Muscle Fatigue - Science topic

I would imagine PharmaLegacy could do it.

How do you plan to do that? You can't test both legs at the exact same time. (Maybe you could, but it wouldn't be easy, and it would probably affect your results.) One leg has to be tested before the other. I suppose you could alternate back and forth as to which leg is tested first during a break from the fatiguing task.

fatigue is task dependent, and each test measures a factor that contributes to fatigue, you should analyze your task and see what factor the fatigue could be attributed to, then a dynamic test or an isometric test will give you different results. it has been seen that the rate of force development is more useful for analyzing muscle damage. I recommend you to read: translating fatigue to human performance - Enoka 2016 - Rate of force development as a measure of muscle damage - Peñailillo 2015 and Fatigue and recovery measured with dynamic properties versus isometric force: effects of exercise intensity - Krugger 2019

Hi James,

In MS, inflammation of the meninges allows for immune cells and cytokines to breach the blood-brain-barrier and contact an immunoprivileged site -the CNS. Because the CNS is an immunopriviledged site, there has been no deletion of auto-reactive B cells and T cells during development, thus cells with the potential to react with CNS determinants are now allowed to do so, and this causes MS (short story, I hope I have not offended anyone with by brevity).

In MG, there is molecular mimicry and also in many cases, a very unique context of paraneoplastic syndrome secondary to carcinoma of the thymus. Thymus is where the T cells develop and undergo tolerance induction. This cancer allows for factors to be made that allow the developing T cells to evade tolerance and now react with AchR and other muscle related factors. The MG can be successfully eliminated by a thymectomy in most instances. So one of my former colleagues had a daughter with MG, there was no cancer, but interestingly, when they removed her thymus, her MG disappeared.

Kind regards, Lora

In regards to your first question, I think it is because a change in EMG parameters provides very little precision in identifying the physiological changes induced by fatigue. Supraspinal, spinal, and even muscle membrane properties are known to be altered by fatigue and each would be expected to influence EMG. For your second question, I believe research using EMG during fatigue has shown great variance in its response. In addition, the intensity (submaximal or maximal) of the fatiguing isometric contraction would be influential on the expected response. If the goal is simply to detect fatigue, while there are several proposed definitions, I believe an exercise-induced decrease in muscle force or power is most widely accepted at least with regard to "performance" fatigue. Hope this helps.

Shrinking concretes are the result of the interaction of the actin filaments with myosin. Therefore, they appear short in length and completely overlapped, and the increase in the number of myosin heads affects the contraction force and muscle stiffness.

This may help as well related to EMG analysis of the lower back region.

Measurement of Low Back Muscle Fatigue and Recovery Time During and After Isometric Endurance Test Advances in Physical Ergonomics and Human Factors 2016 pp 297-308

A strong correlation between frequency content of the EMG signal and TOI (Tissue Oxidation Index) was established, r = 0.78 (right) and r = 0.90 (left). hese findings suggest that the fatigue resulting from sustained isometric exercise are related to a decrease in oxygenation level following by the increasing time of contraction of the ESM (Erector Spinae Muscle)

A better way to look at fatigue in the biceps is to use the median frequency fatigue of muscle using surface electrocardiography. See paper

There are several functional neuroimaging techniques ( e.g. near infrared spectroscopy, EEG, MEG, fMRI and etc) can be used to monitor both physical and mental fatigue. These techniques are chosen for the particular application based on their spatial and temporal resolution and mobility. The following references are for two different studies on fatigue:

[1] K. M. Ranjana and P. Raja, "Effects of Mental Fatigue on the Development of Physical Fatigue: A Neuroergonomic Approach," Human Factors, vol. 56, pp. 645-656, 2014/06/01 2013.

[2] M. Tanaka, A. Ishii, and Y. Watanabe, "Neural effect of physical fatigue on mental fatigue: a magnetoencephalography study," Fatigue: Biomedicine, Health & Behavior, vol. 4, pp. 104-114, 2016.

