Degradation of energy cost with fatigue induced by trail running: effect of distance.

PURPOSE: The effect of trail running competitions on cost of running (Cr) remains unclear and no study has directly examined the effect of distances in similar conditions on Cr. Accordingly, the aims of this study were to (i) assess the effect of trail running races of 40-170 km on Cr and (ii) to assess whether the incline at which Cr is measured influences changes in Cr. METHODS: Twenty trail runners completed races of < 100 km (SHORT) and 26 trail runners completed races of > 100 km (LONG) on similar courses and environmental conditions. Oxygen uptake, respiratory exchange ratio, ventilation, and blood lactate were measured before and after the events on a treadmill with 0% (FLAT) and 15% incline (UH) and Cr was calculated. RESULTS: Cr increased significantly after SHORT but not LONG races. There was no clear relationship between changes in Cr and changes in ventilation or blood lactate. There was a significant correlation (r = 0.75, p < 0.01) between changes in FLAT and UH Cr, and the change in Cr was not affected by the incline at which Cr was measured. CONCLUSION: The distance of the trail running race, but not the slope at which it is measured, influence the changes in Cr with fatigue. The mechanism by which Cr increases only in SHORT is not related to increased cost of breathing.

Effects of endurance cycling training on neuromuscular fatigue in healthy active men. Part II: Corticospinal excitability and voluntary activation.

This study investigated the effects of 9-week endurance cycling training on central fatigability and corticomotor excitability of the locomotor muscles. Fourteen healthy participants undertook three incremental fatiguing cycling tests to volitional exhaustion (EXH): (i) before training (PRE), (ii) after training at the same absolute power output as PRE (POSTABS) and (iii) after training at the same percentage of V̇O2max as PRE (POSTREL). At baseline (i.e. before cycling), every 5 min during cycling and immediately at EXH, a neuromuscular evaluation including a series of 5-s knee extensions at 100, 75 and 50% of maximal voluntary knee extension (MVC) was performed. During each contraction, transcranial magnetic and peripheral nerve stimuli were elicited to obtain motor evoked potential (MEP), silent period (SP) and compound muscle action potential (Mmax) and to calculate voluntary activation (VA). The MEP·Mmax-1 ratio recorded from vastus lateralis at 100 and 50% MVC did not show any difference between conditions. At 75% MVC, MEP exhibited significantly lower values in POSTABS and POSTREL compared to PRE at baseline (P = 0.022 and P = 0.011, respectively) as well as at 25% of time to EXH of PRE (P = 0.022) for POSTREL. No adaptations, either at baseline or during cycling, were observed for VA and SPs. In conclusion, endurance training may result in some adaptations in the corticomotor responses when measured at rest or with low level of fatigue, yet these adaptations do not translate into attenuation of central fatigue at a similar cycling workload or at exhaustion.

Effects of the foot strike pattern on muscle activity and neuromuscular fatigue in downhill trail running.

Minimizing musculo-skeletal damage and fatigue is considered paramount for performance in trail running. Our purposes were to investigate the effects of the foot strike pattern and its variability on (a) muscle activity during a downhill trail run and (b) immediate and delayed neuromuscular fatigue. Twenty-three runners performed a 6.5-km run (1264 m of negative elevation change). Electromyographic activity of lower-limb muscles was recorded continuously. Heel and metatarsal accelerations were recorded to identify the running technique. Peripheral and central fatigue was assessed in knee extensors (KE) and plantar flexors (PF) at Pre-, Post-, and 2 days post downhill run (Post2d). Anterior patterns were associated with (a) higher gastrocnemius lateralis activity and lower tibialis anterior and vastus lateralis activity during the run and (b) larger decreases in KE high-frequency stimulus-evoked torque Post and larger decrements in KE MVC Post2d. High patterns variability during the run was associated with (a) smaller decreases in KE Db100 Post and MVC Post2d and (b) smaller decreases in PF MVC Post and Post2d. Anterior patterns increase the severity of KE peripheral fatigue. However, high foot strike pattern variability during the run reduced acute and delayed neuromuscular fatigue in KE and PF.

