Muscle fatigue: what, why and how it influences muscle function
TL;DR: Experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue are reviewed, providing insight into the rate‐limiting adjustments that constrain muscle function during fatiguing contractions.
Abstract: Much is known about the physiological impairments that can cause muscle fatigue. It is known that fatigue can be caused by many different mechanisms, ranging from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor command in the motor cortex, and that there is no global mechanism responsible for muscle fatigue. Rather, the mechanisms that cause fatigue are specific to the task being performed. The development of muscle fatigue is typically quantified as a decline in the maximal force or power capacity of muscle, which means that submaximal contractions can be sustained after the onset of muscle fatigue. There is even evidence that the duration of some sustained tasks is not limited by fatigue of the principal muscles. Here we review experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue. Selected comparisons of tasks, groups of individuals and interventions with the task-failure approach can provide insight into the rate-limiting adjustments that constrain muscle function during fatiguing contractions.
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TL;DR: Time domain, frequency domain, time-frequency and time-scale representations, and other methods such as fractal analysis and recurrence quantification analysis are described succinctly and are illustrated with their biomechanical applications, research or clinical alike.
694 citations
Cites background from "Muscle fatigue: what, why and how i..."
...Although simple to determine, results obtained in this manner depend also on psychological factors like motivation, associated with task conditions (Enoka, 1995; Enoka and Duchateau, 2008)....
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TL;DR: A unified taxonomy and a novel assessment approach to addressing distinct aspects of fatigue and fatigability in clinical and research settings are proposed and it is suggested that many research questions may be better addressed by using multiple measures.
Abstract: Fatigue is commonly reported in many neurologic illnesses, including multiple sclerosis, Parkinson disease, myasthenia gravis, traumatic brain injury, and stroke. Fatigue contributes substantially to decrements in quality of life and disability in these illnesses. Despite the clear impact of fatigue as a disabling symptom, our understanding of fatigue pathophysiology is limited and current treatment options rarely lead to meaningful improvements in fatigue. Progress continues to be hampered by issues related to terminology and assessment. In this article, we propose a unified taxonomy and a novel assessment approach to addressing distinct aspects of fatigue and fatigability in clinical and research settings. This taxonomy is based on our current knowledge of the pathophysiology and phenomenology of fatigue and fatigability. Application of our approach indicates that the assessment and reporting of fatigue can be clarified and improved by utilizing this taxonomy and creating measures to address distinct aspects of fatigue and fatigability. We review the strengths and weaknesses of several common measures of fatigue and suggest, based on our model, that many research questions may be better addressed by using multiple measures. We also provide examples of how to apply and validate the taxonomy and suggest directions for future research.
617 citations
Cites background from "Muscle fatigue: what, why and how i..."
...Even among studies that define fatigue, there is a considerable range of definitions.(41) Attempts to remedy this situation by adding modifiers to the term fatigue are similarly limited by the lack of standards to anchor these terms....
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TL;DR: A case is made for a unified definition of fatigue to facilitate its management in health and disease and the proposed framework provides a foundation to address the many gaps in knowledge of how laboratory measures of fatigue and fatigability affect real-world performance.
Abstract: Despite flourishing interest in the topic of fatigue-as indicated by the many presentations on fatigue at the 2015 Annual Meeting of the American College of Sports Medicine-surprisingly little is known about its effect on human performance. There are two main reasons for this dilemma: 1) the inability of current terminology to accommodate the scope of the conditions ascribed to fatigue, and 2) a paucity of validated experimental models. In contrast to current practice, a case is made for a unified definition of fatigue to facilitate its management in health and disease. On the basis of the classic two-domain concept of Mosso, fatigue is defined as a disabling symptom in which physical and cognitive function is limited by interactions between performance fatigability and perceived fatigability. As a symptom, fatigue can only be measured by self-report, quantified as either a trait characteristic or a state variable. One consequence of such a definition is that the word fatigue should not be preceded by an adjective (e.g., central, mental, muscle, peripheral, and supraspinal) to suggest the locus of the changes responsible for an observed level of fatigue. Rather, mechanistic studies should be performed with validated experimental models to identify the changes responsible for the reported fatigue. As indicated by three examples (walking endurance in old adults, time trials by endurance athletes, and fatigue in persons with multiple sclerosis) discussed in the review, however, it has proven challenging to develop valid experimental models of fatigue. The proposed framework provides a foundation to address the many gaps in knowledge of how laboratory measures of fatigue and fatigability affect real-world performance.
