Early ventilation-heart rate breakpoint during incremental cycling exercise.

Previous observations having reported a transient hypoxia at the onset of incremental exercise, we investigated the existence of concomitant ventilatory and heart rate (HR) breakpoints.33 subjects executed a maximal cycling exercise with averaging for successive 5-s periods of HR, ventilation, tidal volume (VT), mean inspiratory flow rate (VT/Ti), and end-tidal partial pressures of O2 (PETO2) and CO2. In 10 subjects, the transcutaneous partial pressure of O2 (PtcO2) was recorded and the venous blood lactic acid (LA) concentration measured.At the beginning of exercise, PETO2 decreased, reaching a nadir, then progressively increased until the exercise ended. PtcO2 varied in parallel. Whether or not a 0-W cycling period preceded the incremental exercise, the rate of changes in VE, VT, VT/Ti and HR significantly increased when the nadir PO2 was reached. The ventilatory/ HR breakpoint was measured at 33±4% of VO2max, whereas the ventilatory threshold (VTh) was detected at 67±4% of VO2max and LA began to increase at 45 to 50% of VO2max.During incremental cycling exercise, we identified the existence of HR and ventilatory breakpoints in advance of both lactate and ventilatory thresholds which coincided with modest hypoxia and hypercapnia.

Chronic fatigue syndrome: acute infection and history of physical activity affect resting levels and response to exercise of plasma oxidant/antioxidant status and heat shock proteins.

OBJECTIVES: A history of high-level physical activity and/or acute infection might constitute stress factors affecting the plasma oxidant-antioxidant status and levels of heat shock proteins (HSPs) in patients with chronic fatigue syndrome (CFS). DESIGN: This case-control study compared data from 43 CFS patients to results from a matched control group of 23 healthy sedentary subjects. SETTING AND SUBJECTS: Five patients had no relevant previous history (group I). Eighteen had practised high-level sport (group II), and severe acute infection had been diagnosed in nine patients (group III). A combination of sport practice and infection was noted in 11 patients (group IV). INTERVENTIONS: After examination at rest, all subjects performed a maximal cycling exercise test. Plasma levels of two markers of oxidative stress [thiobarbituric acid reactive substances (TBARS) and reduced ascorbic acid (RAA)] and both HSP27 and HSP70 were measured. RESULTS: At rest, compared with the control group, the TBARS level was higher in groups II, III and IV patients, and the RAA level was lower in groups III and IV. In addition, HSP70 levels were significantly lower in all CFS groups, compared with controls, but negative correlations were found between resting HSP27 and HSP70 levels and the history of physical activity. After exercise, the peak level of TBARS significantly increased in groups II, III and IV, and the variations in HSP27 and HSP70 were attenuated or suppressed, with the greatest effects in groups III and IV. CONCLUSION: The presence of stress factors in the history of CFS patients is associated with severe oxidative stress and the suppression of protective HSP27 and HSP70 responses to exercise.

EMG changes in thigh and calf muscles in fin swimming exercise.

Because previous researchers have reported a reduced lactic acid production that accompanies a delayed or an absent ventilatory threshold (VTh) in water-based exercise, we hypothesized that the metaboreflex, activated by muscle acidosis, might be absent in fin swimming. This motor response, delaying the occurrence of fatigue, is characterized by a decreased median frequency (MF) of electromyographic (EMG) power spectrum. Seven healthy subjects performed a maximal fin swimming exercise protocol with simultaneous recordings of surface EMGs in VASTUS MEDIALIS (VM), TIBIALIS ANTERIOR (TA) and GASTROCNEMIUS MEDIALIS (GM). We computed the root mean square (RMS) and MF and recorded the compound evoked muscle potential (M-wave) in VM. We also measured the propulsive force and oxygen uptake (VO (2)), and determined VTh. VTh was absent in 4/7 subjects and measured at 70-90% of VO (2max) in the other three. In the three studied muscles, the global EMG activity (RMS) increased while the MF decreased in proportion of VO (2), the MF changes being significantly higher in VM (-29%) and GM (-39%) than in TA (-19%). Because no M-wave changes were noted, the MF decline was attributed to the recruitment of low-frequency, fatigue-resistant motor units. Our most important finding is the persistence of the metaboreflex even in a situation of reduced muscle acidosis.

Pulmonary oedema in healthy SCUBA divers: new physiopathological pathways.

