Biomedical subjects

Yves Jammes

Publications and source records attributed to Yves Jammes.

14 recordsLinked to original sources

PubMed2003

Breath-hold training of humans reduces oxidative stress and blood acidosis after static and dynamic apnea.

Repeated epochs of breath-holding were superimposed to the regular training cycling program of triathletes to reproduce the adaptative responses to hypoxia, already described in elite breath-hold divers [Respir. Physiol. Neurobiol. 133 (2002) 121]. Before and after a 3-month breath-hold training program, we tested the response to static apnea and to a 1-min dynamic forearm exercise executed during apnea (dynamic apnea). The breath-hold training program did not modify the maximal performances measured during an incremental cycling exercise. After training, the duration of static apnea significantly lengthened and the associated bradycardia was accentuated; we also noted a reduction of the post-apnea decrease in venous blood pH and increase in lactic acid concentration, and the suppression of the post-apnea oxidative stress (increased concentration of thiobarbituric acid reactive substances). After dynamic apnea, the blood acidosis was reduced and the oxidative stress no more occurred. These results suggest that the practice of breath-holding improves the tolerance to hypoxemia independently from any genetic factor.

Acidosis, Respiratory↗

PubMed2003

Changes in neuromuscular function after training by functional electrical stimulation.

We examined whether the neuromuscular function of rectus femoris (RF) and flexor digitorum brevis (FDB) in humans was modified after a 6-week training period of functional electrical stimulation (FES), and whether any effects persisted at the end of a 6-week post-FES recovery period. In both the stimulated and contralateral nonstimulated muscles, we recorded the muscle force, surface electromyogram, and M wave, and also measured the root mean square (RMS) and the median frequency (MF) during static contraction sustained until exhaustion at 60% of maximal voluntary contraction (MVC). FES was performed with symmetric biphasic pulses, with a ramp modulation of both the stimulation frequency and pulse duration. No changes in MCV and endurance time to exhaustion occurred in nonstimulated muscles, whereas a significant MVC increase occurred immediately after FES in RF (+14 +/- 5%) and FDB (+13 +/- 5%), these effects persisting 6 weeks after the end of FES. In FDB, FES also elicited a significant increase in endurance time to exhaustion (+18 +/- 7%). The M-wave characteristics never varied after FES, but a marked attenuation occurred in the MF decrease and the RMS increase measured at endurance time to sustained 60% MVC, especially in FDB, which contains the higher proportion of type II fibers. These data indicate that FES improves muscle function and elicits changes in central muscle activation. The benefits of FES were greater in FDB, which is highly fatigable, and persisted for at least a 6-week period.

Action Potentials↗

PubMed2003

Reliability of burst superimposed technique to assess central activation failure during fatiguing contraction.

Recording a superimposed electrically-induced contraction at the limit of endurance during voluntary contraction is used as an indicator of failure of muscle activation by the central nervous system and discards the existence of peripheral muscle fatigue. We questioned on the reliability of this method by using other means to explore peripheral muscle failure. Fifteen normal subjects sustained handgrip at 60% of maximal voluntary contraction (MVC) until exhaustion. During sustained contraction, the power spectrum analysis of the flexor digitorum surface electromyogram allowed us to calculate the leftward shift of median frequency (MF). A superimposed 60 Hz 3 s pulse train (burst superimposition) was delivered to the muscle when force levelled off close to the preset value. Immediately after the fatigue trial had ended, the subject was asked to perform a 5 s 60% MVC and we measured the peak contractile response to a 60 Hz 3 s burst stimulation. Recordings of the compound evoked muscle action potential (M-wave) allowed us to explore an impairment of neuromuscular propagation. A superimposed contraction was measured in 7 subjects in their two forearms, whereas it was absent in the 8 others. Despite these discrepancies, all subjects were able to reproduce a 3 s 60% MVC immediately after the fatigue trial ended and there was no post-fatigue decrease of contraction elicited by the 60 Hz 3 s burst stimulation, as well as no M-wave decrease in amplitude and conduction time. Thus, there was no indication of peripheral muscle fatigue. MF decrease was present in all individuals throughout the fatiguing contraction and it was not correlated with the magnitude of superimposed force. These observations indicate that an absence of superimposed electrically-induced muscle contraction does not allow us to conclude the existence of a sole peripheral muscle fatigue in these circumstances.

