Controlled twitch mouth pressure reliably predicts twitch esophageal pressure

The present study hypothesized that twitch mouth pressure (TwPmo) can reliably predict intrathoracic pressure swings reflected by twitch esophageal pressure (TwPes) using a controlled and automated trigger technique. TwPmo, TwPes, and transdiaphragmatic pressure (TwPdi) following bilateral anterior magnetic phrenic nerve stimulation were measured in 21 healthy subjects using an inspiratory pressure trigger (0.5kPa, experiment 1), an expiratory pressure trigger (0.5kPa, experiment 2), an inspiratory flow trigger (40ml/s, experiment 3), and no trigger at relaxed functional residual capacity (experiment 4). TwPmo and TwPes were correlated as follows: r=0.99, p<0.0001 (experiment 1); r=0.67, p=0.001 (experiment 2); r=0.96, p<0.0001 (experiment 3); no correlation (experiment 4). Bland and Altman analysis revealed most narrow limits of agreement for TwPmo and TwPes in experiment 1: bias (range) 0.15kPa (-0.03 to 0.32). TwPmo is an excellent predictor for TwPes when using a fully automated and controlled inspiratory pressure trigger. Thus, measurement of TwPmo could become a standard means assessing inspiratory muscle strength.     

Characteristics of diaphragmatic fatigue during exhaustive exercise until task failure

The diaphragm was postulated to fatigue relatively early during exhaustive whole body exercise without further loss in contractility as exercise proceeds towards task failure. Diaphragmatic contractility was investigated prior/during/after exhaustive whole body exercise until task failure by using lung volume corrected twitch transdiaphragmatic pressure (TwPdi(c)) during magnetic phrenic nerve stimulation (every 45s). Eleven cyclists exercised to exhaustion (workloads ≥85% maximal oxygen uptake; 20.7±9.8min). Individual post hoc calculation of TwPdi(c) was conducted (diaphragmatic contractility versus lung volume). Diaphragmatic fatigue (i.e. TwPdi reduction baseline/recovery ≥10%) occurred in 9/11 subjects (82% "fatiguers"; baseline/recovery TwPdi(c) -16±13%, p<0.01). Fatiguers TwPdi(c) was: baseline: 2.99±0.40kPa, exercise-onset: 2.98±0.41kPa, initial third: 2.80±0.67kPa, second third: 2.54±0.55kPa, final third-task failure: 2.51±0.44kPa, recovery: 2.50±0.52kPa. Diaphragmatic contractility and lung volume (rest) were strongly related (r(2)=0.98, mean TwPdi(c) gradient 0.78kPa/l). To conclude, diaphragmatic contractility (lung volume corrected) decreases relatively early (initial two thirds) during exhaustive exercise and remains preserved towards task failure. This confirms previous assumptions postulating that respiratory performance is sustained without further fatigue of the primary inspiratory muscle.     

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

We investigated whether the inspiratory muscles affect maximal incremental exercise performance using a placebo-controlled, crossover design. Six cyclists each performed six incremental exercise tests. For three trials, subjects exercised with proportional assist ventilation (PAV). For the remaining three trials, subjects underwent sham respiratory muscle unloading (placebo). Inspiratory muscle pressure (P(mus)) was reduced with PAV (-35.9+/-2.3% versus placebo; P<0.05). Furthermore, V(O2) and perceptions of dyspnea and limb discomfort at submaximal exercise intensities were significantly reduced with PAV. Peak power output, however, was not different between placebo and PAV (324+/-4W versus 326+/-4W; P>0.05). Diaphragm fatigue (bilateral phrenic nerve stimulation) did not occur in placebo. In conclusion, substantially unloading the inspiratory muscles did not affect maximal incremental exercise performance. Therefore, our data do not support a role for either inspiratory muscle work or fatigue per se in the limitation of maximal incremental exercise.     

