Biomedical subjects

Y Jammes

Publications and source records attributed to Y Jammes.

At least 37 records · Page 2Linked to original sources

PubMed2001

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.

Adult↗

PubMed2000

Response of the rabbit diaphragm to tendon vibration.

To evaluate the potential role of diaphragmatic muscle spindles in the act of breathing, we have recorded the electromyograms of the diaphragm and the external intercostal muscle in the third interspace during high-frequency mechanical vibration (50 Hz) of the central tendon in eight anesthetized, spontaneously breathing rabbits. Vibration induced a consistent, clear-cut increase in the inspiratory activity recorded from the external intercostal, thus indicating that the mechanical stimulus applied to the diaphragm was strong enough to trigger muscle spindles at distant sites. However, vibration did not elicit any alteration in costal or crural diaphragmatic activity in any animal. Similarly, when vibration was applied during hyperventilation-induced apnea, activity was recorded in the external intercostal but not in the diaphragm. These observations support the traditional view that the diaphragm is poorly endowed with muscle spindles and that these play little or no significant role in the act of breathing.

Animals↗

PubMed2000

Influence of oxygen supply on activation of group IV muscle afferents after low-frequency muscle stimulation.

Anaerobic muscle metabolism and local release of inflammatory mediators play key roles in the mechanism of postfatigue-induced activation of group IV muscle afferents. The present study focused on activation of these muscle afferents after a 3-min period of low-frequency muscle stimulation (LFMS) in different conditions of muscle oxygenation, such as occur in patients with respiratory insufficiency and subjects living at high altitude. In anesthetized rabbits, spontaneous activity of group IV afferents (conduction velocity = 1.52 +/- 0.13 m.s(-1)) from the tibialis anterior muscle was recorded at rest (baseline) and then after LFMS under normoxic (PaO(2) = 113 mmHg), hyperoxic (PaO(2) = 186 mmHg), or hypoxic (PaO(2) = 35 mmHg) conditions. The maximal force decay at the end of LFMS did not differ significantly with respect to conditions of muscle oxygenation. Compared with normoxia, hypoxia significantly increased the baseline activity of group IV muscle afferents, whereas no effect was noted when hypoxia followed a period of hyperoxia. LFMS-induced activation of group IV afferents occurred in all circumstances, except when hypoxia was first tested. The activation of group IV muscle afferents after LFMS was markedly reduced when hypoxia followed normoxia (+14% versus +27%) or hyperoxia (+55% versus +144%), whereas it was accentuated when hyperoxia followed hypoxia (+25% versus +8%). We concluded that the sensorimotor control of skeletal muscles may be altered during acute hypoxia but facilitated after reoxygenation.

Animals↗

PubMed2000

Changes in maximal performance of inspiratory and skeletal muscles during and after the 7.1-MPa Hydra 10 record human dive.

During the 7.1-MPa hydrogen-helium-oxygen record human dive, we tested the hypothesis that the increased ambient pressure would alter the maximal muscle performance, specifically that breathing dense gas would lead to fatigue of the respiratory muscle. A group of hand muscles (adductor pollicis, AP) and the inspiratory muscles (IM) were studied in three professional divers. Maximal voluntary contractions (MVC) of AP and maximal inspiratory pressure (P(i(max))) generated by IM were measured prior to the dive, during compression and decompression, and then 1 and 2 months after the dive. The decrease in MVC (-22%) was significant at 3.1 MPa, i.e. at the beginning of the introduction of hydrogen into the breathing mixture, whereas P(i(max)) fell progressively during the dive and decompression (maximal DeltaP(i(max)) = -55%), a significant reduction still being measured 1 month after the dive. The altered IM function was attributed to the consequences of long-term ventilatory loading, a condition associated with breathing a dense gas. The transient decrease in MVC of the skeletal muscle would indicate a possible effect of the hyperbaric environment, possibly the high partial pressure of hydrogen, on neuromuscular drive.

Diving↗

PubMed2000

Operation Everest III (Comex '97): modifications of cardiac function secondary to altitude-induced hypoxia. An echocardiographic and Doppler study.