513 citations
Cites background from "Muscle fatigue: what, why and how i..."
...Indeed, much of the literature on the physiology of fatigue is focused on exploiting a range of experimental protocols to quantify the capabilities of the neuromuscular system in various contexts (18,22,34,46,59)....
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TL;DR: The high correlations found between mechanical (velocity and countermovement jump height losses) and metabolic (lactate, ammonia) measures of fatigue support the validity of using velocity loss to objectively quantify neuromuscular fatigue during resistance training.
Abstract: SANCHEZ-MEDINA, L., and J. J. GONZALEZ-BADILLO. Velocity Loss as an Indicator of Neuromuscular Fatigue during Resistance Training. Med. Sci. Sports Exerc., Vol. 43, No. 9, pp. 1725-1734, 2011. Purpose: This study aimed to analyze the acute mechanical and metabolic response to resistance exercise protocols (REP) differing in the number of repetitions (R) performed in each set (S) with respect to the maximum predicted number (P). Methods: Over 21 exercise sessions separated by 48-72 h, 18 strength-trained males (10 in bench press (BP) and 8 in squat (SQ)) performed 1) a progressive test for one-repetition maximum (1RM) and load-velocity profile determination, 2) tests of maximal number of repetitions to failure (12RM, 10RM, 8RM, 6RM, and 4RM), and 3) 15 REP (S R(P): 3 6(12), 3 8(12), 3 10(12), 3 12(12), 3 6(10), 3 8(10), 3 10(10), 3 4(8), 3 6(8), 3 8(8), 3 3(6), 3 4(6), 3 6(6), 3 2(4), 3 4(4)), with 5-min interset rests. Kinematic data were registered by a linear velocity transducer. Blood lactate and ammonia were measured before and after exercise. Results: Mean repetition velocity loss after three sets, loss of velocity pre-post exercise against the 1-mIs j1 load, and countermovement jump height loss (SQ group) were significant for all REP and were highly correlated to each other (r = 0.91-0.97). Velocity loss was significantly greater for BP compared with SQ and strongly correlated to peak postexercise lactate (r = 0.93-0.97) for both SQ and BP. Unlike lactate, ammonia showed a curvilinear response to loss of velocity, only increasing above resting levels when R was at least two repetitions higher than 50% of P. Conclusions: Velocity loss and metabolic stress clearly differs when manipulating the number of repetitions actually performed in each training set. The high correlations found between mechanical (velocity and coun- termovement jump height losses) and metabolic (lactate, ammonia) measures of fatigue support the validity of using velocity loss to
510 citations
Cites background or methods from "Muscle fatigue: what, why and how i..."
...0 †62 T 14 †††71 T 11 3 8[12] 32....
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...maximal number of repetitions to failure (12RM, 10RM, 8RM, 6RM, and 4RM), and 3) 15 REP (S R[P]: 3 6[12], 3 8[12], 3 10[12],...
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...All these sessions were conducted on separate days, with 48 h of recovery time except the initial 1RM test, the XRM assessments, and the 3 12[12], 3 10[10], 3 8[8], and 3 6[6] REP (i....
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...12[12], 3 10[12], 3 10[10], 3 8[10], 3 8[8], and...
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..., 8 of 12 possible repetitions with a given load (8[12]) compared with performing all repetitions (12[12])....
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TL;DR: The need to understand sex‐based differences in fatigability to shed light on the benefits and limitations that fatigability can exert for men and women during daily tasks, exercise performance, training and rehabilitation in both health and disease is emphasized.
Abstract: Sex-related differences in physiology and anatomy are responsible for profound differences in neuromuscular performance and fatigability between men and women. Women are usually less fatigable than men for similar intensity isometric fatiguing contractions. This sex difference in fatigability, however, is task specific because different neuromuscular sites will be stressed when the requirements of the task are altered, and the stress on these sites can differ for men and women. Task variables that can alter the sex difference in fatigability include the type, intensity and speed of contraction, the muscle group assessed and the environmental conditions. Physiological mechanisms that are responsible for sex-based differences in fatigability may include activation of the motor neurone pool from cortical and subcortical regions, synaptic inputs to the motor neurone pool via activation of metabolically sensitive small afferent fibres in the muscle, muscle perfusion and skeletal muscle metabolism and fibre type properties. Non-physiological factors such as the sex bias of studying more males than females in human and animal experiments can also mask a true understanding of the magnitude and mechanisms of sex-based differences in physiology and fatigability. Despite recent developments, there is a tremendous lack of understanding of sex differences in neuromuscular function and fatigability, the prevailing mechanisms and the functional consequences. This review emphasizes the need to understand sex-based differences in fatigability to shed light on the benefits and limitations that fatigability can exert for men and women during daily tasks, exercise performance, training and rehabilitation in both health and disease.