INTRODUCTION: The mechanism of immersion pulmonary oedema occurring in healthy divers is a matter of debate. Among consecutive injured divers admitted to our hyperbaric centre, we analysed prospective data about pulmonary oedema. METHOD: A total of 22 divers suffering from immersion pulmonary oedema without cardiac disease were included. The occurrence of events was compared to the diving conditions as assessed by diving-computer. Each patient underwent a clinical examination, laboratory tests, thoracic CT scan and echocardiography. RESULTS: The median age was 49 years, with a higher proportion of women, in comparison with the data of the French diving federation. The common feature was the occurrence of respiratory symptoms during the ascent after median dive duration of 29 min with strenuous exercise and/or psychological stress. Most of the dives were deep (37 msw-121 fsw) in cool water (15 degrees C-59 degrees F). The average inspired oxygen partial pressure was 0.99 bar. Progression was rapidly favourable, and the medical check-up after clinical recovery was normal. CONCLUSION: Immersion, body cooling, hyperoxia, increased hydrostatic pressure and strenuous exercise likely combine to induce pulmonary oedema in patients without cardiac disease. This study underlines new physiopathological tracks related to the frequent occurrence of symptoms noticed in the last part of the ascent and a higher incidence in women.

Chronic fatigue syndrome combines increased exercise-induced oxidative stress and reduced cytokine and Hsp responses.

OBJECTIVES: As heat shock proteins (Hsp) protect the cells against the deleterious effects of oxidative stress, we hypothesized that Hsp expression might be reduced in patients suffering from chronic fatigue syndrome (CFS) who present an accentuated exercise-induced oxidative stress. DESIGN: This case-control study compared nine CFS patients to a gender-, age- and weight-matched control group of nine healthy sedentary subjects. INTERVENTIONS: All subjects performed an incremental cycling exercise continued until exhaustion. We measured ventilation and respiratory gas exchange and evoked compound muscle potential (M-wave) recorded from vastus lateralis. Repetitive venous blood sampling allowed measurements of two markers of oxidative stress [thiobarbituric acid reactive substances (TBARS) and reduced ascorbic acid (RAA)], two cytokines (IL-6 and TNF-alpha) and two Hsp (Hsp27 and Hsp70) at rest, during maximal exercise and the 60-min recovery period. RESULTS: Compared with controls, resting CFS patients had low baseline levels of RAA and Hsp70. Their response to maximal exercise associated (i) M-wave alterations indicating reduced muscle membrane excitability, (ii) early and accentuated TBARS increase accompanying reduced changes in RAA level, (iii) absence of significant increase in IL-6 and TNF-alpha, and (iv) delayed and marked reduction of Hsp27 and Hsp70 variations. The post-exercise increase in TBARS was accentuated in individuals having the lowest variations of Hsp27 and Hsp70. CONCLUSIONS: The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress, which might result from delayed and insufficient Hsp production.

Fin swimming improves respiratory gas exchange.

Data in the literature suggest that compared to dry-land exercise fin swimming might delay the activation of the anaerobic metabolism. To verify this hypothesis, we explored indirect indices such as the oxygen pulse (VO(2)/HR), carbon dioxide production (VCO(2)), and ventilatory threshold, comparing fin swimming exercise to dry-land cycling. Thirteen participants, experienced or inexperienced in fin swimming, completed an incremental fin swimming exercise and a maximal exercise on a cycloergometer with breath-by-breath measurements of heart rate (HR), ventilation (VE), tidal volume (VT), VO(2), VCO(2), and VO(2)/HR and determination of the ventilatory threshold and maximal oxygen uptake (VO(2)max). Compared to dry-land cycling exercise, fin swimming resulted in elevated or absent ventilatory threshold. Although VO(2)max did not differ in either condition, in fin swimming the maximal HR value was lower (-18%, p=0.0072), maximal VO(2)/HR higher (+20%, p=0.0325), and maximal VCO(2) lower (-17%, p=0.0071). We also measured significant reduction of VE, VT, and HR variations for the same VO(2) increase. This study suggests that the anaerobic muscle metabolism might be delayed in fin swimming. An attenuated chemoreflex drive to the heart and respiratory centres exerted by muscle metabolites might explain the depressed cardiopulmonary response to fin swimming.

Statins alter oxidant-antioxidant status and lower exercise-induced oxidative stress.