Adult↗

PubMed2003

Hyperbaric hyperoxia induces a neuromuscular hyperexcitability: assessment of a reduced response in elite oxygen divers.

We compared the changes in compound muscle mass action potential (M-wave) recorded in vastus lateralis in response to hyperbaric hyperoxia (HBO) in nine combat divers who dived daily while breathing 100% O2 or O2-enriched mixture (O2 divers) to those measured in eight recreational divers who dived occasionally using compressed air/21% O2 (air divers). The O2 divers completed a 6-h HBO exposure in which the inspired oxygen pressure (PiO2) varied from 1.15 to 2.7 absolute atmospheres (ATA), PiO2 being maintained at 1.15 ATA throughout the first 2-h period, whereas the air divers only completed a 2-h HBO exposure with PiO2 constant at 1.15 ATA. Before HBO exposure, there were no intergroup differences between baseline M-wave characteristics (amplitude and duration), but the conduction time was significantly shorter in O2 divers compared with air divers. After 90 min of HBO (1.15 ATA) the air divers demonstrated neuromuscular hyperexcitability, as evidenced by an increased M-wave amplitude (13%, P<0.01 versus baseline), shortened M-wave duration (5%, P<0.05 versus baseline), and reduced conduction time (5%, P<0.01 versus baseline). In O2 divers, similar HBO-induced M-wave changes were only observed when PiO2 was greater than 1.50 ATA. We conclude that HBO elicites neuromuscular hyperexcitability, attenuated in elite O2 divers.

Action Potentials↗

PubMed2003

EMG signs of neuromuscular fatigue related to the ventilatory threshold during cycling exercise.

We questioned whether electromyographic (EMG) signs of neuromuscular fatigue accompany the changes in respiratory variables measured at the ventilatory threshold (VTh) during exercise on a cycloergometer. This was based on the assumption that the activation of muscle afferents sensitive to accumulation of lactate and potassium is suspected to elicit both the EMG signs of fatigue and hyperventilation. In 39 subjects performing an incremental cycling, the EMG estimates of neuromuscular fatigue in vastus lateralis were a non-linear increase in root mean square (RMS), a decrease in median frequency (MF), a non-linear increase in low-frequency EMG energies (EL), and/or a decrease in high-frequency energies (EH). VTh was determined from a non-linear increase in VCO2 [VTh(VCO2 slope)] and an increased value of the respiratory equivalent for oxygen [VTh(VE/VO2)]. We measured a significant increase in venous blood concentration of lactate and potassium, and a significant pHv fall at VTh. One EMG estimate of fatigue was detected in 33/39 individuals and two EMG estimates in 17 subjects. Highly significant positive correlations were found between the oxygen uptakes corresponding to each EMG estimate and to each detection criterion of VTh. These observations suggest that the activation of muscle sensory pathways contribute to the mechanism of VTh.

Acidosis, Lactic↗

PubMed2002

Comparison between the effects of chronic and acute hypoxemia on muscle afferent activities from the tibialis anterior muscle.