Caro Giuseppe,

La perdita di tono è legata alla perdita di massa muscolare, ma non è sempre così. Nella mia esperienza, dopo un esercizio molto eccentrico, la rigidità delle mucose diminuisce molto, il che può essere inteso come una condizione delle proprietà contrattili del muscolo (mancanza di ritorno dell'energia elastica)

From my previous experience working with Dr. Petrofsky in Loma Linda University on functional electrostimulation, I expect this goal is reachable within 5 years.

These questions by Dan Robbins are very good that you can also use as guidelines.

For mental cognitive testing, you may want to look at the Uchida-Kraepelin test. The Wisconsin Card Sorting Test and the Tower of London are also commonly used to assess flexibility and planning. Good luck!

Hussin, thank you for this. I would like to use in as an example in a course..

Hi

what do you mean

other than

VO2, VE and respiratory exchange ratio (RER)

Cheers @KlausBlishke

There is a high correlation between the legs to height. but there are other factors that also affect the balance of the body. Remember the principle of balance! muscle and ligament strength, density tulaang also influential. in this case the height (leg length also contributes to balance. So high it would be unstable (but check out, if a tall, thin or muscular?), when a tall, thin it will be more volatile and more increases the risk of injury, but if the height is great , muscles strong, broad pedestal base, it will be stable and less risk of injury.

Not a simple answer. Recovery programmes require an individualised approach focussed on the goals of the athlete, their training/competition schedule and the

environment they are in.

CWI temperature and duration should follow such guidelines. However most research is conducted ~10-15 deg C for ~10-15 mins

Dear,

Check out this:

Thank you, but unfortunately none of these links were opened

Dear Carel Bron,

we recently used the system from Cometa (http://www.cometasystems.com),  the Gereonics miniturized electrodes (http://www.gereonics.com/biopotentialelectrodes.html) and the EMG Easy Report software (http://merlobioengineering.com/emg-easy-report/) to assess the motion pattern (onset/offset time and activity profile) of muscles that control the motion of the scapula (Picture attached) and to obtain normal reference data for shoulder and upper limb muscles during reaching movements.

Miniaturized electrode were used to prevent crosstalk and placed according to Basmajian & Blanc. Muscle onset was computed according to Merlo et al 2003, IEEE Trans. Biomed Eng.

I hope it can help.

I am the main author of the EMG Easy Report software, thus I have a conflict of interest to discolse.

Kind regards.

Andrea Merlo

Disability is not the same as having back pain and is driven by independent variables, including, for example pain catastrophizing and emotional suppression.  You might want to look at this literature and may find it of use.

Robert Stehle gave an excellent explanation for your findings.

It is possible to prevent myofibrils from over-contracting by slight cross-linking of the actin to myosin (Biochemistry. 1993 Jul 20;32(28):7255-63. A structural and kinetic study on myofibrils prevented from shortening by chemical cross-linking. Herrmann C1, Sleep J, Chaussepied P, Travers F, Barman T.) which will allow you to measure something like the 'true' MgATPase rate under quasi isometric conditions.

The phosphate assay is OK, but it may be easier to use a linked assay in a spectrophotometer cuvette using pyruvate kinase and Phosphoenol pyruvate to replenish the ATP using the ADP produced by the myofibrils. Lactate dehydrogenase in the solution turns pyruvate, the product of the previous reaction, into lactate. The lactate dehydrogenase causes oxidation of NADH to NAD+ which can be detected continuously at 340 nm in a spectrophotometer or by fluorescence. The rate of absorption change is proportional to the ATPase. The assay works well at room temperature. This assay is insensitive to Pi contamination, so this is a real advantage. Look up 'linked-assay, ATP and NAD'. There are plenty of publications giving the required conditions etc.

As Richard Lieber says, contractility is not the same as the ATPase rate.

Yes, I agree with opinion which Parth Shah has been mentioned. Method of indentation (dynamic indentation is better because their more informative and convenient in case of biotissues diagnostics than static ones) is good. See, please, for example, our paper "Method for in vivo estimation of viscoelastic characteristics of skeletal muscules"  // Russian Journal of Biomechanics. – 2007. – Vol. 11, № 1. – P. 44–53.

