Search

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.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.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.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.

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.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.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; P0.001). Prefrontal cortex and quadriceps oxygenation were increased (+5.3 ± 8.6 and +2.6 ± 3.0 μmol·cm at task failure, respectively; P0.01) 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%; P0.01) and normoxia (-10% ± 7%; P0.05). 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; P0.05).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.

Despite interest in the possibility of females outperforming males in ultraendurance sporting events, little is known about the sex differences in fatigue during prolonged locomotor exercise. This study investigated possible sex differences in central and peripheral fatigue in the knee extensors and plantar flexors resulting from a 110-km ultra-trail-running race.Neuromuscular function of the knee extensors and plantar flexors was evaluated via transcranial magnetic stimulation (TMS) and electrical nerve stimulation before and after an ultra-trail-running race in 20 experienced ultraendurance trail runners (10 females and 10 males matched by percent of the winning time by sex) during maximal and submaximal voluntary contractions and in relaxed muscle.Maximal voluntary knee extensor torque decreased more in males than in females (-38% vs -29%, P = 0.006) although the reduction in plantar flexor torque was similar between sexes (-26% vs -31%). Evoked mechanical plantar flexor responses decreased more in males than in females (-23% vs -8% for potentiated twitch amplitude, P = 0.010), indicating greater plantar flexor peripheral fatigue in males. Maximal voluntary activation assessed by TMS and electrical nerve stimulation decreased similarly in both sexes for both muscle groups. Indices of knee extensor peripheral fatigue and corticospinal excitability and inhibition changes were also similar for both sexes.Females exhibited less peripheral fatigue in the plantar flexors than males did after a 110-km ultra-trail-running race and males demonstrated a greater decrease in maximal force loss in the knee extensors. There were no differences in the magnitude of central fatigue for either muscle group or TMS-induced outcomes. The lower level of fatigue in the knee extensors and peripheral fatigue in the plantar flexors could partly explain the reports of better performance in females in extreme duration running races as race distance increases.

Purpose - The well-established central deficit in ultraendurance running races is not understood. The use of transcranial magnetic stimulation (TMS) in parallel with peripheral nerve stimulation provides insight into the source of these central changes. The aims of this study were to determine the presence and magnitude of voluntary activation deficits, especially supraspinal deficits, after a mountain trail-running race and to determine whether this can be explained by simultaneous changes in corticospinal excitability and intracortical inhibition. Methods - Neuromuscular function (TMS and femoral nerve electrical stimulation) of the knee extensors was evaluated before and after a 110-km ultratrail in 25 experienced ultraendurance trail runners during maximal and submaximal voluntary contractions and in relaxed muscle. Results - Voluntary activation assessed by both femoral nerve electrical stimulation (−26%) and TMS (−16%) decreased and were correlated (P < 0.01). Decreases in potentiated twitch and doublet amplitudes were correlated with decreased voluntary activation assessed by TMS (P < 0.05). There was increased motor-evoked potential (MEP) amplitude (P < 0.05) without change in cortical silent period (CSP) elicited by TMS at optimal stimulus intensity. Conversely, CSP at suboptimal TMS intensity increased (P < 0.05) without concurrent change in MEP amplitude. Conclusions - The present results demonstrate the development of a large central activation deficit assessed by TMS, indicating that cortical motoneurons are severely impaired in their ability to fire at optimal frequency or be fully recruited after an ultraendurance running race. MEP and CSP responses suggest a shift in the sigmoidal MEP–stimulus intensity relationship toward larger MEP at higher TMS intensity without change in inflection point of the curve and a left shift in the CSP–stimulus intensity relationship.

AB Introduction: Prolonged and strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Although a consensus exists regarding the decrease in diastolic function, the existence of a decrease in systolic function by a PSE remains controversial, probably due to the transient tachycardia and changes in loading conditions observed upon the completion of exercise. Therefore, the objective was to evaluate LV systolic function before and after a PSE using two-dimensional speckle tracking echocardiography not only at rest but also during incremental tests to adjust heart rates (HR). Methods and Results: Sixteen healthy young men (23 +/- 3 yr old) performed a 3-h period of intensity-controlled upright cycling. LV strain (S), systolic strain rate (SR), rotation, and systolic rotational rate were evaluated by two-dimensional speckle tracking echocardiography before and after a 3-h period of PSE at rest and during incremental tests. Posttest evaluation was performed once the HR had returned to the pretest value. Under resting conditions, parameters of systolic function were either unchanged or increased after the PSE. However, during the incremental test, all LV systolic SR and apical rotational rates were decreased after PSE (radial SR at workload 3 (W3): 2.21 +/- 0.12.s-1 vs 1.87 +/- 0.10.s-1, P < 0.01 and apical rotational rate at W3: 128 +/- 28 deg.s-1 vs 105 +/- 26 deg.s-1, P < 0.05). Regression analyses between LV systolic SR and HR showed lower y-intercepts without differences in slopes, suggesting a decrease of both global and regional systolic functions irrespective of HR after the PSE. Conclusion: Our findings based on LV S and SR data during incremental tests demonstrate that the 3-h period of PSE induces LV systolic dysfunction