Acute and delayed peripheral and central neuromuscular alterations induced by a short and intense downhill trail run.

Downhill sections are highly strenuous likely contributing to the development of neuromuscular fatigue in trail running. Our purpose was to investigate the consequences of an intense downhill trail run (DTR) on peripheral and central neuromuscular fatigue at knee extensors (KE) and plantar flexors (PF). Twenty-three runners performed a 6.5-km DTR (1264-m altitude drop) as fast as possible. The electromyographic activity of vastus lateralis (VL) and gastrocnemius lateralis (GL) was continuously recorded. Neuromuscular functions were assessed Pre-, Post-, and 2-day Post-DTR (Post2d). Maximal voluntary torques decreased Post (∼ -19% for KE, ∼ -25% for PF) and Post2d (∼ -9% for KE, ∼ -10% for PF). Both central and peripheral dysfunctions were observed. Decreased KE and PF voluntary activation (VA), evoked forces, VL M-wave amplitude, and KE low-frequency fatigue were observed at Post. Changes in VL M-wave amplitude were negatively correlated to VL activity during DTR. Changes in PF twitch force and VA were negatively correlated to GL activity during DTR. The acute KE VA deficit was about a third of that reported after ultramarathons, although peripheral alterations were similar. The prolonged force loss seems to be mainly associated to VA deficit likely induced by the delayed inflammatory response to DTR-induced ultrastructural muscle damage.

Contraction velocity influence the magnitude and etiology of neuromuscular fatigue during repeated maximal contractions.

This study aimed to compare the magnitude and etiology of neuromuscular fatigue during maximal repeated contractions performed in two contraction modes (concentric vs isometric) and at two contraction velocities (30/s vs 240°/s). Eleven lower limb-trained males performed 20 sets of maximal contractions at three different angular velocities: 0°/s (KE0), 30/s (KE30), and 240°/s (KE240). Cumulated work, number of contraction, duty cycle, and contraction time were controlled. Torque, superimposed and resting twitches, as well as gas exchange, were analyzed. Increasing contraction velocity was associated with greater maximal voluntary torque loss (KE0: -9.8 ± 3.9%; KE30: -16.4 ± 8.5%; KE240: -32.6 ± 6.3%; P < 0.05). Interestingly, the torque decrease was similar for a given cumulated work. Compared with KE0, KE240 generated a greater evoked torque loss (Db100: -24.3 ± 5.3% vs -5.9 ± 6.9%; P < 0.001), a higher O2 consumption (23.7 ± 6.4 mL/min/kg vs 15.7 ± 3.8 mL/min/kg; P < 0.001), but a lower voluntary activation (VA) loss (-4.3 ± 1.6% vs -11.2 ± 4.9%; P < 0.001). The neuromuscular perturbations were intermediate for KE30 (Db100: -10.0 ± 6.8%; VA: -7.2 ± 2.8%). Although the amount of mechanical work cumulated strongly determined the magnitude of torque decrease, the contraction velocity and mode influenced the origin of the neuromuscular fatigue. The metabolic stress and peripheral fatigue increased but reduction of VA is attenuated when the contraction velocity increased from 0°/s to 240°/s.

Hemolysis induced by an extreme mountain ultra-marathon is not associated with a decrease in total red blood cell volume.