"Both oral carnosine and beta-alanine (β-ALA) supplementation have been explored to raise muscle carnosine levels. Regarding β-ALA, there are several potential issues with its supplementation; the first of which is its poor conversion rate to carnosine. By dividing the molar increase in muscle carnosine by the total molar amount of β-ALA, Stegenet al. (23) were able to calculate β-ALA supplementation efficiency. They reported that only 2.80% of ingested β-ALA was incorporated into muscle carnosine, with 95%-96% being metabolized by non-carnosine directed pathways. Also, β-ALA requires a loading phase of up

to 10 wks (3,16), and that users commonly report up to 1 hr of paresthesia shortly after ingestion (20). Similar to β-ALA, carnosine supplementation has several challenges. Due to individual differences in plasma carnosinase levels, there is significant variability in response to carnosine ingestion. Both Asatoor et al. (2) and Gardner et al. (15) were unable to detect any notable carnosine in plasma after administration of a high dose of carnosine, ~60 mg·kg-1 body weight and 4 g, respectively. Gardner and colleagues (15) further noted that large quantities (e.g., up to 14% of the dose) of ingested carnosine was lost in urine. Everaert et al.

(13) observed a considerable non-responder rate to oral carnosine supplementation, noting that in non-responders the plasma carnosinase protein content was ~2 fold higher, and the protein content had ~1.5 fold higher activity compared with the responders. Oral carnosine (17) supplementation fails to substantially elevate plasma carnosine levels, and despite a high

absorption rate in the gastrointestinal tract, ingested carnosine is susceptible to hydrolysis via plasma carnosinase, thus making it inefficient at increasing muscle carnosine levels"

Use an activity monitor.  They are quite good for and should give you a reliable assessment of extent of physical movement, as a proxy of fatigue.

Hi Egwuonwo,

Usually the raw data of EMG is Microvolt. Then we will do the signal processing (feature extraction) of the raw data such as noise reduction, filtering, rectification to get the RMS then amplitude normalization. From EMG we will get the final data in MPF (Mean Power Frequency) or %MVC (Maximum Voluntary Contraction).

Thanks for the material Marcelo, really useful for me...

Hi Marcelo,

There is many reports out there. Here are some recent papers:

Age-Related Changes in Dynamic Postural Control and Attentional Demands are Minimally Affected by Local Muscle Fatigue http://www.ncbi.nlm.nih.gov/pubmed/26834626

Acute effects of muscle fatigue on anticipatory and reactive postural control in older individuals: a systematic review of the evidence http://www.ncbi.nlm.nih.gov/pubmed/24978932

Biomechanical reorganisation of stepping initiation during acute dorsiflexor fatigue http://www.ncbi.nlm.nih.gov/pubmed/21605984

Impact of ankle muscle fatigue and recovery on the anticipatory postural adjustments to externally initiated perturbations in dynamic postural control http://www.ncbi.nlm.nih.gov/pubmed/23111432

Those a few recent studies, and you can go from there to access many more.

Hope this helps. Norbert

Es una cuestión muy difícil de poder objetivar, dado que lo que se mide en concentración plasmática del cuerpo. La concentración plasmática no nos permite cuantificar la cantidad de lactato producido por el músculo activo, salvo que sepamos cuánta es la masa de músculo activo. Además la relación entre nivel de lactato y nivel de fatiga, además de endeble es indivual y no sirve para comparar el nivel de fatiga entre dos personas a partir de los datos de lactatemía de cada una de esas dos personas

Hi Selva

If you want to make sense of these, you will need to carefully explain the experiment, including: which muscle, electrode positioning, load level (fraction of maximal), duration of the exercise, level of pain felt by the volunteer, recording of the torque generated, details of the subjects, and more. My suggestion is that look at the SENIAM guildlines for this. If you are unsure, you may also see one of my pubs on this topic - in IEEE TNSRE in 2012.

Remember- the association of spectrum and fatigue is known, but weak. 

All the best

During maximal intensity exercise, such as sprinting, ATP is re-synthesized from phosphocreatine and anaerobic glycolysis, while aerobic metabolism plays an important role as duration is increased and/or high intensity exercise bouts are repeated. Interestingly, the concentration of ATP never drops below 60-70% of the resting concentration, i.e. the ATP pool of the muscle is preserved, although in some muscle fibres, ATP may drop to zero (see refs below).This is dependent on fiber type. For furthter reading, please see the papers below

Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK, Nevill AM. Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. J Physiol. 1995 Jan 15;482 ( Pt 2):467-80.

