equivalent to that present in a high-protein meal, had little effect on serum glucose or insulin concentrations

2) When leucine was ingested with glucose, it attenuated the serum glucose response and strongly stimulated additional insulin secretion.

In English please
This shows there is some data that leucine when combined glucose, may increase insulin levels but other hormonal levels change too.

Personal note
If you have ever looked at insulin data (I am currently doing this for a study), it varies much more than you would imagine. Your body is CONSTANTLY adjusting insulin and the "anti-insulin" hormones by the second.

History lesson
As far as I could tell, this below is the first one I can find discussiong leucine and insulin stimulation, published in AJP in 1983.

L-leucine methyl ester stimulates insulin secretion and islet glutamate dehydrogenase

The huge downside of this one is that it used perifusion of collagenase-isolated mouse pancreatic islets. In other words, isolated cells in fluid. While ths is a a great START, many many times these data do not translate to whole human (in-vivo) studies.

The final word
I give this one a (drum roll please................)
Plausible

It may happen, but I am not convinced that adding a few grams of leucine or BCAAs to your nutrition is going to dramatically affect insulin levels. Again, this is a supplement, so get your nutrition in line with real food first before you decide to add any fancy supplements.

Comments on this issue of Bustin' Broscience.
Let me know if you this is useful and any feedback you have!
Rock on
Mike T Nelson


REFERENCES

Leucine Supplementation of Drinking Water Does Not Alter Susceptibility to Diet-Induced Obesity in Mice,

Ali Nairizi, Pengxiang She, Thomas C. Vary and Christopher J. Lynch., Penn State Hershey Institute for Diabetes and Obesity and the Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, PA 17033

Branched-chain amino acids (BCAA), Leu, and the signaling pathways they regulate have been reported to either improve or worsen adiposity and insulin sensitivity. Therefore, it is unclear whether dietary supplementation of Leu would be beneficial. To help address this question, we examined the effect of adding Leu (150 mmol/L; Expt. 1 and Expt. 2) or BCAA (109 mmol/L of each; Expt. 3) to the drinking water on diet-induced obesity (induced with a 60-kJ% fat diet) in singly housed C57BL6/J male mice for at least 14 wk. Liquid and solid food intakes were evaluated weekly along with body weight. During the last few weeks, several blood samples were taken at different times for plasma glucose, total cholesterol, or Leu measurements.

Metabolic rate by indirect calorimetry, locomotor activity by light beam breaking, body composition by H1-NMR, and insulin tolerance were also determined. Compared with control, supplementation did not affect body weight, food intake, oxygen consumption, locomotor activity, body composition, insulin tolerance, or total cholesterol. In fed mice, this method of Leu supplementation only increased plasma Leu by 76% when the supplemented group was compared with control. On the other hand, after overnight food deprivation, the plasma Leu did not differ between these 2 groups, even though the mice in the supplemented group had continuous access to Leu-containing water during the solid food deprivation.


CONCLUSION: Taken together, the results do not provide evidence that either Leu or Branched-chain amino acids supplementation of drinking water ameliorates diet-induced obesity in mice, although it may improve glycemia.

Leucine, when ingested with glucose, synergistically stimulates insulin secretion and lowers blood glucose

Auteur(s) / Author(s)
KALOGEROPOULOU Dionysia (1 2) ; LAFAVE Laura ; SCHWEIM Kelly ; GANNON Mary C. (1 2 3) ; NUTTALL Frank Q. (1 2) ;