The reflex loops initiated by the activation of muscle afferents are altered by a reduction of the oxygen supply. This has been shown in different mammalian species under experimental conditions of acute or chronic hypoxemia. In the present study in rats, we compared the effects of acute and chronic hypoxemia on the activity of afferents from the tibialis anterior muscle to investigate the existence of possible adaptive mechanisms to hypoxaemia. The activity in groups I and II (mechanosensitive) and groups III and IV (mechano- and mostly chemosensitive) muscle afferents was recorded under conditions of normoxaemia and acute and chronic hypoxemia. Chronic hypoxaemia was achieved by exposing the rats for 45 consecutive days to a gas mixture containing 10% oxygen in nitrogen, whereas acute hypoxaemia was limited to a 1-h exposure to a 10% oxygen mixture. Different test agents: muscle stimulation (MS), arterial injection of KCl or lactic acid and tendon vibrations, were used to activate muscle afferents. Both acute and chronic hypoxaemia suppressed the post-MS activation of groups III and IV muscle afferents and significantly depressed the response of these afferents to KCl and lactic acid. The pattern of response of mechanosensitive afferents to mechanical tendon vibration was similar under the three conditions but chronic hypoxemia significantly reduced the response to 10-50 Hz vibrations. We conclude that inhibitory effects on muscle metabosensitive afferents occurred in the first minutes following acute hypoxemia and was prolonged with chronic hypoxemia. Our data also suggest that chronic hypoxemia depresses mechanosensitive muscle afferents. This may explain the observation that sensorimotor control of skeletal muscles is often markedly impaired in hypoxemic humans.

Action Potentials↗

PubMed2002

Reduced oxidative stress and blood lactic acidosis in trained breath-hold human divers.

We hypothesized that the repetition of brief epochs of hypoxemia in elite human breath-hold divers could induce an adaptation of their metabolic responses, resulting in reduced blood acidosis and oxidative stress. Trained divers who had a 7-10 year experience in breath-hold diving, and were able to sustain apnea up to 440 sec at rest, were compared to control individuals who sustained apnea for 145 sec at the most. The subjects sustained apnea at rest (static apnea), and then, performed two 1-min dynamic forearm exercises whether they breathed (control exercise) or sustained apnea (dynamic apnea). We measured arterial blood gases, venous blood pH, and venous blood concentrations of lactic acid, thiobarbituric acid reactive substances (TBARS), and two endogenous anti-oxidants (reduced glutathione, GSH, and reduced ascorbic acid, RAA). In control subjects, the three experimental conditions elicited an increase in blood lactic acid concentration and an oxidative stress (increased TBARS, decreased GSH and RAA concentrations). In divers, the changes in lactic acid, TBARS, RAA, and GSH concentrations were markedly reduced after static and dynamic apnea, as well as after control exercise. Thus, human subjects involved in a long duration training programme of breath-hold diving have reduced post-apnea as well as post-exercise blood acidosis and oxidative stress, mimicking the responses of diving animals.

Acidosis, Lactic↗

PubMed2002

Conventional mechanical ventilation of healthy lungs induced pro-inflammatory cytokine gene transcription.

We investigated the potential inflammatory reaction induced by mechanical ventilation (MV) using 10 ml/kg tidal volume and no positive end-expiratory pressure (PEEP) in control (C, n = 8), spontaneously breathing (SB, n = 12) and mechanically ventilated (MV, n = 12) rabbits with normal lungs. After 6 h (MV and SB groups) or immediately (C group), lungs were removed for measurement of wet-to-dry (W/D) weight ratio and for bronchoalveolar lavage (BAL). Pulmonary mechanics were also studied. MV animals developed a modest but significant (P < 0.01) impairment of arterial blood oxygenation and had higher W/D lung weight ratio than C ones. In MV group, BAL macrophage count was greater (P < 0.05) than in SB one. MV induced an upregulation of MCP-1, TNF-alpha, and IL-1beta gene transcription (mRNAs), without significant elevation of the corresponding protein cytokines in the BAL supernatant, except for MCP-1 (P < 0.05). These data suggest that MV, even using moderate tidal volume, elicits a pro-inflammatory stimulus to the lungs.

Analysis of Variance↗

PubMed2002

Interactions between endogenous nitric oxide and hypoxemia in activation of group IV muscle afferents.