Bogdanis GC, Nevill ME, Lakomy HK, Boobis LH. Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans.Acta Physiol Scand. 1998 Jul;163(3):261-72.

Nevill AM, Jones DA, McIntyre D, Bogdanis GC, Nevill ME.A model for phosphocreatine resynthesis. J Appl Physiol (1985). 1997 Jan;82(1):329-35.

Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK. Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise. J Appl Physiol (1985). 1996 Mar;80(3):876-84.

Hellsten Y, Richter EA, Kiens B, Bangsbo J. AMP deamination and purine exchange in human skeletal muscle during and after intense exercise. J Physiol. 1999 Nov 1;520 Pt 3:909-20.

Söderlund K, Hultman E. ATP and phosphocreatine changes in single human muscle fibers after intense electrical stimulation. Am J Physiol. 1991 Dec;261(6 Pt 1):E737-41.

Gray SR, Söderlund K, Ferguson RA. ATP and phosphocreatine utilization in single human muscle fibres during the development of maximal power output at elevated muscle temperatures. J Sports Sci. 2008 May;26(7):701-7. doi: 10.1080/02640410701744438.

I am unaware of any questionnaire/scale/rating that has been demonstrated to be reliable and valid for the assessment of  muscle fatigue. Muscle fatigue is formally defined as a "reduction in strength or a failure to maintain force output". To demonstrate a valid instrument, one would have compare questionnaire/scale/rating values against simultaneously-measured strength values. I am unaware that anyone has done this, probably because there are many physiological mechanisms for muscle fatigue and it is unlikely that one single psychosocial measure could encompass the effects of all these fatigue mechanisms.

Hello Leticia, it depends of what body mass is you or your athlete losing... lean mass, bone mass, fat mass? It is very important to know if there is an unbalance nutrition, over trainning, etc...

Hello Angel,

As you obviously know, muscle contraction / force / work production, especially in situ, is a complex process and hence fatigue can be due to several factors and dependent on how measured, temperature, isometric, isotonic etc.

Thus, as a start, it would be worth giving some serious thinking. As I recall, in our paper Roots et al 2009 in J Appl Physiol we considered accumulation of Pi as a possibility.

Hope this comment is useful,

KW

Keeping in mind R. Bianchi's remark on burnout and depression, and being highly cautious on "prediction", you may read:

Activated immune-inflammatory pathways are associated with long-standing depressive symptoms: Evidence from gene-set enrichment analyses in the Young Finns Study

ARTICLE in JOURNAL OF PSYCHIATRIC RESEARCH 71:120-125 · OCTOBER 2015 

It is interesting question as you want to see the relationship of fatigue and frailty.You have to measure the MVIC strength of quadriceps muscle and fraily of quadriceps muscle.

These papers may help:

EFFECTS OF LOWER EXTREMITY AND TRUNK MUSCLES RECRUITMENT ON SERRATUS ANTERIOR MUSCLE ACTIVATION IN HEALTHY MALE ADULTS

RELATIONSHIPS BETWEEN CORE STRENGTH, HIP EXTERNAL ROTATOR MUSCLE STRENGTH, AND STAR EXCURSION BALANCE TEST PERFORMANCE IN FEMALE LACROSSE PLAYERS

An Investigation of Simulated Core Muscle Activation during Running and its Effect on Knee Loading and Lower Extremity Muscle Activation Using OpenSim

Multiple papers:

and

We need more information. One, is the "signal" an electromyographic signal?  If so, what kind of electrodes are being used, indwelling or surface? Is "MPF" median power frequency or mean power frequency or neither? What is happening to the amplitude of the "signal"? What is the work task? One with a constant power output? What muscle group is involved? Is the "signal" from one or all muscles in the muscle group?

Dear Justin,

To investigate the muscle fatigue I use "the shift" of frequential parameters calculated from the EMG signal.

For exemple see abstract of my student.