Data on effects of statins on resting oxidant-antioxidant status are contradictory and no study has been published on the effects of statins on exercise-induced oxidative stress. We carried out a 6-month longitudinal study in 10 dyslipidemic patients receiving 10 mg/day atorvastatin and 13 healthy sedentary subjects. Thiobarbituric acid reactive substances (TBARS) and reduced ascorbic acid (RAA) were measured in plasma at rest and every 5 minutes after submaximal isometric thumb adduction and handgrip sustained until exhaustion. At inclusion, resting TBARS and RAA levels in controls and patients did not differ and exercise increased TBARS and decreased RAA. Atorvastatin reduced resting TBARS and RAA levels in a time-dependent but lipid-independent manner. The main effect was a post-exercise increase in TBARS, without affecting the post-exercise RAA levels. The reduction in oxidative stress occurred earlier in oxidative muscles involved in thumb adduction. In conclusion, atorvastatin lowers resting oxidant-antioxidant activity: exercise-induced oxidative stress occurs mainly in muscles having a high oxidative capacity.

Effect of long-term atorvastatin treatment on the electrophysiological and mechanical functions of muscle.

OBJECTIVE: To study alterations in muscle function combining physiological, electrophysiological and metabolic measurements in patients receiving a statin at various dosages during long-term therapy. MATERIAL: A 3-month (D0, D30 and D90) longitudinal physiological and electrophysiological muscle study was performed in 26 patients receiving 10, 40 or 80 mg/day atorvastatin. METHOD: All subjects performed maximal (MVC) and submaximal (60% MVC) isometric thumb adduction, handgrip and knee extension exercises during the recording of surface electromyograms (EMG) of the adductor pollicis (AP), flexor digitorum (FD) and vastus lateralis (VL). The compound muscle potential (M-wave) evoked by direct muscle stimulation was measured at rest and after 60% MVCs and the EMG power spectrum was analyzed during sustained effort. Blood was sampled from an antecubital vein for measurements of pH, lactate and potassium levels after thumb adduction and handgrip exercises. The measurements were repeated on Day 0 (D0), D30 and D90. RESULTS: Atorvastatin did not affect the MVC and endurance time to fatigue. Post-exercise M-wave alterations in the AP began at D30 with the 80 mg/day treatment and there was a reduced or suppressed leftward shift in the EMG power spectrum in the AP and VL with all 3 dosages. In the AP, the EMG changes appeared earlier (D30) with 80 mg/day whereas they only occurred at D90 on the lower dosages. Atorvastatin had no effect on the maximal postexercise variations in pHv and lactate but it significantly reduced the maximal increase in plasma potassium concentration after thumb adduction and handgrip exercise, the effects being only present at D90 on 10 mg/day but occurring as early as D30 with higher dosages. CONCLUSION: A 3-month atorvastatin treatment did not affect the maximal performance of skeletal muscle during voluntary efforts but EMG analysis revealed a reduced muscle excitability and an attenuated adaptation to fatigue. These effects prevailed in muscles containing the largest proportion of slow-oxidative fibers and were associated with a reduced outward flow of potassium.

Chronic electrostimulation after nerve repair by self-anastomosis: effects on the size, the mechanical, histochemical and biochemical muscle properties.

This study tests the effects of chronic electrostimulation on denervated/reinnervated skeletal muscle in producing an optimal restoration of size and mechanical and histochemical properties. We compared tibialis anterior muscles in four groups of rats: in unoperated control (C) and 10 weeks following nerve lesion with suture (LS) in the absence of electrostimulation and in the presence of muscle stimulation with either a monophasic rectangular current (LSEm) or a biphasic modulated current (LSEb). The main results were (1) muscle atrophy was reduced in LSEm (-26%) while it was absent in LSEb groups (-8%); (2) the peak twitch amplitude decreased in LS and LSEm but not in LSEb groups, whereas the contraction time was shorter; (3) muscle reinnervation was associated with the emergence of type IIC fibers and proportions of types I, IIA and IIB fibers recovered in the superficial portion of LSEb muscles; (4) the ratio of oxidative to glycolytic activities decreased in the three groups with nerve injury and repair; however, this decrease was more accentuated in LSEm groups. We conclude that muscle electrostimulation following denervation and reinnervation tends to restore size and functional and histochemical properties during reinnervation better than is seen in unstimulated muscle.

Evidence that free radical generation occurs during scorpion envenomation.

