Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading

Fothergill, D. M., and N. A. Carlson. Effects ofN₂O narcosis on breathing andeffort sensations during exercise and inspiratory resistive loading.J. Appl. Physiol. 81(4):1562-1571, 1996.The influence of nitrous oxide(N₂O) narcosis on the responses toexercise and inspiratory resistive loading was studied in thirteen maleUS Navy divers. Each diver performed an incremental bicycle exercisetest at 1 ATA to volitional exhaustion while breathing a 23%N₂O gas mixture and a nonnarcoticgas of the same PO₂, density, andviscosity. The same gas mixtures were used during four subsequent30-min steady-state submaximal exercise trials in which the subjectsbreathed the mixtures both with and without an inspiratory resistance(5.5 vs. 1.1 cmH₂O ^· s ^· l¹at 1 l/s). Throughout each test, subjective ratings of respiratory effort (RE), leg exertion, and narcosis were obtained with acategory-ratio scale. The level of narcosis was rated between slightand moderate for the N₂O mixturebut showed great individual variation. Perceived leg exertion and thetime to exhaustion were not significantly different with the twobreathing mixtures. Heart rate was unaffected by the gas mixture andinspiratory resistance at rest and during steady-state exercise but wassignificantly lower with the N₂O mixture during incremental exercise (P < 0.05). Despite significant increases in inspiratory occlusionpressure (13%; P < 0.05),esophageal pressure (12%; P < 0.001), expired minute ventilation (4%;P < 0.01), and the work rate ofbreathing (15%; P < 0.001) when the subjects breathed the N₂O mixture,RE during both steady-state and incremental exercise was 25% lowerwith the narcotic gas than with the nonnarcotic mixture(P < 0.05). We conclude that the narcotic-mediated changes in ventilation, heart rate, and RE induced by23% N₂O are not of sufficientmagnitude to influence exercise tolerance at surface pressure.Furthermore, the load-compensating respiratory reflexes responsible formaintaining ventilation during resistive breathing are not depressed byN₂O narcosis.

     

Phrenic motoneuron discharge during sustained inspiratory resistive loading

Iscoe, Steve. Phrenic motoneuron discharge duringsustained inspiratory resistive loading. J. Appl.Physiol. 81(5): 2260-2266, 1996.I determinedwhether prolonged inspiratory resistive loading (IRL) affects phrenicmotoneuron discharge, independent of changes in chemical drive. Inseven decerebrate spontaneously breathing cats, the discharge patternsof eight phrenic motoneurons from filaments of one phrenic nerve weremonitored, along with the global activity of the contralateral phrenicnerve, transdiaphragmatic pressure, and fractional end-tidalCO₂ levels. Discharge patterns during hyperoxic CO₂ rebreathingand breathing against an IRL (2,500-4,000cmH₂O ^· l^{1 ·} s)were compared. During IRL, transdiaphragmatic pressure increased andthen either plateaued or decreased. At the highest fractional end-tidalCO₂ common to both runs,instantaneous discharge frequencies in six motoneurons were greaterduring sustained IRL than during rebreathing, when compared at the sametime after the onset of inspiration. These increased dischargefrequencies suggest the presence of a load-induced nonchemical drive tophrenic motoneurons from unidentified source(s).

     

Ultrasound evaluation of piglet diaphragm function before and after fatigue

Kocis, Keith C., Peter J. Radell, Wayne I. Sternberger, JaneE. Benson, Richard J. Traystman, and David G. Nichols. Ultrasound evaluation of piglet diaphragm function before and after fatigue. J. Appl. Physiol. 83(5):1654-1659, 1997.Clinically, a noninvasive measure of diaphragmfunction is needed. The purpose of this study is to determine whetherultrasonography can be used to 1)quantify diaphragm function and 2)identify fatigue in a piglet model. Five piglets were anesthetized withpentobarbital sodium and halothane and studied during the followingconditions: 1) baseline (spontaneous breathing); 2) baseline + CO₂ [inhaledCO₂ to increase arterial PCO₂ to 50-60 Torr (6.6-8kPa)]; 3) fatigue + CO₂ (fatigue induced with 30 minof phrenic nerve pacing); and 4)recovery + CO₂ (recovery after 1 hof mechanical ventilation). Ultrasound measurements of the posteriordiaphragm were made (inspiratory mean velocity) in the transverseplane. Images were obtained from the midline, just inferior to thexiphoid process, and perpendicular to the abdomen. M-mode measures weremade of the right posterior hemidiaphragm in the plane just lateral tothe inferior vena cava. Abdominal and esophageal pressures weremeasured and transdiaphragmatic pressure (Pdi) was calculated duringspontaneous (Sp) and paced (Pace) breaths. Arterial blood gases werealso measured. Pdi(Sp) and Pdi(Pace)during baseline + CO₂ were 8 ± 0.7 and 49 ± 11 cmH₂O, respectively, anddecreased to 6 ± 1.0 and 27 ± 7 cmH₂O,respectively, during fatigue + CO₂. Mean inspiratory velocityalso decreased from 13 ± 2 to 8 ± 1 cm/s during theseconditions. All variables returned to baseline during recovery + CO₂. Ultrasonography can beused to quantify diaphragm function and identify piglet diaphragm fatigue.