Prolonged running is known to induce hemolysis. It has been suggested that hemolysis may lead to a significant loss of red blood cells; however, its actual impact on the erythrocyte pool is unknown. Here, we test the hypothesis that prolonged running with high hemolytic potential decreases total red blood cell volume (RCV). Hemolysis (n = 22) and RCV (n = 19) were quantified in ultra-marathon runners before and after a 166-km long mountain ultra-endurance marathon (RUN) with 9500 m of altitude gain/loss. Assessment of total hemoglobin mass (Hbmass) and RCV was performed using a carbon monoxide rebreathing technique. RUN induced a marked acute-phase response and promoted hemolysis, as shown by a decrease in serum haptoglobin (P < 0.05). Elevated serum erythropoietin concentration and reticulocyte count after RUN were indicative of erythropoietic stimulation. Following RUN, runners experienced hemodilution, mediated by a large plasma volume expansion and associated with a large increase in plasma aldosterone. However, neither Hbmass nor RCV were found to be altered after RUN. Our findings indicate that mechanical/physiological stress associated with RUN promotes hemolysis but this has no impact on total erythrocyte volume. We therefore suggest that exercise 'anemia' is entirely due to plasma volume expansion and not to a concomitant decrease in RCV.

Comparison of skin and shoe marker placement on metatarsophalangeal joint kinematics and kinetics during running.

This study investigated the effects of marker placement (skin- vs shoe-mounted) on metatarsophalangeal joint (MTP) kinematics and kinetics during running. Fifteen trained men ran on a 15-m track at 10 and 13 km/h with three (low, standard and high stiffness) shoe longitudinal bending stiffnesses (LBS). Reflective markers were fixed on the shoe upper, and on the skin using holes cut in the shoe. Three-dimensional marker positions and ground reaction forces were recorded at 200 and 2000 Hz, respectively. Kinematic and kinetic parameters were analyzed using one-dimensional metrics (statistical parametric mapping). MTP joint was less dorsiflexed at midstance ([57% to 100%] of braking phase and [0% to 48%] of pushing phase), and the MTP joint plantarflexion moment was higher ([22% to 55%] of pushing phase) with the shoe markerset in comparison with the skin markerset. The effect of LBS on MTP angle was found to be significant for a larger percentage of each stride using the shoe markerset compared to the skin markerset. However, the effect of LBS on plantarflexion moment was significant with the shoe markerset only. The effect of running speed on MTP angle was significant for a larger percentage of each stride with the skin markerset. This study demonstrates that the placement of markers influences the measurement of MTP kinematics and kinetics and that these effects are mediated by other variables such as LBS or running speed. It is concluded that the shoe markerset does not fully reflect the movement of the MTP joint.

Time-dependent effect of acute hypoxia on corticospinal excitability in healthy humans.

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.

Central and peripheral fatigue kinetics during exhaustive constant-load cycling.

The kinetics of central and peripheral fatigue development during an intensive constant-load cycling exercise was evaluated to better understand the mechanisms of task failure. Thirteen males cycled to exhaustion at 80% of maximal power output in intermittent bouts of 6 min of exercise with 4-min break between bouts to assess quadriceps fatigue with maximal voluntary contractions and single (1 Hz), paired (10 and 100 Hz) potentiated and interpolated magnetic stimulations of the femoral nerve (TwQ). Surface electromyographic signals (EMG) of the quadriceps muscles were recorded during stimulations and cycling. Total cycling duration (TCD) was 27 min 38 s±7 min 48 s. The mechanical response evoked by magnetic stimulation decreased mostly during the first half of TCD (TwQ1 Hz reduction: -34.4±12.2% at 40% TCD and -44.8±9.2% at exhaustion; P<0.001), while a reduction in maximum voluntary activation was present toward the end of exercise only (-5.4±4.8% and -6.4±5.6% at 80% TCD and exhaustion, respectively; P<0.01). The increase in quadriceps EMG during cycling was significantly correlated to the TwQ reduction for the rectus femoris (r(2) =0.20 at 1 Hz, r(2) =0.47 at 100 Hz, all P≤0.001). We conclude that peripheral fatigue develops early during constant-load intense cycling and is compensated by additional motor drive, while central fatigue appears to be associated with task failure.

Fatigue after short (100-m), medium (200-m) and long (400-m) treadmill sprints.

