An Introduction to Acute Fatigue within Sport


Muscle fatigue most often occurs during strenuous dynamic physical activity (James, Scheurmann & Smith, 2010) and within sport, can be explained as a reduction of maximal force or power that is associated with sustained exercise, or the inability to produce or maintain a required force or power output (Celine et al., 2011).


Neuromuscular fatigue is a vast topic of research and though many of the causes are still obscure, it is agreed to be the result of a combination of central and peripheral factors (Allen, Lamb, & Westerblad, 2008; Enoka & Duchateau, 2008; Fitts, 1994; Waldron & Highton, 2014).

Vaguely put, central fatigue is related to the brain and central nervous system while peripheral fatigue is to do with the muscles themselves and the substances related to contracting them.

In a few more words, central fatigue is related to reduced central motor drive of the central nervous system (CNS) due to changes in the synaptic concentration of neurotransmitters and therefore its ability to recruit available motor units (Davis and Bailey, 1997).

Peripheral fatigue on the other hand, relates to limitations of muscle capacity through biochemical changes (Waldron & Highton, 2014), such as an increase in blood lactate concentration and hydrogen ion accumulation (Mohr, Krustup & Bangsbo, 2003). It occurs at, or distal to, the neuromuscular junction and is thought to be linked to several mechanisms such as failure of excitation-contraction coupling, a disruption in neuromuscular transmission and the inhibition of muscle contraction through either the build-up or depletion of metabolites (Kent-Braun, 1999).


Lactate and hydrogen ions (H+) production is the result of glucose breakdown. If a sufficient amount of oxygen is not available to the working muscles then hydrogen ion concentrations begin to rise and the muscles, including blood flow to the muscles, become acidic. This acidic environment blocks neuromuscular transmission (signal to and from the brain and muscle), slowing down the individual in order to allow more oxygen to get to the working muscles.

Decreased work rate within sports has been affiliated with reduction in muscle glycogen content (Saltin, 1991) while other factors such as physiological changes within the muscle cell, dehydration and a reduction of recruitable muscle fibres for force production have also been suggested (Saltin, 1973; Jacobs et al., 1982; Bangsbo, 1994). Sjersted and Sjoogard (2000) hypothesized that the sarcolemma was one of the sites of fatigue due to its inability of maintaining sodium and potassium concentrations during repeated stimulation. As a result of inefficiency of the sodium/potassium pump, potassium concentrations increase outside the membrane, in turn decreasing the amount within the membrane. This leads to depolarization of the cell, thus reducing action potential amplitude.

Recovery from peripheral fatigue where it relates to metabolic factors and impairments in neuromuscular transmission is known as high frequency fatigue and has been shown to occur within shorts periods of time following exhaustive exercise (Bruton, Lannergren, & Westerblad, 1998; Saltin, Radegran, Koskolou, & Roach, 1998). Low frequency fatigue on the other hand, is related to peripheral fatigue due to impairments within the excitation-contraction coupling process, and occurs as a result of repeated short intervals of repeated muscle stimulation. This type of fatigue is more prominent following eccentric exercise and is likely the cause of a longer lasting neuromuscular fatigue (Keeton & Binder-Macleod, 2006).


Fatigue within sports is primarily identified through a decline in performance (Reilly, 1994). A fatigue effect has been reported to be noticeable in soccer, particularly within the second half due to an observation of decreased work rate (Reilly and Thomas, 1976). Bangsbo et al (1991) reported a 5% greater distance covered within the first half by professional soccer players,

Fatigue been shown to impair sprinting mechanics and joint stability. Such a combination of factors is likely to predispose players to injury during tasks that have high mechanical demands. (Greig, 2009). Fatigue leads to altered movement patterns of athletes into more stressful positions (Borotikar et al., 2008), and has been reported to be a direct contributor towards injuries such anterior cruciate ligament (ACL) injury via promotion of high risk biomechanics (McLean & Samorezov, 2009)

With advancements in team sports performance analysis such as player tracking technology, fatigue is a popular topic of interest and has usually been associated with variables such as running performance, distance covered from baseline, along with reported changes in neuromuscular force or sprinting ability (Rampinini et al., 2011). Basic physiological measures such as heart rate and blood lactate provide a useful index of overall physiological strain and anaerobic energy yield in response to high intensity situations respectively (Reilly & Thomas, 1997; Reilly, 1997). Thus, combining these variables with a measurement in decrease of muscular force overtime within match play may help indicate acute neuromuscular fatigue.


