Chantal Guillot

Matched adaptations of electrophysiological, physiological, and histological properties of skeletal muscles in response to chronic hypoxia

This study tried to differentiate the consequences of chronic hypoxia on the electrophysiological and physiological properties and the histological characteristics of slow and fast muscles in rats. Animals inhaled a 10% O2 concentration for a 1-month period. Then, slow [soleus (SOL)] and fast [extensor digitorum longus (EDL)] muscles were analyzed in vitro by physiological and electrophysiological measurements and histological analyses. The results were compared to those obtained in corresponding muscles of an age-matched normoxic group. After exposure to hypoxia: (1) in SOL, there was a tendency to elevated Fmax, a significant increase in twitch force and tetanic frequency and a shortening of M-wave duration, and a reduced percentage of type I fibres, whereas the proportion of type IIa fibres doubled; (2) in EDL, Fmax and tetanic frequency were lowered, the muscle became less resistant to fatigue, and the proportion of type IId/x fibres was halved. Then, after 1 month of hypoxia, in the SOL muscle, both the contractile and histological properties resemble those of a fast muscle. By contrast, the EDL became slower, despite its histology was modestly affected. Reduced muscle use in hypoxia could explain the tendency for deteriorating adaptations in EDL, and the faster properties of SOL could result from hypoxia-induced inhibition of the growth-related fast-to-slow shift in muscle fibre types.

A randomized, single-blind crossover comparison of the effects of chronic DDD and dual sensor VVIR pacing mode on quality-of-life and cardiopulmonary performance in complete heart block

The aim of this study was to compare DDD and dual sensor VVIR (activity and QT) pacing modes in complete AV block (CAVB). Eighteen patients (14 men and 4 women, aged 70 ± 6.5 years) implanted with a dual chamber, dual sensor pacemaker for CAVB with normal sinus node chronotropic function were studied. A quality‐of‐life and cardiovascular symptom questionnaire, and a treadmill exercise test were completed after a period of VVIR and a period of DDD pacing, each lasting 1 month. Overall quality‐of‐life and cardiovascular symptoms did not significantly differ, though three patients felt discomfort during VVIR mode. There was no significant statistical difference in Cardiopulmonary parameters. DDD and VVIR modes yielded the following respective data: maximum heart rate = 105.7 ± 21.8 beats/minute versus 107.6 ± 21.6 beats/minute (NS); maximum workload = 60 ± 33.4 W versus 59.3 ± 37.8 W (NS); treadmill duration = 10.1 ± 3.8 minute versus 10.1 ± 3.6 minute (NS); oxygen consumption at anaerobic threshold = 14.6 ± 4.1 ml/kg per minute versus 14.9 ± 4.6 mL/kg per minute (NS); maximum minute ventilation = 49.6 ± 9 L/min versus 46 ± 12 L/min (NS); and respiratory quotient = 1.08 ± 0.15 versus 1.08 ± 0.13 (NS). We conclude that, during a 1‐month follow‐up period, no difference was found between DDD and dual sensor VVIR (QT and activity) pacing modes in CAVB patients with regard to quality‐of‐life and Cardiopulmonary performance, though a trend toward an increased sense of well being was noted with the DDD mode.

Depressed fatigue-induced oxidative stress in chronic hypoxemic humans and rats

It was already documented that acute hypoxemia reduces the oxidative stress following static as well as dynamic handgrip bouts in humans. Then, we examined if chronic hypoxemia could produce the same effect in patients suffering from chronic respiratory insufficiency. In rats, we studied the respective consequence of a one-month exposure to normobaric hypoxia on two muscles (soleus, SOL, and extensor digitorum longus, EDL) which have high and low aerobic metabolism, respectively. Compared to healthy humans, the resting level of erythrocyte reduced glutathione (GSH) was significantly lower in chronic hypoxemic patients, and after a handgrip contraction sustained at 50% of maximal until exhaustion the GSH level and plasma thiobarbituric acid reactive substances (TBARS) did not vary. A 20-min period of oxygen supplementation partly restored the post-handgrip oxidative stress. Compared to control rats, SOL muscle of hypoxemic animals had lower intra-muscular resting level of GSH; after a 3-min muscle stimulation (MS) leading to fatigue, TBARS did not vary in SOL and EDL and the GSH decrease was absent in SOL whereas it persisted in EDL. We concluded that chronic hypoxemia depressed the fatigue-induced oxidative stress, the effects prevailing in muscles having a high oxygen demand.