The aim of this study was to compare the aetiology of neuromuscular fatigue following maximal sprints of different distances. It was hypothesized that increasing the distance would modify the type of peripheral and induce central fatigue. 11 subjects performed 100-, 200- and 400-m sprints on a motorized instrumented treadmill. Neuromuscular function, evaluated before (Pre), 30 s after (Post), and 5 and 30 min after the sprints (Post5 and Post30), consisted in determining maximal voluntary knee extensors torque (MVC), maximal voluntary activation of the knee extensors (%AL), maximal compound muscle action potential amplitude and duration on vastus lateralis, single twitch (Tw), and low- (Db10) and high-frequency torque. Compared with peak values, running speed decreased by 8%, (P < 0.01), 20% (P < 0.001) and 39% (P < 0.001) at the end of the 100-, 200- and 400-m sprints, respectively. MVC was not altered following 100 and 200 m, but decreased by 14% (P < 0.001) after the 400 m, was still depreciated Post5 (-11%, P < 0.01) and went back to initial values Post30. A decrease in %AL (-6.0%, P < 0.01) was observed Post5 for the 400 m. Tw, Db10 and low-to-high doublets ratio decreased Post-sprints and were not recovered Post30 after all sprints. Single maximal sprints of 100-400 m did not alter sarcolemmal excitability but induced progressive and substantial low-frequency fatigue and a slight reduction in neural drive with increasing sprint duration. Despite altered single or paired stimulations, MVC strength loss was detected only after the 400 m.

Physiological and biological factors associated with a 24 h treadmill ultra-marathon performance.

The purpose of this study was to examine the physiological and biological factors associated with ultra-endurance performance. Fourteen male runners volunteered to run on a treadmill as many kilometers as possible over a 24-h period (24TR). Maximal oxygen uptake (VO(2max)), velocity associated with VO(2max)(VO(2max)) and running economy (RE) at 8 km/h were measured. A muscle biopsy was also performed in the vastus lateralis muscle. The subjects ran 149.2 ± 15.7 km in 18 h 39 ± 41 min of effective attendance on the treadmill, corresponding to 39.4 ± 4.2% of . Standard multiple-regression analysis showed that performance was significantly (R(2) = 0.82; P = 0.005) related to VO(2max) and specific endurance, i.e. the average speed sustained over the 24TR expressed in . VO(2max) was associated with a high capillary tortuosity (R(2) = 0.66; P = 0.01). Specific endurance was significantly related to RE and citrate synthase activity. It is concluded that a high VO(2max) and an associated developed capillary network are essential for ultra-endurance running performance. The ability to maintain a high %VO(2max) over a 24TR is another factor associated with performance and is mainly related to RE and high mitochondrial oxidative capacity in the vastus lateralis.

[Exercise therapy and myopathies]. / Thérapie par l'exercice et myopathies.

Since the first consensus papers published early in the 2000s, a growing number of recent publications has shown that adapted physical activity is not only safe in the context of myopathy but also potentially effective as a therapeutic tool. After a short recall of the different exercise modalities, the mechanical strain they induce and the expected muscular benefits, the present paper reviews the different studies related to exercise therapy in myopathic patients and provides a critical analysis of the topic. Myopathies are rare diseases with many different etiologies and a large number of training modalities which could be useful for the different muscular challenges have been proposed. We have chosen to focus on several specific training modalities and to discuss the results from the most recent papers. The purpose of this review is to, firstly, update physical training guidelines for patients with myopathy and, secondly, highlight some common pitfalls associated with this strategy. This is particularly important for medical and allied professionals involved in prescribing and managing exercise therapy protocols.

Effect of acute hypoxia on central fatigue during repeated isometric leg contractions.

