Effect of acute hypoxia on respiratory muscle fatigue in healthy humans

<p>Abstract</p> <p>Background</p> <p>Greater diaphragm fatigue has been reported after hypoxic versus normoxic exercise, but whether this is due to increased ventilation and therefore work of breathing or reduced blood oxygenation per se remains unclear. Hence, we assessed the effect of different blood oxygenation level on isolated hyperpnoea-induced inspiratory and expiratory muscle fatigue.</p> <p>Methods</p> <p>Twelve healthy males performed three 15-min isocapnic hyperpnoea tests (85% of maximum voluntary ventilation with controlled breathing pattern) in normoxic, hypoxic (SpO₂= 80%) and hyperoxic (FiO₂= 0.60) conditions, in a random order. Before, immediately after and 30 min after hyperpnoea, transdiaphragmatic pressure (P_di,tw) was measured during cervical magnetic stimulation to assess diaphragm contractility, and gastric pressure (P_ga,tw) was measured during thoracic magnetic stimulation to assess abdominal muscle contractility. Two-way analysis of variance (time x condition) was used to compare hyperpnoea-induced respiratory muscle fatigue between conditions.</p> <p>Results</p> <p>Hypoxia enhanced hyperpnoea-induced P_di,twand P_ga,twreductions both immediately after hyperpnoea (P_di,tw: normoxia -22 ± 7% vs hypoxia -34 ± 8% vs hyperoxia -21 ± 8%; P_ga,tw: normoxia -17 ± 7% vs hypoxia -26 ± 10% vs hyperoxia -16 ± 11%; all <it>P </it>< 0.05) and after 30 min of recovery (P_di,tw: normoxia -10 ± 7% vs hypoxia -16 ± 8% vs hyperoxia -8 ± 7%; P_ga,tw: normoxia -13 ± 6% vs hypoxia -21 ± 9% vs hyperoxia -12 ± 12%; all <it>P </it>< 0.05). No significant difference in P_di,twor P_ga,twreductions was observed between normoxic and hyperoxic conditions. Also, heart rate and blood lactate concentration during hyperpnoea were higher in hypoxia compared to normoxia and hyperoxia.</p> <p>Conclusions</p> <p>These results demonstrate that hypoxia exacerbates both diaphragm and abdominal muscle fatigability. These results emphasize the potential role of respiratory muscle fatigue in exercise performance limitation under conditions coupling increased work of breathing and reduced O₂transport as during exercise in altitude or in hypoxemic patients.</p

MEASUREMENT OF EFFECTIVE ALVEOLAR CARBON-DIOXIDE TENSION DURING SPONTANEOUS BREATHING IN NORMAL SUBJECTS AND PATIENTS WITH CHRONIC AIRWAYS OBSTRUCTION

Background - The measurement of effective alveolar carbon dioxide tension (PACo(2)eff) is still a matter of debate. It has, however, become common practice to use arterial instead of alveolar CO2, tension for computing alveolar oxygen tension (PAO(2)) and physiological dead space, not only in normal subjects but also in patients. The purpose of this study was to estimate alveolar CO2 tension during spontaneous breathing with a new bedside technique which is simple and non-invasive, and to compare these values with arterial CO2 tension measured in normal subjects and patients with chronic airways obstruction. Methods - The subjects breathed quietly through the equipment assembly (mouthpiece, monitoring ring, Fleisch transducer head) connected to a pneumotachograph and a fast response infrared CO2 analyser. The method is a computerised calculation of the volume weighted effective alveolar CO2 tension obtained from the simultaneously recorded expiratory flow and CO2 concentration versus time curves. An arterial blood sample was taken to measure Paco(2) for comparison during the study. Results - The results showed a mean difference (PAco(2)eff-Paco(2)) of -0.205 kPa in 20 normal subjects and -0.460 kPa in 46 patients. The 95% confidence interval of the bias was -0.029 to - 0.379 kPa in normal subjects and -0.213 to -0.707 kPa in patients. The limits of agreement between PACO(2)eff and Pace, were 0.526 to -0.935 in normal subjects and 1.170 to -2.088 in patients. Conclusions - The volume weighted effective alveolar Pco(2) in normal subjects and patients with chronic airways obstruction the classical equations for estimating dead space and intrapulmonary shunt

Inspiratory pressure support prolongs exercise induced lactataemia in severe COPD

Background-A physiological benefit from pulmonary rehabilitation in chronic obstructive pulmonary disease (COPD) is more probable if exercise is performed above the lactate threshold. This study was undertaken to investigate whether it was possible to extend the lactataemia of exercise using non-invasive inspiratory pressure support (IPS). Methods-Plasma lactate levels were measured in eight men with severe COPD who performed two treadmill walks at an identical constant work rate to a condition of severe dyspnoea; the second walk was supported by IPS. Results-Mean plasma lactate levels before the free and IFS assisted walks were 1.65 mmol/l and 1.53 mmol/l, respectively (p = NS). Lactate levels increased during both walks to 2.96 mmol/l and 2.42 mmol/l , respectively (p = 0.01 for each) but the duration of the IPS assisted walk was significantly greater than the free walk (13.6 minutes versus 5.5 minutes, p = 0.01). Conclusions-Patients with severe COPD can sustain exercise induced lactataemia for longer if assited with IPS. This technique may prove to be at useful adjunct in pulmonary rehabilitation