Expiratory flow limitation and intrinsic positive end-expiratory pressure in obesity

Breathing at very low lung volumes might beaffected by decreased expiratory airflow and air trapping. Our purposewas to detect expiratory flow limitation (EFL) and, as a consequence, intrinsic positive end-expiratory pressure(PEEP_i) in grossly obesesubjects (OS). Eight OS with a mean body mass index (BMI) of 44 ± 5 kg/m² and six age-matchednormal-weight control subjects (CS) were studied in different bodypositions. Negative expiratory pressure (NEP) was used to determineEFL. In contrast to CS, EFL was found in two of eight OS in the uprightposition and in seven of eight OS in the supine position. DynamicPEEP_i and mean transdiaphragmatic pressure (mean Pdi) were measured in all six CS and in six of eight OS.In OS, PEEP_i increased from 0.14 ± 0.06 (SD) kPa in the upright position to 0.41 ± 0.11 kPa inthe supine position (P < 0.05) anddecreased to 0.20 ± 0.08 kPa in the right lateral position(P < 0.05, compared with supine),whereas, in CS, PEEP_i wassignificantly smaller (<0.05 kPa) in each position. In OS, mean Pdiin each position was significantly larger compared with CS. Mean Pdiincreased from 1.02 ± 0.32 kPa in the upright position to 1.26 ± 0.17 kPa in the supine position (not significant) and decreasedto 1.06 ± 0.26 kPa in the right lateral position(P < 0.05, compared with supine),whereas there were no significant changes in CS. We conclude that in OS1) tidal breathing can be affectedby EFL and PEEP_i;2) EFL andPEEP_i are promoted by the supineposture; and 3) the increaseddiaphragmatic load in the supine position is, in part, related toPEEP_i.

     

Effects of unilateral lesions of retrotrapezoid nucleus on breathing in awake rats

Akilesh, Manjapra R., Matthew Kamper, Aihua Li, and EugeneE. Nattie. Effects of unilateral lesions of retrotrapezoid nucleuson breathing in awake rats. J. Appl.Physiol. 82(2): 469-479, 1997.In anesthetizedrats, unilateral retrotrapezoid nucleus (RTN) lesions markedlydecreased baseline phrenic activity and the response toCO₂ (E. E. Nattie and A. Li.Respir. Physiol. 97: 63-77,1994). Here we evaluate the effects of such lesions on restingbreathing and on the response to hypercapnia and hypoxia inunanesthetized awake rats. We made unilateral injections [24 ± 7 (SE) nl] of ibotenic acid (IA; 50 mM), an excitatoryamino acid neurotoxin, in the RTN region(n = 7) located by stereotaxic coordinates and by field potentials induced by facial nervestimulation. Controls (n = 6) receivedRTN injections (80 ± 30 nl) of mock cerebrospinal fluid. A secondcontrol consisted of four animals with IA injections (24 ± 12 nl)outside the RTN region. Injected fluorescent beads allowed anatomicidentification of lesion location. Using whole body plethysmography, wemeasured ventilation in the awake state during room air, 7%CO₂ in air, and 10%O₂ breathing before and for 3 wkafter the RTN injections. There was no statistically significant effectof the IA injections on resting room air breathing in the lesion groupcompared with the control groups. We observed no apnea. The response to7% CO₂ in the lesion groupcompared with the control groups was significantly decreased, by 39%on average, for the final portion of the 3-wk study period. There wasno lesion effect on the ventilatory response to 10%O₂. In this unanesthetized model,other areas suppressed by anesthesia, e.g., the reticular activatingsystem, hypothalamus, and perhaps the contralateral RTN, may providetonic input to the respiratory centers that counters the loss of RTNactivity.

