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Purpose: Prolonged cycling exercise performance in normoxia is limited because of both peripheral and central neuromuscular impairments. It has been reported that cerebral perturbations are greater during short-duration exercise in hypoxia compared with normoxia. The purpose of this study was to test the hypothesis that central deficits are accentuated in hypoxia compared with normoxia during prolonged (three bouts of 80 min separated by 25 min) whole-body exercise at the same relative intensity., Methods: Ten subjects performed two sessions consisting of three 80-min cycling bouts at 45% of their relative maximal aerobic power in normoxia and hypoxia (FiO2 = 0.12). Before exercise and after each bout, maximal voluntary force, voluntary activation assessed with nerve stimulation and transcranial magnetic stimulation, corticospinal excitability (motor evoked potential), intracortical inhibition (cortical silent period), and electrical (M-wave) and contractile (twitch and doublet peak forces) properties of the knee extensors were measured. Prefrontal and motor cortical oxygenation was also recorded during each cycling bout in both conditions., Results: A significant but similar force reduction (≈-22%) was observed at the end of exercise in normoxia and hypoxia. The modifications of voluntary activation assessed with transcranial magnetic stimulation and nerve stimulation, motor evoked potential, cortical silent period, and M-wave were also similar in both conditions. However, cerebral oxygenation was reduced in hypoxia compared with normoxia., Conclusion: These findings show that when performed at the same relative low intensity, prolonged exercise does not induce greater supraspinal fatigue in hypoxia compared with normoxia. Despite lower absolute exercise intensities in hypoxia, reduced brain O2 availability might contribute to similar amounts of central fatigue compared with normoxia.

Introduction: The central nervous system can play a critical role in limiting exercise performance during hypoxic conditions. Hypocapnia, which is associated with hypoxia-induced hyperventilation, may affect cerebral perfusion. We hypothesized that CO2 clamping during hypoxic isometric knee extensions would improve cerebral oxygenation and reduce central fatigue., Methods: Fifteen healthy men (mean ± SD: age, 25 ± 8 yr; body mass, 72 ± 11 kg; height, 179 ± 7 cm) performed intermittent isometric knee extensions at ∼50% of maximal voluntary contraction to task failure in normoxia, hypoxia with CO2 clamping (arterial O2 saturation, 80% ± 2%; end-tidal CO2 partial pressure, 40 ± 2 mm Hg), and hypoxia without CO2 clamping (arterial O2 saturation, 80% ± 3%). Transcranial magnetic stimulation and femoral nerve electrical stimulation were used to assess central and peripheral determinants of fatigue. Prefrontal cortex and quadriceps femoris oxygenation were monitored by multichannel near-infrared spectroscopy., Results: Exercise duration was reduced to a similar extent in hypoxia with CO2 clamping (997 ± 460 s) or hypoxia without CO2 clamping (929 ± 412 s) compared to normoxia (1473 ± 876 s; P < 0.001). Prefrontal cortex and quadriceps oxygenation were increased (+5.3 ± 8.6 and +2.6 ± 3.0 μmol·cm at task failure, respectively; P < 0.01) during hypoxia with CO2 clamping compared to hypoxia without CO2 clamping. Transcranial magnetic stimulation maximal voluntary activation decreased to a greater extent at task failure in hypoxia without CO2 clamping (-18% ± 8%) compared to hypoxia with CO2 clamping (-9% ± 9%; P < 0.01) and normoxia (-10% ± 7%; P < 0.05). Conversely, exercise-induced peripheral fatigue was larger in hypoxia with CO2 clamping than in hypoxia without CO2 clamping (e.g., Db10-to-Db100 ratio of 0.54 ± 0.12 and 0.63 ± 0.11 at task failure, respectively; P < 0.05)., Conclusion: The results demonstrate that CO2 clamping can alter central and peripheral mechanisms that contribute to neuromuscular fatigue during hypoxic isometric knee extensions in men. Hypocapnia impairs cerebral oxygenation and central drive but exerts a protective effect against fatigability in muscles.