I am open to collaborate with you if necessary.

Neuromuscular Response of Young Boys Versus Men during Sustained Maximal Contraction

Renaud Halin · Philippe Germain · Stephane Bercier · Bronislaw Kapitaniak · Olivier Buttelli

ABSTRACT: This study was designed to compare neuromuscular response between boys and men during sustained maximal voluntary contraction (MVC). Fifteen boys (YB, 10.5 +/- 0.9 yr) and 12 men (AM, 21.5 +/- 4.5 yr) participated in the experiment. Arm's cross sectional area (CSA) and maximal force (F(max)) of elbow flexor were measured before subjects performed a 30-s sustained MVC. Mean power frequency (MPF) and muscle fiber conduction velocity (MFCV) were calculated from myoelectric signals of the biceps brachii. F(max)/CSA, MPF, and MFCV changes were expressed by slopes of linear regressions. Maximal MPF (I-MPF) and MFCV (I-MFCV) were derived from the intercept of each regression. AM had significantly greater F(max)/CSA (P < 0.05), I-MPF (P < 0.05), and I-MFCV (P < 0.01) than YB. F(max)/CSA (P < 0.001), MPF (P < 0.001), and MFCV (P < 0.01) declined significantly more for AM than YB. MPF/MFCV ratio increased, i.e., MPF decreased more than MFCV, for both groups but this was significantly (P < 0.001) more pronounced for AM. Taken together, those results suggest that more fatigable Type II motor units are involved in men, resulting in greater lactic acid and ions accumulations during fatigue. This difference in muscle's metabolic and ionic state could be responsible for a greater reflex-induced decrease of motor units firing rates in men compared with boys. This firing rate decrease could be explained using the "muscular wisdom" hypothesis and would express a nervous command adaptation to sustain a maximal contraction.

Medicine &amp Science in Sports &amp Exercise 06/2003; 35(6):1042-8. DOI:10.1249/01.MSS.0000069407.02648.47 · 3.98 Impact Factor

Interesting idea , but it is difficult to conclude that clinically . Possible symptoms may be subjective . recording EMG in response to same ammount of stimulus , may be done to add more objectivity .

i am not an expert in this field .

Corben JS, Cerrone SA, Soviero JE, Kwiecien SY, Nicholas SJ, McHugh MP. Performance Demands in Softball Pitching: A Comprehensive Muscle Fatigue Study. Am J Sports Med. 2015 Jun 24. pii: 0363546515588179. [Epub ahead of print]

Severijns D, Lamers I, Kerkhofs L, Feys P. Hand grip fatigability in persons with multiple sclerosis according to hand dominance and disease progression. J Rehabil Med. 2015;47(2):154-60. doi: 10.2340/16501977-1897.

Anumula SK, Beku C, Murthy YSN. Measurement of reliability in grip strength. International Journal of Healthcare Sciences. 2014;1(1):1-6.

Neu D, Mairesse O, Montana X, Gilson M, Corazza F, Lefevre N, Linkowski P, Le Bon O, Verbanck P. Dimensions of pure chronic fatigue: psychophysical, cognitive and biological correlates in the chronic fatigue syndrome. Eur J Appl Physiol. 2014;114(9):1841-51. doi: 10.1007/s00421-014-2910-1.

White C, Dixon K, Samuel D, Stokes M. Handgrip and quadriceps muscle endurance testing in young adults. Springerplus. 2013;2:451. doi: 10.1186/2193-1801-2-451.

Roberts HC, Denison HJ, Martin HJ, Patel HP, Syddall H, Cooper C, Sayer AA. A review of the measurement of grip strength in clinical and epidemiological studies: towards a standardised approach. Age Ageing. 2011;40(4):423-9. doi: 10.1093/ageing/afr051.

by inhibiting the HMG-coA reductase you are also inhibiting the formation of co-enzyme Q10. the article above is a good one. 

On the most basic of levels, Borg's perceived exertion scale (6-20) measures overall fatigue during a task, and correlates quite well with HR.

I have not seen any publication on physiological work load  of Quarry workers Of Nigerian Quarry Industry but Indian work is available in Ergonomics journal around 1988 to 1999 during this period.   