During Operation Everest III (Comex '97), to assess the consequences of altitude-induced hypoxia, eight volunteers were decompressed in a hypobaric chamber, with a decompression profile simulating the climb of Mount Everest. Cardiac function was assessed using a combination of M-mode and two-dimensional echocardiography, with continuous and pulsed Doppler at 5,000, 7,000, and 8,000 m as well as 2 d after return to sea level (RSL). On simulated ascent to altitude, aortic and left atrial diameters, left ventricular (LV) diameters, and right ventricular (RV) end-systolic diameter fell regularly. Heart rate (HR) increased at all altitudes accompanied by a decrease in stroke volume; in total, cardiac output (Q) remained unchanged. LV filling was assessed on transmitral and pulmonary venous flow profiles. Mitral peak E velocity decreased, peak A velocity increased, and E/A ratio decreased. Pulmonary venous flow velocities showed a decreased peak D velocity, a decreased peak S velocity, and a reduction of the D/S ratio. Systolic pulmonary arterial pressure (Ppa) showed a progressive and constant increase, as seen on the elevation of the right ventricular/right atrial (RV/RA) gradient pressure from 19.0 +/- 2.4 mm Hg at sea level up to 40.1 +/- 3.3 mm Hg at 8,000 m (p < 0.05), and remained elevated 2 d after recompression to sea level (SL) (not significant). In conclusion, this study confirmed the elevation of pulmonary pressures and the preservation of LV contractility secondary to altitude-induced hypoxia. It demonstrated a modification of the LV filling pattern, with a decreased early filling and a greater contribution of the atrial contraction, without elevation of LV end-diastolic pressure.

Adult↗

PubMed2000

Effects of prolonged hypobaric hypoxia on human skeletal muscle function and electromyographic events.

This study tested the hypothesis that a prolonged decrease in arterial oxygen pressure in resting or contracting skeletal muscles alters their ability to develop force through an impairment of energy-dependent metabolic processes and also through an alteration of electrophysiological events. The experiment was conducted during a 32-day simulated ascent of Mt. Everest (8848 m altitude) (Everest III Comex '97), which also allowed testing of the effects of re-oxygenation on muscle function. Maximal voluntary contractions (MVCs) of the flexor digitorum, and static handgrips sustained at 60% of MVC, were performed by eight subjects before the ascent (control), then during the stays at simulated altitudes of 5000 m, 6000 m and 7000 m, and finally 1 day after the return to 0 m. The evoked muscle compound action potential (M-wave) was recorded at rest and during the manoeuvres at 60% of MVC. The changes in median frequency of electromyographic (EMG) power spectra were also studied during the contraction at 60% of MVC. In four individuals, transient re-oxygenation during the ascent allowed us to test the reversibility of hypoxia-induced MVC and M-wave changes. At rest, a significant decrease in M-wave amplitude was noted at 5000 m. This effect was associated with a prolonged M-wave conduction time at 6000 m and an increased M-wave duration at 7000 m, and persisted after the return to 0 m. Re-oxygenation did not modify the changes in M-wave characteristics. A significant decrease in MVC was measured only during the ascent (-10 to -24%) in the non-dominant forearm of subjects who underwent re-oxygenation; this intervention slightly improved muscle strength at 6000 m and 7000 m. During the ascent and after the return to 0 m, there was a significant reduction of the median frequency decrease throughout contraction at 60% of MVC compared with the EMG changes measured before the ascent. It is concluded that prolonged exposure to hypoxia slows the propagation of myopotentials and alters sensorimotor control during sustained effort. Re-oxygenation did not affect the hypoxia-induced EMG changes and had a modest influence on muscle strength.

Adult↗

PubMed1999

Activation of respiratory afferents by resistive loaded breathing modifies somatosensory evoked potentials to median nerve stimulation in humans.

The cortical projections of respiratory afferents (vagus and respiratory muscle nerves) are well documented in humans. It is also shown that their activation during loaded breathing modifies the perception of tactile sensation as well as the motor drive to skeletal muscles. The effects of expiratory or inspiratory loaded breathing on somatosensory evoked potentials (SEPs) elicited by median nerve stimulation were studied in eight healthy subjects. No significant changes occurred in latencies of N20, N30 and P40 throughout the expiratory loading period, except for a significant lengthening in P1 latency compared with unloaded breathing. However, inspiratory loading induced a significant increase in peak latency of N20, N30 and P40 components. We suggest that projections of inspiratory afferents from the diaphragm and the intercostal muscles, activated by inspiratory loading, could be responsible for the lengthened latency of median nerve SEP components. Thus, respiratory afferents very likely interact with pathways of the somatosensory system.

