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This book surveys the research evidence into exercise-induced fatigue and discusses how knowledge of fatigue can be applied in sport and exercise contexts. The book examines the different \"types\" of fatigue and the difficulties of identifying which types are prevalent during different types of exercise. It introduces the fundamental science of fatigue, focusing predominantly on physiological and neuromuscular aspects, and explores key topics in detail, such as energy depletion, lactic acid, dehydration, electrolytes and minerals, and the perception of fatigue.-- From publisher's description.

Maximal central motor drive is known to decrease during prolonged exercise although it remains to be determined whether a supraspinal deficit exists, and if so, when it appears. The purpose of this study was to evaluate corticospinal excitability and muscle voluntary activation before, during and after a 4-h cycling exercise. Ten healthy subjects performed three 80-min bouts on an ergocycle at 45% of their maximal aerobic power. Before exercise and immediately after each bout, neuromuscular function was evaluated in the quadriceps femoris muscles under isometric conditions. Transcranial magnetic stimulation was used to assess voluntary activation at the cortical level (VATMS), corticospinal excitability via motor-evoked potential (MEP) and intracortical inhibition by cortical silent period (CSP). Electrical stimulation of the femoral nerve was used to measure voluntary activation at the peripheral level (VAFNES) and muscle contractile properties. Maximal voluntary force was significantly reduced after the first bout (13 ± 9%, P<0.01) and was further decreased (25 ± 11%, P<0.001) at the end of exercise. CSP remained unchanged throughout the protocol. Rectus femoris and vastus lateralis but not vastus medialis MEP normalized to maximal M-wave amplitude significantly increased during cycling. Finally, significant decreases in both VATMS and VAFNES (∼ 8%, P<0.05 and ∼ 14%, P<0.001 post-exercise, respectively) were observed. In conclusion, reductions in VAFNES after a prolonged cycling exercise are partly explained by a deficit at the cortical level accompanied by increased corticospinal excitability and unchanged intracortical inhibition. When comparing the present results with the literature, this study highlights that changes at the cortical and/or motoneuronal levels depend not only on the type of exercise (single-joint vs. whole-body) but also on exercise intensity and/or duration.

Exercise-induced fatigue causes changes within the central nervous system that decrease force production capacity in fatigued muscles. The impact on unrelated, non-exercised muscle performance is still unclear. The primary aim of this study was to examine the impact of a bilateral forearm muscle contraction on the motor function of the distal and unrelated ankle plantar-flexor muscles. The secondary aim was to compare the impact of maximal and submaximal forearm contractions on the non-fatigued ankle plantar-flexor muscles. Maximal voluntary contractions (MVC) of the forearm and ankle plantar-flexor muscles as well as voluntary activation (VA) and twitch torque of the ankle plantar-flexor muscles were assessed pre-fatigue and throughout a 10-min recovery period. Maximal (100 % MVC) and submaximal (30 % MVC) sustained isometric handgrip contractions caused a decreased handgrip MVC (to 49.3 ± 15.4 and 45.4 ± 11.4 % of the initial MVC for maximal and submaximal contraction, respectively) that remained throughout the 10-min recovery period. The fatigue protocols also caused a decreased ankle plantar-flexor MVC (to 77 ± 8.3 and 92.4 ± 6.2 % of pre-fatigue MVC for maximal and submaximal contraction, respectively) and VA (to 84.3 ± 15.7 and 97.7 ± 16.1 % of pre-fatigue VA for maximal and submaximal contraction, respectively). These results suggest central fatigue created by the fatiguing handgrip contraction translated to the performance of the non-exercised ankle muscles. Our results also show that the maximal fatigue protocol affected ankle plantar-flexor MVC and VA more severely than the submaximal protocol, highlighting the task-specificity of neuromuscular fatigue.

Previous studies attempted to compare the effectiveness of isokinetic and isotonic training. However, they have provided conflicting results. The purpose of this study was to compare the effects of isotonic versus isokinetic standardized concentric strength training programs of the knee extensors on the neuromuscular system. The standardization of these two training programs was ensured by the equalization of the total external amount of work performed and the mean angular movement velocity. Thirty healthy male students were randomly assigned to the isotonic (IT; n  = 11), the isokinetic (IK; n  = 11) or the control (C; n  = 8) group. Both IT and IK groups trained their dominant lower leg 3 sessions/week for 8 weeks on a dynamometer. The IT group exercised using a preset torque of 40% of the maximal voluntary isometric torque at 70° (0° = leg in horizontal position). The IK group exercised at a velocity ranging between 150° and 180° s −1 . Isotonic, isokinetic and isometric tests were performed on a dynamometer before and after strength training. Surface electromyographic activity of vastus lateralis , vastus medialis , rectus femoris , semitendinosus and biceps femoris muscles was recorded during the tests. Significant strength increases in both dynamic and static conditions were noticed for IT and IK groups without any significant difference between the two trained groups. Agonist muscle activity also increased with training but no change in antagonist muscle co-activity was observed. The two training methods could be proposed by clinicians and athletic coaches to improve concentric muscle strength in dynamic and static conditions.