     

Does resistive loading decrease diaphragmatic contractility before task failure?

While sustaining a load that leads to taskfailure, it is unclear whether diaphragmatic fatigue developsprogressively or occurs only at task failure. We hypothesized thatincremental loading produces a progressive decrease in diaphragmaticcontractility ever before task failure. Ten subjectsgenerated 60% of maximal transdiaphragmatic pressure(Pdi_max) for 2 min, 4 min, anduntil task failure. Before loading, 20 min after each period ofloading, and ~20 h after the last period of loading,Pdi_max, nonpotentiated andpotentiated Pdi twitch pressure(Pdi_tw), and the pattern of respiratory muscle recruitment during aCO₂ challenge were recorded. Sensation of inspiratory effort at the 4th min of the task-failure protocol was greater than at the same time in the preceding 4-min protocol. Surprisingly, potentiatedPdi_tw andPdi_max were reduced after 2 min ofloading and decreased further after 4 min of loading and after taskfailure; nonpotentiated Pdi_tw wasreduced after 4 min of loading and after task failure. The gastricpressure contribution to tidal breathing during aCO₂ challenge decreased progressively in relation to duration of the preceding loading period,whereas expiratory muscle recruitment progressively increased. A restperiod of ~20 h after task failure was not sufficient to normalizethese alterations in respiratory muscle recruitment or fatigue-inducedchanges in diaphragmatic contractility. In conclusion, while sustaininga mechanical load, the diaphragm progressively fatigued, ever beforetask failure, and when challenged the rib cage-to-diaphragmaticcontribution to tidal breathing and recruitment of the expiratorymuscles increased pari passu with duration of the preceding loading.

     

N-acetylcysteine administration alters the response to inspiratory loading in oxygen-supplemented rats

Supinski, G. S., D. Stofan, R. Ciufo, and A. DiMarco.N-acetylcysteine administrationalters the response to inspiratory loading in oxygen-supplemented rats.J. Appl. Physiol. 82(4): 1119-1125, 1997.Based on recent studies, it has been suggested that free radicals are elaborated in the respiratory muscles during strenuous contractions and contribute to the development of muscle fatigue. If this theory is correct, then it should be possible toattenuate the development of diaphragm fatigue and/or delay theonset of respiratory failure during loaded breathing by administering afree radical scavenger. The purpose of the present experiment was,therefore, to examine the effect ofN-acetylcysteine (NAC), a free radicalscavenger and glutathione precursor, on the evolution of respiratoryfailure in decerebrate unanesthetized rats breathing against a largeinspiratory resistive load. We compared the inspiratory volume andpressure generation over time in animals pretreated with either salineor NAC (150 mg/kg) and then loaded until respiratory arrest. Afterarrest, the diaphragm was excised, and samples were assayed for reduced(GSH) and oxidized glutathione. As a control, we also assessedrespiratory function and glutathione concentrations in groups ofnonloaded saline- and NAC-treated animals. We found that NAC-treatedanimals were able to tolerate loading better than the saline-treatedgroup, maintaining higher inspiratory pressures and sustaining higherinspired volumes. Administration of NAC also increased the time thatanimals could tolerate loading before the development of respiratoryarrest. In addition, although saline-treated loaded animals hadsignificant reductions in diaphragmatic GSH levels compared withunloaded controls, the magnitude of this reduction was blunted by NACadministration (i.e., GSH averaged 965 ± 113, 568 ± 83, 907 ± 39, and 784 ± 61 nmol/g for unloaded-saline, loaded-saline,unloaded-NAC, and loaded-NAC groups, P < 0.05, with the value for the loaded-saline group lower than thevalues for the two unloaded groups; GSH for the loaded-NAC group was not different, however, from unloaded controls). These data demonstrate that administration of NAC, a free radical scavenger, slows the rate ofdevelopment of respiratory failure during inspiratory resistiveloading.