     

Important role of carotid afferents in control of breathing

The purpose of the present study was todetermine the effect on breathing in the awake state of carotid bodydenervation (CBD) over 1-2 wk after denervation. Studies werecompleted on adult goats repeatedly before and1) for 15 days after bilateral CBD (n = 8),2) for 7 days after unilateral CBD(n = 5), and3) for 15 days after sham CBD(n = 3). Absence of ventilatorystimulation when NaCN was injected directly into a common carotidartery confirmed CBD. There was a significant(P < 0.01) hypoventilation during the breathing of room air after unilateral and bilateral CBD. Themaximum Pa_CO2 increase (8 Torr forunilateral and 11 Torr for bilateral) occurred ~4 days afterCBD. This maximum was transient because by 7 (unilateral)to 15 (bilateral) days after CBD, Pa_CO2 was only 3-4 Torr above control.CO₂ sensitivity was attenuated from control by 60% on day 4 afterbilateral CBD and by 35% on day 4 after unilateral CBD. This attenuation was transient, because CO₂ sensitivity returned tocontrol temporally similar to the return ofPa_CO2 during the breathing of room air.During mild and moderate treadmill exercise 1-8 days afterbilateral CBD, Pa_CO2 was unchanged fromits elevated level at rest, but, 10-15 days after CBD,Pa_CO2 decreased slightly from restduring exercise. These data indicate that1) carotid afferents are animportant determinant of rest and exercise breathing and ventilatoryCO₂ sensitivity, and2) apparent plasticity within theventilatory control system eventually provides compensation for chronicloss of these afferents.

     

Conservation of bronchiolar wall area during constriction and dilation of human airways

Mitchell, R. W., E. Rühlmann, H. Magnussen, N. M. Muñoz, A. R. Leff, and K. F. Rabe. Conservation ofbronchiolar wall area during constriction and dilation of humanairways. J. Appl. Physiol. 82(3):954-958, 1997.We assessed the effect of smooth musclecontraction and relaxation on airway lumen subtended by the internalperimeter(A_i)and total cross-sectional area (A_o)of human bronchial explants in the absence of the potential lungtethering forces of alveolar tissue to test the hypothesis thatbronchoconstriction results in a comparable change ofA_i andA_o.Luminal area (i.e.,A_i) andA_owere measured by using computerized videomicrometry, and bronchial wallarea was calculated accordingly. Images on videotape were captured;areas were outlined, and data were expressed as internal pixel numberby using imaging software. Bronchial rings were dissected in 1.0- to1.5-mm sections from macroscopically unaffected areas of lungs frompatients undergoing resection for carcinoma, placed in microplate wellscontaining buffered saline, and allowed to equilibrate for 1 h.Baseline, A_o[5.21 ± 0.354 (SE)mm²], andA_i(0.604 ± 0.057 mm²) weremeasured before contraction of the airway smooth muscle (ASM) withcarbachol. MeanA_inarrowed by 0.257 ± 0.052 mm²in response to 10 µM carbachol (P = 0.001 vs. baseline). Similarly, A_onarrowed by 0.272 ± 0.110 mm²in response to carbachol (P = 0.038 vs. baseline; P = 0.849 vs. change inA_i).Similar parallel changes in cross-sectional area forA_iandA_owere observed for relaxation of ASM from inherent tone of otherbronchial rings in response to 10 µM isoproterenol. We demonstrate aunique characteristic of human ASM; i.e., both luminal and totalcross-sectional area of human airways change similarly on contractionand relaxation in vitro, resulting in a conservation of bronchiolarwall area with bronchoconstriction and dilation.

     

Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans

Honda, Y., H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. Effect of priorO₂ breathing on ventilatoryresponse to sustained isocapnic hypoxia in adult humans.J. Appl. Physiol. 81(4):1627-1632, 1996.Sixteen healthy volunteers breathed 100%O₂ or room air for 10 min in random order, then their ventilatory response to sustained normocapnic hypoxia (80% arterial O₂saturation, as measured with a pulse oximeter) was studied for 20 min.In addition, to detect agents possibly responsible for the respiratorychanges, blood plasma of 10 of the 16 subjects was chemically analyzed.1) Preliminary O₂ breathing uniformly andsubstantially augmented hypoxic ventilatory responses.2) However, the profile ofventilatory response in terms of relative magnitude, i.e., biphasichypoxic ventilatory depression, remained nearly unchanged.3) Augmented ventilatory incrementby prior O₂ breathing wassignificantly correlated with increment in the plasma glutamine level.We conclude that preliminary O₂administration enhances hypoxic ventilatory response without affectingthe biphasic response pattern and speculate that the excitatory aminoacid neurotransmitter glutamate, possibly derived from augmentedglutamine, may, at least in part, play a role in this ventilatoryenhancement.