Hello Vitor,

thanks for your answer, but I managed to program it myself and had it checked by a further expert...

Regards,

Niklas

P.S. Attached is the Matlab Function, Sample Data and Sample Script to calculate Dimitov-Index and Kim Index (Kim et al., 2013, International Journal of Precision Engineering and Manufacturing)

I agree with both. Due to the highest energy demand of brain, the hypoxic condition will severely affect tissue metabolism causing derangements.  

Hi Nicola,

Interesting question! Have you come across the Reflotron system? It may be your best bet. Unfortunately the i-STAT device only does CK-MB, but you may be interested in some of the variables it can offer. Equally, the IPRO doesn’t do CK, though does provide markers like testosterone, cortisol, IGA, IL-6 and CRP using salivary samples that are used as part of workload monitoring systems too.

Links to each of these devices are attached. I hope that this is of some help.

Cheers,

Geoff

Any survey, including the BORG scale, will be pretty vague and vary a lot between individuals. Monitoring the MEDIAN FREQUENCY of an EMG signal would be more sensitive to a change in fatigue status.

Gleeson, M.; Bishop, N.C.; Stensel, D.J.; Lindley, M.R.; Mastana, S.S.; Nimmo, M.A. The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol, 11, 607-615.

I am no expert in this field but have heard about "fatigue syndrome", the underlying (despite <proximate>) mechanisms mostly are unclear / not elucidated yet. At least when it comes to <find ultrastructural parameters> (in hum. diagnostics, e.g. muscle biopsies) with a clinical diagnosis of "fatigue".

Usually this syndrome is said to include a variety of symptoms as a consequence of diverse chronic diseases (e. g. cancer, and others) <Neurasthenia> perhaps can be seen as one kind of independent <fatigue >.

@ Marcel: Sorry for not being exhaustive...one for sure should "dig" into literature references and reports available. Regards, Wolfgang

I've been doing a literature review on mechanical disruption and impairments to the E-C coupling process as a result of contraction-induced injury and information from Friden et al. (1983) and Warren et al. (1993, 2001) was very insightful! Fantastic piece of research. Thank you

There might be a difference in intentionality and awareness. Concealment (e.g. of negative feeelings like shame or frustration) is something I may decide to enact, intentionally and fully conscious about what I do Irealize my feeling, but others hould not..Deception is about negating the negative feeling, lying to myself," oh no not me", like an automatized response, not a willful act. Before even reaklizing, the negative feeling is pushed away, suppressed as a psychoanalist might say. As a strategy, concealment is fuly compatible with awareness and management of painful sensations, while deception is not.

I wonder of this helps - good luck!

Muscle fatigue or neuromuscular fatigue is defined as a decrease in maximal voluntary contraction (MVC) torque/force/power that can be produced by a muscle group. To identify if an experimental manipulation induces muscle fatigue, you will need to measure MVCs pre-post intervention. If MVC decreases, you demonstrates presence of muscle fatigue. However you do not know the origin of muscle fatigue.

Muscle fatigue can be caused by a central (fatigue) or peripheral (fatigue) component. Central fatigue corresponds to a decrease in maximal voluntary activation level (inhibition of the central motor drive, measured by the twitch interpolation tehnique) and peripheral fatigue to all changes at or distal to the neuromuscular junction. Briefly, to measure these central and peripheral components you can use various stimulation techniques such as peripheral nerve stimulation, transcranial magnetic stimulation and the twitch interpolation technique.

Also, muscle fatigue and mental fatigue are two different phenomena. Mental fatigue does not induce a decrease in MVC but increase your perception of effort and will impair your performance (during endurance exercise) independently of any impairment of neuromuscular function. When you are mentally fatigued, your neuromuscular system is still able to produce a maximal force, but effort is perceived higher.

In addition to the increase of lactic acid and the reduction of muscular glycogen, the MAIN cause of muscular fatigue is the change of ph in the microenvironment. If we measured the ph level inside the muscle cells, where the myosin head interacts with the actin filament, we would note a physiological ph level. But when the exercise is extreme, that is when too many times the ATP has been hydrolyzed, H+ ions increases and the ph level may low from 7 to 4. Because the myosin head has an optimal conformation at ph 7-7.2, ph 4 levels brakes the contractile event, because each enzyme needs for an optimal ph to act. This is a transitory condition, but it’s sufficient to prevent the exercise continuation.