     

Functional role and structure of the scalene: an accessory inspiratory muscle in hamster

Fournier, Mario, and Michael I. Lewis. Functional roleand structure of the scalene: an accessory inspiratory muscle inhamster. J. Appl. Physiol. 81(6):2436-2444, 1996.Although the scalene muscle (Sca) is a primaryinspiratory muscle in humans, its respiratory function in other speciesis less clear. The electromyographic (EMG) activity of the Sca wasstudied during resting ventilation (eupnea) in both the awake andanesthetized hamster and after a variety of respiratory challenges inthe anesthetized animal. The EMG activities of the medial Sca and thecostal diaphragm were compared. The medial Sca, the major component ofthe Sca, originates from cervical transverse processes 2 to 5 andinserts primarily onto rib 4, with a small segment onto rib 3. In both the anesthetized and awake animal, the Sca was always silent during quiet breathing. WithCO₂-stimulated hyperpnea, the Scawas always recruited during inspiration in phase with the diaphragm.Active recruitment of the Sca was also observed after resistive loading and total airway occlusion. After ipsilateral phrenicotomy, the Sca waspersistently recruited during eupnea. The specificity of the EMGsignals was tested both by excluding cross contamination from other ribcage muscles and by selective denervation studies. Muscle spindles wereidentified in the medial Sca histochemically, suggesting that therespiratory activity of the Sca can also be modulated by changes inmuscle length and/or load. These results indicate that the Scafunctions as an accessory inspiratory muscle in the hamster and mayplay an important role in conditions of chronic load.

     

Phrenic motoneuron firing rates before, during, and after prolonged inspiratory resistive loading

Road, J. D., and A. M. Cairns. Phrenic motoneuronfiring rates before, during, and after prolonged inspiratory resistive loading. J. Appl. Physiol. 83(3):776-783, 1997.Phrenic motoneuron firing rates during briefinspiratory resistive loading (IRL) are high, and nearly all themotoneurons are recruited. Diaphragmatic fatigue has been difficult todemonstrate during IRL. Furthermore, evidence from studies in limbmuscles has shown variable motoneuron responses to prolongedhigh-intensity loads. We studied phrenic motoneuron firing ratesbefore, during, and after prolonged IRL in anesthetized rabbits. Of 117 phrenic axons, only 2 axons were not recruited; 41 axons were silentduring unloaded breathing but were recruited at higher loads. Silentaxons showed a more rapid increase in firing rate as the loadincreased. Phrenic motoneuron firing rates increased throughout theperiod of loading, whereas airway pressure swings did not. Afterprolonged IRL, higher motoneuron firing rates were needed during briefloads to produce the same airway pressure. No evidence of a decline inmotoneuron firing rates was seen at any point. We conclude that therespiratory muscles can be shown to demonstrate physiological responsesconsistent with fatigue during prolonged IRL, and activation rates arehigh and remain so throughout this prolonged loading.

     

Cervical magnetic stimulation as a method to discriminate between diaphragm and rib cage muscle fatigue

Inspiratory muscle fatigue can probablydetermine hypercapnic respiratory failure. Diaphragm fatigue isdetected by electrical phrenic stimulation (ELS), but there is nosimple tool to assess rib cage muscle (RCM) fatigue. Cervical magneticstimulation (CMS) costimulates the phrenic nerves and RCM. We reasonedthat changes in transdiaphragmatic pressure twitch (Pdi,tw) with CMSand ELS should be different after selective diaphragm vs. RCM fatigue. Five volunteers performed inspiratory resistive tasks while voluntarily uncoupling diaphragm and RCM. BaselinePdi,tw_ELS andPdi,tw_CMS were 28.57 ± 1.68 and 32.83 ± 2.92 cmH₂O. Afterselective diaphragm loading,Pdi,tw_ELS andPdi,tw_CMS were reduced by 39 and26%, with comparable decreases in gastric pressure twitch (Pga,tw).Esophageal pressure twitch (Pes,tw) was better preserved with CMS.Therefore Pes,tw/Pga,tw was lower with ELS than CMS (1.24 ± 0.16 vs. 1.73 ± 0.11, P = 0.05). After selectiveRCM loading, there was no diaphragm fatigue, butPes,tw_CMS was significantlyreduced (30%). These findings support the role of rib cagestiffening by CMS-related RCM contraction in the ELS-CMSdifferences and suggest that CMS can be used to assess RCM fatigue.