Contradictory results regarding the effect of hypoxia on cortex excitability have been reported in healthy subjects, possibly depending on hypoxia exposure duration. We evaluated the effects of 1- and 3-h hypoxia on motor corticospinal excitability, intracortical inhibition, and cortical voluntary activation (VA) using transcranial magnetic stimulation (TMS). TMS to the quadriceps cortex area and femoral nerve electrical stimulations were performed in 14 healthy subjects. Motor-evoked potentials (MEPs at 50-100% maximal voluntary contraction; MVC), recruitment curves (MEPs at 30-100% maximal stimulator power output at 50% MVC), cortical silent periods (CSP), and VA were measured in normoxia and after 1 (n = 12) or 3 (n = 10) h of hypoxia (Fi(O(2)) = 0.12). One-hour hypoxia did not modify any parameters of corticospinal excitability but reduced slightly VA, probably due to the repetition of contractions 1 h apart (96 ± 4% vs. 94 ± 4%; P = 0.03). Conversely, 3-h hypoxia significantly increased 1) MEPs of the quadriceps muscles at all force levels (+26 ± 14%, +24 ± 12%, and +27 ± 17% at 50, 75, and 100% MVC, respectively; P = 0.01) and stimulator power outputs (e.g., +21 ± 14% at 70% maximal power), and 2) CSP at all force levels (+20 ± 18%, +18 ± 19%, and +14 ± 22% at 50, 75, and 100% MVC, respectively; P = 0.02) and stimulator power outputs (e.g., +9 ± 8% at 70% maximal power), but did not modify VA (98 ± 1% vs. 97 ± 3%; P = 0.42). These data demonstrate a time-dependent hypoxia-induced increase in motor corticospinal excitability and intracortical inhibition, without changes in VA. The impact of these cortical changes on physical or psychomotor performances needs to be elucidated to better understand the cerebral effects of hypoxemia.

It has been shown that the ability of humans to maintain a quiet standing posture is degraded after fatigue of the muscles at the ankle. Yet, it has also been shown that skin stimulation at the ankle could improve postural performance. In the present study, we addressed the issue of the interaction of these two effects. Subjects were tested with the eyes closed in four conditions of quiet stance: with or without skin stimulation and before and after a fatigue protocol. The skin was stimulated with a piece of medical adhesive tape on the Achilles' tendon. The fatigue protocol consisted of multiple sets of ankle plantar flexion of both legs on stool. Without fatigue, we did not observe a significant effect of the tape. With fatigue, subjects decreased their postural performance significantly, but this effect was cancelled out when a piece of tape was glued on the Achilles' tendon. This indicated that the beneficial effect of the tape was unveiled by the degraded postural performance after fatigue. We conclude that, when the muscular sensory input flow normally relevant for the postural system is impaired due to fatigue, the weight of cutaneous information increases for the successful representation of movements in space to adjust postural control., (Copyright © 2011 Elsevier B.V. All rights reserved.)

The present study aimed to assess whether high intensity exhaustive eccentric (ECC) exercise was associated with a greater decrease in muscle oxygenation compared to high intensity exhaustive concentric (CON) exercise during maximal isokinetic knee extensions. On two separate days, ten recreationally active participants performed maximal isokinetic concentric (KE(CON)) and eccentric (KE(ECC)) knee extension exercises at 60°s(-1) until exhaustion. Muscle oxygenation profile and activity were acquired continuously from the vastus lateralis (VL) muscle using near-infrared spectroscopy, along with surface electromyography (sEMG). The torque output was significantly greater during KE(ECC) (P<0.01). Total time to exhaustion was longer in ECC condition (P<0.01). The decrease in tissue oxygenation index observed between the beginning and end-exercise values was significantly greater during KE(ECC) than during KE(CON) (P<0.05) while total haemoglobin volume did not differ significantly. KE(ECC) resulted in a significant increase in end-exercise integrated sEMG (P<0.05). We propose that the associated higher intramuscular pressure may have compressed blood vessels and led to a greater decrease in tissue oxygenation index. The observed end-exercise increase in neural drive during KE(ECC) may have occurred to prevent from muscle performance decrease. These results suggest that, over time, repeated maximal ECC actions induce a greater O(2) extraction compared to maximal CON actions., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

This study aimed to reveal the neural and muscular adjustments following a repeated-sprint (RS) running exercise. Sixteen subjects performed a series of neuromuscular tests before, immediately after and 30 min (passive recovery) post-RS exercise (12 x 40 m sprints interspaced by 30 s of passive recovery). Sprint times significantly lengthened over repetitions (+17% from the first to the last sprint; P < 0.05). After RS running exercise, maximal voluntary contraction torque of the plantar flexors (-11 +/- 7.3%), muscle activation (twitch interpolation) (-2.7 +/- 3.4%) and soleus maximal M-wave amplitude (-20 +/- 17%) were significantly (P < 0.05) reduced but returned close to baseline after 30 min. Both soleus EMG activity and maximal Hoffmann reflex normalized with respect to M-wave amplitude did not change during the whole experiment. From pre- to post-RS exercise, evoked twitch response was characterized by lower peak torque and maximal rate of torque development (-13 and -11%, respectively, P < 0.05), but was not different from baseline after recovery. Peak tetanus at 20 and 80 Hz were 17 and 8% lower (P < 0.05) in the fatigued state, respectively. Acute muscle fatigue induced by RS running exercise is mainly peripheral as the short-term (30 min) recovery pattern of plantar flexors contractile properties follows that of the voluntary force-generating capacity.