Although it is well established that symptomatology, morbidity and death following scorpion envenomation are due to increases in neurotransmitter release secondary to toxins binding to voltage-sensitive sodium channels, the mechanism by which venom action is involved in damaging heart, liver, lungs and kidneys remains unclear. We hypothesized that scorpion toxins could induce the generation of high levels of free radicals responsible for membrane damage in organs targeted by venom action. We have investigated lipid peroxidation in different organs, through the evaluation of thiobarbituric acid reactive substances (TBARS), after experimental envenomation of rats by toxic fractions of Androctonus australis Hector venom. We have shown that scorpion toxins cause considerable lipid peroxidation in most vital organs. We also evaluated the protective effects of antioxidants in mice injected with lethal doses of toxins. Among the drugs tested, N-acetylcysteine (NAC) was effective in protecting the mice when injected prior to toxin application. However, the free radical scavenging properties of NAC seem less implicated in these protective effects than its ability to increase the fluidity of bronchial secretions. We therefore conclude that free radical generation only plays a minor role in the toxicity of scorpion venom.

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise.

OBJECTIVES: Because the muscle response to incremental exercise is not well documented in patients suffering from chronic fatigue syndrome (CFS), we combined electrophysiological (compound-evoked muscle action potential, M wave), and biochemical (lactic acid production, oxidative stress) measurements to assess any muscle dysfunction in response to a routine cycling exercise. DESIGN: This case-control study compared 15 CFS patients to a gender-, age- and weight-matched control group (n=11) of healthy subjects. INTERVENTIONS: All subjects performed an incremental cycling exercise continued until exhaustion. MAIN OUTCOME MEASURES: We measured the oxygen uptake (VO2), heart rate (HR), systemic blood pressure, percutaneous O2 saturation (SpO2), M-wave recording from vastus lateralis, and venous blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid (LA), and three markers of the oxidative stress (thiobarbituric acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic acid, RAA). RESULTS: Compared with control, in CFS patients (i) the slope of VO2 versus work load relationship did not differ from control subjects and there was a tendency for an accentuated PvO2 fall at the same exercise intensity, indicating an increased oxygen uptake by the exercising muscles; (ii) the HR and blood pressure responses to exercise did not vary; (iii) the anaerobic pathways were not accentuated; (iv) the exercise-induced oxidative stress was enhanced with early changes in TBARS and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration markedly increased during the recovery period. CONCLUSIONS: The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients.

Increased diaphragmatic strength and tolerance to fatigue after bilateral lung transplantation: an electromyographic study.

We evaluated the diaphragmatic function of seven patients with severe chronic respiratory failure before and after a bilateral lung transplantation (BLT), with follow-up at one year of pulmonary function tests, maximal inspiratory mouth pressure (MIP) and surface diaphragmatic electromyogram (Edi). The patients were asked to sustain target inspiratory pressures at -15, -30, and -50 cmH(2)O. We measured the endurance time (Tlim) to sustain inspiratory efforts and the power spectrum density function of Edi at each inspiratory maneuver. The Edi power spectra was analysed in terms of median frequency (MF), total power (TP) and energies in high-and low-frequency bands (EL and EH). Before BLT, a defect of the diaphragmatic function was evident: MIP was 62+/-7% of the predicted value and the Tlim measured at each inspiratory effort was very short ( 13+/-1 s, 10+/-1 s and 8+/-1 s at pressures of -15, -30, and -50 cmH(2)O, respectively). One month after BLT, the Tlim began to increase at all target inspiratory pressures and at 6 months MIP recovered to normal values. One month after BLT, there was a significant decrease in TP measured at the beginning of each inspiratory efforts and also an increase in the concomitant MF value. BLT markedly accentuated the maximal variations of TP, MF and low-frequency Edi energy. Some hypotheses are raised to explain this dramatic improvement in diaphragmatic function after BLT.

Electromyographic signs of neuromuscular fatigue are concomitant with further increase in ventilation during static handgrip.