     

Effect of inspiratory muscle fatigue on breathing pattern during inspiratory resistive loading

The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.     

Preferential fatigue of the rib cage muscles during inspiratory resistive loaded ventilation

Because the inspiratory rib cage muscles are recruited during inspiratory resistive loaded breathing, we hypothesized that such loading would preferentially fatigue the rib cage muscles. We measured the pressure developed by the inspiratory rib cage muscles during maximal static inspiratory maneuvers (Pinsp) and the pressure developed by the diaphragm during maximal static open-glottis expulsive maneuvers (Pdimax) in four human subjects, both before and after fatigue induced by an inspiratory resistive loaded breathing task. Tasks consisted of maintaining a target esophageal pressure, breathing frequency, and duty cycle for 3-5 min, after which the subjects maintained the highest esophageal pressure possible for an additional 5 min. After loading, Pinsp decreased in all subjects [control, -128 +/- 14 (SD) cmH2O; with fatigue, -102 +/- 18 cmH2O; P less than 0.001, paired t test]. Pdimax was unchanged (control, -192 +/- 23 cmH2O; fatigue, -195 +/- 27 cmH2O). These data suggest that 1) inability to sustain the target during loading resulted from fatigue of the inspiratory rib cage muscles, not diaphragm, and 2) simultaneous measurement of Pinsp and Pdimax may be useful in partitioning muscle fatigue into rib cage and diaphragmatic components.     

Ventilatory response to exercise in subjects breathing CO2 or HeO2

Babb, T. G. Ventilatory response to exercise insubjects breathing CO₂ orHeO₂.J. Appl. Physiol. 82(3): 746-754, 1997.To investigate the effects of mechanical ventilatory limitationon the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycleergometry to exhaustion once while breathing room air; once whilebreathing 3% CO₂-21%O₂-balanceN₂; and once while breathing HeO₂ (79% He and 21%O₂). Minute ventilation(E) and respiratory mechanics weremeasured continuously during each 1-min increment in work rate (10 or20 W). Data were analyzed at rest, at ventilatory threshold (VTh),and at maximal exercise. When the subjects were breathing 3%CO₂, there was an increase(P < 0.001) inE at rest and at VTh but not duringmaximal exercise. When the subjects were breathingHeO₂,E was increased(P < 0.05) only during maximalexercise (24 ± 11%). The ventilatory response to exercise belowVTh was greater only when the subjects were breathing 3% CO₂(P < 0.05). Above VTh, theventilatory response when the subjects were breathingHeO₂ was greater than whenbreathing 3% CO₂(P < 0.01). Flow limitation, aspercent of tidal volume, during maximal exercise was greater(P < 0.01) when the subjects werebreathing CO₂ (22 ± 12%) thanwhen breathing room air (12 ± 9%) or when breathingHeO₂ (10 ± 7%)(n = 7). End-expiratory lung volumeduring maximal exercise was lower when the subjects were breathingHeO₂ than when breathing room airor when breathing CO₂(P < 0.01). These data indicate thatolder subjects have little reserve for accommodating an increase inventilatory demand and suggest that mechanical ventilatory constraintsinfluence both the magnitude of Eduring maximal exercise and the regulation ofE and respiratory mechanics duringheavy-to-maximal exercise.

     

Threshold effects of respiratory muscle work on limb vascular resistance

The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (Q(L)) and utilized the changes in mouth twitch pressure (DeltaP(M)T) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 +/- 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1-3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and Q(L), limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control (P > 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 +/- 12% reduction in P(M)T with bilateral phrenic nerve stimulation. During the fatigue trial, Q(L) and LVR were unchanged from baseline at minute 1, but LVR rose 36% and Q(L) fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and Q(L) returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and Q(L), whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in Q(L). We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions.     