The aim of this study was to determine whether and how young participants modulate their postural response to compensate for postural muscle fatigue during predictable but externally initiated continuous and oscillatory perturbations. Twelve participants performed ten postural trials before and after an ankle muscle fatigue protocol. Each postural trial was 1 min long and consisted of continuous backward and forward oscillations of the platform. Fatigue was induced by intermittent, bilateral isometric contractions of the ankle plantar- and dorsiflexors until the force production was reduced to 50 % of the pre-fatigue maximal voluntary contraction. Changes in the center of mass (COM) displacement, center of pressure (COP) displacement, and anterior–posterior location of the COP within the base of support were quantified as well as the activity of the tibialis anterior (TA), medial gastrocnemius (MG), quadriceps, and hamstring. All participants demonstrated postural stability post-fatigue by maintaining the displacement of their COM. Everyone also demonstrated a general forward shift in the anterior–posterior location of the COP within the base of support; however, two distinct postural modifications, corresponding to either an immediate fatigue-induced increase or decrease in the COP displacement during the backward platform translation, were recorded immediately post-fatigue. The changes in muscle onset latencies lasted beyond the recovery of the force production of the fatigued postural muscles. By 10 min post-fatigue, the participants showed a decrease in the COP displacement as well as an earlier activation of the postural muscles and an increased TA/MG co-activation relative to pre-fatigue. Although different strategies were used, the participants were able to adjust to and overcome postural muscle fatigue and remain balanced during the postural perturbations regardless of the direction of the platform movement. These adjustments lasted beyond the recovery of the ankle muscle force production indicating that they may be part of a centrally mediated protective response as opposed to a peripherally induced limitation to performance.

With regard to intermittent training exercise, the effects of the mode of recovery on subsequent performance are equivocal. To compare the effects of 3 types of recovery intervention on peak torque (PT) and electromyographic (EMG) activity of the knee extensor muscles after fatiguing isokinetic intermittent concentric exercise. Crossover study. Research laboratory. Eight elite judo players (age = 18.4 ± 1.4 years, height = 180 ± 3 cm, mass = 77.0 ± 4.2 kg). Participants completed 3 randomized sessions within 7 days. Each session consisted of 5 sets of 10 concentric knee extensions at 80% PT at 120°/s, with 3 minutes of recovery between sets. Recovery interventions were passive, active, and electromyostimulation. The PT and maximal EMG activity were recorded simultaneously while participants performed isokinetic dynamometer trials before and 3 minutes after the resistance exercise. The PT and maximal EMG activity from the knee extensors were quantified at isokinetic velocities of 60°/s, 120°/s, and 180°/s, with 5 repetitions at each velocity. The reduction in PT observed after electromyostimulation was less than that seen after passive (P < .001) or active recovery (P < .001). The reduction in PT was less after passive recovery than after active recovery (P < .001). The maximal EMG activity level observed after electromyostimulation was higher than that seen after active recovery (P < .05). Electromyostimulation was an effective recovery tool in decreasing neuromuscular fatigue after high-intensity, intermittent isokinetic concentric exercise for the knee extensor muscles. Also, active recovery induced the greatest amount of neuromuscular fatigue.

The concept of fatigue refers to a class of acute effects that can impair motor performance, and not to a single mechanism. A great deal is known about the peripheral mechanisms underlying the process of fatigue, but our knowledge of the roles of the central structures in that process is still very limited. During fatigue, it has been shown that peripheral apparatus is capable of generating adequate force while central structures become insufficient/sub-optimal in driving them. This is known as central fatigue, and it can vary between muscles and different tasks. Fatigue induced by submaximal isometric contraction may have a greater central component than fatigue induced by prolonged maximal efforts. We studied the changes in regional cerebral blood flow (rCBF) of brain structures after sustained isometric muscle contractions of different submaximal force levels and of different durations, and compared them with the conditions observed when the sustained muscle contraction becomes fatiguing. Changes in cortical activity, as indicated by changes in rCBF, were measured using positron emission tomography (PET). Twelve subjects were studied under four conditions: (1) rest condition; (2) contraction of the m. biceps brachii at 30% of MVC, sustained for 60 s; (3) contraction at 30% of MVC, sustained for 120 s, and; (4) contraction at 50% of MVC, sustained for 120 s. The level of rCBF in the activated cortical areas gradually increased with the level and duration of muscle contraction. The fatiguing condition was associated with predominantly contralateral activation of the primary motor (MI) and the primary and secondary somatosensory areas (SI and SII), the somatosensory association area (SAA), and the temporal areas AA and AI. The supplementary motor area (SMA) and the cingula were activated bilaterally. The results show increased cortical activation, confirming that increased effort aimed at maintaining force in muscle fatigue is associated with increased activation of cortical neurons. At the same time, the activation spread to several cortical areas and probably reflects changes in both excitatory and inhibitory cortical circuits. It is suggested that further studies aimed at controlling afferent input from the muscle during fatigue may allow a more precise examination of the roles of each particular region involved in the processing of muscle fatigue.