We questioned if a non-linear increase in ventilation defining a ventilatory threshold (V(Th)) accompanied the electromyographic (EMG) signs of neuromuscular fatigue. Indeed, the intramuscular accumulation of metabolites may activate the afferent nervous pathways responsible for both the 'muscle wisdom' phenomenon and the respiratory centre activation. During inframaximal (50%) handgrip sustained until exhaustion, minute ventilation (V(E)), V(E)/V(O2) and V(E)/V(CO2) ratios were measured simultaneously with surface EMG of the 'flexor digitorum' muscle. V(Th) was defined as a non-linear V(E) increase and/or an abrupt V(E)/V(O2) increase without any concomitant increase in the V(E)/V(CO2) ratio. Handgrip was repeated during complete arterial blood flow interruption in order to suppress any venous return from the exercising forearm. In both control and blood flow interruption conditions, an abrupt increase in the V(E)/V(O2) ratio was measured in the majority of trials (13 of 15 and 14 of 15, respectively) and the EMG signs of neuromuscular fatigue (a decline in median frequency and/or a non-linear increase in low-frequency EMG energies, E(L)) were concomitant with the V(Th) determination. Thus, V(Th) occurs during sustained static contraction and is concomitant with EMG signs of neuromuscular fatigue. Neurogenic factors seem to be responsible for the two responses which persist despite the absence of any release of metabolites in the circulation.

Combined in situ analysis of metabolic and myoelectrical changes associated with electrically induced fatigue.

Electrical muscle stimulation (Mstim) at a low or high frequency is associated with failure of force production, but the exact mechanisms leading to fatigue in this model are still poorly understood. Using 31P magnetic resonance spectroscopy (31PMRS), we investigated the metabolic changes in rabbit tibialis anterior muscle associated with the force decline during Mstim at low (10 Hz) and high (100 Hz) frequency. We also simultaneously recorded the compound muscle mass action potential (M-wave) evoked by direct muscle stimulation, and we analyzed its post-Mstim variations. The 100-Hz Mstim elicited marked M-wave alterations and induced mild metabolic changes at the onset of stimulation followed by a paradoxical recovery of phosphocreatine (PCr) and pH during the stimulation period. On the contrary, the 10-Hz Mstim produced significant PCr consumption and intracellular acidosis with no paradoxical recovery phenomenon and no significant changes in M-wave characteristics. In addition, the force depression was linearly linked to the stimulation-induced acidosis and PCr breakdown. These results led us to conclude that force failure during 100-Hz Mstim only results from an impaired propagation of muscle action potentials with no metabolic involvement. On the contrary, fatigue induced by 10-Hz Mstim is closely associated with metabolic changes with no alteration of the membrane excitability, thereby underlining the central role of muscle energetics in force depression when muscle is stimulated at low frequency. Finally, our results further indicate a reduction of energy cost of contraction when stimulation frequency is increased from 10 to 100 Hz.

Effect of muscle electrostimulation on afferent activities from tibialis anterior muscle after nerve repair by self-anastomosis.

Numerous previous studies were devoted to the regeneration of motoneurons toward a denervated muscle after nerve repair by self-anastomosis but, to date, few investigations have evaluated the regeneration of sensory muscle endings. In a previous electrophysiological study (Decherchi et al., 2001) we showed that the functional characteristics of tibialis anterior muscle afferents are affected after self-anastomosis of the peroneal nerve even when the neuromuscular preparation was not chronically stimulated. The present study examines the regeneration of groups I-II (mechanosensitive) and groups III-IV (metabosensitive) muscle afferents by evaluating the recovery of their response to different test agents after self-anastomosis combined or not with chronic muscle stimulation for a 10-weeks period. We compared five groups of rats: C, control; L, nerve lesion without suture; LS, nerve lesion with suture; LSE(m): nerve lesion plus chronic muscle stimulation with a monophasic rectangular current; and LSE(b): nerve lesion plus chronic stimulation with a biphasic current with modulations of pulse duration and frequency, eliciting a pattern of activity resembling that delivered by the nerve to the muscle. Compared to the control group, (1) muscle kept only its original weight in the LSE(b) group, (2) in the LS group the response curve to tendon vibration was shifted toward the highest mechanical frequencies and the response of groups III-IV afferents after fatiguing muscle stimulation lowered, (3) in the LSE(m) group, the pattern of activation of mechanoreceptors by tendon vibrations was altered as in the LS group, and the response of metabosensitive afferents to KCl injections was markedly reduced, (4) in the LSE(b) group, the response to tendon vibration was not modified and the activation of metabosensitive units by increased extracellular potassium chloride concentration was conserved. Both LSE(b) and LSE(m) conditions were ineffective to maintain the post muscle stimulation activation of metabosensitive units as well as their activation by injected lactic acid solutions. Our data indicate that chronic muscle electrostimulation partially favors the recovery of mechano- and metabosensitivity in a denervated muscle and that biphasic modulated currents seem to provide better results.

Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise.

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 m altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 m by a mean of 23% (P<0.05), at 8000 m by 79% (P<0.01) and at 8848 m by 94% (P<0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P<0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P<0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P<0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P<0.05). At 6000 m, the LP was enhanced further from 23 (P<0.05) to 66% (P<0.01), and after RSL from 81 (P<0.01) to 232% (P<0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 m, but decreased after RSL by 32% (P<0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise.

Effects of chronic hypoxemia on the afferent nerve activities from skeletal muscle.

An acute reduction of the oxygen supply to contracting muscles not only affects their metabolism but also modifies their sensorimotor control through changes in afferent discharge of the group I and group III-IV nerve fibers, the latter playing a pivotal role in the protective mechanisms against muscle fatigue. The effects of chronic hypoxemia on the muscle sensitivity are totally unknown. In the present study, group I fibers (mechanosensory afferents) and group III-IV fibers (mechanosensory and chemosensory afferents) from the anterior tibial muscle were recorded in normoxemic and chronic hypoxemic rats. Hypoxemic rats breathed for 45 d a gas mixture containing 9.5 to 10% O(2) in N(2). The data were compared with those obtained in normoxemic animals of the same age. To activate the different muscle afferents, we used different test agents, including electrically induced fatigue (EIF), KCl, lactic acid injections, as well as tendon vibrations. The conduction velocity of all nerve fibers was significantly (p < 0.01) higher in hypoxemic rats than in the normoxemic group. Chronic hypoxemia significantly depressed the response of the group III-IV muscle afferents to KCl injections and even abolished their response to lactic acid and EIF. However, the response to tendon vibrations of the group I afferents was similar in hypoxemic and normoxemic rats. These results suggest that chronic hypoxemia markedly alters the chemosensitivity of the group III-IV muscle afferents, which may explain the higher fatigability of hypoxemic subjects.

Interindividual variability of surface EMG changes during cycling exercise in healthy humans.

We studied surface electromyogram (SEMG) changes during 1-h endurance cycling in 12 healthy subjects of whom five were involved in mountain bike training programme. The work load was set at 50% of the predicted maximal heart rate. The surface EMG and the compound evoked muscle action potential (M-wave) from the vastus lateralis muscle were recorded at rest, during the 1-h cycling period, and the 20-min recovery period. The root mean square (RMS) and the median frequency (MF) of SEMG power spectrum were computed. In all subjects, there was no shift in the median frequency throughout the cycling period and the increase in RMS remained stable. In subjects untrained to endurance cyclism, the M-wave duration increased at the end of the cycling period and these changes persisted for a consecutive 15-min period during recovery of exercise. By contrast, in trained mountain bikers the M-wave duration decreased after 2 min of exercise--the effect persisting for 2 min during recovery. These data suggest that the interpretation of M-wave changes during cycling must take into consideration the sport practices of the subjects and also that SEMG power spectrum and M-wave explore different electrophysiological events.

Is a short trial of prone positioning sufficient to predict the improvement in oxygenation in patients with acute respiratory distress syndrome?

OBJECTIVE: To determine whether a 1-h trial of prone positioning is sufficient to identify responders. DESIGN: Prospective clinical cohort study in a medico-surgical ICU in a teaching hospital. PATIENTS: 49 patients with acute respiratory distress syndrome. INTERVENTIONS: A 6-h period of prone positioning. MEASUREMENTS AND RESULTS: Baseline measurements (blood gas analysis and respiratory parameters) were evaluated in supine position just prior to turning the patients prone. Measurements were then repeated 1 h after the beginning of prone positioning (PP1h) and at the end of the 6-h period of prone positioning (PP6h). The last measurements were performed 1 h after repositioning the patients supine. Prone position induced an increase in the PaO2/FIO2 ratio (p < 0.001). A response (increase in PaO2/FIO2 ratio of at least 20 % at PP1h and/or at PP6h) was observed in 37 of 49 patients (76%). Twenty-seven of these patients (73%) were responders at PP1h while 10 (27%) were responders only at PP6h- In all, two-thirds of the patients were considered persistent responders. However, whereas the PaO2/FIO2 ratio decreased significantly 1 h after repositioning the fast responders supine, the PaO2/ FIO2 ratio remained unchanged after repositioning slow responders. CONCLUSIONS: A short-term trial of prone positioning does not appear a sufficient method to identify patients who would benefit from the postural treatment.