Diaphragm thickening during inspiration

Cohn, David, Joshua O. Benditt, Scott Eveloff, and F. DennisMcCool. Diaphragm thickening during inspiration.J. Appl. Physiol. 83(1): 291-296, 1997.Ultrasound has been used to measure diaphragm thickness(T_di) in thearea where the diaphragm abuts the rib cage (zone of apposition).However, the degree of diaphragm thickening during inspiration reportedas obtained by one-dimensional M-mode ultrasound was greater than thatpredicted by using other radiographic techniques. Becausetwo-dimensional (2-D) ultrasound provides greater anatomic definitionof the diaphragm and neighboring structures, we used this technique toreevaluate the relationship between lung volume andT_di. We firstestablished the accuracy and reproducibility of 2-D ultrasound bymeasuring T_diwith a 7.5-MHz transducer in 26 cadavers. We found thatT_di measured byultrasound correlated significantly with that measured by ruler (R² = 0.89), withthe slope of this relationship approximating a line of identity(y = 0.89x + 0.04 mm). The relationship between lung volume andT_di was thenstudied in nine subjects by obtaining diaphragm images at the fivetarget lung volumes [25% increments from residual volume (RV) tototal lung capacity (TLC)]. Plots ofT_di vs. lungvolume demonstrated that the diaphragm thickened as lung volumeincreased, with a more rapid rate of thickening at the higher lungvolumes[T_di = 1.74 vital capacity (VC)² + 0.26 VC + 2.7 mm] (R² = 0.99; P < 0.001) where lung volumeis expressed as a fraction of VC. The mean increase inT_di between RVand TLC for the group was 54% (range 42-78%). We conclude that2-D ultrasound can accurately measureT_di and that theaverage thickening of the diaphragm when a subject is inhaling from RVto TLC using this technique is in the range of what would be predictedfrom a 35% shortening of the diaphragm.

     

Differential respiratory muscle recruitment induced by clonidine in awake goats

The purpose of this study was to test thehypothesis that dysrhythmic breathing induced by the₂-agonist clonidine isaccompanied by differential recruitment of respiratory muscles. Inadult goats (n = 14) electromyographic(EMG) measurements were made from inspiratory muscles (diaphragm andparasternal intercostal) and expiratory muscles [triangularissterni (TS) and transversus abdominis (Abd)]. EMG of thethyroarytenoid (TA) muscle was used as an index of upper airway(glottal) patency. Peak EMG activities of all spinal inspiratory andexpiratory muscles were augmented by central and peripheralchemoreceptor stimuli. Phasic TA was apparent in the postinspiratoryphase of the breathing cycle under normoxic conditions. Duringdysrhythmic breathing episodes induced by clonidine, TS and Abdactivities were attenuated or abolished, whereas diaphragm andparasternal intercostal activities were unchanged. There was no tonicactivation of TS or Abd EMG during apneas; however, TA activity becametonic throughout the apnea. We conclude that1) ₂-adrenoceptor stimulationresults in differential recruitment of respiratory muscles duringrespiratory dysrhythmias and 2) apneas are accompanied by active glottic closure in the awake goat.

     

Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans

Kayser, Bengt, Pawel Sliwinski, Sheng Yan, Mirek Tobiasz,and Peter T. Macklem. Respiratory effort sensation during exercisewith induced expiratory-flow limitation in healthy humans. J. Appl. Physiol. 83(3): 936-947, 1997.Nine healthy subjects (age 31 ± 4 yr) exercised with andwithout expiratory-flow limitation (maximal flow ~1 l/s). Wemonitored flow, end-tidal PCO₂, esophageal (Pes) and gastric pressures, changes in end-expiratory lungvolume, and perception (sensation) of difficulty in breathing. Subjectscycled at increasing intensity (+25 W/30 s) until symptom limitation.During the flow-limited run, exercise performance was limited in allsubjects by maximum sensation. Sensation was equally determined byinspiratory and expiratory pressure changes. In both runs, 90% of thevariance in sensation could be explained by the Pes swings (differencebetween peak inspiratory and peak expiratory Pes). End-tidalPCO₂ did not explain any variance insensation in the control run and added only 3% to the explained variance in the flow-limited run. We conclude that in healthy subjects,during normal as well as expiratory flow-limited exercise, the pleuralpressure generation of the expiratory muscles is equally related to theperception of difficulty in breathing as that of the inspiratorymuscles.