Background Understanding soccer players’ match-related fatigue and recovery profiles likely helps with developing conditioning programs that increase team performance and reduce injuries and illnesses. In order to improve match recovery (the return-to-play process and ergogenic interventions) it is also pivotal to determine if match simulation protocols and actual match-play lead to similar responses. Objectives (1) To thoroughly describe the development of fatigue during actual soccer match play and its recovery time course in terms of physiological, neuromuscular, technical, biochemical and perceptual responses, and (2) to determine similarities of recovery responses between actual competition (11 vs. 11) and match simulations. Methods A first screening phase consisted of a systematic search on PubMed (MEDLINE) and SportDiscus databases until March 2016. Inclusion criteria were: longitudinal study with soccer players; match or validated protocol; duration > 45 min; and published in English. Results A total of 77 eligible studies ( n  = 1105) were used to compute 1196 effect sizes (ES). Half-time assessments revealed small to large alterations in immunological parameters (e.g. leukocytes, ES = 1.9), a moderate decrement in insulin concentration (ES = − 0.9) and a small to moderate impairment in lower-limb muscle function (ES = − 0.5 to − 0.7) and physical performance measures (e.g. linear sprint, ES = − 0.3 to − 1.0). All the systematically analyzed fatigue-related markers were substantially altered at post-match. Hamstrings force production capacity (ES = − 0.7), physical performance (2–4%, ES = 0.3−0.5), creatine kinase (CK, ES = 0.4), well-being (ES = 0.2−0.4) and delayed onset muscle soreness (DOMS, ES = 0.6–1.3) remained substantially impaired at G + 72 h. Compared to simulation protocols, 11 vs. 11 match format (CK, ES = 1.8) induced a greater magnitude of change in muscle damage (i.e. CK, ES = 1.8 vs. 0.7), inflammatory (IL-6, ES = 2.6 vs. 1.1) and immunological markers and DOMS (ES = 1.5 vs. 0.7) than simulation protocols at post-assessments. Neuromuscular performances at post-match did not differ between protocols. Conclusion While some parameters are fully recovered (e.g. hormonal and technical), our systematic review shows that a period of 72 h post-match play is not long enough to completely restore homeostatic balance (e.g. muscle damage, physical and well-being status). The extent of the recovery period post-soccer game cannot consist of a ‘one size fits all approach’. Additionally, the ‘real match’ (11 vs. 11 format) likely induces greater magnitudes of perceptual (DOMS) and biochemical alterations (e.g. muscle damage), while neuromuscular alterations were essentially similar. Overall, coaches must adjust the structure and content of the training sessions during the 72-h post-match intervention to effectively manage the training load within this time-frame.

Short-duration sprints (<10 seconds), interspersed with brief recoveries (<60 seconds), are common during most team and racket sports. Therefore, the ability to recover and to reproduce performance in subsequent sprints is probably an important fitness requirement of athletes engaged in these disciplines, and has been termed repeated-sprint ability (RSA). This review (Part I) examines how fatigue manifests during repeated-sprint exercise (RSE), and discusses the potential underpinning muscular and neural mechanisms. A subsequent companion review to this article will explain a better understanding of the training interventions that could eventually improve RSA. Using laboratory and field-based protocols, performance analyses have consistently shown that fatigue during RSE typically manifests as a decline in maximal/mean sprint speed (i.e. running) or a decrease in peak power or total work (i.e. cycling) over sprint repetitions. A consistent result among these studies is that performance decrements (i.e. fatigue) during successive bouts are inversely correlated to initial sprint performance. To date, there is no doubt that the details of the task (e.g. changes in the nature of the work/recovery bouts) alter the time course/magnitude of fatigue development during RSE (i.e. task dependency) and potentially the contribution of the underlying mechanisms. At the muscle level, limitations in energy supply, which include energy available from phosphocreatine hydrolysis, anaerobic glycolysis and oxidative metabolism, and the intramuscular accumulation of metabolic by-products, such as hydrogen ions, emerge as key factors responsible for fatigue. Although not as extensively studied, the use of surface electromyography techniques has revealed that failure to fully activate the contracting musculature and/or changes in inter-muscle recruitment strategies (i.e. neural factors) are also associated with fatigue outcomes. Pending confirmatory research, other factors such as stiffness regulation, hypoglycaemia, muscle damage and hostile environments (e.g. heat, hypoxia) are also likely to compromise fatigue resistance during repeated-sprint protocols.