Independence of exercise-induced diaphragmatic fatigue from ventilatory demands

Exercise-induced diaphragmatic fatigue (DF) manifests after - rather than during - exercise. This suggests that DF reflects post-exercise diaphragm-shielding. This study tested the physiological hypothesis that diaphragmatic force-generation undergoes similar regulations during either whole-body-exercise or controlled hyperventilation, but differs during recovery. Ten trained subjects (VO2(max) 60.3+/-6.4 ml/kg/min) performed: I, cycling exercise (maximal workload: 85% VO2(max)); II, controlled hyperventilation (exercise breathing pattern) followed by recovery. Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF occurred following exercise, while hyperventilation enhanced diaphragmatic force-generation (TwPdi-rest 2.28+/-0.58 vs. 2.52+/-0.54, TwPdi-end-recovery: 1.94+/-0.32 kPa vs. 2.81+/-0.49 kPa, both p<0.05). TwPdi was comparable between the two protocols until recovery (p>0.05, RM-ANOVA) whereby it underwent a progressive increase. In conclusion, TwPdi progressively increases and is subject to similar regulations during exercise versus controlled hyperventilation, but differs markedly during recovery. Here, DF occurred after exercise while TwPdi increased subsequent to hyperventilation. Therefore, ventilatory demands regulate diaphragmatic force-generation during exercise, whereas DF must be attributed to non-ventilatory controlled feedback mechanisms.     

New physiological insights into exercise-induced diaphragmatic fatigue

Data on the dynamic process and time-point of manifestation of exercise-induced diaphragmatic fatigue (DF) are lacking. Therefore, this study was aimed assessing dynamic changes of diaphragmatic strength during exercise and determining the time-point of DF manifestation. Fourteen trained subjects (maximal oxygen uptake (VO2(max)) 59.3+/-5.5 ml/min/kg) performed standardized exercise protocols (maximal workload: 85% VO2(max)) followed by recovery (6 min). Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF was induced (TwPdi-rest: 2.34+/-0.26 versus TwPdi-end-recovery 2.01+/-0.21 kPa, p<0.01). TwPdi progressively increased during exercise (TwPdi-rest: 2.34+/-0.26 versus TwPdi-maximal-workload: 3.28+/-0.38 kPa, p<0.001). DF was detectable immediately after exercise-termination (TwPdi-maximal-workload: 3.28+/-0.38 versus TwPdi-early-recovery 2.55+/-0.34 kPa, p<0.001). TwPdi during exercise was highly correlated to workload, VO2(max) and dyspnea (r=0.96/r=0.92/r=0.97; all p<0.0001). In conclusion, diaphragmatic strength progressively increases with increasing workload, and DF manifests after - rather than during - exercise. In addition, TwPdi is highly correlated to key-measures of ergospirometry, approving the physiological thesis that muscle strength is progressively enhanced and escapes fatiguing failure during high-intensity exercise performance.     

Respiratory muscle strength and cough capacity in patients with Duchenne muscular dystrophy

The function of inspiratory muscles is crucial for effective cough as well as expiratory muscles in patients with Duchenne muscular dystrophy (DMD). However, there is no report on the correlation between cough and inspiratory muscle strength. To investigate the relationships of voluntary cough capacity, assisted cough techniques, and inspiratory muscle strength as well as expiratory muscle strength in patients with DMD (n= 32). The vital capacity (VC), maximum insufflation capacity (MIC), maximal inspiratory pressure (MIP), and maximal expiratory pressure (MEP) were measured. Unassisted peak cough flow (UPCF) and three different techniques of assisted PCF were evaluated. The mean value of MICs (1918 +/- 586 mL) was higher than that of VCs (1474 +/- 632 mL) (p < 0.001). All three assisted cough methods showed significantly higher value than unassisted method (212 +/- 52 L/min) (F = 66.13, p < 0.001). Combined assisted cough technique (both manual and volume assisted PCF; 286 +/- 41 L/min) significantly exceeded manual assisted PCF (MPCF; 246 +/- 49 L/ min) and volume assisted PCF (VPCF; 252 +/- 45 L/min) (F = 66.13, p < 0.001). MIP (34 +/- 13 cmH2O) correlated significantly with both UPCF and all three assisted PCFs as well as MEP (27 +/- 10 cmH2O) (p < 0.001). Both MEP and MIP, which are the markers of respiratory muscle weakness, should be taken into account in the study of cough effectiveness.     

