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!

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"

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.

Z Health Tesimonial and Performance Research for March: Central Fatigue part 1

Z Health Testimonial Time!

My name is Gail Jensen and I've enjoyed strength training and its benefits for years. Recently, I was diagnosed with bone spurs and a herniated disc in my cervical spine. As a result, I was experiencing a significant loss of strength and endurance in my right tricep probably because one of the spurs is pinching a nerve. Surgery is an option but I am fearful of my future in strength training with such a drastic procedure. I decided to investigate my options and was referred to Mike Nelson by a friend whose opinion I value.

Mike is a Master in Z Health and I was fascinated with his insight into my problem(s)! The tricep problem was obvious at our session but Mike also discovered that my left glute and abs were not firing properly, either. He remedied the situation on the spot with the glute-ab issues and gave me an exercise regimen to help regain the strength in my tricep ( I have lost a fair amount of muscle mass) and my thumb and forefinger no longer tingle!

I have followed his advice religiously and I am making daily strength gains. I've had several days of relatively little pain and I feel much stronger! The pain has also subsided. Thanks, Mike! I also hope to take Z Health classes myself so I can recognize more fully the importance of the neuromuscular aspect of exercise.

Gail Jensen, Alexandria, Minnesota

Special thanks to Gail for making the long couple hour plus drive down and being diligent on doing her exercises. Awesome work Gail!! It is not always this "easy" but many times it is with the correct information/skills.

If you need more Z Health information or want to set up an appointment for yourself, see this link below and click this link Email Mike T Nelson

Z Health in Minnesota

On to the science! The series of new research on fatigue and why do muscles get tired blazes on.

Neuromuscular fatigue following high versus low-intensity eccentric exercise of biceps brachii muscle.

Gauche E, Couturier A, Lepers R, Michaut A, Rabita G, Hausswirth C. Laboratory of Biomechanics and Physiology, Research Department, National Institute of Sport and Physical Education, INSEP, 11 Avenue du Tremblay, 75012 Paris, France.


PURPOSE: This study investigated neuromuscular fatigue following high versus low-intensity eccentric exercise corresponding to the same amount of work.

METHODS: Ten volunteers performed two eccentric exercises of the elbow flexors: a high-intensity versus a low-intensity exercise. Maximal voluntary contraction torque and surface electromyography of the biceps brachii muscle were recorded before, immediately and 48h after exercises. Maximal voluntary activation level, neural (M-wave) and contractile (muscular twitch) properties of the biceps brachii muscle were analysed using electrical stimulation techniques.


RESULTS: Maximal voluntary contraction torque was significantly (P<0.01) style="font-weight: bold;">


CONCLUSION: High and low-intensity eccentric exercises with the same amount of work induced the same reduction in maximal strength capacities of the biceps brachii muscles. The magnitude of peripheral and central fatigue was very similar in both conditions.

My Notes: Interesting. I would not have guessed they would be the same in both conditions.

The Role of Impaired Mitochondrial Lipid Oxidation in Obesity.

Rogge MM.


Obesity represents a disruption in balancing fuel intake with energy expenditure in favor of energy conservation. Adiposity is known to be carefully regulated and, over time, highly resistant to major changes, raising questions about how energy homeostasis can become dysregulated in favor of fat accumulation. In obesity, the excess lipid accumulation represents a surfeit of energy, but those who are obese often experience rapid fatigue and decreased physical endurance, reflecting an energy deficiency. To develop an explanation for this apparent contradiction in energy homeostasis and the chronic overeating relative to energy used in obesity, a review of the literature was conducted.


The resulting model of obesity is based on a growing body of research demonstrating that altered mitochondrial energy production, particularly in skeletal muscles, is a major anomaly capable of setting off a chain of metabolic events leading to obesity. Alterations in skeletal muscle mitochondria distribution and their oxidative and glycolytic energy capacities in obesity are described. The metabolic responses of obese and normal individuals to exercise are contrasted, and the effects of weight loss on energy production are presented.