     

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.

     

Periodic breathing induced on demand in awake newborn lamb

Canet, Emmanuel, Jean-Paul Praud, and Michel A. Bureau.Periodic breathing induced on demand in awake newborn lamb. J. Appl. Physiol. 82(2): 607-612, 1997.Spontaneous periodic breathing, although a common feature infullterm and preterm human infants, is scarce in other newborn mammals.The aim of this study was to induce periodic breathing in lambs. Four10-day-old and two <48-h-old awake lambs were instrumented withjugular catheters connected to an extracorporeal membrane lung aimed atcontrolling arterial PCO₂(Pa_CO2). ArterialPO₂(Pa_O2) was set and maintained at thedesired level by changing inspiredO₂ fraction and providingO₂ through a small catheter intothe "apneic" lung. At a criticalPa_O2/Pa_CO2combination, the four 10-day-old lambs exhibited periodic breathingthat could be initiated, terminated, and reinitiated on demand. In the2-day-old lambs with low chemoreceptor gain, periodic breathing washardly seen, regardless of the trials done to find the criticalPO₂/PCO₂combination. We conclude that periodic breathing can be induced inlambs and depends on criticalPa_O2/Pa_CO2combinations and maturity of the chemoreceptors.

     

Effect of different levels of hyperoxia on breathing in healthy subjects

Becker, Heinrich F., Olli Polo, Stephen G. McNamara, MichaelBerthon-Jones, and Colin E. Sullivan. Effect of different levelsof hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683-1690, 1996.Wehave recently shown that breathing 50%O₂ markedly stimulates ventilationin healthy subjects if end-tidal PCO₂(PET_CO2) ismaintained. The aim of this study was to investigate apossible dose-dependent stimulation of ventilation byO₂ and to examine possiblemechanisms of hyperoxic hyperventilation. In eight normalsubjects ventilation was measured while they were breathing 30 and 75%O₂ for 30 min, withPET_CO2 being held constant.Acute hypercapnic ventilatory responses were also tested in thesesubjects. The 75% O₂ experimentwas repeated without controllingPET_CO2 in 14 subjects, andin 6 subjects arterial blood gases were taken at baseline and at theend of the hyperoxia period. Minute ventilation(I) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75%O₂ without any control onPET_CO2 led toa 16% increase inI, butPET_CO2 decreased by3.6 Torr (9%). There was a linear correlation(r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, withI more than doubling after 30 min of75% O₂. If isocapnia is notmaintained, hyperventilation is attenuated by a decrease in arterialPCO₂. There is a correlation betweenhyperoxic and hypercapnic ventilatory responses. On the basis of datafrom the literature, we concluded that the Haldane effect seems to bethe major cause of hyperventilation duringboth isocapnic and poikilocapnichyperoxia.

     

Ventilatory response to helium-oxygen breathing during exercise: effect of airway anesthesia