368 citations
Cites background from "Muscle fatigue: what, why and how i..."
...This activity-induced reduction in force or power is known as muscle fatigue (Gandevia 2001, Enoka & Duchateau 2008, Kent-Braun et al. 2012) or fatigability (Kluger et al. 2013)....
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...A functionally relevant approach has been to vary the task requirements and environment of a fatiguing contraction in order to stress different sites (or the same site at a different rate) within the neuromuscular system (Hunter et al. 2004a, Enoka & Duchateau 2008)....
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...Despite recent developments in our understanding of the mechanisms of muscle fatigue [e.g. (Gandevia 2001, Enoka & Duchateau 2008, Kent-Braun et al. 2012)], there is still a tremendous lack of knowledge and appreciation of sex-based differences in fatigability and the prevailing mechanisms under…...
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References
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TL;DR: Evidence for "central" fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it.
Abstract: Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal cha...
3,200 citations
TL;DR: In order to stimulate further adaptation toward a specific training goal(s), progression in the type of resistance training protocol used is necessary and emphasis should be placed on multiple-joint exercises, especially those involving the total body.
Abstract: In order to stimulate further adaptation toward a specific training goal(s), progression in the type of resistance training protocol used is necessary. The optimal characteristics of strength-specific programs include the use of both concentric and eccentric muscle actions and the performance of both single- and multiple-joint exercises. It is also recommended that the strength program sequence exercises to optimize the quality of the exercise intensity (large before small muscle group exercises, multiple-joint exercises before single-joint exercises, and higher intensity before lower intensity exercises). For initial resistances, it is recommended that loads corresponding to 8-12 repetition maximum (RM) be used in novice training. For intermediate to advanced training, it is recommended that individuals use a wider loading range, from 1-12 RM in a periodized fashion, with eventual emphasis on heavy loading (1-6 RM) using at least 3-min rest periods between sets performed at a moderate contraction velocity (1-2 s concentric, 1-2 s eccentric). When training at a specific RM load, it is recommended that 2-10% increase in load be applied when the individual can perform the current workload for one to two repetitions over the desired number. The recommendation for training frequency is 2-3 d x wk(-1) for novice and intermediate training and 4-5 d x wk(-1) for advanced training. Similar program designs are recommended for hypertrophy training with respect to exercise selection and frequency. For loading, it is recommended that loads corresponding to 1-12 RM be used in periodized fashion, with emphasis on the 6-12 RM zone using 1- to 2-min rest periods between sets at a moderate velocity. Higher volume, multiple-set programs are recommended for maximizing hypertrophy. Progression in power training entails two general loading strategies: 1) strength training, and 2) use of light loads (30-60% of 1 RM) performed at a fast contraction velocity with 2-3 min of rest between sets for multiple sets per exercise. It is also recommended that emphasis be placed on multiple-joint exercises, especially those involving the total body. For local muscular endurance training, it is recommended that light to moderate loads (40-60% of 1 RM) be performed for high repetitions (> 15) using short rest periods (< 90 s). In the interpretation of this position stand, as with prior ones, the recommendations should be viewed in context of the individual's target goals, physical capacity, and training status.
2,845 citations
"Muscle fatigue: what, why and how i..." refers background in this paper
...This concept is analogous to the principle of specificity that characterizes the adaptations evoked by several weeks of physical training (Kraemer et al. 2002; Aagaard & Bangsbo, 2006)....
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Journal Article•
2,160 citations
TL;DR: Intracellular stimulation of individual motoneurones ensured functional isolation of the muscle units innervated by them in pentobarbitone‐anaesthetized cats.
Abstract: 1. A variety of physiological properties of single motor units have been studied in the gastrocnemius muscle (primarily in the medial head) of pentobarbitone-anaesthetized cats. Intracellular stimulation of individual motoneurones ensured functional isolation of the muscle units innervated by them.