It has previously been shown that both hypoxemia and nitric oxide (NO) synthase blockade depress the activation of group IV muscle afferents after muscle stimulation (MS). In the present study, we questioned whether hypoxemia exerts a specific inhibitory influence, independently from its effects on endogenous NO formation. This hypothesis was tested in two groups of anesthetized rabbits in which we examined the effects of hypoxemia, and then of subsequent NO synthase blockade by N(G)-nitro-L-arginine methyl ester (L-NAME), and vice versa. In each protocol, group IV afferent activity was recorded from the resting tibialis anterior muscle and after 3-min periods of MS that elicited a significant decrease in muscle force. NO synthase blockade in normoxemia suppressed the group IV afferent response to MS, and hypoxemia alone significantly reduced the post-MS activation of these nerve afferents (+18% vs. +28% in normoxemia). In hypoxemic rabbits, further NO synthase blockade abolished the post-MS activation of group IV afferents. Moreover, when hypoxemia followed the NO synthase blockade, MS significantly reduced the discharge of group IV afferents (-28%). Thus, while these muscle afferents are activated after fatiguing muscle contractions when the endogenous NO production is present, they are deactivated by hypoxemia when NO production is blocked. We conclude that endogenous NO production and hypoxemia exert opposite effects on the activation of the group IV afferents. Our data anticipate the neuromuscular side effects of treatments using exogenous NO or drugs acting on endogenous NO production.

Animals↗

PubMed2002

The post-exercise oxidative stress is depressed by acetylsalicylic acid.

In order to assess whether oxidative stress occurs after fatiguing dynamic contractions of a small forearm muscle group, we estimated the kinetics of changes in some of its biomarkers (thiobarbituric acid reactive substances or TBARS; plasma reduced ascorbic acid or RAA; erythrocyte reduced glutathione or GSH). We also tested the hypothesis that acetylsalicylic acid (ASA) may compete with endogenous radical targets, attenuating the post-exercise oxidative stress. Seven male subjects successively performed a 3-min dynamic handgrip exercise with the dominant and then the contralateral forearm. Blood samples were taken from an antecubital vein in each exercising forearm. Biochemical analyses, including the concentration measurements of lactic acid, potassium, and oxidative stress markers were performed at rest and then during the 30-min period of recovery following each exercise. The same day, exercises were repeated after ingestion of a single dose (10 mg/kg) of ASA, and the same exercises were performed after a 3-day ASA treatment (30 mg/kg/day). In control condition, the changes in TBARS, RAA and GSH were already significant immediately after the end of the forearm exercise. They culminated after 5 min, and control values were recovered by a 30-min rest period. We verified that repeated bouts failed to alter the post-exercise variations. ASA did not modify the lactic acid production significantly, though the 3-day ASA treatment significantly reduced the efflux of potassium (-74%, P < 0.05), and the post-exercise variations of TBARS (-45%, P < 0.01), RAA (-44%, P < 0.01) and GSH (-48%, P < 0.01). These results suggest that the dynamic handgrip exercise is a good model for studying the post-exercise oxidative stress and also that ASA seems to offer an efficient protection against oxidative stress and the changes in membrane permeability to potassium.

Adult↗

PubMed2002

Surface diaphragmatic electromyogram changes after laparotomy.

The aim of this human study was to objective cliaphragmatic electromyogram (EMG) changes after supraombilical laparotomy. The surface diapbragmatic FMG was recorded in patients (before and after laparotomy), and in healthy volunteers, during standardized inspiratory efforts sustained at -30 cmH2O (Muller manoeuvres). The quantitative EMG analysis showed significant postoperative modifications: the root mean square (RMS) increased and the median frequency (ME) decreased. These modifications are compatible with an altered diaphragmatic excitability and/or a reduced central drive to the diaphragm.

Abdomen↗

PubMed2002

Acute hypoxemia does not increase the oxidative stress in resting and contracting muscle in humans.

In healthy humans sustaining static handgrip at 60% of maximal voluntary contraction (MVC) until exhaustion, we measured the venous blood concentration of reduced ascorbic acid (RAA) and thiobarbituric acid reactive substances (TBARS), respectively, used as markers of the post-exercise oxidative stress and lipid peroxidation. Measurements were conducted in normoxemia, then during a 30-min period of hypoxemia (PaO2 = 56 mmHg) produced by inhalation of an hypoxic gas mixture. Compared to normoxemia, hypoxemia did not significantly modify the resting concentrations of TBARS and RAA, and did not affect the consumption of ascorbic acid after 60% MVC but suppressed the post-exercise TBARS increase. We conclude that acute hypoxemia does not modify the production of oxygen free radicals after strenuous static efforts and even seems to attenuate the lipid peroxidation.