The present study was designed to investigate if the suggested greater fatigability during repeated exercise in the afternoon, compared to the morning, represents a true time-of-day effect on fatigability or a consequence of a higher initial power. In a counterbalanced order, eight subjects performed a repeated-sprint test [10 x (6 s of maximal cycling sprint + 30 s of rest)] on three different occasions between: 08:00-10:00, 17:00-19:00, and 17:00-19:00 h controlled (17:00-19:00 h(cont), i.e., initial power controlled to be the same as the two first sprints of the 08:00-10:00 h trial). Power output was significantly (p < 0.05) higher for sprints 1, 2, and 3 in the afternoon than in the morning (e.g., sprint 1: 23.3 +/-1 versus 21.2 +/-1 W.kg(-1)), but power decrement for the 10 sprints was also higher in the afternoon. Based on the following observations, we conclude that this higher power decrement is a consequence of the higher initial power output in the afternoon. First, there was no difference in power during the final five sprints (e.g., 20.4 +/-1 versus 19.7 +/-1 W.kg(-1) for sprint 10 in the afternoon and morning, respectively). Second, the greater decrement in the afternoon was no longer present when participants were producing the same initial power output in the afternoon as in the morning. Third, electromyographic activity of the vastus lateralis decreased during the exercise (p < 0.05), but without a time-of-day effect.

There is still conflicting evidence about the influence of fatigue on trunk reflex activity. The aim of this study was to measure response latency and amplitude changes of lumbar and abdominal muscles after heavy external force perturbation applied to the trunk in the sagittal plane before and after back muscle fatigue, in expected and unexpected conditions. Ten healthy subjects in a semi-seated position, torso upright in a specific apparatus performed an intermittent back muscle fatigue protocol. EMG reflex activity of erector spinae (ES) and external oblique muscles were recorded in unexpected and in expected (self pre-activation) conditions. After fatigue, the normalized reflex amplitude of ES increased in expected and unexpected conditions (P<0.05) while ES response latency was slightly decreased. Reflexes latencies for ES were systematically shorter (P<0.05) of 25% in expected compared to unexpected conditions. These findings suggest that a large external force perturbation would elicit higher paraspinal magnitude responses and possible earlier activation in order to compensate the loss of muscular force after fatigue. Because of the seated position the postural adjustments were probably not triggered and thus explain the lack of abdominal activation. The self-anticipated pre-activation in order to counteract perturbations was not affected by fatigue illustrating the natural muscular activation to maintain trunk stability., ((c) 2009 Elsevier Ltd. All rights reserved.)

This study aimed to determine whether the time-course of maximal resting H-reflex amplitude (H(max)) recovery after a prolonged moderate-intensity muscle contraction differs according to the optimal stimulation intensity used (predetermined vs. readjusted). Thirteen males performed a sustained isometric plantar flexion at 40% of their maximal voluntary contraction torque output until exhaustion. H(max) of the soleus muscle was recorded before and 2, 6, 10, and 14 min after the end of the contraction, then normalized by the respective maximal M-wave to form the H(max)/M(max) ratio. During recovery, pre- and redetermined optimal stimulation intensities (mini-recruitment curve drawn before each recovery measurement) were applied randomly to measure H(max). When using redetermined stimulation intensities, normalized H-reflex values were systematically greater (+11, +16, +15, and +15% after 2-, 6-, 10-, and 14-min recovery periods, respectively) than those obtained with the predetermined intensity. Keeping the stimulation intensity constant to evoke H(max) after a sustained muscle contraction can underestimate the H-reflex facilitation occurring after exhaustive exercise. It is therefore more appropriate to redefine the optimal stimulation intensity to evoke H(max) (using mini-recruitment curves) when the purpose is to analyze spinal modulation during the recovery phase.