(1) Endocrine, Metabolism and Nutrition Section, VA Medical Center, Minneapolis, MN 55417, ETATS-UNIS
(2) Department of Medicine, University of Minnesota, Minneapolis, MN 55455, ETATS-UNIS
(3) Department of Food Science & Nutrition, University of Minnesota, St. Paul, MN 55108, ETATS-UNIS
Résumé / Abstract
Our laboratory is interested in the metabolic effects of ingested proteins. As part of this research, we currently are investigating the metabolic effects of ingested individual amino acids. The objective of the current study was to determine whether leucine stimulates insulin and/or glucagon secretion and whether, when it is ingested with glucose, it modifies the glucose, insulin, or glucagon response. Thirteen healthy subjects (6 men and 7 women) were studied on 4 different occasions. Subjects were admitted to the special diagnostic and treatment unit after a 12-hour fast. They received test meals at 8:00 AM. On the first occasion, they received water only. Thereafter, they received 25 g glucose or 1 mmol/kg lean body mass leucine or 1 mmol/kg lean body mass leucine plus 25 g glucose in random order. Serum leucine, glucose, insulin, glucagon, and α-amino nitrogen concentrations were measured at various times during a 2.5-hour period after ingestion of the test meal. The amount of leucine provided was equivalent to that present in a high-protein meal, that is, that approximately present in a 350-g steak. After leucine ingestion, the leucine concentration increased 7-fold; and the α-amino nitrogen concentration increased by 16%. Ingested leucine did not affect the serum glucose concentration. When leucine was ingested with glucose, it reduced the 2.5-hour glucose area response by 50%. Leucine, when ingested alone, increased the serum insulin area response modestly. However, it increased the insulin area response to glucose by an additional 66%; that is, it almost doubled the response. Ingested leucine stimulated an increase in glucagon. Ingested glucose decreased it. When ingested together, the net effect was essentially no change in glucagon area. In summary, leucine at a dose equivalent to that present in a high-protein meal, had little effect on serum glucose or insulin concentrations but did increase the glucagon concentration. When leucine was ingested with glucose, it attenuated the serum glucose response and strongly stimulated additional insulin secretion. Leucine also attenuated the decrease in glucagon expected when glucose alone is ingested. The data suggest that a rise in glucose concentration is necessary for leucine to stimulate significant insulin secretion. This in turn reduces the glucose response to ingested glucose.


L-leucine methyl ester stimulates insulin secretion and islet glutamate dehydrogenase

AJP - Endocrinology and Metabolism, Vol 245, Issue 4 338-E346, Copyright © 1983 by American Physiological Society

P. Knudsen, H. Kofod, A. Lernmark and C. J. Hedeskov

Column perifusion of collagenase-isolated mouse pancreatic islets was used to study the dynamics of insulin release in experiments lasting for several hours. The methyl esters of L-leucine and L-arginine were synthesized. Whereas L-arginine methyl ester (L-arginine OMe) had no effect, L-leucine OMe stimulated the release of insulin. The effect of L-leucine OMe was maximal at 5 mmol/liter. Whereas the Km for glucose-stimulated insulin release was unaffected by 1 mmol/liter L-leucine OMe, the maximal release of D-glucose was increased by the amino acid derivative that appeared more effective than L-leucine. L-Leucine OMe was also a potent stimulus of insulin release from the perfused mouse pancreas. In the presence of 10 mmol/liter L-glutamine, 1 mmol/liter L-leucine OMe induced a 50- to 75-fold increase in insulin release. A similar stimulatory effect was also observed in column-perifused RIN 5F cells, a cloned rat islet tumor cell line. A twofold increase in islet glutamate dehydrogenase activity was induced by 5 mmol/liter L-leucine OMe, a larger effect than that of L-leucine (P less than 0.02), whereas L-arginine OMe had a small inhibitory effect. We conclude that L-leucine OMe is a potent stimulus of insulin secretion and that its effect on the beta-cells may be exerted by activating islet glutamate dehydrogenase.

Performance Research for April : Central Fatigue during Exercise part 2

More info for yas on why do you actually stop a heavy training set, high intensity exercise etc.

I have some comments to get to yet on the treadmill post, so hang in there with me. Excellent comments by all and much appreciated!

I am excited that I have 7 exercise tests for the Energy Drink study in the lab this week, which brings me closer to wrapping up the data collection portion, although it equals more cat naps in my car and more coffee.