Adult↗

PubMed1999

Reflex inhibition of canine inspiratory intercostals by diaphragmatic tension receptors.

1. Electrical stimulation of phrenic afferent fibres in the dog elicits a reflex inhibition of efferent activity to the inspiratory intercostal muscles. However, electrical stimulation has a poor selectivity, so the sensory receptors responsible for this inhibition were not identified. 2. In the present studies, cranial forces were applied during spontaneous inspiration to the abdominal surface of the central, tendinous portion of the canine diaphragm to activate tension mechanoreceptors in the muscle. Vagal afferent inputs were eliminated by vagotomy. 3. The application of force to the central tendon caused a graded, reflex reduction in inspiratory intercostal activity, especially in external intercostal activity. This reduction was commonly associated with a decrease in inspiratory duration and was invariably attenuated after section of the cervical dorsal roots. 4. In contrast, no change in inspiratory intercostal activity was seen when high frequency mechanical vibration was applied to the central tendon to stimulate diaphragmatic muscle spindles. 5. These observations provide strong evidence that tension receptors in the diaphragm, but not muscle spindles, induce reflex inhibition of inspiratory intercostal activity. The expression of this reflex probably involves supraspinal structures.

Animals↗

PubMed1999

M-wave changes after high- and low-frequency electrically induced fatigue in different muscles.

The mechanisms of fatigue-induced changes in evoked compound muscle action potential (M-waves) are not well documented. In rats, isolated fast-glycolytic (tibialis anterior, or TA) and slow-oxidative muscles (soleus, or SOL) were stimulated repetitively at a low (10-Hz) or high (80-Hz) rate. Decreased amplitude and prolonged duration of M-waves were only significant after high-frequency fatigue in TA and SOL muscles; that is, in the conditions in which an influx of calcium was measured. On the other hand, maximal force failure and maximal lactic acid increase in the bath medium occurred in TA muscle after high- and low-frequency fatigue trials. Postfatigue increase in potassium concentration occurred in all circumstances. Thus, M-wave alterations depend mainly on the stimulation paradigm and not on the muscle type, and cannot be used as a marker of changes in intracellular potassium or lactate ions. This amplifies understanding of the significance of M-wave changes in human exercise protocols.

Animals↗

PubMed1999

Decrease of subcutaneous adipose tissue lipolysis after exposure to hypoxia during a simulated ascent of Mt Everest.

The purpose of this study was to examine the effects of prolonged hypoxia on adipose tissue lipolysis, in relation to the weight loss usually observed at high altitude. Eight male subjects were exposed for 31 days to gradually increasing hypobaric hypoxia up to the equivalent altitude of 8848 m (Mt Everest) in a decompression chamber, after 7 days at 4350 m for altitude pre-acclimatization. A biopsy of subcutaneous adipose tissue was performed before and after hypoxic exposure, to study in vitro changes in adipose tissue sensitivity. Fat mass, adipocyte volume and spontaneous lipolysis were not impaired by the exposure to hypoxia. The in vitro lipolytic response to epinephrine, isoproterenol, growth hormone (GH) and parathormone (PTH) decreased significantly (P<0.01, P<0.05, P<0.01 and P<0.01 respectively), as did the plasma concentration of free fatty acid (P<0.01). The anti-lipolytic effect promoted by alpha2-adrenergic receptor stimulation (epinephrine with propranolol) was greater after hypoxia (P<0.05), while the anti-lipolytic activity of insulin was decreased (P<0.01). In conclusion, prolonged exposure to hypobaric hypoxia led to a potent reduction in lipid mobilization, through a decrease in the efficiency of beta-adrenergic, GH and PTH lipolytic pathways, as well as an increment in the alpha2-adrenergic-receptor-mediated anti-lipolytic effects.