Krishnan, Bharath S., Ron E. Clemens, Trevor A. Zintel,Martin J. Stockwell, and Charles G. Gallagher. Ventilatory response to helium-oxygen breathing during exercise: effect of airwayanesthesia. J. Appl. Physiol. 83(1):82-88, 1997.The substitution of a normoxic helium mixture(HeO₂) for room air (Air) during exercise results in a sustained hyperventilation, which is present evenin the first breath. We hypothesized that this response is dependent onintact airway afferents; if so, airway anesthesia (Anesthesia) shouldaffect this response. Anesthesia was administered to the upper airwaysby topical application and to lower central airways by aerosolinhalation and was confirmed to be effective for over 15 min. Subjectsperformed constant work-rate exercise (CWE) at 69 ± 2 (SE) % maximal work rate on a cycle ergometer on three separate days: twiceafter saline inhalation (days 1 and3) and once after Anesthesia(day 2). CWE commenced after a briefwarm-up, with subjects breathing Air for the first 5 min (Air-1),HeO₂ for the next 3 min, and Airagain until the end of CWE (Air-2). The resistance of the breathingcircuit was matched for Air andHeO₂. BreathingHeO₂ resulted in a small butsignificant increase in minute ventilation(I) anddecrease in alveolar PCO₂ in both theSaline (average of 2 saline tests; not significant) and Anesthesiatests. Although Anesthesia had no effect on the sustainedhyperventilatory response to HeO₂breathing, theI transientswithin the first six breaths ofHeO₂ were significantly attenuatedwith Anesthesia. We conclude that theI response to HeO₂ is not simply due to areduction in external tubing resistance and that, in humans, airwayafferents mediate the transient but not the sustained hyperventilatoryresponse to HeO₂ breathing duringexercise.

     

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.

     

Lung resistance and elastance in spontaneously breathing preterm infants: effects of breathing pattern and demographics

Reported values of lung resistance(RL) and elastance (EL) in spontaneouslybreathing preterm neonates vary widely. We hypothesized that thisvariability in lung properties can be largely explained by both inter-and intrasubject variability in breathing pattern and demographics.Thirty-three neonates receiving nasal continuous positive airwaypressure [weight 606-1,792 g, gestational age (GA) of25-33 wk, 2-49 days old] were studied. Transpulmonary pressure was measured by esophageal manometry and airway flow by facemask pneumotachography. Breath-to-breath changes in RL andEL in each infant were estimated by Fourier analysis ofimpedance (Z) and by multiple linear regression (MLR).RL_MLR (RL_MLR = 0.85 × RL_Z 0.43; r² = 0.95) and EL_MLR(EL_MLR = 0.97 × EL_Z + 8.4; r² = 0.98) werehighly correlated to RL_Z andEL_Z, respectively. Both RL(mean ± SD; RL_Z = 70 ± 38, RL_MLR = 59 ± 36 cmH₂O · s · l¹)and EL (EL_Z = 434 ± 212, EL_MLR = 436 ± 210 cmH₂O/l)exhibited wide intra- and intersubject variability.Regardless of computation method, RL was found to decreaseas a function of weight, age, respiratory rate (RR), and tidal volume(VT) whereas it increased as a function ofRR · VT and inspiratory-to-expiratorytime ratio (TI/TE). EL decreasedwith increasing weight, age, VT and female gender andincreased as RR and TI/TE increased. Weconclude that accounting for the effects of breathing patternvariability and demographic parameters on estimates of RLand EL is essential if they are to be of clinical value.Multivariate statistical models of RL and ELmay facilitate the interpretation of lung mechanics measurements inspontaneously breathing infants.

     