To determine whether hypoxia has a direct influence on the central command independently of the working muscles, 16 subjects performed intermittent isometric unilateral knee extensions until exhaustion either in normobaric hypoxia (inspired O(2) fraction=0.11, arterial oxygen saturation approximately 84%) or in normoxia while the knee extensor muscles were exposed to circulatory occlusion with a 250 mmHg cuff. Among the subjects, 11 also performed the tests in hypoxia and normoxia without occlusion. Single electrical stimulations were regularly delivered to the femoral nerve to measure the changes in the knee extensor peak twitch force. With the cuff, the average slope of decrease in peak twitch did not depend on the inspired oxygen fraction. Performance was slightly but significantly lower during hypoxia than in normoxia (8.2+/-2.6 vs 9.4+/-3.1 repetitions, P<0.05) with the cuff on. The number of repetitions was much higher during hypoxia with maintaining leg blood flow (15.6+/-4.5 repetitions) than with circulatory occlusion in normoxia. In conclusion, this study showed that a direct effect of hypoxia in reducing the motor drive to the working muscles exists but this effect is moderate.

Fatigue and neuromuscular diseases.

PURPOSE: To identify the role of fatigue, its evaluation and its causes in the pathophysiology context of acquired or hereditary neuromuscular diseases of the spinal anterior horn cell, peripheral nerve, neuromuscular junction and muscle. MATERIAL AND METHODS: A literature review has been done on Medline with the following keywords: neuromuscular disease, peripheral neuropathy, myopathy, fatigue assessment, exercise intolerance, force assessment, fatigue scale and questionnaire, then with the terms: Fatigue Severity Scale, Chalder Fatigue Scale, Fatigue Questionnaire, Piper Fatigue Scale, electromyography and the combination of the word Fatigue with the following terms: Amyotrophic Lateral Sclerosis (ALS), Post-Polio Syndrome (PPS), Guillain-Barre Syndrome, Immune Neuropathy, Charcot-Marie-Tooth Disease, Myasthenia Gravis (MG), Metabolic Myopathy, Mitochondrial Myopathy, Muscular Dystrophy, Facioscapulohumeral Dystrophy, Myotonic Dystrophy. RESULTS: Fatigue is a symptom very frequently reported by patients. Fatigue is mainly evaluated by strength loss after an exercise, by change in electromyographic activity during a given exercise and by questionnaires that takes into account the subjective (psychological) part of fatigue. Due to the large diversity of motor disorders, there are multiple clinical expressions of fatigue that differ in their presentation, consequences and therapeutic approach. CONCLUSION: This review shows that fatigue has to be taken into account in patients with neuromuscular diseases. In this context, pathophysiology of fatigue often implies the motor component but the disease evolution and the physical obligates of daily life also induce an important psychological component.

Transcranial magnetic stimulation intensity affects exercise-induced changes in corticomotoneuronal excitability and inhibition and voluntary activation.

Transcranial magnetic stimulation (TMS) of the motor cortex during voluntary contractions elicits electrophysiological and mechanical responses in the target muscle. The effect of different TMS intensities on exercise-induced changes in TMS-elicited variables is unknown, impairing data interpretation. This study aimed to investigate TMS intensity effects on maximal voluntary activation (VATMS), motor-evoked potentials (MEPs), and silent periods (SPs) in the quadriceps muscles before, during, and after exhaustive isometric exercise. Eleven subjects performed sets of ten 5-s submaximal isometric quadriceps contractions at 40% of maximal voluntary contraction (MVC) strength until task failure. Three different TMS intensities (I100, I75, I50) eliciting MEPs of 53 ± 6%, 38 ± 5% and 25 ± 3% of maximal compound action potential (Mmax) at 20% MVC were used. MEPs and SPs were assessed at both absolute (40% baseline MVC) and relative (50%, 75%, and 100% MVC) force levels. VATMS was assessed with I100 and I75. When measured at absolute force level, MEP/Mmax increased during exercise at I50, decreased at I100 and remained unchanged at I75. No TMS intensity effect was observed at relative force levels. At both absolute and relative force levels, SPs increased at I100 and remained stable at I75 and I50. VATMS assessed at I75 tended to be lower than at I100. TMS intensity affects exercise-induced changes in MEP/Mmax (only when measured at absolute force level), SPs, and VATMS. These results indicate a single TMS intensity assessing maximal voluntary activation and exercise-induced changes in corticomotoneuronal excitability/inhibition may be inappropriate.