Other ways include monitoring training load through session RPE’s (rate of perceived exertion) or/and RSI (Reactive strength index). These are easily obtained through a set of numbers based on session time and perceived exertion or using a jump mat and monitoring jump performance which is custom for most professional athletes particularly within team sports. An example and some uses for these two methods are summarised in the below picture.


Sport scientists and S&C coaches may prefer to use other methods of further analysis through a combination of the above mentioned factors or equations such as the Fatigue Index equation (Fitzsimons, Dawson, Ward & Wilkinson, 1993) based on peak running speed/peak force produced and sum of general running speeds or gneral force produced, depending on the athlete being monitored.

Charcot-Marie-Tooth Disease (CMT): Brief Etiology, Clinical Presentation and Rehabilitative considerations.

CMT is a genetically heterogenous disorder which effects the motor and sensory peripheral nerves and may also be known clinically as Hereditary Motor and Sensory Neuropathy (HMSN); in the rare occasion where it only effects motor nerves, it is recognised as Distal Hereditary Motor Neuro(no)pathy (dHMN) (Pareyson & Marchesi, 2009). It is one of the most common hereditary neuromuscular disorders with an occurrence of 40 incidences in every 100,000 individuals (Martyn & Hughes, 1997). CMT is caused by mutation of genes responsible for encoding various proteins such as compact/non-compact myelin, Schwann cells and axons which are involved in everyday functions of the body such as mitochondrial metabolism, axonal transport and maintenance of myelin (Barisic et al., 2008; Szigeti & Lupski, 2009; Hoogendijk et al., 1994). Regardless of the defects that primarily effect the myelin or axon, the common end pathway seen of CMT is degenerative process at the axon involving the largest and longest fibres (Pareyson, Scaori & Laura, 2006; Schrerer & Wrabetz, 2009; Krajewski et al., 2000).


Figure 1. Visual representation of the location of the axon and myelin (

Unlike early onset foot conditions such as Congenital Talipes Equinovarus (Clubfoot) which is treated within the first years of birth (Dobbs & Gurnett, 2009), CMT usually occurs over the first 2 decades of life and then progresses relatively thereafter over decades, and neither is it restricted to the feet as it may progress from the feet to the entire lower limb region and even the upper limbs in some subtypes of the condition (Pareyson & Marchesi, 2009).

Though the diagnostic process may be complicated, there are at least 25 specific genes that have been identified to be associated with CMT and 70% of patients are now able to receive a precise molecular genetic diagnosis. The process generally includes identification and definition of the clinical phenotype, identification of the inheritance pattern, electrophysiological examination and a molecular analysis (Pareyson & Marchesi, 2009). The molecular diagnosis can be significantly aided by clinical information/findings of the patients including the age of CMT onset, severity of the disease and presence of uncommon features which still may be associated with CMT such as optic atrophy, vocal cord palsy and glaucoma (Shy et al, 2005; Pareyson, Scaori & Laura, 2006; Barisic et al., 2008; Reilly, 2007; Szigeti & Lupski, 2009).

Based on nerve conduction studies and nerve pathology, CMT can be classified into two types: Demyelinating CMT which is characterised by slow nerve conduction velocities (<35 m/s in the upper limb motor nerves) and is further split into CMT-1 or CMT-4. This split is based on inheritance identification, with CMT-1 presenting itself as autosomal dominant (defect in a dominant non sex specific chromosome) and CMT-4 as autosomal recessive (defect in a recessive non sex specific chromosome). The second type of CMT is axonal and these are characterised by relatively faster nerve conduction velocities (>35 m/s) and pathological evidence of chronic axonal degeneration. Autosomal dominant forms such as CMT-1, CMT-2, dHMN are the most common expressions of CMT in cases while autosomal recessive forms are slightly more rare and severe with an early onset and can be either demyelinating or axonal such as CMT-4, AR-CMT-2 and AR-dHMN. (Ouvrier, Geevasingha, & Ryan, 2007; Vallat, Tazir, Magdelaine, & Sturtz, 2005). However, with the knowledge of CMT being consistently further enhanced, research has begun to find many subtypes in between some of the above mentioned, most importantly CMT-X or x linked CMT (CMT-X1), which is a form of the disease carried by the parent in the x-chromosome (responsible for determining the child’s sex) and is then passed down. This type of CMT cannot be transferred from male to male (therefore a son cannot inherit this from his father) but it is still found to be more common in men (Pareyson, Scaori & Laura, 2006; Barisic et al., 2008).