In my opinion the best "indirect" blood markers of muscle damage are Creatine kinase (CK) and (Mb). Although they peak at different time points (Mb: 6hrs after; CK: 1 day after exercise).

I prefer to quantify the muscle damage using the fluorescent (loss in dystrophin staining) or electron transmission microscopy (Z-disk streaming). Have a look to this article. Macaluso F, Isaacs AW, Myburgh KH. Preferential type II muscle fiber damage from plyometric exercise. J Athl Train. 2012 Jul-Aug;47(4):414-20.

Dear Béres

Take a look at this link. If you cannot open the full text just contact me

I am not an exercise scientists, but your question reminded me of a project we (three of us) undertook many years ago. I give a brief outline below, if interested.

We had already developed a complex mechanics recording system to record evoked and voluntary isometric contractions of human elbow flexors at a wide range of elbow angles. One subject undertook a regular daily isotonic elbow flexion (against maximal load) in one forelimb and we wanted to monitor the time course of change in performance (weight flexed), strength (Max vol force) at different elbow angles and any change in contraction speed (twitch, rate etc) in ~weekly expts. The exercise routine continued for ~6 weeks and experimental recordings for >20 weeks - as I recall.

During six weeks of exercise, after a latency, max (weight) performance increased 100% (doubled), MVF increased 20-25% but there were no changes in cont speed etc. It took ~20 weeks for return of MVF to normal. So there was a learning period - may be.

So, I think performance, strength (force), speed etc need to be cosidered with due care, compared against similar measurements under control conditions.

Hope some of this at least makes sense.

I have observed that feedlot cattle on zilpaterol get progressively fatigued. They may be good at the feedlot and then arrive at the slaughter plant stiff and sore footed. Some animals are more affected than others. You may want to look at lactate and CPK.

A.V. Hill's theory that lactic acid causes muscle fatigue and "burn" has largely been dismissed. Fatigue is a complicated phenomenon, and lactate production probably has little to do with it. The literature on this is long and complicated, but accumulation of inorganic phosphate may be a major player.

In any case, lactate will not "burn" through thick or thin filaments. In fact, it is less acidic than pyruvate - its precursor which is always abundant in the cell.

The idea is to use an easy and quick tool (with other ones) on a daily basis with rugby league players in order to monitor training load. This technique is widely used in Australia (and in a few rugby union teams in France) but I can't find any scientific evidence supporting its effectiveness/reliability.

Some teams also use flight time and contact time data during vertical jump tests but these measurements can be highly affected by impairments at the peripheral level (especially in team-sports athletes).

We can also measure the maximal number of touches an athlete can perform with his/her index over a short period time (about 30 sec) but I think it's easier to find reference on isometric handgrip strength...

Hi Frank,

I want to thank you so much for your answer

I have calculated the mean RMS during each 6s sprint according to Mendezet al. (2007). Fatigue responses during repeated sprints matched for initial mechanical output. Medicine and science in sports and exercise, 39(12), 2219-2225.

Best regards

I have had the Chronic Fatigue Syndrome/ME since getting the 1957 Asian flu. I was six years old at the time. It was relapsing/remitting the first twenty years (except for some muscle problems that showed up in Oct 1957 that have been with me ever since) . It has been permanent the last 35 years. It is definitely NOT a psychological disorder. The type of fatigue is different from a normal person's experience of it. In fact, I have felt as many as six or seven types of fatigue simultaneously. I can give very plausible physiological causes for all of them--they have absolutely nothing to do with state of mind. NOTHING!