Congrats to all the new RKCs that passed this past weekend! Sorry I was not able to stop down there, but excellent work! If anyone is around here for the next one and is interested in a Z Health session to optimize your performance, drop me a line---first come first serve.

On to the studies....

Voluntary activation and cortical activity during a sustained maximal contraction: an fMRI study.

Post M, Steens A, Renken R, Maurits NM, Zijdewind I. Department of Medical Physiology, University Medical Center Groningen, University of Groningen, The Netherlands. Marijn.post@med.umcg.nl


Motor fatigue is an exercise-induced reduction in the force-generating capacity. The underlying mechanisms can be separated into factors residing in the periphery or in the central nervous system. We designed an experiment in which we investigated central processes underlying motor fatigue by means of magnetic resonance imaging in combination with the twitch interpolation technique. Subjects performed a sustained maximal abduction (2 min) with the right index finger. Brain activation was recorded with an MR scanner, together with index finger abduction force, EMG of several hand muscles and interpolated twitches.


Mean activity per volume was calculated for the primary motor cortex and the secondary motor areas (supplementary motor, premotor, and cingulate areas) as well as mean force and mean rectified EMG amplitude. Results showed a progressive decline in maximal index finger abduction force and EMG of the target muscles combined with an increase in brain activity in the contralateral primary motor cortex and secondary motor areas. Analysis of the twitches superimposed on the sustained contraction revealed that during the contraction the voluntary drive decreased significantly.


CONCLUSION: In conclusion, our data showed that despite an increase in brain activity the voluntary activation decreased. This suggests that, although the central nervous system increased its input to the relevant motor areas, this increase was insufficient to overcome fatigue-related changes in the voluntary drive.

My Notes: Hmmm, perhaps we are seeing a blend of peripheral and central fatigue out in the really real world?

Estimation of critical torque using intermittent isometric maximal voluntary contractions of the quadriceps in humans.

Burnley M. Department of Sport and Exercise Science, Aberystwyth University, Ceredigion, United Kingdom. mhb@aber.ac.uk


To determine whether the asymptote of the torque-duration relationship (critical torque) could be estimated from the torque measured at the end of a series of maximal voluntary contractions (MVCs) of the quadriceps, eight healthy men performed eight laboratory tests. Following familiarization, subjects performed two tests in which they were required to perform 60 isometric MVCs over a period of 5 min (3 s contraction, 2 s rest), and five tests involving intermittent isometric contractions at approximately 35-60% MVC, each performed to task failure. Critical torque was determined using linear regression of the torque impulse and contraction time during the submaximal tests, and the end-test torque during the MVCs was calculated from the mean of the last six contractions of the test.


During the MVCs voluntary torque declined from 263.9 +/- 44.6 to 77.8 +/- 17.8 N x m. The end-test torque was not different from the critical torque (77.9 +/- 15.9 N x m; 95% paired-sample confidence interval, -6.5 to 6.2 N x m). The root mean squared error of the estimation of critical torque from the end-test torque was 7.1 N x m. Twitch interpolation showed that voluntary activation declined from 90.9 +/- 6.5% to 66.9 +/- 13.1% (P < style="font-weight: bold;">indicating the development of both central and peripheral fatigue.

CONCLUSION: These data indicate that fatigue during 5 min of intermittent isometric maximal voluntary contractions of the quadriceps leads to an end-test torque that closely approximates the critical torque.

My notes: see my comment above!

Active Release Technique (ART), Z Health, Hands on Work (Massage, Guided Exericse)

What are your thoughts about ART?

This was a good question that I received about 3 times in the past week, so I thought I would address it here.

It is a general question, so I will answer it in relation to general prinicples. Again, everything needs to be custom to the athletes that you work with of course.

For more info, click the links below

Get Off the Foam Roller

Myth Busters-Painful Soft Tissue Work

Some have believed based on my posts above that I am against soft tissue/hands on work; and that is not true at all. I am against PAINFUL soft tissue work!