In this study we investigated the contribution of muscle activation to the impairment of fine force control with fatigue. In three experiments, we manipulated muscle activation and measured force variability before and after a fatigue protocol. When muscle activation was left free (subjects had to match the same absolute force pre- and post-fatigue), fatigue increased muscle activation at moderate force levels only, and force variability increased regardless of the level of force. When muscle activation was controlled (subjects had to match the same electromyographic activity), fatigue no longer increased force variability, except at low force levels. When voluntary muscle activation was suppressed (muscles were electrically stimulated), force variability was unaffected by fatigue. We conclude that the impairment of force steadiness with fatigue is mainly due to the increase in muscle activation at moderate forces, but there are other central sources of force fluctuation present at low force levels.

This study aimed to measure time course of postactivation potentiation during intermittent submaximal fatiguing isometric contractions in 2 groups of subjects with different physical training history. Fifteen men subjects (8 endurance-trained athletes [END] and 7 power-trained athletes [POW]) performed a 10-minute intermittent (5-second contraction, 5-second rest) knee extension exercise at 50% of their maximal voluntary isometric contraction. Mechanical (peak twitch torque, Pt) and electrophysiological (M-wave) responses following electrical stimulation of the femoral nerve were measured at rest and every 10 s throughout exercise. Vastus lateralis (VL) muscle activity (root mean square, RMS) was recorded during each contraction, and the RMS/M ratio was calculated. A significant increase in Pt (+52%, p < 0.01) was observed in both groups during the first minute of the exercise. Thereafter Pt decreased dramatically (p < 0.05) in POW whereas it remained above baseline values in END until the end of exercise. The VL RMS/M ratio increased from 7 minutes of exercise for the entire population of subjects, but showed a tendency toward greater and earlier increase in POW. Our study showed the effectiveness of an intermittent submaximal preconditioning protocol to induce similar potentiation (5-10 repetitions of 5-second submaximal contraction at 50% MVC of knee-extensors) for 2 groups of trained-individuals with different muscular profiles (END vs. POW). The enhanced fatigue resistance of endurance athletes allows the potentiating effect to prevail longer over the fatigue effect during all the 10-minute exercise. The proposed conditioning protocol (moderate-intensity, short-duration intermittent exercise) as an interesting alternative compared to MVC is adequate to warm all athletes and increase sports performance.

To achieve task goals in the various contexts of everyday life, the CNS has to adapt to short time scale changes in the properties of the neuromuscular system, such as those induced by fatigue. Here we investigated how humans preserve task success despite fatigue-induced changes within the neuromuscular system, when they have to aim at a target as fast and as accurately as possible. In such a task, subjects generally choose a compromise between speed and accuracy that has been formalized as Fitts's law. We first characterized the effect of fatigue on Fitts's law in an experiment where participants had to perform fast but accurate elbow movements aimed at targets of different sizes, before and after a fatiguing exercise that reduced maximal voluntary force by approximately 30%. We found that movements were slower to guarantee task success in the presence of fatigue. We then used an optimal control model to determine how fatigue-induced changes in variables such as noise in motor commands, muscle contraction and relaxation times, and the gain between neural activation and muscle force may contribute to changes in Fitts's law with fatigue. We concluded that the observed behavior was not due to the lack of available force, but very likely reflected the fact that the CNS uses the same optimal strategy with a fatigued neuromuscular plant that notably exhibits increased signal-dependent noise in motor commands. This strategy appears necessary to preserve task success in the presence of acute changes in the neuromuscular system.

This study aimed to assess the capacity of recurrence quantification analysis (RQA) to detect potentiation and to determine the fatigue components to which RQA is sensitive. Fifteen men were divided in two groups [8 endurance-trained athletes (END) and 7 power-trained athletes (POW)]. They performed a 10-min intermittent (5s contraction, 5s rest) knee extension exercise at 50% of their maximal voluntary isometric contraction. Muscular fatigue and potentiation were evaluated with neurostimulation technique. Mechanical (peak torque, Pt) and electrophysiological (M-wave) responses following electrical stimulation of the femoral nerve were measured at rest and every 10s throughout exercise. Vastus lateralis muscle activity (root mean square, RMS) was recorded during each contraction, and RMS was normalized to M-wave area (RMS/M). During contraction, muscle activity was analyzed with RQA to obtain the percentage of determinism (%Det). At the beginning of exercise, a significant Pt increase (+52%, P<0.001) was observed in both groups, indicating potentiation. At this time, %Det remained constant in both groups, indicating that RQA did not detect potentiation. Thereafter, Pt decreased in POW from 5min 30s of exercise (-30%, P<0.001), reflecting impairment in excitation-contraction coupling, and %Det increased from 3min 30s (P<0.01). In END, Pt remained high and %Det was unchanged. These two results indicated that RQA detected the peripheral component of fatigue. Conversely, RQA did not detect central adaptation to fatigue since %Det remained constant when a significant increase in RMS/M (P<0.01) appeared in END.