Chest wall and lung volume estimation by optical reflectance motion analysis

Cala, S. J., C. M. Kenyon, G. Ferrigno, P. Carnevali, A. Aliverti, A. Pedotti, P. T. Macklem, and D. F. Rochester. Chest wall and lung volume estimation by optical reflectance motion analysis.J. Appl. Physiol. 81(6):2680-2689, 1996.Estimation of chest wall motion by surfacemeasurements only allows one-dimensional measurements of the chestwall. We have assessed an optical reflectance system (OR), which tracksreflective markers in three dimensions (3-D) for respiratory use. Weused 86 (6-mm-diameter) hemispherical reflective markers arrangedcircumferentially on the chest wall in seven rows between the sternalnotch and the anterior superior iliac crest in two normal standingsubjects. We calculated the volume of the entire chest wall andcompared inspired and expired volumes with volumesobtained by spirometry. Marker positions were recorded by four TVcameras; two were 4 m in front of and two were 4 m behind the subject.The TV signals were sampled at 100 Hz and combined with gridcalibration parameters on a personal computer to obtain the 3-Dcoordinates of the markers. Chest wall surfaces were reconstructed bytriangulation through the point data, and chest wall volume wascalculated. During tidal breathing and vital capacity maneuvers andduring CO₂-stimulated hyperpnea, there was a very close correlation of the lung volumes(VL) estimated by spirometry[VL(SP)] and OR[VL(OR)]. Regressionequations of VL(OR)(y) vs.VL(SP)(x,BTPS in liters) for the two subjects were given by y = 1.01x  0.01 (r = 0.996) andy = 0.96x + 0.03 (r = 0.997), and byy = 1.04x + 0.25 (r = 0.97) andy = 0.98x + 0.14 (r = 0.95) for the two maneuvers,respectively. We conclude spirometric volumes can be estimated veryaccurately and directly from chest wall surface markers, and wespeculate that OR may be usefully applied to calculations of chest wallshape, regional volumes, and motion analysis.

     

Regulation of the epithelial Na+ channel by intracellular Na+

The hypothesis that the intracellularNa⁺ concentration([Na⁺]_i)is a regulator of the epithelialNa⁺ channel (ENaC) was tested withthe Xenopus oocyte expression systemby utilizing a dual-electrode voltage clamp.[Na⁺]_iaveraged 48.1 ± 2.2 meq (n = 27)and was estimated from the amiloride-sensitive reversal potential.[Na⁺]_iwas increased by direct injection of 27.6 nl of 0.25 or 0.5 MNa₂SO₄.Within minutes of injection,[Na⁺]_istabilized and remained elevated at 97.8 ± 6.5 meq(n = 9) and 64.9 ± 4.4 (n = 5) meq 30 min after theinitial injection of 0.5 and 0.25 MNa₂SO₄,respectively. This increase of[Na⁺]_icaused a biphasic inhibition of ENaC currents. In oocytes injected with0.5 MNa₂SO₄(n = 9), a rapid decrease of inwardamiloride-sensitive slope conductance(g_Na) to 0.681 ± 0.030 of control within the first 3 min and a secondary, slowerdecrease to 0.304 ± 0.043 of control at 30 min were observed.Similar but smaller inhibitions were also observed with the injectionof 0.25 MNa₂SO₄.Injection of isotonicK₂SO₄(70 mM) or isotonicK₂SO₄made hypertonic with sucrose (70 mMK₂SO₄-1.2M sucrose) was without effect. Injection of a 0.5 M concentration ofeitherK₂SO₄,N-methyl-D-glucamine (NMDG) sulfate, or 0.75 M NMDG gluconate resulted in a much smaller initial inhibition (<14%) and little or no secondary decrease. Thusincreases of[Na⁺]_ihave multiple specific inhibitory effects on ENaC that can betemporally separated into a rapid phase that was complete within 2-3 min and a delayed slow phase that was observed between 5 and 30 min.

     

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.

     

Predicting body cell mass with bioimpedance by using theoretical methods: a technological review

De Lorenzo, A., A. Andreoli, J. Matthie, and P. Withers.Predicting body cell mass with bioimpedance by using theoretical methods: a technological review. J. Appl.Physiol. 82(5): 1542-1558, 1997.The body cellmass (BCM), defined as intracellular water (ICW), was estimated in 73 healthy men and women by total body potassium (TBK) and by bioimpedancespectroscopy (BIS). In 14 other subjects, extracellular water (ECW) andtotal body water (TBW) were measured by bromide dilution and deuteriumoxide dilution, respectively. For all subjects, impedance spectral datawere fit to the Cole model, and ECW and ICW volumes were predicted byusing model electrical resistance terms R_E andR_I in an equation derived from Hanai mixture theory,respectively. The BIS ECW prediction bromide dilution wasr = 0.91, standard error of theestimate (SEE) 0.90 liter. The BIS TBW prediction of deuterium spacewas r = 0.95, SEE 1.33 liters. The BISICW prediction of the dilution-determined ICW wasr = 0.87, SEE 1.69 liters. The BIS ICWprediction of the TBK-determined ICW for the 73 subjects wasr = 0.85, SEE = 2.22 liters. Theseresults add further support to the validity of the Hanai theory, theequation used, and the conclusion that ECW and ICW volume can bepredicted by an approach based solely on fundamental principles.