All of the ART therapists that I have met so far have been great and extremely knowledgeable. Some do painful soft tissue work and others do not (although they are much less common). I don't believe pain is needed to get a result and will actually diminish your results. You are normally seeing an ART person to get out of pain or change a motor pattern/pain.

Don't try to blow up the safe when you just need the correct combination to open the door.

Here is another great post by Carl Valle at Elite Track and my response to it.

Soft Tissue Therapy by Carl Valle (click the title to open it)


My response to Carl.

Hi there Carl! Thanks for the kinds words as it means a lot coming from someone such as yourself.

In relation to experience with athletes that is an excellent point. To date, I have done a fair amount of Z Health sessions (I do have the exact number documented and not pulled out of thin air if you need further info).

Note that when I say Z Health this may apply to dynamic joint mobility work, visual testing/movements, vestibular work or even hands on work (which means that I am holding
tissue/joint/muscle in a specific orientation while they perform an exercise).

I agree that most of these are not what would be considered high level athletes and more weekend warriors types. I was able do a session with a recent Olympic competitor and was able to get her out of pain for the first time in years (see link below)

Z Health and Marathon Running

The same principles would apply to high level athletes.

I agree 100% that soft tissue work done correctly can have HUGE changes for people. No question about that!

You point about most businesses is a good one. I do run a business in the private sector.

Clients/athletes come to a professional in the field for results. My guarantee is that if I can’t get your pain to less than a 2 on a 1-10 scale in ONE session, it is FREE. No results=no money for me=out of business.

Down with foam rollers! Preach on.

Yes, there is research on eccentric stimuli to help encourage remodeling, esp in the case of
tendonOSIS as you know. I like to think upstream—-what causes tension on the muscles/tendons?

Control from the nervous system, so if we can alter that signal, over time the structures will adapt.

Carl said “..but the direct approach WITH motor changes and other elements is a full approach.”

Yes! I have had cases where I’ve needed to do hands on (touch an athlete just as you would touch them to guide them during an exericse) to get a result. In one specific case I held the hamstrings in a specific orientation with the athlete doing an opposite elbow circle (joint mobility), with her head turned to the right and eyes in the up position.

Her hamstrings worked much better afterward and total time of the drill was about 1 minute (getting to that point was about 40 minutes in that case though). She had to follow up and do a similar drill (without hands on work) 3xs a day for about 3-4 weeks for it to “stick”—there is never a free lunch

In general, I do the minimal approach to get the maximal results. Precise joint mobility work seems to get me there about 70% of the time ( I mean 72.8958859% of the time, hehee). The more times I work with athletes and as their movement progresses, the more other work they will need—hands on (guided exercises), visual (eyes held in a specific position), and vestibular (head motions) ; but with all things “it depends” as I may skip around depending on the client. I like to start simple and then only add complexity when the simple looking things do not work.


I hope that answers the ART question!

Any follow up points, thoughts, clarifications, please post them in the comments below.
Thanks!
Mike T Nelson

Performance Research for April : Central Fatigue and Exercise part 1

Treadmill Update
I updated the post the other day in an attempt to better explain my treadmill thoughts; so go back and check it out if you have not done so

Get Off the Treadmill!

General Update
All is going well, just stupid busy and up at 4:30am tomorrow for more testing again in the lab for my Energy Drink study, which is good. Getting close to the end now.

Some new studies for all of you related to central/peripheral fatigue. Enjoy and see my comments below each one.

Fatigue alters in vivo function within and between limb muscles during locomotion.

Higham TE, Biewener AA. Department of Biological Sciences, Clemson University, 132 Long Hall, Clemson, SC 29634, USA. thigham@clemson.edu


Muscle fatigue, a reduction in force as a consequence of exercise, is an important factor for any animal that moves, and can result from both peripheral and/or central mechanisms. Although much is known about whole-limb force generation and activation patterns in fatigued muscles under sustained isometric contractions, little is known about the in vivo dynamics of limb muscle function in relation to whole-body fatigue. Here we show that limb kinematics and contractile function in the lateral (LG) and medial (MG) gastrocnemius of helmeted guineafowl (Numida meleagris) are significantly altered following fatiguing exercise at 2ms-1 on an inclined treadmill.