Value of Bronchial Challenge in Scuba Diving Candidates

Bronchial challenges were effected with carbachol in 76 subjects who were candidates for a scuba diving group. Bronchial reactivity was assessed through airway resistance and forced expiratory volume in 1 sec (FEV1) measurements. Medical interrogation had revealed symptoms of recent (RA) or ancient (AA) asthma, or allergic rhinitis (AL). Nearly half of the subjects (47%) presented bronchial hyperresponsiveness (BHR), which was much more frequent in the RA group, but whose strength did not depend on clinical presentation. Prevalence of BHR was fairly high (36%) in the AL group. BHR constituted a contraindication to scuba diving because it may promote pulmonary barotrauma.

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.

Increased asymptomatic airway hyper-responsiveness in obese individuals.

Objective. Asymptomatic airway hyper-responsiveness (AHR) represents a risk of further accelerated decline in lung function, and of asthma. Due to the fact that rare and contradictory results exist concerning the impact of obesity on BHR, we re-assessed the prevalence of bronchial hyper-responsiveness (BHR) in a large cohort of 60 lean, 84 overweight, and 360 class 1–3 obese non-asthmatic individuals, by coupled plethysmography and spirometry. Methods. Baseline-specific airway conductance (SGaw) and spirometric values were measured and then a methacholine challenge testing (MCT) was performed and considered as positive when a ≥200% increase in specific airway resistance (SRaw = 1/SGaw) was reached. Results. Compared to lean and overweight subjects, obese subjects of any class presented about a twice more frequent AHR (∼ 50% in obese vs. 17 and 26% in lean and overweight subjects, respectively). However, the bronchial sensitivity (methacholine dose doubling SRaw) and the shape of the relationship between SGaw and cumulative methacholine doses were the same in the five groups of individuals. Conclusion. The present data show a more frequent AHR in obese subjects. The association of plethysmography with spirometry, by taking into account the bronchodilator effect of the lung inflation (preceding the expiratory flow measurement) in some individuals, permitted to include some MCT which would have been otherwise excluded.

One-Year Occupational Exposure to a Cold Environment Alters Lung Function

Abstract 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 [ddot]C to + 10 [ddot]C) and spent approximately 25% of that time at +3 [ddot]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 [ddot]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.

Same efficacies of ipratropium and salbutamol in reversing methacholine-induced bronchoconstriction

Efficacy of salbutamol (S) was compared to that of ipratropium (I) or to their association, after methacholine challenge testing (MCT). MCT was performed in 4 groups of 10 patients suspected to suffer from asthma; mean changes in FEV1, maximal midexpiratory flow rate (MMFR), and airway resistance (Raw) were the same in all groups. After MCT, the group 1 patients inhaled S and then I, 10 min later; both drugs were given in the reverse order to the group 2 patients. The group 3 patients inhaled a mixture of both drugs just after MCT; the group 4 patients were not given any bronchodilator till the 20th min after MCT, when they inhaled S. Short-term (10 min) bronchodilator effects of S, I or S + I on spirometric variables were of the same magnitude and Raw returned to its baseline value. Further improvement (10–20 min) in FEV1 was mainly due to spontaneous recovery, whereas further increase in MMFR was due also to bronchodilator actions of drugs. It is concluded that ipratropium could be proposed as an alternative bronchodilator to salbutamol after MCT.

Transient hypoxia: Ventilatory response after vagotomy and during artificial phasic inflation

The early ventilatory response to transient hypoxia was examined in the anaesthetized rabbit. In intact spontaneously breathing animals, an increase in tidal volume (VT) with an accompanying slight increase in inspiratory duration (TI) and a decrease in the expiratory duration (TE) was observed. After vagotomy, the ventilatory response was distinguished by a greater increase inVT and a significant decrease inTI andTE.In another group of artificially ventilated rabbits, an increase in inspiratory volume with a simultaneous decrease in breathing frequency was found to involve a smaller reflex increase in phrenic inspiratory discharge after onset of transient hypoxia.These observations suggest that afferents from pulmonary vagal stretch receptors inhibit those from arterial chemoreceptors.