Usefulness of phrenic nerve stimulation to measure upper airway collapsibility in normal awake subjects

Upper airway (UA) collapsibility can be characterized during sleep by looking at the changes in inspiratory flow limitation (IFL) with changing nasal pressure. IFL can be induced during wakefulness using phrenic nerve stimulation (PNS) applied during exclusive nasal breathing. The aim of the study was to evaluate the possibility of measuring UA critical pressure (Pcrit) in normal awaked subjects using electrical PNS (EPNS) or bilateral anterior magnetic phrenic stimulation (BAMPS). Instantaneous flow, esophageal (Peso) and mask pressures (Pmask), and genioglossal (GG) end-expiratory EMG activity were recorded in 13 normal subjects (4F, 9M) with randomly changing Pmask (0 to -20 cmH2O). For each trial, we examined the relationship between maximal inspiratory flow (Vtmax) of IFL twitches and the corresponding Pmask. Pcrit could be determined in 12 subjects (mean -33.5 +/- 16.3 cmH2O). No difference in Pcrit values was found between the EPNS and BAMPS methods but the strength of the Vtmax/Pmask relationship was higher with BAMPS. GG end-expiratory EMG activity increased with decreasing Pmask but no significant relationship was found between the slope of the GG end-expiratory EMG activity/Pmask relationship and Pcrit. We conclude that: (1) Pcrit can be measured during wakefulness in normal using PNS: (2) Pcrit measurements may be easier and more reliable with BAMPS than EPNS: and (3) Pcrit does not seem to be influenced by the pressure-related changes in GG end-expiratory EMG.     

Effect of inspiratory muscle work on peripheral fatigue of locomotor muscles in healthy humans

The work of breathing required during maximal exercise compromises blood flow to limb locomotor muscles and reduces exercise performance. We asked if force output of the inspiratory muscles affected exercise-induced peripheral fatigue of locomotor muscles. Eight male cyclists exercised at ≥ 90% peak O₂ uptake to exhaustion (CTRL). On a separate occasion, subjects exercised for the same duration and power output as CTRL (13.2 ± 0.9 min, 292 W), but force output of the inspiratory muscles was reduced (−56% versus CTRL) using a proportional assist ventilator (PAV). Subjects also exercised to exhaustion (7.9 ± 0.6 min, 292 W) while force output of the inspiratory muscles was increased (+80% versus CTRL) via inspiratory resistive loads (IRLs), and again for the same duration and power output with breathing unimpeded (IRL-CTRL). Quadriceps twitch force ( Q _tw), in response to supramaximal paired magnetic stimuli of the femoral nerve (1–100 Hz), was assessed pre- and at 2.5 through to 70 min postexercise. Immediately after CTRL exercise, Q _tw was reduced −28 ± 5% below pre-exercise baseline and this reduction was attenuated following PAV exercise (−20 ± 5%; P < 0.05). Conversely, increasing the force output of the inspiratory muscles (IRL) exacerbated exercise-induced quadriceps muscle fatigue ( Q _tw=−12 ± 8% IRL-CTRL versus −20 ± 7% IRL; P < 0.05). Repeat studies between days showed that the effects of exercise per se , and of superimposed inspiratory muscle loading on quadriceps fatigue were highly reproducible. In conclusion, peripheral fatigue of locomotor muscles resulting from high-intensity sustained exercise is, in part, due to the accompanying high levels of respiratory muscle work.     

Respiratory response to inspiratory resistive load changes in patients with obstructive sleep apnea syndrome

Patients with OSA have many episodes of increased airway resistance because of repeated collapses of upper airways during night. The aim of this work was to evaluate respiratory response during chemical stimulation without and with added inspiratory resistive load (10 cmH2O/L/sec). The studies were performed during quiet breathing with air and during hypercapnic and hypoxic rebreathing tests without and with inspiratory resistive loading in 23 obese (BMI = 34.4 +/- 4.3 kg/m2) patients with OSA and in 10 healthy subjects with similar weight (BMI = 32.4 +/- 4.3 kg/m2). The measurements of respiratory responses (ventilation, mouth occlusion pressure) were performed with the use of computerized equipment. During quiet breathing in response to added load an increase of P0.1 in controls and in OSA patients was observed. During hypercapnic stimulation the ventilatory response with additional load decreased in patients as well as in controls. The slope of mouth occlusion pressure response increased significantly in controls (from 4.40 to 6.83 cmH2O/kPa, p < 0.001) and slightly weaker in OSA patients (from 4.21 to 5.43 cmH2O/kPa, p < 0.05). Although the difference between the slopes was not significant, we found that the absolute increase of P0.1 measured at point 8 kPa of PEtCO2 during loaded breathing was significantly smaller in OSA patients in comparison to controls. (2.1 vs. 10.3 cm H2O; p < 0.001). During hypoxic stimulation occlusion pressure responses were similar in both examined groups. In conclusion we postulate that OSA patients have impaired respiratory compensation of additional inspiratory load, what was demonstrated during hypercapnic rebreathing test.     