The two most significant findings were that the variation in muscle force generation, measured directly from the muscles' tendons, increased significantly with fatigue, and fascicle shortening in the proximal MG, but not the distal MG, decreased significantly with fatigue. We suggest that the former is a potential mechanism for decreased stability associated with fatigue. The region-specific alteration of fascicle behaviour within the MG as a result of fatigue suggests a complex response to fatigue that probably depends on muscle-aponeurosis and tendon architecture not previously explored.


CONCLUSION: These findings highlight the importance of studying the integrative in vivo dynamics of muscle function in response to fatigue.

My Notes: This study shows once again that studies done in isolation and in a petri dish may not (heck, are usually) not the same as those done in the whole body. Everything affects everything in the body. Dr. Cobb likes to say "all the body, all the time"

Brain activation in multiple sclerosis: a BOLD fMRI study of the effects of fatiguing hand exercise.

White A, Lee J, Light A, Light K. Department of Exercise & Sport Science and Brain Institute, University of Utah, Salt Lake City, Utah, USA.


BackgroundMultiple sclerosis (MS) patients experience fatigue as a chronic symptom that decreases quality of life. Commonly, fatigue in MS patients is manifested as decreased motor function during or after physical activity and is associated with changes in brain metabolism.ObjectiveTo determine brain activation patterns in MS patients and healthy controls during a simple motor task before and after fatiguing hand-grip exercise.MethodsFunctional magnetic resonance imaging (fMRI) scans were conducted on 10 MS patients and 13 healthy controls during 4-finger flexion and extension in rested and fatigued states.


ResultsBefore the fatigue protocol, MS patients had greater activation in the contralateral primary motor cortex, insula, and cingulate gyrus than controls. Following fatiguing exercise, controls showed increased activation of precentral gyrus and insula while patients did not show any activation increases and actually decreased activity to the insula.


CONCLUSION: Results indicate that before fatiguing exercise, MS patients marshaled more brain activation compared to controls, which may represent functionally adaptive changes in response to demyelination. This increased activation may suggest that patients require more effort to perform even simple motor tasks, possibly because peripheral or central signals for fatigue are chronically enhanced. When fatigued further by muscle contraction, brain activation cannot be further increased.

My Notes: Sounds like the brain is having to work over time to attempt to make up for this difference. I would expect to see changes in the brain and coordination patterns then long term.

Mechanisms of fatigue induced by isometric contractions in exercising humans and in mouse isolated single muscle fibres.

Place N, Bruton JD, Westerblad H. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. nicolas.place@ki.se


1. Muscle fatigue (i.e. the decrease in muscle performance during exercise) has been studied extensively using a variety of experimental paradigms, from mouse to human, from single cell to whole-body exercise. Given the disparity of models used to characterize muscle fatigue, it can be difficult to establish whether the results of basic in vitro studies are applicable to exercise in humans. 2. In the present brief review, our attempt is to relate neuromuscular alterations caused by repeated or sustained isometric contraction in humans to changes in excitation-contraction (E-C) coupling observed in intact single muscle fibres, where force and the free myoplasmic [Ca(2+)] can be measured. 3. Accumulated data indicate that impairment of E-C coupling, most likely located within muscle fibres, accounts for the fatigue-induced decrease in maximal force in humans, whereas central (neural) fatigue is of greater importance for the inability to continue a sustained low-intensity contraction.


Based on data from intact single muscle fibres, the fatigue-induced impairment in E-C coupling involves: (i) a reduced number of active cross-bridges owing to a decreased release of Ca(2+); (ii) a decreased sensitivity of the myofilaments to Ca(2+); and/or (iii) a reduced force produced by each active cross-bridge. 4.


