Abdominal muscle fatigue following exercise in chronic obstructive pulmonary disease

<p>Abstract</p> <p>Background</p> <p>In patients with chronic obstructive pulmonary disease, a restriction on maximum ventilatory capacity contributes to exercise limitation. It has been demonstrated that the diaphragm in COPD is relatively protected from fatigue during exercise. Because of expiratory flow limitation the abdominal muscles are activated early during exercise in COPD. This adds significantly to the work of breathing and may therefore contribute to exercise limitation. In healthy subjects, prior expiratory muscle fatigue has been shown itself to contribute to the development of quadriceps fatigue. It is not known whether fatigue of the abdominal muscles occurs during exercise in COPD.</p> <p>Methods</p> <p>Twitch gastric pressure (TwT10Pga), elicited by magnetic stimulation over the 10^ththoracic vertebra and twitch transdiaphragmatic pressure (TwPdi), elicited by bilateral anterolateral magnetic phrenic nerve stimulation were measured before and after symptom-limited, incremental cycle ergometry in patients with COPD.</p> <p>Results</p> <p>Twenty-three COPD patients, with a mean (SD) FEV₁40.8(23.1)% predicted, achieved a mean peak workload of 53.5(15.9) W. Following exercise, TwT₁₀Pga fell from 51.3(27.1) cmH₂O to 47.4(25.2) cmH₂O (p = 0.011). TwPdi did not change significantly; pre 17.0(6.4) cmH₂O post 17.5(5.9) cmH₂O (p = 0.7). Fatiguers, defined as having a fall TwT10Pga ≥ 10% had significantly worse lung gas transfer, but did not differ in other exercise parameters.</p> <p>Conclusions</p> <p>In patients with COPD, abdominal muscle but not diaphragm fatigue develops following symptom limited incremental cycle ergometry. Further work is needed to establish whether abdominal muscle fatigue is relevant to exercise limitation in COPD, perhaps indirectly through an effect on quadriceps fatigability.</p

Respiratory muscle strength as a predictive biomarker for survival in amyotrophic lateral sclerosis

Rationale: Biomarkers for survival in amyotrophic lateral sclerosis (ALS) would facilitate the development of novel drugs. Although respiratory muscle weakness is a known predictor of poor prognosis, a comprehensive comparison of different tests is lacking. Objectives: To compare the predictive power of invasive and noninvasive respiratory muscle strength assessments for survival or ventilator-free survival, up to 3 years. Methods: From a previously published report respiratory muscle strength measurements were available for 78 patients with ALS. Time to death and/or ventilation were ascertained. Receiver operating characteristic analysis was used to determine the cutoff point of each parameter. Measurements and Main Results: Each respiratory muscle strength assessment individually achieved statistical significance for prediction of survival or ventilator-free survival. In multivariate analysis sniff trans-diaphragmatic and esophageal pressure, twitch trans-diaphragmatic pressure (Tw Pdi), age, and maximal static expiratory mouth pressure were significant predictors of ventilation-free survival and Tw Pdi and maximal static expiratory mouth pressure for absolute survival. Although all measures had good specificity, there were differing sensitivities. All cutoff points for the VC were greater than 80% of normal, except for prediction of 3-month outcomes. Sequential data showed a linear decline for direct measures of respiratory muscle strength, whereas VC showed little to no decline until 12 months before death/ventilation. Conclusions: The most powerful biomarker for mortality stratification was Tw Pdi, but the predictive power of sniff nasal inspiratory pressure was also excellent. A VC within normal range suggested a good prognosis at 3 months but was of little other value

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

Inspiratory muscle maximum relaxation rate measured from submaximal sniff nasal pressure in patients with severe COPD

Background: Slowing of the inspiratory muscle maximum relaxation rate (MRR) is a useful index of severe inspiratory muscle loading and potential fatigue and has been measured from the oesophageal pressure during sniffs in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate whether it is possible to measure MRR and detect slowing using sniff nasal pressure in patients with COPD and to investigate the relationship between sniff oesophageal and sniff nasal MRR. Methods: Eight patients with severe COPD (mean FEV(1) 0.7 l; 26% predicted) were studied. Each subject performed submaximal sniff manoeuvres before and after walking to a state of severe dyspnoea on a treadmill. Oesophageal and gastric pressures were measured using balloon tipped catheters and nasal pressure was measured using an individually modelled nasal cast. MRR (% pressure fall/10 ms) was determined for each sniff and any change following exercise was reported as percentage of baseline to allow comparison of sniff nasal and oesophageal MRR. Results: At rest the mean (SE) sniff Poes MRR was 7.1 (0.3) and the mean Pnasal MRR was 8.6 (0.1). At 1 minute following exercise there was a mean decrease in sniff Poes MRR of 33.7% (range 20.7–53.4%) and a mean decrease in sniff Pnasal MRR of 28.2% (range 8.1–52.8%). The degree of slowing and time course of recovery was similar, with both returning to baseline values within 5–10 minutes. A separate analysis of the sniff pressures using only the nasal pressure traces demonstrated a similar pattern of slowing and recovery. Conclusions: It is possible to detect slowing of the inspiratory muscles non-invasively using sniff nasal pressures in patients with COPD. This could be a useful technique with which to measure severe and potentially fatiguing inspiratory muscle loading, both in clinical settings and during exercise studies

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 IPS 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 assisted with IPS. This technique may prove to be a useful adjunct in pulmonary rehabilitation.


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