Figure 2. Some of the most common symptoms of CMT

Due to most forms of CMT being an autosomal disorder, it is not specific to gender and effects both men and women equally (Dyck, Chance, Lebo & Carney, 1993). All muscles and muscle fiber types are effected with the distal muscles being effected the most severely (Tsairis, 1974; Borg & Ericson-Gripenstedt, 2002; Erikson, Ansved & Borg, 1998). Symptoms include muscle wastage, muscle weakness, atrophy in the lower limb muscles (particularly the calves), reduced (or absent) deep tendon reflexes, change in gait with difficulty in walking/running, arched feet with development of ‘hammer toes’ and muscle cramps. In some cases, the hands are also affected, along with the fore arms, leading to hand tremors and a clawed hand posture. Sensory loss generally follows a similar pathway (from lower to upper limb) causing loss of sensation within the feet and hands in terms of pain, vibration and touch (Shy et al, 2005; Pareyson, Scaori & Laura, 2006; Barisic et al., 2008; Jani-Acsadi, Krajewski, & Shy, 2008; Reilly, 2007; Szigeti & Lupski, 2009). Onset has been recorded in some cases at such early age that it has caused hypotonia (‘floppy baby syndrome’) and delayed motor development, whilst in other cases, CMT has not fully expressed itself until much later on in life (Pareyson & Marchesi, 2009).

Rehabilitative Considerations

Unfortunately, there is currently still no effective or known drug therapy for CMT, leaving treatment limited to rehabilitation therapy or surgical procedures in the case of skeletal deformities or soft tissue abnormalities, while clinical and animal trials are still currently in the works (Young, De Jonghe, Stögbauer, & Butterfass‐Bahloul, 2008; Sackley et al, 2009). This means the management of CMT in patients requires an interdisciplinary approach with the collaboration of a neurologist, physiotherapist/qualified strength coach and other professionals (Erikson, Ansved & Borg, 1998).

The biggest implication of training patients with a neuromuscular disease such as CMT is the ‘overwork hypothesis’ within which research has pointed towards weakness being further induced from resistance training or general overload (Vinci et al., 2003; van Pomeren et al., 2009). This originated from the study of Kilmer et al., (1994) who observed an increase in injury after a high intensity home based resistance training programme, and concluded that increases in training frequency, volume and particularly intensity is a major risk for patients suffering a neuromuscular disease. Lindeman et al., (1995) found improvements in strength and functional ability after a moderate -high intensity training programme in CMT patients, suggesting that high intensity training is possibly a grey area for training prescription.

Chetlin et al., (2004) observed a twelve week home based resistance training programme focused on improving strength, body composition and activities of daily living, and found that activities of daily living and strength were significantly improved from baseline in both men and women. The programme used in the experimental design placed emphasis on the knee and elbow extensors and flexors, with resistance exercises such as tricep extensions, bicep curls, leg extensions and leg curls. This suggests that moderate exercises can be safe and effective for CMT patients to improve strength and performance in day to day activities.

Though it is yet to be a proven method of rehabilitative therapy for CMT patients, it has been theorised that passive stretching of the ankle flexors and extensors could be prescribed within programming to help counteract tendon retractions and improve it’s reflex ability (Refshauge et al., 2006). Matjacić and Zupan, (2006) also observed the effects of passive stretching along with exercises aimed at general muscle strengthening and balance either guided by a physical therapist or by the set balance apparatus, over a twelve-session intervention and concluded postural and dynamic balance training to be a useful training modality to improve balance and mobility. They suggested this may be due to an improvement in utilisation of compensatory balance and movement strategies of the proximal muscle groups as the distal lower limbs wiuld have been significantly weakened due to CMT.

Patients with CMT have also been reported to present reduced peak oxygen consumption (Vo2 Max) values and a generally decreased aerobic capacity and it has been suggested moderate aerobic exercise may improve functional ability and aerobic capacity but this is yet to be further studied and proven (El Mhandi et al., 2007).