     

Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery

Verbitsky, O., J. Mizrahi, M. Levin, and E. Isakov.Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery. J. Appl. Physiol. 83(2):333-337, 1997.The influence of acute ingestion ofNaHCO₃ on fatigue and recovery ofthe quadriceps femoris muscle after exercise was studied in six healthymale subjects. A bicycle ergometer was used for exercising under three loading conditions: test A, loadcorresponding to maximal oxygen consumption; testB, load in test A + 17%; test C, load intest B but performed 1 h after acuteingestion of NaHCO₃.Functional electrical stimulation (FES) was applied to provokeisometric contraction of the quadriceps femoris. The resulting kneetorque was monitored during fatigue (2-min chronic FES) and recovery (10-s FES every 10 min, for 40 min). Quadriceps torques were higher inthe presence of NaHCO₃(P < 0.05): withNaHCO₃ the peak, residual, andrecovery (after 40 min) normalized torques were, respectively, 0.68 ± 0.05 (SD), 0.58 ± 0.05, and 0.73 ± 0.05; withoutNaHCO₃ the values were 0.45 ± 0.04, 0.30 ± 0.06, and 0.63 ± 0.06. The increasedtorques obtained after acute ingestion ofNaHCO₃ indicate the possibleexistence of improved nonoxidative glycolysis in isometric contraction,resulting in reduced fatigue and enhanced recovery.

     

Chest wall motion during tidal breathing

De Groote, A., M. Wantier, G. Cheron, M. Estenne, and M. Paiva. Chest wall motion during tidal breathing. J. Appl. Physiol. 83(5): 1531-1537, 1997.We have used an automaticmotion analyzer, the ELITE system, to study changes inchest wall configuration during resting breathing in five normal,seated subjects. Two television cameras were used to record thex-y-z displacements of 36 markers positioned circumferentiallyat the level of the third (S₁) and fifth(S₂) costal cartilage, corresponding to the lung-apposedrib cage; midway between the xyphoid process and thecostal margin (S₃), corresponding to the abdomen-apposedrib cage; and at the level of the umbilicus (S₄).Recordings of different subsets of markers were made by submitting thesubject to five successive rotations of 45-90°. Each recordinglasted 30 s, and three-dimensional displacements of markers wereanalyzed with the Matlab software. At spontaneous end expiration,sections S_1-3 were elliptical but S₄ wasmore circular. Tidal changes in chest wall dimensions were consistentamong subjects. For S_1-2, changes during inspirationoccurred primarily in the cranial and ventral directions and averaged3-5 mm; displacements in the lateral direction were smaller(1-2 mm). On the other hand, changes at the level ofS₄ occurred almost exclusively in the ventral direction. Inaddition, both compartments showed a ventral displacement of theirdorsal aspect that was not accounted for by flexion of the spine. Weconclude that, in normal subjects breathing at rest in the seatedposture, displacements of the rib cage during inspiration are in thecranial, lateral outward, and ventral directions but that expansion ofthe abdomen is confined to the ventral direction.

     

A model of the spontaneously breathing patient: applications to intrinsic PEEP and work of breathing

Schuessler, Thomas F., Stewart B. Gottfried, and Jason H. T. Bates. A model of the spontaneously breathing patient: applications to intrinsic PEEP and work of breathing.J. Appl. Physiol. 82(5):1694-1703, 1997.Intrinsic positive end-expiratory pressure(PEEP_i) and inspiratory work ofbreathing (WI) are important factors in the management of severe obstructive respiratory disease. Weused a computer model of spontaneously breathing patients with chronicobstructive pulmonary disease to assess the sensitivity of measurementtechniques for dynamic PEEP_i(PEEP_{i dyn}) andWI to expiratory muscle activity(EMA) and cardiogenic oscillations (CGO) on esophageal pressure.Without EMA and CGO, bothPEEP_{i dyn} andWI were accurately estimated(r = 0.999 and 0.95, respectively). Addition of moderate EMA causedPEEP_{i dyn} andWI to be systematically overestimated by 141 and 52%, respectively. Furthermore, CGOintroduced large random errors, obliterating the correlation betweenthe true and estimated values for bothPEEP_{i dyn}(r = 0.29) andWI (r = 0.38). Thus the accurateestimation of PEEP_{i dyn} andWI requires steps to be taken toameliorate the adverse effects of both EMA and CGO. Taking advantage ofour simulations, we also investigated the relationship betweenPEEP_{i dyn} and staticPEEP_i(PEEP_{i stat}). ThePEEP_{i dyn}/PEEP_{i stat}ratio decreased as stress adaptation in the lung was increased,suggesting that heterogeneity of expiratory flow limitation isresponsible for the discrepancies betweenPEEP_{i dyn} andPEEP_{i stat} thathave been reported in patients with severe airwayobstruction.