Adipose Tissue↗

PubMed1999

Changes in airway resistance induced by nasal or oral intermittent positive pressure ventilation in normal individuals.

Nasal intermittent positive-pressure ventilation (nIPPV) is used for the treatment of respiratory failure in patients with neuromuscular disease. The aim of the present study was to demonstrate that nIPPV may activate nose receptors, the consequence of which being reflex changes in lung resistance. The changes in interrupter resistances (Rint) in response to nIPPV were tested before and after local anaesthesia of the nasal mucosa in normal subjects. They were compared to the Rint changes induced by oral intermittent positive-pressure ventilation (oIPPV) in the same individuals. Rint was measured during 10-min periods of nIPPV or oIPPV at a constant rate (15 L x min(-1)), but at two different stroke volumes (0.8 and 1.2 L). Inspired temperature and relative humidity were held constant. nIPPV with 1.2 L (17 mL x kg(-1)) significantly increased the Rint value (+22%). This effect disappeared after nose anaesthesia or after inhalation of a cholinergic antagonist. oIPPV never changed Rint, even though the associated hypocapnia was present and more accentuated than during nIPPV. Adding CO2 to the inspired gas during nIPPV and oIPPV trials suppressed the Rint changes. The present study suggests the existence of a nasopulmonary bronchoconstrictor reflex elicited through the stimulation of nasal mechanoreceptors, their activity being markedly influenced by the changes in expired CO2 concentration.

Adult↗

PubMed1999

Passive expiratory flow-volume curve is not an accurate method to measure the respiratory time constant in rabbits.

BACKGROUND: In mechanically ventilated patients, inspiration is forced by an externally applied positive pressure whereas expiration remains passive and depends on the time constant of the total respiratory system (tau), which constitutes an important determinant of mechanical ventilation. The end-inspiratory occlusion technique is one of the easiest methods to obtain tau values in ventilated patients, especially infants, but its accuracy is not well established. The aim of this study was to compare in anesthetized, paralyzed rabbits tau values given by the end-inspiratory occlusion technique (tau(rs)) to tau values obtained by references methods for measurements (i.e. the product of static lung compliance by airway resistance: tau(ref)) during carbachol-induced bronchospasm eliciting marked modifications of the respiratory mechanics. METHODS: Comparisons were made in the basal state and after carbachol-induced bronchoconstriction in seven New Zealand adult rabbits. This procedure resulted in a wide range of expiratory time constants. A pneumotachograph was used to measure expiratory flow and volume before and after end-inspiratory occlusion. The slope of the flow volume curve gave tau(rs). Then tau(rs) was compared with tau(ref) (which ranged from 0.30 to 1.96 s). RESULTS: Statistical analysis revealed a weak correlation between the two methods, and a size-dependent bias of tau(rs) measurements. CONCLUSIONS: The end-inspiratory occlusion technique leads to a systemic bias in measurements of respiratory time constant, especially when the resistance of the respiratory system is elevated.

Airway Resistance↗

PubMed1999

Inhaled nitric oxide and vasoconstrictors in acute respiratory distress syndrome.

It has been suggested that the increase in PO(2) observed with nitric oxide (NO) should be enhanced by the addition of a vasoconstrictor agent. The vasoconstrictor used in combination with NO should mimic or enhance hypoxic vasoconstriction. The aim of this study was to evaluate the respiratory and hemodynamic effects of norepinephrine (a nonspecific vasoconstrictor), almitrine bismesylate (a specific pulmonary vasoconstrictor), and inhaled NO, alone or together. During a 6-mo period, 16 patients presenting with ARDS were prospectively investigated. On inclusion, no patient was receiving cardiovasoactive drugs. The protocol consisted of seven consecutive phases: baseline, norepinephrine (in order to obtain a 3 mm Hg rise in mean pulmonary arterial pressure [Ppa]), almitrine bismesylate (16 micrograms/kg/min), inhaled NO (20 ppm delivered during inspiration), norepinephrine + inhaled NO, almitrine bismesylate + inhaled NO, almitrine bismesylate + norepinephrine + inhaled NO. General factorial analysis of variance showed that inhaled NO and almitrine bismesylate increased oxygenation (p < 0.0001). Norepinephrine had no effect on oxygenation. A synergistic effect between inhaled NO and almitrine bismesylate was found (p < 0.05), whereas norepinephrine did not affect the response to inhaled NO. Nitric oxide produced a significant decrease in Ppa and pulmonary vascular resistances (PVRI) (p < 0.0001). Both almitrine bismesylate and norepinephrine induced an increase in Ppa (p < 0.0001). Norepinephrine increased PVRI (p < 0.002), whereas almitrine bismesylate had no effect on PVRI. The present results support the hypothesis that a selective pulmonary vasoconstrictor enhances the increase in oxygenation induced by inhaled NO, whereas norepinephrine attenuates this effect.