     

Effect of oxygen tension and rate of pressure reduction during decompression on central gas bubbles

Reinertsen, R. E., V. Flook, S. Koteng, and A. O. Brubakk.Effect of oxygen tension and rate of pressure reduction duringdecompression on central gas bubbles. J. Appl.Physiol. 84(1): 351-356, 1998.Reduction inascent speed and an increase in theO₂ tension in the inspired airhave been used to reduce the risk for decompression sickness. It haspreviously been reported that decompression speed andO₂ partial pressure are linearly related for human decompressions from saturation hyperbaric exposures. The constant of proportionality K(K = rate/partial pressure of inspiredO₂) indicates the incidence ofdecompression sickness. The present study investigated the relationshipamong decompression rate, partial pressure of inspiredO₂, and the number of central gasbubbles after a 3-h dive to 500 kPa while breathing nitrox with an O₂ content of 35 kPa. Weused transesophageal ultrasonic scanning to determine the number ofbubbles in the pulmonary artery of pigs. The results show that, for agiven level of decompression stress, decompression rate andO₂ tension in the inspired air canbe traded off against each other by using pulmonary artery bubbles asan end point. The results also seem to confirm that decompressions thathave a high K value are morestressful.

     

Normalized metabolic stress for 31P-MR spectroscopy studies of human skeletal muscle: MVC vs. muscle volume

Fowler, M. D., T. W. Ryschon, R. E. Wysong, C. A. Combs, andR. S. Balaban. Normalized metabolic stress for³¹P-MR spectroscopy studies ofhuman skeletal muscle: MVC vs. muscle volume. J. Appl.Physiol. 83(3): 875-883, 1997.A criticalrequirement of submaximal exercise tests is the comparability ofworkload and associated metabolic stress between subjects. In thisstudy, ³¹P-magnetic resonancespectroscopy was used to estimate metabolic strain in the soleus muscleduring dynamic, submaximal plantar flexion in which target torque was10 and 15% of a maximal voluntary contraction (MVC). In 10 healthy,normally active adults, (PCr + P_i)/PCr, where PCr isphosphocreatine, was highly correlated with power output normalized tothe volume of muscle in the plantar flexor compartment(r = 0.89, P < 0.001). The same variable was also correlated, although less strongly(r = 0.78, P < 0.001), with power normalized toplantar flexor cross-sectional area. These findings suggest thatcomparable levels of metabolic strain can be obtained in subjects ofdifferent size when the power output, or stress, for dynamic plantarflexion is selected as a function of plantar flexor muscle volume. Incontrast, selecting power output as a function of MVC resulted in apositive linear relationship between (PCr + P_i)/PCr and thetorque produced, indicating that metabolic strain was increasing ratherthan achieving constancy as a function of MVC. These findings providenew insight into the design of dynamic muscle contraction protocolsaimed at detecting metabolic differences between subjects of differentbody size but having similar blood flow capacity and mitochondrialvolume per unit of muscle.