Comparison of microvascular filtration in human arms with and without postmastectomy oedema

Oedema is caused by impaired lymphatic drainage and/or increased microvascular filtration. To assess a postulated role for the latter in postmastectomy oedema, filtration was studied in the forearms of 14 healthy subjects and 22 patients with chronic, unilateral arm oedema caused by surgical and radiological treatment for breast cancer. A new non-contact optical device (the Perometer) and a conventional mercury strain gauge were used simultaneously to record forearm swelling rates caused by microvascular filtration during applied venous congestion. Filtration rate (FR) per 100 ml tissue was measured over 10-15 min at a venous pressure of 30 cmH2O, a pressure reached in the dependent forearm (FR30), and then at 60 cmH2O (FR60). Apparent filtration capacity of 100 ml soft tissue (CFCa) was calculated from FR60 - FR30/30, after adjustment for bone volume. The Perometer and strain gauge gave similar results in normal and oedematous arms. Mean CFCa in healthy subjects was (3.8+/-0.4) x 10(-3) ml (100 ml)-1 cmH2O-1 min-1, close to literature values. In the patients, FR30 was 47 % lower in the oedematous forearm than in the opposite, unaffected forearm (P = 0.04). FR60 showed a similar trend but did not reach significance (P = 0.15). The values of CFCa of (2.2+/-0.5) x 10(-3) ml (100 ml)-1 cmH2O-1 min-1 in the oedematous arm and (2.8+/-0.5) x 10(-3) ml (100 ml)-1 cmH2O-1 min-1 in the unaffected arm were not significantly different (P = 0.47). When differences in arm volume on the two sides were taken into account, the total fluid load on the lymphatic system of the oedematous forearm was (411.0+/-82.2) x 10(-3) ml min-1 at 30 cmH2O and (1168+/-235.6) x 10(-3) ml min-1 at 60 cmH2O, similar to the normal side, namely (503.7+/-109.3) 10(-3) ml min-1 and (1063+/-152.0) x 10(-3) ml min-1, respectively (P >/= 0.50). The filtration capacity of the entire oedematous forearm (CFCa scaled up by total soft tissue volume), (25.4+/-6.2) x 10(-3) ml cmH2O-1 min-1, was not significantly greater than that of the normal forearm, (18.3+/-2.6) x 10(-3) ml cmH2O-1 min-1 (P = 0.40). The results indicate that no major change occurs in the microvascular hydraulic permeability-area product of the forearm, or in the total filtration load on the lymph drainage system during dependency, in the arm with postmastectomy oedema compared with the normal arm. This argues against a significant haemodynamic contribution to postmastectomy oedema.     

The effect of sleep on reflex genioglossus muscle activation by stimuli of negative airway pressure in humans.