This study was designed to characterize the effect of fatigue on the relationship between muscular force and its variability over a broad range of submaximal forces. Eight participants had to match 4 levels of isometric force from 7 to 53% of their maximal capabilities. This task was repeated before and after a fatigue protocol that induced a loss of maximal force of approximately 31%. We found that, despite an increase in force variability that was proportional to the force level, the linear scaling of force variability with mean force was preserved during fatigue. Because this linear scaling is a prerequisite for optimal sensorimotor control models, our results broaden the explanatory power of these models to the fatigue case, while at the same time offering new routes towards understanding how the central nervous system adapts to fatigue.

The present experiment was designed to test the hypothesis that fatigue-induced impairment in movement accuracy is caused by a decrease in muscle cocontraction rather than a reduced ability to produce muscular force. Seven participants performed fast and accurate elbow extensions aimed at a target, before and after a fatigue protocol. The inertia of the manipulandum was decreased after the fatigue protocol so that the ratio of required to available force during movements was identical pre- and post-fatigue. After the fatigue protocol, movement endpoint accuracy decreased and movement endpoint variability increased. These alterations were associated with a decrease in cocontraction. We concluded that the impairment of movement accuracy during fatigue could not be explained by the lack of available force, but was likely to be due to a fatigue-induced decrease in muscular cocontraction. We then speculate that fatigue influences the relative weights of accuracy and energy economy in the optimisation of sensorimotor control.

The main purpose of this study was to investigate the modulations in H-reflex and V-wave responses (spinal loop properties) induced by prolonged locomotion activities. The second purpose was to compare the development of central fatigue between continuous and intermittent running modes. Eleven males randomly performed two 90-min running exercises either continuously (CONT, first ventilatory threshold) or intermittently (INT, 150 s at a velocity 20% higher than that during CONT/30 s of recovery). Neuromuscular tests of the plantar flexors [including M-wave and H-reflex at rest and M-wave and V-wave during maximal voluntary contraction (MVC)] were performed before and 5 and 30 min after the running exercises. During MVC, the torque significantly decreased (P < 0.05) from preexercise to 5 and 30 min postexercise (-11 and -9%, respectively), as did the RMS/M ratio (-11 and -13%, respectively) and the V/M ratio (-19 and -37%, respectively) for the soleus muscle. At rest, the H/M ratio also decreased significantly (P < 0.001) from preexercise to 5 and 30 min postexercise (-61 and -55%, respectively). Last, no difference in the alteration of spinal loop properties was noted between CONT and INT. In conclusion, the results regarding H-reflex and V-wave suggest for the first time a modulation in spinal loop properties after prolonged running.

The present study investigated whether muscular monocarboxylate transporter (MCT) 1 and 4 contents are related to the blood lactate removal after supramaximal exercise, fatigue indexes measured during different supramaximal exercises, and muscle oxidative parameters in 15 humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (gamma(2)), which denoted the blood lactate removal ability. Fatigue indexes were calculated during 1-min all-out (FI(AO)) and repeated 10-s (FI(Sprint)) cycling sprints. Biopsies were taken from the vastus lateralis muscle. MCT1 and MCT4 contents were quantified by Western blots, and maximal muscle oxidative capacity (V(max)) was evaluated with pyruvate + malate and glutamate + malate as substrates. The results showed that the blood lactate removal ability (i.e., gamma(2)) after a 1-min all-out test was significantly related to MCT1 content (r = 0.70, P < 0.01) but not to MCT4 (r = 0.50, P > 0.05). However, greater MCT1 and MCT4 contents were negatively related with a reduction of blood lactate concentration at the end of 1-min all-out exercise (r = -0.56, and r = -0.61, P < 0.05, respectively). Among skeletal muscle oxidative indexes, we only found a relationship between MCT1 and glutamate + malate V(max) (r = 0.63, P < 0.05). Furthermore, MCT1 content, but not MCT4, was inversely related to FI(AO) (r = -0.54, P < 0.05) and FI(Sprint) (r = -0.58, P < 0.05). We concluded that skeletal muscle MCT1 expression was associated with the velocity constant of net blood lactate removal after a 1-min all-out test and with the fatigue indexes. It is proposed that MCT1 expression may be important for blood lactate removal after supramaximal exercise based on the existence of lactate shuttles and, in turn, in favor of a better tolerance to muscle fatigue.