     

Reduced oxidation rates of ingested glucose during prolonged exercise with low endogenous CHO availability

Jeukendrup, Asker E., Lars B. Borghouts, Wim H. M. Saris,and Anton J. M. Wagenmakers. Reduced oxidation rates of ingested glucose during prolonged exercise with low endogenous CHO availability. J. Appl. Physiol. 81(5):1952-1957, 1996.This study investigated the effect of endogenouscarbohydrate (CHO) availability on oxidation rates of ingested glucoseduring moderate-intensity exercise. Seven well-trained cyclistsperformed two trials of 120 min of cycling exercise in random order at57% maximal O₂ consumption. Preexercise glycogen concentrations were manipulated byglycogen-lowering exercise in combination with CHO restriction[low-glycogen (LG) trial] or CHO loading[moderate-to-high-glycogen (HG) trial]. In the LG and HGtrials, subjects ingested 4 ml/kg body wt of an 8% corn-derivedglucose solution of high natural¹³C abundance at the start,followed by boluses of 2 ml/kg every 15 min. The third trial, in whichpotato-derived glucose was ingested, served as a control test forbackground correction. Exogenous glucose oxidation rates werecalculated from the ¹³C enrichmentof the ingested glucose and of the breathCO₂. Total CHO oxidation was lowerin the LG trial than in the HG trial during 60-120 min of exercise[84 ± 7 (SE) vs. 116 ± 8 g;P < 0.05]. Exogenous CHOoxidation in this period was 28% lower in the LG trial compared withthe HG trial. Maximal exogenous oxidation rates were also lower(P < 0.05) in the LG trial (0.64 ± 0.05 g/min) than in the HG trial (0.88 ± 0.04 g/min). Thisdecreased utilization of exogenous glucose was accompanied by increased plasma free fatty acid levels (2-3 times higher) and lower insulin concentrations. It is concluded that glycogen-lowering exercise, performed the evening before an exercise bout, in combination with CHOrestriction leads to a reduction of the oxidation rate of ingestedglucose during moderate-intensity exercise.

     

Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue

Babcock, Mark A., David F. Pegelow, Bruce D. Johnson, andJerome A. Dempsey. Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue. J. Appl.Physiol. 81(5): 2156-2164, 1996.We usedbilateral phrenic nerve stimulation (BPNS; at 1, 10, and 20 Hz atfunctional residual capacity) to compare the amount of exercise-induceddiaphragm fatigue between two groups of healthy subjects, a high-fitgroup [maximal O₂consumption (O_{2 max}) = 69.0 ± 1.8 ml ^· kg^{1 ·} min¹,n = 11] and a fit group(O_{2 max} = 50.4 ± 1.7 ml ^· kg^{1 ·} min¹,n = 13). Both groups exercised at88-92% O_{2 max}for about the same duration (15.2 ± 1.7 and 17.9 ± 2.6 min forhigh-fit and fit subjects, respectively,P > 0.05). The supramaximal BPNS test showed a significant reduction (P < 0.01) in the BPNS transdiaphragmatic pressure (Pdi) immediatelyafter exercise of 23.1 ± 3.1% for the high-fit group and23.1 ± 3.8% (P > 0.05)for the fit group. Recovery of the BPNS Pdi took 60 min in both groups.The high-fit group exercised at a higher absolute workload, whichresulted in a higher CO₂production (+26%), a greater ventilatory demand (+16%) throughout theexercise, and an increased diaphragm force output (+28%) over theinitial 60% of the exercise period. Thereafter, diaphragm force outputdeclined, despite a rising minute ventilation, and it was not differentbetween most of the high-fit and fit subjects. In summary, the high-fitsubjects showed diaphragm fatigue as a result of heavy enduranceexercise but were also partially protected from excessive fatigue,despite high ventilatory requirements, because their hyperventilatoryresponse to endurance exercise was reduced, their diaphragm wasutilized less in providing the total ventilatory response, and possiblytheir diaphragm aerobic capacity was greater.