The present study was designed to determine the effect of sleep on reflex pharyngeal dilator muscle activation by stimuli of negative airway pressure in human subjects. Intra-oral bipolar surface electrodes were used to record genioglossus electromyogram (EMG) responses to 500 ms duration pressure stimuli of 0 and -25 cmH2O applied, via a face-mask, in four normal subjects. Stimuli were applied during early inspiration in wakefulness and in periods of non-rapid-eye-movement (non-REM) sleep, defined by electroencephalographic (EEG) criteria. The rectified and integrated EMG responses to repeated interventions were bin averaged for the 0 and -25 cmH2O stimuli applied in wakefulness and sleep. Response latency was defined as the time when the EMG activity significantly increased above prestimulus levels. Response magnitude was quantified as the in ratio of the EMG activity for an 80 ms post-stimulus period to an 80 ms prestimulus period; data from after the subject's voluntary reaction time for tongue protrusion (range, 150-230 ms) were not analysed. Application of the -25 cmH2O stimuli caused genioglossus muscle activation in wakefulness and sleep, but in all subjects response magnitude was reduced in sleep (mean decrease, 61%; range, 52-82%; P = 0.011, Student's paired t test). In addition, response latency was increased in sleep in each subject (mean latency awake, 38 ms; range, 30-50 ms; mean latency asleep, 75 ms; range, 40-110 ms; P = 0.072, Student's paired t test). Application of the -25 cmH2O stimuli caused arousal from sleep on 90% occasions, but in all cases the reflex genioglossus muscle responses (maximum latency, 110 ms) always proceeded any sign of EEG arousal (mean time to arousal, 643 ms; range, 424-760 ms). These results show that non-REM sleep attenuates reflex genioglossus muscle activation by stimuli of negative airway pressure. Attenuation of this reflex by sleep may impair the ability of the upper airway to defend itself from suction collapse by negative pressures generated during inspiration; this may have implications for the pathogenesis of obstructive sleep apnoea.     

Constant mean airway pressure with different patterns of positive pressure breathing during the adult respiratory distress syndrome

Twenty-one ARDS patients were divided into two groups of severity according to FIO2 and PEEP required to maintain an adequate gas exchange. The 10 most severe patients (group A) underwent continuous positive pressure ventilation (CPPV) (I/E 3:1) with the mean airway pressure maintained at 21 +/- 6.2 cmH2O. The PEEP values were 12.6 +/- 4.3 cmH2O during CPPV and 6.5 +/- 3.7 cmH2O during IRV (p less than 0.01). Eleven less severe ARDS patients (group B) underwent CPPV and positive pressure spontaneous breathing (CPAP) at constant mean airway pressure of 14.3 +/- 3.8 cmH2O. The PEEP was 7 +/- 2.5 cmH2O during CPPV and 14.9 +/- 4.3 cmH2O during CPAP (p less than 0.001). In five patients of each group, the SF6 shunt was measured as representative of true shunt. The results showed that gas exchange, including true shunt, and haemodynamics did not change between CPPV and IRV and between CPPV and CPAP tests. Taken with previous work on mean airway pressure, our results further support the concept that the main determinant of oxygenation and haemodynamics is the mean airway pressure, irrespective of the PEEP level and of the mode of ventilation.     

Effect of increased diaphragm activation on diaphragm power spectrum center frequency

Increased transdiaphragmatic pressure, reduced muscle blood flow, and increased duty cycle have all been associated with a reduction in the center frequency (CFdi) of the diaphragm's electrical activity (EAdi). However, the specific influence of diaphragm activation on CFdi is unknown. We evaluated whether increased diaphragm activation would result in a greater decline in the CFdi when pressure-time product (PTPdi) was kept constant. Five healthy subjects performed periods of intermittent quasi-static diaphragmatic contractions with a fixed duty cycle. In separate runs, subjects targeted transdiaphragmatic pressures (Pdi) by performing end-inspiratory holds with the glottis open and expulsive maneuvers at end-expiratory lung volume (EELV). Diaphragm activation and pressures were measured with an electrode array and balloons mounted on an esophago-gastric catheter, respectively. The EAdi, which was 25+/-8%(S.D.) of maximum at EELV, increased to 61+/-8% (P<0.001) when an identical Pdi (averaging 31+/-13 cmH2O) was generated at a higher lung volume (77% of inspiratory capacity). The latter was associated with a 17% greater decline in CFdi (P=0.012). In order to reproduce at EELV, the decrease in CFdi observed at the increased lung volume, a two-fold increase in PTPdi was required. We conclude that CFdi responds specifically to increased diaphragm activation when pressure-time product remains constant.     

Chest wall volume changes during inspiratory loaded breathing

We assessed the effect of inspiratory loaded breathing (ILB) on respiratory muscle strength and investigated the extent to which respiratory muscle fatigue is associated with chest wall volume changes during ILB. Twelve healthy subjects performed ILB at 76 ± 11% of maximal inspiratory mouth pressure (MIP) for 1h. MIP and breathing pattern during 3 min of normocapnic hyperpnea (NH) were measured before and after ILB. Breathing pattern and chest wall volume changes were assessed by optoelectronic plethysmography. After ILB, six subjects decreased MIP significantly (-16 ± 10%; p < 0.05), while the other six subjects did not (0 ± 7%, p = 0.916). Only subjects with decreased MIP after ILB lowered end-expiratory rib cage volume (volume at which inspiration is initiated) below resting values during ILB. During NH after ILB, tidal volume was smaller in subjects with decreased MIP (-19 ± 16%, p < 0.05), while it remained unchanged in the other group (-3 ± 11%, p = 0.463). These results suggest that respiratory muscle fatigue depends on the lung volume from which inspiratory efforts are made during ILB.     