Effect of Sleep Extension on the Subsequent Testosterone, Cortisol and Prolactin Responses to Total Sleep Deprivation and Recovery.

Total sleep deprivation (TSD) in humans is associated with altered hormonal levels, which may have clinical relevance. Less is known about the effect of an extended sleep period before TSD on these hormonal changes. Fourteen subjects participated in two experimental counterbalanced conditions (randomised cross-over design): extended sleep (21.00-07.00 h time in bed, EXT) and habitual sleep (22.30-07.00 h time in bed, HAB). For each condition, subjects performed two consecutive phases: six nights of either EXT or HAB. These nights were followed by 3 days in the sleep laboratory with blood sampling at 07.00 and 17.00 h at baseline (B-07.00 and B-17.00), after 24 and 34 h of continuous awakening (24 h-CA, 34 h-CA) and after one night of recovery sleep (R-07.00 and R-17.00) to assess testosterone, cortisol, prolactin and catecholamines concentrations. At 24 h of awakening, testosterone, cortisol and prolactin concentrations were significantly lower compared to B-07.00 and recovered basal levels after recovery sleep at R-07.00 (P < 0.001 for all). However, no change was observed at 34 h of awakening compared to B-17.00. No effect of sleep extension was observed on testosterone, cortisol and catecholamines concentrations at 24 and 34 h of awakening. However, prolactin concentration was significantly lower in EXT at B-07.00 and R-07.00 compared to HAB (P < 0.05, P < 0.001, respectively). In conclusion, 24 h of awakening inhibited gonadal and adrenal responses in healthy young subjects and this was not observed at 34 h of awakening. Six nights of sleep extension is not sufficient to limit decreased concentrations of testosterone and cortisol at 24 h of awakening but may have an impact on prolactin concentration.

Why does knee extensor muscles torque decrease after eccentric-type exercise?

AIM: The purpose of this study was to re-examine central and peripheral origins of neuromuscular fatigue after a highly strenuous eccentric exercise of the knee extensor muscles (KE) using both voluntary/evoked contractions and electromyographic recordings (EMG). METHODS: Before, and 30 min after 15 min of intermittent one-logged downhill running, maximal percutaneous electrical stimulations (single twitch, 0.5 s tetanus at 20 Hz and 80 Hz) were applied to the femoral nerve of 10 male subjects. Electrically evoked superimposed twitches were delivered during isometric maximal voluntary contraction (MVC) to determine maximal voluntary activation (%VA). Vastus lateralis (VL), vastus medialis (VM) and biceps femoris (BF) EMG were recorded during MVC and quantified using the root mean square (RMS) value. M-wave characteristics were also determined. RESULTS: KE MVC and %VA decreased significantly with fatigue (-19.6+/-6.1%; P<0.001 and -7.8+/-6.6%; P<0.01, respectively). Peak tetanus tension at 20 and 80 Hz (P20 and P80, respectively) declined (P<0.001), concurrently with a decrement of the P20 x P80(-1) ratio (-37.3+/-16.6%; P<0.001). Antagonist muscle coactivation, RMS to M-wave peak-to-peak amplitude and MVC x P80(-1) ratios were unchanged after the fatiguing exercise. CONCLUSIONS: The results reveal that part of the large loss in MVC may have a central origin but most of the MVC decrement is due to the presence of low-frequency fatigue while possible contractile failure cannot be excluded.

Mechanisms contributing to knee extensor strength loss after prolonged running exercise.