2. A system for muscle unit classification was developed using a combination of two physiological properties. Almost all of the units studied could be classified into one of three major types, including two groups with relatively short twitch contraction times (types FF and FR, which were differentiable from one another on the basis of sensitivity to fatigue) and one group with relatively long contraction times (type S, which were extremely resistant to fatigue and were differentiable from FF and FR units on the basis of the shape of unfused tetani). Post-tetanic potentiation of twitch responses was observed in all three muscle unit types. The distributions of axonal conduction velocities for motoneurones innervating FF and FR muscle units were essentially the same, while conduction velocities for motoneurones innervating type S units were, in general, slower.
3. Histochemical profiles of muscle units representative of each of the physiological classes present in the gastrocnemius pool were determined using a method of glycogen depletion for muscle unit identification. Each of the physiological categories of muscle units exhibited a corresponding unique set of muscle fibre staining reactions, or histochemical profile. Within each physiological type, all of the units examined had the same histochemical profile. The results generally support the hypothesis that the histochemical characteristics of muscle fibres are meaningfully related to the physiological properties of the same fibres. However, certain limitations in the detailed application of the hypothesis were also apparent.
4. Systematic assessment of the histochemical profiles of relatively large numbers of fibres belonging to single muscle units provided strong support for the hypothesis that all of the muscle fibres innervated by a single α-motoneurone are histochemically identical.
1,514 citations
"Muscle fatigue: what, why and how i..." refers background in this paper
...Since the early observations on the differences in the contractile properties of red and white muscle and the classification of motor units based on fatigability (Buller et al. 1960; Edström & Kugelberg, 1968; Burke et al. 1973), the endurance capacity of muscle, at least in experimental animals with electrically evoked contractions, can depend on the proportion of its muscle fibre types (Cairns et al....
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...…properties of red and white muscle and the classification of motor units based on fatigability (Buller et al. 1960; Edström & Kugelberg, 1968; Burke et al. 1973), the endurance capacity of muscle, at least in experimental animals with electrically evoked contractions, can depend on the…...
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TL;DR: The paper shows that a maximal voluntary effort develops the same tension as a maximal tetanus artificially excited; in the second part the same equality is found to persist during fatigue, implying that in fatigue, too, the limitation of strength is peripheral.
Abstract: In voluntary efforts it is not known for certain whether the force that can be exerted is limited by the capacity of the nervous centres and conducting pathways to deliver motor impulses to the muscle fibres or by the intrinsic contractile properties of the fibres themselves; whether, in fact, a voluntary effort can be bettered by maximal tetanic stimulation of the muscle electrically, or not. Again in fatigue it is undecided whether tension falls because the degree of voluntary innervation drops or because the fibres are biochemically incapable of maintaining their contraction. The experiments described here attempt to settle these questions by comparing directly voluntary tension with that resulting from electrically excited motor volleys. To make a valid comparison in an intact human subject is difficult, but it will be argued that it can be achieved by using a particularly convenient muscle, the adductor of the thumb, and special apparatus. The paper falls into three parts: the first shows that a maximal voluntary effort develops the same tension as a maximal tetanus artificially excited; in the second part the same equality is found to persist during fatigue, implying that in fatigue, too, the limitation of strength is peripheral; finally the effect of ischaemia is described. Preliminary accounts have already appeared (Merton & Pampiglione, 1950; Merton, 1950).
1,437 citations
"Muscle fatigue: what, why and how i..." refers background or methods in this paper
...…used to quantify the development of muscle fatigue is to interrupt the fatiguing exercise with brief maximal contractions (voluntary or electrically evoked) to estimate the decline in the maximal force capacity (Merton, 1954; Bigland-Ritchie et al. 1986b; Hunter et al. 2004b; Søgaard et al. 2006)....
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...A common protocol used to quantify the development of muscle fatigue is to interrupt the fatiguing exercise with brief maximal contractions (voluntary or electrically evoked) to estimate the decline in the maximal force capacity (Merton, 1954; Bigland-Ritchie et al. 1986b; Hunter et al. 2004b; Søgaard et al. 2006)....
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...If activation is inadequate, a few electrical stimuli delivered to the motor nerve during an MVC will evoke additional force from the muscle (Merton, 1954)....
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