Non-linear dependence of interstitial fluid pressure on joint cavity pressure and implications for interstitial resistance in rabbit knee

AIMS: Synovium retains lubricating fluid in the joint cavity. Synovial outflow resistance estimated as dPj/dQs (Pj, joint fluid pressure and Qs trans-synovial flow) is greater, however, than expected from interstitial glycosaminoglycan concentration. This study investigates whether subsynovial fluid pressure increases with intra-articular pressure, as this would reduce the estimated resistance estimate. METHODS: Interstitial fluid pressure (Pif) was measured as a function of distance from the joint cavity in knees of anaesthetized rabbits, using servo-null pressure-measuring micropipettes and using an external 'window'. Joint fluid pressure Pj was either endogenous (-2.4 +/- 0.4 cmH2O, mean +/- SEM) or held at approximately 4, 8 or 15.0 cmH2O by a continuous intra-articular saline infusion that matched the trans-synovial interstitial drainage rate. RESULTS: At endogenous Pj the peri-articular Pif was subatmospheric (-1.9 +/- 0.3 cmH2O, n = 19). At raised Pj the Pif values became positive. Gradient dPif /dx was approximately 20 times steeper across synovium than subsynovium. Pif close to the synovium-subsynovium border (Pif*) increased as a non-linear function of Pj to 1.4 +/- 0.2 cmH2O (n = 23) at Pj = 4.3 +/- 0.1 cmH2O : 2.3 +/- 0.2 cmH2O (n = 17) at Pj = 7.6 +/- 0.2 cmH2O: and 3.0 +/- 0.4 cmH2O (n = 26) at Pj = 15 +/- 0.2 cmH2O (P = 0.03, anova). CONCLUSIONS: Synovial resistivity is approximately 20x subsynovial resistivity. The increase in Pif*with Pj means that true synovial resistance d(Pj-Pif*)/dQs is overestimated 1.5x by dPj/dQs. This narrows but does not eliminate the gap between analysed glycosaminoglycan concentration, 4 mg ml(-1), and the net interstitial biopolymer concentration of 11.5 mg ml(-1) needed to generate the resistance.     

Superiority of nasal mask pressure over mouth pressure, as a surrogate of diaphragm twitch-related esophageal pressure, in healthy humans

Assessing diaphragm function is clinically and physiologically pertinent. It can rely on the measurement of pressure responses to phrenic stimulation. Combining mouth pressure (Pm) with cervical magnetic stimulation (CMS) is painless and easy to perform, but Pm-CMS poorly reflects esophageal pressure (Pes-CMS) because of poor pressure transmission across the airway. We reasoned that the mouth opening and neck flexion that are associated with the measurement of Pm-CMS would impair upper airway dynamics and further hinder pressure transmission. Therefore, we assessed the CMS-related pressure measured in a nasal mask (Pmask; mouth closed) without neck flexion as a possible surrogate of Pes-CMS, in 14 men and 3 women, age 24.5+/-2.2. Pes-CMS was 15.7+/-4.3 cmH2O, significantly higher than Pm-CMS (13.5+/-5.6 cmH2O, P<0.0001) but not different from Pmask-CMS (15.2+/-4.9 cmH2O). The concordance correlation coefficient was low (0.6808) between Pes-CMS and Pm-CMS. It was higher between Pes-CMS and Pmask-CMS (0.8730). Pm-CMS wrongly classified five subjects as abnormal (<10 cmH2O), versus 1 for Pmask and 5 for Pm (P=0.025). Passing and Bablok regressions found no difference between Pes-CMS and Pmask-CMS, but identified a systematic difference and a proportional error between Pes-CMS and Pm-CMS. We conclude that Pmask-CMS is a better surrogate of Pes-CMS than Pm-CMS.     