The present study investigated whether blood lactate removal after supramaximal exercise and fatigue indexes measured during continuous and intermittent supramaximal exercises are related to the maximal muscle oxidative capacity in humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (gamma(2)), which denoted the blood lactate removal ability. Fatigue indexes were calculated during all-out (FI(AO)) and repeated 10-s cycling sprints (FI(Sprint)). Biopsies were taken from the vastus lateralis muscle, and maximal ADP-stimulated mitochondrial respiration (V(max)) was evaluated in an oxygraph cell on saponin-permeabilized muscle fibers with pyruvate + malate and glutamate + malate as substrates. Significant relationships were found between gamma(2) and pyruvate + malate V(max) (r = 0.60, P < 0.05), gamma(2) and glutamate + malate V(max) (r = 0.66, P < 0.01), and gamma(2) and citrate synthase activity (r = 0.76, P < 0.01). In addition, gamma(2), glutamate + malate V(max), and pyruvate + malate V(max) were related to FI(AO) (gamma(2) - FI(AO): r = 0.85; P < 0.01; glutamate + malate V(max) - FI(AO): r = 0.70, P < 0.01; and pyruvate + malate V(max) - FI(AO): r = 0.63, P < 0.01) and FI(Sprint) (gamma(2) - FI(Sprint): r = 0.74, P < 0.01; glutamate + malate V(max) - FI(Sprint): r = 0.64, P < 0.01; and pyruvate + malate V(max) - FI(Sprint): r = 0.46, P < 0.01). In conclusion, these results suggested that the maximal muscle oxidative capacity was related to blood lactate removal ability after a 1-min all-out test. Moreover, maximal muscle oxidative capacity and blood lactate removal ability were associated with the delay in the fatigue observed during continuous and intermittent supramaximal exercises in well-trained subjects.

We tested the hypothesis that O(2) uptake (Vo(2)) kinetics at the onset of heavy exercise would be altered in a state of muscle fatigue and prior metabolic acidosis. Eight well-trained cyclists completed two identical bouts of 6-min cycling exercise at >85% of peak Vo(2) separated by three successive bouts of 30 s of sprint cycling. Not only was baseline Vo(2) elevated after prior sprint exercises but also the time constant of phase II Vo(2) kinetics was faster (28.9 +/- 2.4 vs. 22.2 +/- 1.7 s; P < 0.05). CO(2) output (Vco(2)) was significantly reduced throughout the second exercise bout. Subsequently Vo(2) was greater at 3 min and increased less after this after prior sprint exercise. Cardiac output, estimated by impedance cardiography, was significantly higher in the first 2 min of the second heavy exercise bout. Normalized integrated surface electromyography of four leg muscles and normalized mean power frequency were not different between exercise bouts. Vo(2) and Vco(2) kinetic responses to heavy exercise were markedly altered by prior multiple sprint exercises.

Purpose: The origin of the slow component is not fully understood. The mechanical hypothesis is one of the potential factors, because an increase in external mechanical work with fatigue was previously reported for a constant velocity run. The purpose of this study was to determine whether a change in mechanical work could occur during the development of the VO2 slow component under the effect of fatigue., Methods: Twelve regional-level competitive runners performed a square-wave transition, corresponding to 95% of the speed associated with peak VO2 obtained during an incremental test. The VO2 response was fit with a classical model including two exponential functions. A specific treadmill with three-dimensional force transducers was used to measure the ground reaction force. Kinetic work (W(kin)), potential work (W(pot)), external work (W(ext)), and an index of internal work (W(int)) per unit of distance were quantified continuously., Results: During the slow component of VO2, a significant increase in W (P< 0.01), no change in W, and a significant decrease in W and W index (P< 0.05, P< 0.001, respectively) were observed., Conclusion: The present study showed that the slow component of VO2 did not result partly from a change in mechanical work under the effect of fatigue. Nevertheless, the decrease in stride frequency (P< 0.001) and contact time (P< 0.001) suggested an alternative mechanical explanation. The slow component during running may be due to the cost of generating force or to alterations in the storage and recoil of elastic energy, and not to the external mechanical work.