The aim of this study was to identify the mechanisms that contribute to the decline in knee extensor (KE) muscles strength after a prolonged running exercise. During the 2 days preceding a 30-km running race [duration 188.7 +/- 27.0 (SD) min] and immediately after the race, maximal percutaneous electrical stimulations (single twitch, 0.5-s tetanus at 20 and 80 Hz) were applied to the femoral nerve of 12 trained runners. Superimposed twitches were also delivered during isometric maximal voluntary contraction (MVC) to determine the level of voluntary activation (%VA). The vastus lateralis electromyogram was recorded. KE MVC decreased from pre- to postexercise (from 188.1 +/- 25.2 to 142.7 +/- 29.7 N x m; P < 0.001) as did %VA (from 98.8 +/- 1.8 to 91.3 +/- 10.7%; P < 0.05). The changes from pre- to postexercise in these two variables were highly correlated (R = 0.88; P < 0.001). The modifications in the mechanical response after the 80-Hz stimulation and M-wave peak-to-peak amplitude were also significant (P < 0.001 and P < 0.05, respectively). It can be concluded that 1) central fatigue, neuromuscular propagation, and muscular factors are involved in the 23.5 +/- 14.9% reduction in MVC after a prolonged running bout at racing pace and 2) runners with the greatest KE strength loss experience large activation deficit.

Assessment of low-frequency fatigue with two methods of electrical stimulation.

The aim of this study was to compare the use of transcutaneous vs. motor nerve stimulation in the evaluation of low-frequency fatigue. Nine female and eleven male subjects, all physically active, performed a 30-min downhill run on a motorized treadmill. Knee extensor muscle contractile characteristics were measured before, immediately after (Post), and 30 min after the fatiguing exercise (Post30) by using single twitches and 0.5-s tetani at 20 Hz (P20) and 80 Hz (P80). The P20-to-P80 ratio was calculated. Electrical stimulations were randomly applied either maximally to the femoral nerve or via large surface electrodes (ES) at an intensity sufficient to evoke 50% of maximal voluntary contraction (MVC) during a 80-Hz tetanus. Voluntary activation level was also determined during isometric MVC by the twitch-interpolation technique. Knee extensor MVC and voluntary activation level decreased at all points in time postexercise (P < 0.001). P20 and P80 displayed significant time x gender x stimulation method interactions (P < 0.05 and P < 0.001, respectively). Both stimulation methods detected significant torque reductions at Post and Post30. Overall, ES tended to detect a greater impairment at Post in male and a lesser one in female subjects at both Post and Post30. Interestingly, the P20-P80 ratio relative decrease did not differ between the two methods of stimulation. The low-to-high frequency ratio only demonstrated a significant time effect (P < 0.001). It can be concluded that low-frequency fatigue due to eccentric exercise appears to be accurately assessable by ES.

Alterations of neuromuscular function after an ultramarathon.

Neuromuscular fatigue of the knee extensor (KE) and plantar flexor (PF) muscles was characterized after a 65-km ultramarathon race in nine well-trained runners by stimulating the femoral and tibial nerves, respectively. One week before and immediately after the ultramarathon, maximal twitches were elicited from the relaxed KE and PF. Electrically evoked superimposed twitches of the KE were also elicited during maximal voluntary contractions (MVCs) to determine maximal voluntary activation. MVC and maximal voluntary activation decreased significantly after the ultramarathon (-30.2 +/- 18.0% and -27.7 +/- 13.0%, respectively; P < 0.001). Surprisingly, peak twitch increased after the ultramarathon from 15.8 +/- 6.3 to 19.7 +/- 3.3 N. m for PF (P < 0.01) and from 131.9 +/- 21.2 to 157.1 +/- 35.9 N for KE (P < 0.05). Also, shorter contraction and half-relaxation times were observed for both muscles. The compound muscle action potentials (M wave) were not significantly altered by the ultramarathon with the exception of the soleus, which showed a slightly higher M-wave amplitude after the running. From these results, it can be concluded that 65 km of running 1) severely depressed the maximal voluntary force capacity mainly because of a decrease in maximal voluntary activation, 2) potentiated the twitch mechanical response, and 3) did not change significantly the M-wave characteristics.