Pulmonary flow-resistive work during hydrostatic loading

This paper focuses upon flow-resistive pulmonary work during upright immersion, and during changes in the air delivery pressure. Nine male non-smokers (aged 26.2 +/- 3.5 years), with normal lung function history, performed spontaneous respiration while seated in air (control) and during total immersion. During the immersed state subjects were supplied with air at four hydrostatic pressures: mouth pressure (PM; simulating a mouth-held demand regulator), lung centroid pressure (PLC; + 1.33 kPa relative to the sternal notch), and 0.98 kPa (10 cmH2O) above and below the lung centroid pressure. Inspiratory, expiratory and total flow-resistive pulmonary work were computed from the integration of transpulmonary pressure (difference between oesophageal and mouth pressure) with respect to lung volume change. When breathing air delivered at mouth pressure, immersion significantly elevated all total flow-resistive pulmonary work components (P less than 0.05). Each increment in breathing pressure resulted in a progressive reduction in expiratory and total flow-resistive pulmonary work, so that when air was provided at lung centroid pressure and lung centroid pressure +0.98 kPa both components were similar to control values (P greater than 0.05). Inspiratory was always less than expiratory pulmonary work. During immersion inspiratory pulmonary work was significantly reduced when air supply pressure was increased above mouth pressure (P less than 0.05). Subsequent pressure increments failed to produce further changes in inspiratory pulmonary work. The difference in response between the inspiratory and expiratory components of total flow resistive pulmonary work was attributed primarily to the volume-dependence of the expiratory component.     

Inspiratory resistive loading after all-out exercise improves subsequent performance

We have previously shown that post-exercise inspiratory resistive loading (IRL) reduces blood lactate ([Lac_b⁻]). In this study, we tested the hypothesis that IRL during recovery could improve subsequent exercise performance. Eight healthy men underwent, on different days, two sequential 30-s, cycle ergometer Wingate tests. During the 10-min recovery period from test 1, subjects breathed freely or through an inspiratory resistance (15 cm H₂O) with passive leg recovery. Arterialized [Lac_b⁻] values, perceptual scores (Borg), cardiac output by impedance cardiography (QT), and changes in the deoxygenation status of the M. vastus lateralis by near-infrared spectroscopy (ΔHHb), were recorded. [Lac_b⁻] was significantly reduced after 4 min of recovery with IRL (peak [Lac_b⁻] 12.5 ± 2.3 mmol l⁻¹ with free-breathing vs. 9.8 ± 1.5 mmol l⁻¹ with IRL). Effort perception was reduced during late recovery with IRL compared with free-breathing. Cardiac work was increased with IRL, since heart rate and QT were elevated during late recovery. Peripheral muscle reoxygenation, however, was significantly impaired with IRL, suggesting that post-exercise convective O₂ delivery to the lower limbs was reduced. Importantly, IRL had a dual effect on subsequent performance, i.e., improvement in peak and mean power, but increased fatigue index (P < 0.05). Our data demonstrate that IRL after a Wingate test reduces post-exercise effort perception and improves peak power on subsequent all-out maximal-intensity exercise.     

Lymph capillary pressure of rat intestinal villi during fluid absorption.

A newly developed intestinal preparation is described for determining lymph capillary pressure (PL) in the villi in vivo and in vitro. Determination of PL provided an estimate of tissue fluid pressure in the villi. PL was related to the fluid absorption rate and increased by lymphatic obstruction. During fluid absorption from isotonic mucosal fluid, PL was 1.4 +/- 0.5 or 1.1 +/- 0.4 cmH2O determined in vivo or in vitro, respectively. Both pressures were essentially in the same range as that (0.7 +/- 0.3--1.3 +/- 0.5 cmH2O) in which the mucosal fluid was isotonic Na2SO4 solution or Na-free solutions from which little fluid absorption occurred. This range of pressures may be taken as the normal tissue fluid pressure in the villi. At a high rate of fluid absorption from hypotonic mucosal fluid, PL increased to 5.2 +/- 1.4 cmH2O and tissue fluid pressure was also similarly increased. It is concluded that the fluid absorptive process by the epithelium could not develop an appreciable hydrostatic pressure in the villus tissue space or in the lymphatics.