CONCLUSION: In conclusion, data from single muscle fibre studies can be used to increase our understanding of fatigue mechanisms in some, but not all, types of human exercise. To further increase the understanding of fatigue mechanisms in humans, we propose future studies using in vitro stimulation patterns that are closer to the in vivo situation.

My Notes: Um, see my comments above about in vitro (petri dish/bench testing) and in vivio (in the body testing). The reality is that research is a back and forth method or in the clinical world they call it "bench top to bed side"

Get Off the Treadmill!

The "Get Off" series continues (add your own bad joke here_____)

Seems like the past one about foam rollers was like poking a hornet's nest with a big stick; so it should be interesting to see what happens here.

In case you missed the first installment, see the post below

Get Off the Foam Roller

Stay the heck off the darn treadmill!

I find it incredibly odd that when I used to lift at a commercial gym that people would circle the parking lot for several minutes to find a close parking spot only to go in and get on a treadmill. What? Why don't you just leave your car at home and walk to the gym? Yeah I know there are tons of reasons why this may not be practical, but buy a kettlebell (see the dragon link on the upper right hand side) and get some expert instruction from a local RKC and you are on your way. Yes, you can train your CRF (cardiorespiratory fitness aka "cardio") by using a KB.

If you want more details, see the post below where I challenged Carl Lanore at Super Human Radio about his treadmill usage.

Z Health, Proprioception, Neuroplasticity all on Super Human Radio

Why are treadmills bad news bears?
In short, when you are on a treadmill, your joints are telling your brain you are moving; but the eyes tell your brain--no you are not moving you idiot because you are in the same darn place that you were 20 minutes ago! I think this causes some massive confusion with your nervous system and a decrease in performance.

Just watching people walk off a treadmill in any gym---they look like Ted Kennedy after a late night bender.

If people want more treadmill information, this is one of the many topics covered in the Z Health R Phase Certification; so drop me a line for information.

Editor's Note: (I add the following portion in an attempt to better explain myself. I appreciate the comments!).

I am not against exercise at all. I've spend the better part of the past 17 years (yikes, I can't believe I started college in 1992, ugh) studying physiology/engineering in some form. If someone could put the benefits of exercise in a pill, it would be the best selling drug in history almost over night.

Like all things, I believe there is a correct way and a wrong way to do things. Keep in mind that all forms of exercise have a COST. No free lunch. The cost of doing treadmill work I believe is making your muscles weaker (I will be working on a video to demo this in the next few weeks). The cost of attempting a very heavy deadlift with piss poor form may be a back issue. The correct exercise for your body, done correctly will still cost you fuel (think food) to perform it. You get the idea.

The gait (walking/running pattern) on a treadmill is very close to what we would normally do on flat, non moving ground and this compounds the issue. From many studies, we know that if a major league baseball pitcher decided to throw a baseball that is even just a little bit heavier for his training, it would completely screw up his pitching. Some coaches have completely ruined athlete's careers by doing this! The motor learning process is very precise and using a heavier ball for pitching has a negative transfer to his pitching with a regulation ball.

I think the treadmill is too close to our normal gait and seems to have a negative transfer. Other modes of cardio don't seem to do this probably because they are different enough; so bikes (even stationary ones) don't seem to be an issue and most weight lifting is fine also.

It is a free country and nobody any time soon is going to take your treadmill away from you. You are free to use it, I just ask that people keep careful records to make sure it does not have any negative transfer to them (decrease in performance).

Chasing someone around with a metabolic cart to complete a study would be a total pain in the butt, I agree completely. So far to date I've done over 150 exercise tests and I am glad I don't have to chase anyone around (although there are systems to do that). The cardiorespiratory response appears to be fine as anything that uses lots of muscles in a rhythmic fashion will work.

We know so much about CRF since it is much easier to study then strength and even athletic performance in the lab.

Back to the blog again. If people are interested, I am working on a longer version of this based off the many research studies that I pulled. Not sure when it will be done though.