CONCLUSION: The effect of altered fat oxidation is considered in relation to energy regulation by the central nervous system and the development of major obesity comorbidities, including systemic inflammation, insulin resistance and diabetes, and cardiovascular disease. Recommendations for clinical intervention and additional research are proposed based on the model presented of impaired mitochondrial function in obesity.

My Notes: Look for more research in this area over the next several years as scientist dig deeper into this area. Remember, as Dr. Cobb likes to say "all the body, all the time" It is all connected!

Effect of endurance training on hypothalamic serotonin concentration and performance.

Caperuto EC, dos Santos RV, Mello MT, Costa Rosa LF. Department of Bioscience, Federal University of São Paulo, Baixada Santista, Brazil.


1. Serotonin is a neurotransmitter that modulates several functions, such as food intake, energy expenditure, motor activity, mood and sleep. Acute exhaustive endurance exercise increases the synthesis, concentration and metabolism of serotonin in the brain. This phenomenon could be responsible for central fatigue after prolonged and exhaustive exercise. However, the effect of chronic exhaustive training on serotonin is not known. The present study was conducted to examine the effect of exhaustive endurance training on performance and serotonin concentrations in the hypothalamus of trained rats.


2. Rats were divided into three groups: sedentary rats (SED), moderately trained rats (MOD) and exhaustively trained rats (EXT), with an increase of 200% in the load carried during the final week of training. 3. Hypothalamic serotonin concentrations were similar between the SED and MOD groups, but were higher in the EXT group (P < style="font-weight: bold;">

CONCLUSION: Thus, the present study demonstrates that exhaustive training increases serotonin concentrations in the hypothalamus, together with decreased endurance performance after inadequate recovery time. However, the mechanism underlying these changes remains unknown.

My Notes: Maybe this is the infamous "runners high?"

Performance Research for February: Central Fatigue Round 1

That's right, it is Sat early AM and I am up sharing with you the great readers of this blog some very cool research.

More crazy studies once again! Be sure to read my comments below each one and don't let all the uber geek speak scare you away.

Off to conduct some more testing for the Energy Drink study at the U of MN lab. Science "rolls on."

Joint-specific power production and fatigue during maximal cycling.

Martin JC, Brown NA. Department of Exercise and Sport Science, University of Utah, 250 S. 1850 E. Room 241, Salt Lake City, UT 84112-0920, USA.


Cycling power decreases substantially during a maximal cycling trial of just 30s. It is not known whether movement patterns and joint powers produced at each joint decrease to a similar extent or if each joint exhibits an individual fatigue profile. Changes in movement patterns and/or joint powers associated with overall task fatigue could arise from several different mechanisms or from a complex interplay of these mechanisms. The purpose of this investigation was to determine the changes in movement and power at each joint during a fatiguing cycling trial. Thirteen trained cyclists performed a 30s maximal cycling trial on an isokinetic cycle ergometer at 120rpm. Pedal forces and limb kinematics were recorded.


Joint powers were calculated using a sagittal plane inverse dynamics model and averaged for the initial, middle, and final three second intervals of the trial, and normalized to initial values. Relative ankle plantar flexion power was significantly less than all other joint actions at the middle interval (51+/-5% of initial power; p=0.013). Relative ankle plantar flexion power for the final interval (37+/-3%) was significantly less than the relative knee flexion and hip extension power (p=0.010). Relative knee extension power (41+/-5%) was significantly less than relative hip extension power (55+/-4%) during the final three second interval (p=0.045). Knee flexion power (47+/-5%) did not differ from relative hip extension power (p=0.06).


Conclusion: These changes in power were accompanied by a decrease in time spent extending by each joint with fatigue (i.e., decreased duty cycle, p<0.03). style="font-style: italic;">

My notes: When I read the first part of the abstract and the title, I was super excited! Finally some more cool data to look at the effects of joints on overall performance. I have to admit that I was dissapointed in the conclusion, since I think it just made the whole thing more confusing. Perhaps someone other there can help me out.