Adult↗

PubMedDate not supplied

One-year occupational exposure to a cold environment alters lung function.

Numerous observations have shown that breathing cold air causes bronchospasm and increases respiratory tract secretions in asthmatic patients and normal individuals. However, few studies have been conducted on the respiratory effects of protracted daily exposures to a cold environment. In this 1-yr study, the authors examined individuals who spent 6 hr a day in cold stores (+3 degrees C to + 10 degrees C) and spent approximately 25% of that time at +3 degrees C. The protocol included a questionnaire about clinical symptoms, with measurements of baseline pulmonary function and airway responses to carbachol and to nasal inhalation of cold air (-5 degrees C). Eleven subjects were examined prior to their first occupational exposure to cold, and again following 6 mo and 12 mo of work in the cold environment. Compared with a control group of 6 subjects engaged at the same time but who did not work in cold stores, 6 of 11 individuals who worked 12 mo in a cold environment experienced increased symptoms of rhinitis, sore throat, and cough. Physiological measurements at 6 mo and 12 mo showed a progressive decrease in forced expiratory volume in 1 sec and a progressive increase in the baseline value of central airway resistance. Forced expiratory flow measured between 25% and 75% of vital capacity had decreased at 6 mo, but showed no further change at 12 mo. A progressive enhancement of bronchial reactivity to carbachol was noted at 6 mo and again at 12 mo, but airway response to nasal breathing of cold air did not vary. The authors concluded that 1 yr of daily exposure to a cold occupational environment elicits a modest--but significant--airflow limitation, accompanied by bronchial hyperresponsiveness, with the effects beginning within 6 mo of exposure.

Adult↗

PubMedDate not supplied

High prevalence of reversible airway obstruction in asbestos-exposed workers.

In this retrospective study of 97 male workers exposed to asbestos for 2-50 yr, data were collected on chest x-ray findings and lung function, including lung volumes, forced expiratory flow rates (i.e., forced expiratory volume in 1 sec [FEV1.0], forced expiratory flow measured between 25% and 75% of forced vital capacity [FEF(25-75%)]), airway resistance (R(aw)), carbon monoxide (CO)-diffusing capacity, and the existence of airway obstruction reversible by a beta-adrenergic agonist (RAO). The authors performed multiple-regression analyses to correlate the variations in lung function data with age, smoking habits, duration of asbestos exposure, and time since last exposure. Occupational activities of subjects that might induce specific lung abnormalities were also considered. No significant decrease was seen in lung volumes or CO-diffusing capacity; however, a decrease in FEV1.0 and an increase in R(aw) were measured in 65% of the subjects, and an isolated decrease in FEF(25-75%) occurred in only 18%. There was no difference in lung-function data between subjects who had chest x-ray signs of abnormalities (n = 59) and those who did not (n = 38). A significant relationship was found between the decrease in FEV1.0 and age; however, no correlation was noted between altered lung function and cigarette smoking, duration of asbestos exposure, or time since last exposure. RAO prevalence was higher (34%) than previously reported (9%) in subjects with chronic obstructive pulmonary disease (COPD) who were not exposed to asbestos or outdoor pollution. The RAO prevalence in asbestos-exposed workers was nearly the same as that measured in COPD subjects who lived downtown and who were exposed to outdoor pollution (36%). The high RAO prevalence in asbestos-exposed workers was found in 43% of subjects who were exposed only to asbestos, and in 33% of subjects who were also exposed to air pollution due to their occupational activities. It is hoped that the observations in this study will encourage practitioners to check for RAO in asbestos workers who use inhaled bronchodilators.

Aged↗