In fact, had a I not been a very creative, stubborn person with a great deal of psychological resilience, I never would have finished school, let alone got a PhD in mathematics and have a career as a university professor. I was lucky to be in remission for graduate school.I was also lucky that the worst of the neurocognitive problems didn't start to show up until 22 years ago. I got another infection which set off the usual symptoms permanently shortly after I started teaching in 1978. Over decades, the illness has definitely turned into some type of degenerative neurological/neuromuscular illness. In 1998 I was sent to a mitochondrial specialist. A series of blood test over time on the same day established as fact what I could tell physiologically. Lactic acid builds up and doesn't break down for a day or more afterwards. For me, this has been a major component of the fatigue. No amount of mind over matter will cause lactic acid to break down. You have to wait it out. The specialist ultimately took my view of the mitochondrial dysfunction--it was the result of damage from chronic viral infections in certain muscles. But only certain muscles. We both agreed I don't have typical mitochondrial disease. Also muscle biopsies have established my mitochondria LOOK fine. They just don't work right. The specialist also explained that the reason I feel prostrated, especially the day after doing something, is because my body is reacting to the high levels of reactive oxygen species (ROS) and my body is telling me to go to bed and not move because a great deal of damage is going on that it wants to limit. He also explained the peculiar pain I experience then is from that, too.

A neurologist at MASS General went outside his area of expertise and figured out that high levels of biotin, B-1 and B-2 would speed up the recovery process. He was right. They have. So I've been able to teach several days in a row, if I'm careful of my recovery periods being long enough. I gained another 14 years of my career thanks to his insight.

Recent papers have established mitochondrial dysfunction as a common component of CFS. This is now a well-established scientific medical fact. For more information on this, you can see my paper on mitochondrial dysfunction in CFS posted on the Massachusetts CFIDS-ME & FM Association website http://masscfids.org/resource-library/13/302.

In addition I've had another type of muscle dysfunction problem consistently since Oct 1957. That I haven't found in any other person and I can't find any specialist who has the slightest clue about it. I can't find anything in the medical literature about it, either. It does respond temporarily to bananas and potatoes (for about an hour) and for a while it did to metformin. But that response has faded after the last infection I got and as my insulin-resistance has grown.It is getting worse and worse over time. I'm sure I'm not the only person in the world with the problem, but it clearly isn't anything the medical community has investigated yet. It has been established that it isn't a known genetic illness. As far as I can see, it is from some type of potassium channel dysfunction in my arm and leg muscles combined with something to do with insulin receptors, especially in the muscles that were infected at various times. It does get permanently worse after every infection of muscles or nerves. I decided I have to live to over one hundred in order to find out what is wrong. I hope I do find out before I die. I would really like to know what is going on, even if it is too late to help.

I do strongly recommend that most of you start reading the well-established medical literature on CFS/ME. There are many things wrong with the immune system as well as other components of the body in CFS/ME. This is a very complicated illness with changes in the body that are hard to measure--which is why it is taking so long to understand it.

As for cause--I've been convinced for decades that many different viral and bacterial triggers exist. Certainly in my case, influenza has been a consistent one, but there have been other types--including Coxsackie virus and West Nile virus. I have felt for the last twenty years or so that the defective RNAse-L found in many CFS/ME patients explains a great deal of the causes of the illness. I also have found that excessive response to histamine's effects on the immune system were a major cause of my chronic fever and other immune-system symptoms. I've stopped the chronic fever and other problems since 1985 by taking a H-1 and H-2 blocker. But I can't fix anything else. At least I haven't been smart enough to think of anything.

With respect to the underlying fatigue common in many chronic diseases–one of the causes appears to be elevated circulating interleukin-6 or soluble IL-6 receptor. The fatiguing effects of increased IL-6 have been shown in athletes (http://www.ncbi.nlm.nih.gov/pubmed/15317982) and elevated levels are associated with most inflammatory-based illnesses that present with fatigue. Cytokine-blockers are currently being developed (Chugai Pharmacueticals) that block/reduce the sensations of fatigue. The fatigue has been termed 'cytokine sickness'. Have a look at http://www.ncbi.nlm.nih.gov/pubmed/12895132.

Lactate is an indicator of the rate of glycolysis in the muscle. Interpretation of fatigue based on this measure requires careful consideration of factors such training status, motivation, recovery, fractional utilisation etc. Basically, if you what to know how tired the swimmers feel, ask them; if you want to know the state of the exercising muscle then you need EMG and preferably some measure of central and peripheral activation.