Frontal and motor cortex oxygenation during maximal exercise in normoxia and hypoxia.

Subudhi AW, Miramon BR, Granger ME, Roach RC. University of Colorado at Colorado Springs.


Reductions in prefrontal oxygenation near maximal exertion may limit exercise performance by impairing executive functions that influence the decision to stop exercising; however, it is unknown if deoxygenation also occurs in motor regions that more directly affect central motor drive. Methods Multichannel near infrared spectroscopy (NIRS) was used to compare changes in prefrontal, premotor and motor cortices during exhaustive exercise. Twenty-three subjects performed two sequential, incremental cycle tests (25 W(.)min(-1) ramp) during acute hypoxia (PIO2 = 79 mmHg) and normoxia (PIO2 = 117 mmHg) in an environmental chamber. Test order was balanced and subjects were blinded to chamber pressure.


Results In normoxia, bilateral prefrontal oxygenation was maintained during low- and moderate- intensity exercise, but dropped 9.0 +/- 10.7 % (mean +/- SD; P < power =" 305"> 0.94). In hypoxia, prefrontal oxygenation was reduced 11.1 +/- 14.3% at rest (P < power =" 256"> 0.61), but deoxygenation was greater in prefrontal than in premotor and motor regions (P < style="font-weight: bold;">

Conclusions: Prefrontal, premotor and motor cortex deoxygenation during high-intensity exercise may contribute to an integrative decision to stop exercise. The accelerated rate of cortical deoxygenation in hypoxia may hasten this effect.

My Notes: I thought this was a very interesting study. The effects of pacing (how hard should I work and at what times to get my best time over a fixed distance) have been proposed for awhile, championed by Dr. Noakes. This provides some evidence that the brain is so smart, that if it is being even slightly deprived from oxygen due to exericse, exercise will stop. Remember, the body is survival orientated, not performance orientated; but we can "back door" performance by increasing survival. This is one of the tennets of Z Health.

Opioid-mediated muscle afferents inhibit central motor drive and limit peripheral muscle fatigue development in humans.

Amann M, Proctor LT, Sebranek JJ, Pegelow DF, Dempsey JA. Institute of Physiology, University of Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland. markus.amann@physiol.biol.ethz.ch


We investigated the role of somatosensory feedback from locomotor muscles on central motor drive (CMD) and the development of peripheral fatigue during high-intensity endurance exercise. In a double-blind, placebo-controlled design, eight cyclists randomly performed three 5 km time trials: control, interspinous ligament injection of saline (5K(Plac), L3-L4) or intrathecal fentanyl (5K(Fent), L3-L4) to impair cortical projection of opioid-mediated muscle afferents. Peripheral quadriceps fatigue was assessed via changes in force output pre- versus postexercise in response to supramaximal magnetic femoral nerve stimulation (DeltaQ(tw)). The CMD during the time trials was estimated via quadriceps electromyogram (iEMG). Fentanyl had no effect on quadriceps strength.


Impairment of neural feedback from the locomotor muscles increased iEMG during the first 2.5 km of 5K(Fent) versus 5K(Plac) by 12 +/- 3% (P < style="font-weight: bold;">

Conclusion: Our results emphasize the critical role of somatosensory feedback from working muscles on the centrally mediated determination of central motor drive. Attenuated afferent feedback from exercising locomotor muscles results in an overshoot in central motor drive and power output normally chosen by the athlete, thereby causing a greater rate of accumulation of muscle metabolites and excessive development of peripheral muscle fatigue.

My notes: Yep! For optimal performance you need to know what your muscles are doing! Many that I see have some form of SMA--sensory motor amnesia (coined by Thomas Hanna founder of Somatics); they have very poor feedback on what some of their muscle are doing (this seems to almost always correspond to an area with poor mobility). Many times a Z Health mobility drill will be able increase muscle feedback.