Administration, Inhalation↗

PubMed1999

Inhaled NO and almitrine bismesylate in patients with acute respiratory distress syndrome: effect of noradrenalin.

The combination of inhaled nitric oxide with almitrine bismesylate has been proposed for the management of acute respiratory distress syndrome in order to divert pulmonary blood flow away from poorly ventilated toward well-ventilated areas. The aims of this prospective and comparative study were to: 1) confirm the beneficial effects on oxygenation of this association; 2) evaluate the haemodynamic effects of this association; and 3) evaluate the influence of noradrenaline (a nonspecific vasoconstrictor) on the modification of gas exchange related to inhaled NO and/or almitrine bismesylate. Forty-one sedated paralysed and ventilated patients were investigated. Haemodynamic and blood gas measurements were performed in a fixed order: baseline; inhalation of NO for 30 min.; intravenous infusion of almitrine bismesylate; and concomitant administration of inhaled NO and almitrine bismesylate. Inhaled NO and almitrine bismesylate increased arterial oxygen tension (Pa,O2)/inspiratory oxygen fraction (FI,O2) (p<0.001). The association of inhaled NO with almitrine bismesylate resulted in a dramatic improvement in Pa,O2/FI,O2 (p<0.0001 versus almitrine bismesylate, p<0.05 versus inhaled NO). In patients receiving noradrenalin (n = 19), almitrine bismesylate had no effect on oxygenation. The present study confirmed that the combination of inhaled NO with almitrine bismesylate improved oxygenation, and demonstrated that almitrine bismesylate has no effect on oxygenation in patients receiving noradrenalin.

Administration, Inhalation↗

PubMed1998

Mechanisms of fatigue-induced activation of group IV muscle afferents: the roles played by lactic acid and inflammatory mediators.

We already showed that group IV muscle afferents are activated during electrically-induced fatigue. The purpose of this study is to identify the mechanisms of stimulation of these muscle afferents by electrically-induced fatigue at a high (100 Hz; high frequency fatigue, HFF) or a low rate (10 Hz; low frequency fatigue, LFF) of stimulation. In 23 paralyzed and anaesthetized rabbits, group IV afferent activity from the tibialis anterior muscle was recorded before and after 3-min HFF or 5-min LFF runs eliciting the same force failure. Plasma lactic acid concentration (LA) was also measured in leg venous blood. We tested the effects of dichloroacetate (DCA), which reduces lactic acid production, and of acetylsalicylic acid (ASA), a blocker of cyclooxygenase, on fatigue-induced activation of group IV muscle afferents after HFF and LFF trials. Pretreatment by ASA or DCA did not modify HFF-induced activation of muscle afferents. On the other hand, LFF-induced response was markedly depressed by each pharmacological agent (-44% after ASA and -75% after DCA). We verified that DCA markedly lowered LA production after LFF. The present results show that the activation of group IV muscle afferents by LFF or HFF results from different mechanisms and also demonstrate the major role played by lactic acid production and, to a lesser extent, the release of inflammatory mediators in LFF-induced activation of group IV muscle afferents.

Animals↗

PubMed1998

Resistive loading reduces ventilatory response to strychnine in anesthetized rabbits.