Below are some great treadmill videos for your viewing pleasure that I stole off of Eric Cressey's blog.



I had this one in a presentation years ago---one of my favs!



The rise of "functional treadmill training" Challenge your balance!



Comments? Let me know and post them below.
Rock on
Mike T Nelson

Mental fatigue impairs physical performance in humans

FLzine
I just finished an interview with the fine folks at FLzine.com. I will give you all a heads up once the interview is posted. In it I discuss more mobility fun, why static stretching sucks, and much more.

Mental Fatigue Impairs Performance
Here is something that I have wondered about for years, but until recently never found any data.

When I started working in Technical Services for a major medical device company after my first 7.5 years in college many years ago in a galaxy far far away, I would get grilled all day answering calls from patients, reps, nurse and doctors. They ranged from Ethel that was too close to her microwave and she was trying to hide around the corner closing the door with a broomstick (microwaves and pacemakers are not an issue) to a physician at a device implant who is calling about a certain feature and you can hear the monitors in the background beeping.

I could not understand why I was so tired once I got home even though I sat no my butt all day! Part of this was from just not moving around much at all, but perhaps part of it was "mental fatigue"?

On to the Study
The nice part was the study below was a crossover design, so each subject acted as their own control. This allows you to use less subjects overall as you are only comparing 2 different conditions changes; so one with mental fatigue and the other without.

While it has been argued that a bike to exhaustion is not similar to a time trial format, the vast majority of evidence has been collected using that format. Time trials can be altered too by the subjects (esp. non competitive athletes) learning to pace themselves better.

The performance decrease did not appear to be from the heart/lungs (cardiorespiratory) or muscles! It appears to be all in your head indeed!

If anyone has watched lots of exercise tests to exhaustion will tell you, you need to be very careful what you say to them during a test. I always make it a point to explain everything up front and remind them that it is a max test. Once the test is over half way, I only use encouragement and do not give one group an "option" to quit. My guess is that if someone is working very hard (RPE of a 9 out of 10) and you reminded them that they can stop at any point now because the test is on a volunteer basis, many would just stop even though physically their numbers may be the same!

Other trials have attempted to get around this by giving money for the top performance to make it more competitive.

No mater how you cut it, endurance events at a high level are much about pain management.

Thoughts on the study? Let me know by posting a comment
Rock on
Mike T Nelson


Mental fatigue impairs physical performance in humans

Samuele M. Marcora, Walter Staiano, and Victoria Manning School of Sport, Health and Exercise Sciences, Bangor University, Bangor, Wales, United Kingdom Submitted 4 October 2008 ; accepted in final form 5 January 2009


Mental fatigue is a psychobiological state caused by prolonged periods of demanding cognitive activity. Although the impact of mental fatigue on cognitive and skilled performance is well known, its effect on physical performance has not been thoroughly investigated. In this randomized crossover study, 16 subjects cycled to exhaustion at 80% of their peak power output after 90 min of a demanding cognitive task (mental fatigue) or 90 min of watching emotionally neutral documentaries (control). After experimental treatment, a mood questionnaire revealed a state of mental fatigue (P = 0.005) that significantly reduced time to exhaustion (640 ± 316 s) compared with the control condition (754 ± 339 s) (P = 0.003).


This negative effect was not mediated by cardiorespiratory and musculoenergetic factors as physiological responses to intense exercise remained largely unaffected. Self-reported success and intrinsic motivation related to the physical task were also unaffected by prior cognitive activity. However, mentally fatigued subjects rated perception of effort during exercise to be significantly higher compared with the control condition (P = 0.007). As ratings of perceived exertion increased similarly over time in both conditions (P < style="font-weight: bold;">

CONCLUSION: In conclusion, our study provides experimental evidence that mental fatigue limits exercise tolerance in humans through higher perception of effort rather than cardiorespiratory and musculoenergetic mechanisms. Future research in this area should investigate the common neurocognitive resources shared by physical and mental activity.