In summary, though it may be difficult for a strength coach, physiotherapist or patient to conclude much on exercise prescriptions and recommendations from this brief overview on the current literature in the field of CMT, it is however safe to conclude:

  • Resistance exercise can be beneficial if the patients level of weakness is not severe, and if the rate of progression of the disease is relatively slow.
  • High-intensity resistance exercises/programmes have no advantage over moderate intensity training programmes (Kilmer, 2002).



Barisic, N., Claeys, K. G., Sirotković‐Skerlev, M., Löfgren, A., Nelis, E., De Jonghe, P., & Timmerman, V. (2008). Charcot‐Marie‐Tooth Disease: A Clinico‐genetic Confrontation. Annals of human genetics72(3), 416-441.

Borg, K., & Ericson-Gripenstedt, U. (2002). Muscle biopsy abnormalities differ between Charcot-Marie-Tooth type 1 and 2: reflect different pathophysiology?. Exercise and sport sciences reviews30(1), 4-7.

Chetlin, R. D., Gutmann, L., Tarnopolsky, M. A., Ullrich, I. H., & Yeater, R. A. (2004). Resistance training exercise and creatine in patients with Charcot–Marie–Tooth disease. Muscle & nerve30(1), 69-76.

Dyck, P., Chance, P., Lebo, R., Carney, J. (1993). Hereditary motor and sensory neuropathies. In: Dyck P, Thomas P, editors. Peripheral neuropathy, 3rd ed. Philadelphia: WB Saunders; p 1094- 136.

Dyck, P. J., Karnes, J. L., & Lambert, E. H. (1989). Longitudinal study of neuropathic deficits and nerve conduction abnormalities in hereditary motor and sensory neuropathy type 1. Neurology39(10), 1302-1302.

El Mhandi, L., Calmels, P., Camdessanché, J. P., Gautheron, V., & Féasson, L. (2007). Muscle strength recovery in treated Guillain-Barré syndrome: a prospective study for the first 18 months after onset. American Journal of Physical Medicine & Rehabilitation86(9), 716-724.

Ericson, U., Ansved, T., & Borg, K. (1998). Charcot‐Marie‐Tooth disease type 1 and 2‐an immunohistochemical study of muscle fibre cytoskeletal proteins and a maker for muscle fibre cytoskeletal proteins and a marker for muscle fibre regeneration. European journal of neurology5(6), 545-551.

Herrmann, D. N. (2008). Experimental therapeutics in hereditary neuropathies: the past, the present, and the future. Neurotherapeutics5(4), 507-515.

Hoogendijk, J. E., de Visser, M., Bolhuis, P. A., Hart, A. A., & de Visser, B. W. O. (1994). Hereditary motor and sensory neuropathy type I: clinical and neurographical features of the 17p duplication subtype. Muscle & nerve17(1), 85-90.

Houlden, H., Laura, M., Wavrant–De Vrièze, F., Blake, J., Wood, N., & Reilly, M. M. (2008). Mutations in the HSP27 (HSPB1) gene cause dominant, recessive, and sporadic distal HMN/CMT type 2. Neurology71(21), 1660-1668.

Jani-Acsadi, A., Krajewski, K., & Shy, M. E. (2008, April). Charcot-Marie-Tooth neuropathies: diagnosis and management. In Seminars in neurology (Vol. 28, No. 02, pp. 185-194). © Thieme Medical Publishers.

Kilmer, D. D. (2002). Response to resistive strengthening exercise training in humans with neuromuscular disease. American journal of physical medicine & rehabilitation81(11), S121-S126.

Kilmer, D. D., Wright, N. C., & Aitkens, S. (2005). Impact of a home-based activity and dietary intervention in people with slowly progressive neuromuscular diseases. Archives of physical medicine and rehabilitation86(11), 2150-2156.

Kilmer, D. D., McCrory, M. A., Wright, N. C., Aitkens, S. G., & Bernauer, E. M. (1994). The effect of a high resistance exercise program in slowly progressive neuromuscular disease. Archives of physical medicine and rehabilitation75(5), 560-563.