Breathing through an inspiratory resistance induces a hypoventilation in mammals despite an increased diaphragmatic activity. We showed in previous works that an increase in GABA and endogenous opioid release in the central respiratory network could explain in part the inadequate increase in the inspiratory drive during inspiratory loading. In the present experiment, we speculated about an additional role of glycine, another inhibitory neurotransmitter. The ventilatory effects of the glycine antagonist strychnine were evaluated in two groups of anesthetized rabbits, breathing either through an inspiratory resistive load (IRL) or not (control group). In the control group, strychnine raised (+7%, P < 0.05) the minute ventilation, V, and the rate of increase in integrated diaphragmatic discharge (Edi peak/T peak: +29%, P < 0.01). In the IRL group, strychnine did not change V and produced a lesser increase in Edi peak/T peak (+9%, P < 0.05). In both groups, strychnine induced a tonic diaphragmatic discharge. These data show that there is a weak inhibition of inspiration by glycine during resistive loading, but the effect is modest compared with that observed during unloaded ventilation. Thus, it seems that IRL breathing reduces the efficacy and/or the release of this neurotransmitter in the central nervous system, in this experimental situation.

Airway Resistance↗

PubMed1998

Correlation between surface electromyogram, oxygen uptake and blood lactate concentration during dynamic leg exercises.

Very few data are found in the literature on the adjustment of the motor drive to contracting muscles to their oxygen uptake (V(O2)). The present study examines in seven untrained and trained individuals, who performed a progressive 8 min and two 5 min constant-load cycling exercises, the changes in the ratio between total EMG energy (root mean square or RMS), recorded in a leg extensor (vastus lateralis), to the corresponding V(O2) value and their correlations with the anaerobic threshold (V(O2)AT) and the peak blood lactate concentration. In all circumstances, the RMS/V(O2) ratio began to increase, then it decreased progressively despite V(O2) continued to rise (progressive exercise) or plateaued (constant-load exercises preseted at a sub- or suprathreshold level). The decrease in RMS/V(O2) ratio persisted and it was often accentuated during the first 2 min of the recovery period. In all exercise protocols, the rate of RMS/V(O2) decrease was positively correlated with the initial peak increase in this ratio. During progressive exercise, the peak increase in RMS/V(O2) ratio as well as its rate of decrease were negatively correlated with V(O2)AT. Thus, training and/or the reduction of anaerobic muscle metabolism attenuate the changes in RMS/V(O2) ratio. During constant-load exercise trials, the rate of decrease in RMS/V(O2) ratio was positively correlated with the plateau V(O2) value and also the peak blood lactate concentration. This suggests that information on the magnitude of the anaerobic muscle metabolism play a key role in the mechanisms which adjust RMS to V(O2).

Adolescent↗

PubMed1998

Metabolic and myoelectrical effects of acute hypoxaemia during isometric contraction of forearm muscles in humans: a combined 31P-magnetic resonance spectroscopy-surface electromyogram (MRS-SEMG) study.

1. Failure of muscle force during sustained fatiguing contraction is associated with myoelectrical and metabolic alterations. However, the inter-relationships between these two types of events remain unclear. The purpose of this study was to examine the effects of decreased oxygen availability during sustained contraction on myoelectrical and metabolic changes, thereby addressing the issue of fatigue. 2. 31P-Magnetic resonance spectra and surface electromyograms were simultaneously recorded in six subjects (three women and three men) performing isometric contraction of forearm flexor muscles sustained at 60% maximum value of force under aerobic or acute hypoxaemic conditions (inhalation of a gas mixture containing 12% O2). 3. The 5 min hypoxaemic rest preceding contraction did not affect the phosphocreatine level and pH value. Under both conditions of oxygen availability, the magnitude of metabolic changes remained similar and the duration of contraction was unaffected (similar workload). However, hypoxaemia significantly reduced the rate of changes in integrated surface electromyogram activity measured in the high-frequency band. Correlative analysis of magnetic resonance spectroscopy and surface electromyogram data shows that for a given surface electromyogram change, metabolic variations were always larger under hypoxaemic conditions. 4. These results suggest that hypoxaemia does not alter metabolic changes, i.e. decrease in pH and phosphocreatine during static contraction. The downward shift of the relationships between myoelectrical and metabolic changes under hypoxaemia points to the existence of a better excitation-contraction coupling in acute hypoxaemia compared with normoxia and this is indicative of an adaptative mechanism.

Acute Disease↗