     

Pliometric contraction-induced injury of mouse skeletal muscle: effect of initial length

Hunter, Kam D., and John A. Faulkner. Pliometriccontraction-induced injury of mouse skeletal muscle: effect of initial length. J. Appl. Physiol. 82(1):278-283, 1997.For single pliometric (lengthening) contractionsinitiated from optimal fiber length (L_f), the mostimportant factor determining the subsequent force deficit is the workinput during the stretch. We tested the hypothesis that regardless ofthe initial length, the force deficit is primarily a function of thework input. Extensor digitorum longus muscles of mice were maximallyactivated in situ and lengthened at 2 L_f /s from oneof three initial fiber lengths (90, 100, or 120% of L_f) to one ofthree final fiber lengths (150, 160, or 170% of L_f). Maximalisometric force production was assessed before and after the pliometriccontraction. No single mechanical factor, including thework input(r² = 0.34), was sufficient to explain the differences in force deficits observed among groups. Therefore, the force deficit appears to arisefrom a complex interaction of mechanicalevents. With the data grouped by initial fiber length,the correlation between the average work and the average force deficitwas high(r² = 0.97-0.99). Consequently, differences in force deficits among groups were best explained on the basis of the initial fiber length andthe work input during the stretch.

     

Control of breathing during sleep assessed by proportional assist ventilation

Meza, S., E. Giannouli, and M. Younes. Control ofbreathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3-12, 1998.We used proportional assist ventilation (PAV) to evaluate thesources of respiratory drive during sleep. PAV increases the slope ofthe relation between tidal volume(VT) andrespiratory muscle pressure output (Pmus). We reasoned that ifrespiratory drive is dominated by chemical factors, progressiveincrease of PAV gain should result in only a small increase inVT because Pmus would bedownregulated substantially as a result of small decreases inPCO₂. In the presence of substantialnonchemical sources of drive [believed to be the case inrapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reductionin PCO₂ as the output related to thechemically insensitive drive source is amplified severalfold. Twelvenormal subjects underwent polysomnography while connected to a PAVventilator. Continuous positive air pressure (5.2 ± 2.0 cmH₂O) was administered tostabilize the upper airway. PAV was increased in 2-min steps from 0 to20, 40, 60, 80, and 90% of the subject's elastance and resistance.VT, respiratory rate, minuteventilation, and end-tidal CO₂pressure were measured at the different levels, and Pmus wascalculated. Observations were obtained in stage 2 sleep (n = 12), slow-wave sleep(n = 11), and REM sleep(n = 7). In all cases, Pmus wassubstantially downregulated with increase in assist so that theincrease in VT, althoughsignificant (P < 0.05), was small(0.08 liter at the highest assist). There was no difference in responsebetween REM and non-REM sleep. We conclude that respiratory driveduring sleep is dominated by chemical control and that there is nofundamental difference between REM and non-REM sleep in this regard.REM sleep appears to simply add bidirectional noise to what isbasically a chemically controlled respiratory output.

     

When does the lung die? Kfc, cell viability, and adenine nucleotide changes in the circulation-arrested rat lung

Jones, David R., Randy M. Becker, Steve C. Hoffmann, John J. Lemasters, and Thomas M. Egan. When does the lungdie? K_fc, cellviability, and adenine nucleotide changes in the circulation-arrested rat lung. J. Appl. Physiol. 83(1):247-252, 1997.Lungs harvested from cadavericcirculation-arrested donors may increase the donor pool for lungtransplantation. To determine the degree and time course ofischemia-reperfusion injury, we evaluated the effect ofO₂ ventilation on capillarypermeability [capillary filtration coefficient(K_fc)],cell viability, and total adenine nucleotide (TAN) levels in in situcirculation-arrested rat lungs.K_fc increased with increasing postmortem ischemic time(r = 0.88). Lungs ventilated withO₂ 1 h postmortem had similarK_fc andwet-to-dry ratios as controls. Nonventilated lungs had threefold(P < 0.05) and sevenfold (P < 0.0001) increases inK_fc at 30 and 60 min postmortem compared with controls. Cell viability decreased inall groups except for 30-min postmortemO₂-ventilated lungs. TAN levelsdecreased with increasing ischemic time, particularly in nonventilatedlungs. Loss of adenine nucleotides correlated with increasingK_fc values (r = 0.76). This study indicates thatlungs retrieved 1 h postmortem may have normalK_fc withpreharvest O₂ ventilation. Therelationship betweenK_fc and TANsuggests that vascular permeability may be related to lung TAN levels.