Krajewski, K. M., Lewis, R. A., Fuerst, D. R., Turansky, C., Hinderer, S. R., Garbern, J., & Shy, M. E. (2000). Neurological dysfunction and axonal degeneration in Charcot–Marie–Tooth disease type 1A. Brain123(7), 1516-1527.

Lindeman, E., Leffers, P., Spaans, F., Drukker, J., Reulen, J., Kerckhoffs, M., & Köke, A. (1995). Strength training in patients with myotonic dystrophy and hereditary motor and sensory neuropathy: a randomized clinical trial. Archives of physical medicine and rehabilitation76(7), 612-620.

Martyn, C.N., Hughes, R.A.C. (1997). Epidemiology of peripheral neuropathy. Journal of Neurology, Neurosurgery and Psychiatry. 62: 310–318.

Matjacić, Z., & Zupan, A. (2006). Effects of dynamic balance training during standing and stepping in patients with hereditary sensory motor neuropathy. Disability and rehabilitation28(23), 1455-1459.

Ouvrier, R., Geevasingha, N., & Ryan, M. M. (2007). Autosomal‐recessive and X‐linked forms of hereditary motor and sensory neuropathy in childhood. Muscle & nerve36(2), 131-143.

Pareyson, D., Scaioli, V., & Laurà, M. (2006). Clinical and Electrophysiological Aspects of Charcot-Marie-Tooth Disease. NeuroMolecular Medicine,8(1-2), 3-22.

Raeymaekers, P., Timmerman, V., Nelis, E., De Jonghe, P., Hoogenduk, J. E., Baas, F., & Van Broeckhoven, C. (1991). Duplication in chromosome 17p11. 2 in Charcot-Marie-Tooth neuropathy type 1a (CMT 1a). Neuromuscular Disorders1(2), 93-97.

Refshauge, K. M., Raymond, J., Nicholson, G., & van den Dolder, P. A. (2006). Night splinting does not increase ankle range of motion in people with Charcot-Marie-Tooth disease: a randomised, cross-over trial. Australian Journal of Physiotherapy52(3), 193-199.

Reilly, M. M. (2007). Sorting out the inherited neuropathies. Practical neurology7(2), 93-105.

Sackley, C., Disler, P. B., Turner‐Stokes, L., Wade, D. T., Brittle, N., & Hoppitt, T. (2009). Rehabilitation interventions for foot drop in neuromuscular disease. The Cochrane Library.

Scherer, S. S., & Wrabetz, L. (2008). Molecular mechanisms of inherited demyelinating neuropathies. Glia56(14), 1578-1589.

Shy, M. E. (2006). Therapeutic strategies for the inherited neuropathies. Neuromolecular medicine8(1-2), 255-278.

Shy, M., Lupski, J.R., Chance, P.F., Klein, C.J., Dyck, P.J. (2005). Hereditary motor and sensory neuropathies: an overview of clinical, genetic, electrophysiologic and pathologic features. In: Dyck PJ, Thomas PK, eds. Peripheral neuropathy 4th edn. Philadelphia: Elsevier Saunders. 1623–58.

Szigeti, K., & Lupski, J. R. (2009). Charcot–Marie–Tooth disease. European Journal of Human Genetics17(6), 703-710.

Szigeti, K., Garcia, C. A., & Lupski, J. R. (2006). Charcot-Marie-Tooth disease and related hereditary polyneuropathies: molecular diagnostics determine aspects of medical management. Genetics in Medicine8(2), 86-92.

Tsairis, P. (1974). Muscle Biopsy: A Modern Approach. Archives of Neurology31(2), 143-143.

Vallat, J. M., Tazir, M., Magdelaine, C., & Sturtz, F. (2005). Autosomal-recessive Charcot-Marie-Tooth diseases. Journal of Neuropathology & Experimental Neurology64(5), 363-370.

van Pomeren, M., Selles, R. W., van Ginneken, B. T., Schreuders, T. A., Janssen, W. G., & Stam, H. J. (2009). The hypothesis of overwork weakness in Charcot-Marie-Tooth: a critical evaluation. Journal of rehabilitation medicine41(1), 32-34.

Vinci, P., Esposito, C., Perelli, S. L., Antenor, J. A. V., & Thomas, F. P. (2003). Overwork weakness in Charcot-Marie-Tooth disease. Archives of physical medicine and rehabilitation84(6), 825-827.

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An Introduction to Performance Training.


“One of the misconceptions in the sports world is that a sports person gets in shape by just playing or taking part in his/her chosen sport. If a stationary level of performance, consistent ability in executing a few limited skills is your goal, then engaging only in your sport will keep you there. However, if you want the utmost efficiency, consistent improvement, and balanced abilities sportsmen and women must participate in year round conditioning programs.The bottom line in sports conditioning and fitness training is stress, not mental stress, but adaptive body stress. Sportsmen and women must put their bodies under a certain amount of stress (overload) to increase physical capabilities.” Tancred, 1995

Many people affiliate the term ‘training’ or ‘fitness’ to just strolling into a gym either loaded with weights or treadmills.
But the truth is, the term has such a broad meaning which people have misunderstood so badly, to the extent that they just have no clue what they do in the gym or on a treadmill, but as long as it makes them slightly tired or sweaty, they feel they have achieved something.

How many times have you come across someone in the gym that attempts to bicep curl or tricep pull-down the whole line of weights on the cable machine and sees that as their ultimate sign of progress? How many times have you seen others scoff at people run for a few miles and stick to the lighter weights for multiple reps and sets? How many times have you come across a guy/girl who dead-lifts a phenomenal amount of weight for the size he/she is?

The truth is, each person should be training for their own goals. And the goals vary depending on the person, their sport, their weaknesses/strengths and much more.

However, while the goals of every person may vary, the components of one’s ‘fitness’ or ‘training’ are of few. This means the goals are generally based around these few components.

These include:

1) Power – Exerting maximum muscular contraction/force within the shortest amount of time (A combination of Strength and Speed)
E.g: Weightlifting (to some degree), Wrestling, Judo


2) Strength – How much a muscle can exert itself against resistance.
E.g: Maximal Strength sports – Powerlifting


3) Cardiovascular Endurance – Ability and efficiency of the heart in providing blood and oxygen to the working muscles.
E.g: Marathons

4) Muscular Endurance – Ability and efficiency of a single muscle to contract under a sustained strain.
E.g: Rowing, Boxing

5) Strength Endurance – Ability of a muscle to contract maximally repeatedly.
E.g: Baseball throws, Roundhouse kick


6) Flexibility – Ability of extending range of motion within the body.
E.g: Splits


7) Agility – Ability to perform explosive fast movements within opposite  directions.
E.g: 90 or 180 degree turns/cuts in any field based sports


8) Balance – Ability to control movement of body when either moving or  being still.
E.g: Gymnastics


9) Coordination – The ability to combine all/most of these components effectively to perform a movement.

NOTE: Most sports contain a combination of many components. It is very rare an athlete only possesses just one!

Notice anything missing? Were you looking for something?  Hypertrophy/mass/size?
Well that’s the thing..

Being muscular or aesthetic or ‘dench’ ISN’T a component of fitness. However it may be a by-product of some of the training done by an athlete, or an aid to helping him/her achieve one of the components.


Hence many argue, Bodybuilding not being a sport, but more an art. A deep appreciation for the outward look of muscular symmetry but not with much function to do something within a sport which require skill along with any of the above mentioned components. However bodybuilders themselves may vary individually; some will decide to stay more athletic than the others by working on some of the above mentioned components of fitness.

(This is not a rip off on bodybuilding!)

If your goal is to truly stimulate muscle growth or fat breakdown so that you look more aesthetic and ‘bigger’, then there is no problem with sticking to the principles of training for hypertrophy or lipolysis and cracking on with just that! I stress with sticking to the principles due to it allowing you to not be one of those wanderers who just have a vague idea of the concept of training and freestyle as they go along, but instead, is a person with set goals and an understanding mindset towards where their routines will lead them towards.


Don’t forget! Being powerful doesn’t necessitate you will be extremely muscular and aesthetic either. It’s very easy to think a huge muscular person is very powerful/strong, but that isn’t always the case! Power is a combination of strength AND speed and they will need BOTH. As for their strength, their are many types; is their relative strength compared to others in their weight class up to standard? Well, that’s another question in itself!

Lu xiaojun CHN 77kg
Incredible attempt with a world record 175kg!!! But what does HE weigh? -77kg!

What are YOU training for?