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1.
Human ventilatory response to 8h of euoxic hypercapnia   总被引:1,自引:0,他引:1  
Tansley, John G., Michala E. F. Pedersen, Christine Clar,and Peter A. Robbins. Human ventilatory response to 8 h of euoxic hypercapnia. J. Appl.Physiol. 84(2): 431-434, 1998.Ventilation (E) risesthroughout 40 min of constant elevated end-tidalPCO2 without reaching steady state(S. Khamnei and P. A. Robbins. Respir. Physiol. 81: 117-134, 1990). The present studyinvestigates 8 h of euoxic hypercapnia to determine whetherE reachessteady state within this time. Two protocols were employed:1) 8-h euoxic hypercapnia (end-tidalPCO2 = 6.5 Torr above prestudy value,end-tidal PO2 = 100 Torr) followed by 8-h poikilocapnic euoxia; and2) control, where the inspired gaswas air. Ewas measured over a 5-min period before the experiment and then hourly over a 16-h period. In the hypercapnia protocol,E had notreached a steady state by the first hour(P < 0.001, analysis of variance), but there were no further significant differences inEover hours 2-8 (analysis ofvariance). Efell promptly on return to eucapnic conditions. We conclude that,whereas there is a component of theE responseto hypercapnia that is slow, there is no progressive rise inE throughoutthe 8-h period.

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2.
Duringventilatory acclimatization to hypoxia (VAH), the relationship betweenventilation (E) and end-tidalPCO2 (PETCO2) changes.This study was designed to determine 1) whether these changes can be seenearly in VAH and 2) if these changesare present, whether the responses differ between isocapnic andpoikilocapnic exposures. Ten healthy volunteers were studied by usingthree 8-h exposures: 1) isocapnichypoxia (IH), end-tidal PO2(PETO2) = 55 Torr andPETCO2 held at thesubject's normal prehypoxic value;2) poikilocapnic hypoxia (PH),PETO2 = 55 Torr; and3) control (C), air breathing. TheE-PETCO2relationship was determined in hyperoxia (PETO2 = 200 Torr) beforeand after the exposures. We found a significant increase in theslopes ofE-PETCO2 relationship after both hypoxic exposures compared with control (IH vs.C, P < 0.01; PH vs. C,P < 0.001; analysis of covariance with pairwise comparisons). This increase was not significantly different between protocols IH andPH. No significant changes in theintercept were detected. We conclude that 8 h of hypoxia, whetherisocapnic or poikilocapnic, increases the sensitivity of the hyperoxicchemoreflex response to CO2.

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3.
Ventilatory acclimatization tohypoxia is associated with an increase in ventilation under conditionsof acute hyperoxia(Ehyperoxia) and an increase in acute hypoxic ventilatory response (AHVR). Thisstudy compares 48-h exposures to isocapnic hypoxia( protocol I) with 48-hexposures to poikilocapnic hypoxia ( protocolP) in 10 subjects to assess the importance ofhypocapnic alkalosis in generating the changes observed in ventilatoryacclimatization to hypoxia. During both hypoxic exposures,end-tidal PO2 was maintained at60 Torr, with end-tidal PCO2 held at the subject's prehypoxic level( protocol I) or uncontrolled( protocol P).Ehyperoxiaand AHVR were assessed regularly throughout the exposures.Ehyperoxia(P < 0.001, ANOVA) and AHVR(P < 0.001) increased during thehypoxic exposures, with no significant differences betweenprotocols I andP. The increase inEhyperoxiawas associated with an increase in slope of theventilation-end-tidal PCO2 response(P < 0.001) with no significantchange in intercept. These results suggest that changes in respiratorycontrol early in ventilatory acclimatization to hypoxiaresult from the effects of hypoxia per se and not the alkalosisnormally accompanying hypoxia.

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4.
Moon, Jon K., and Nancy F. Butte. Combined heart rateand activity improve estimates of oxygen consumption and carbon dioxideproduction rates. J. Appl. Physiol.81(4): 1754-1761, 1996.Oxygen consumption(O2) andcarbon dioxide production (CO2) rates were measuredby electronically recording heart rate (HR) and physical activity (PA).Mean daily O2 andCO2 measurements by HR andPA were validated in adults (n = 10 women and 10 men) with room calorimeters. Thirteen linear and nonlinear functions of HR alone and HR combined with PA were tested as models of24-h O2 andCO2. Mean sleepO2 andCO2 were similar to basalmetabolic rates and were accurately estimated from HR alone[respective mean errors were 0.2 ± 0.8 (SD) and0.4 ± 0.6%]. The range of prediction errorsfor 24-h O2 andCO2 was smallestfor a model that used PA to assign HR for each minute to separateactive and inactive curves(O2, 3.3 ± 3.5%; CO2, 4.6 ± 3%). There were no significant correlations betweenO2 orCO2 errors and subject age,weight, fat mass, ratio of daily to basal energy expenditure rate, orfitness. O2,CO2, and energy expenditurerecorded for 3 free-living days were 5.6 ± 0.9 ml · min1 · kg1,4.7 ± 0.8 ml · min1 · kg1,and 7.8 ± 1.6 kJ/min, respectively. Combined HR and PA measured 24-h O2 andCO2 with a precisionsimilar to alternative methods.

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5.
Yan, Sheng, Pawel Sliwinski, and Peter T. Macklem.Association of chest wall motion and tidal volume responses during CO2 rebreathing.J. Appl. Physiol. 81(4):1528-1534, 1996.The purpose of this study is to investigate theeffect of chest wall configuration at end expiration on tidal volume(VT) response duringCO2 rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory andend-inspiratory volume of the rib cage (Vrc,E andVrc,I, respectively) and abdomen (Vab,E and Vab,I, respectively) measured by linearizedmagnetometers were expressed as a function of end-tidalPCO2(PETCO2). The changes inend-expiratory and end-inspiratory volumes of the chest wall(Vcw,E and Vcw,I,respectively) were calculated as the sum of the respectiverib cage and abdominal volumes. The magnetometer coils were placed atthe level of the nipples and 1-2 cm above the umbilicus andcalibrated during quiet breathing against theVT measured from apneumotachograph. TheVrc,E/PETCO2 slope was quite variable among subjects. It was significantly positive (P < 0.05) in fivesubjects, significantly negative in four subjects(P < 0.05), and not different fromzero in the remaining two subjects. TheVab,E/PETCO2slope was significantly negative in all subjects(P < 0.05) with a much smallerintersubject variation, probably suggesting a relatively more uniformrecruitment of abdominal expiratory muscles and a variable recruitmentof rib cage muscles during CO2rebreathing in different subjects. As a group, the meanVrc,E/PETCO2,Vab,E/PETCO2, andVcw,E/PETCO2slopes were 0.010 ± 0.034, 0.030 ± 0.007, and0.020 ± 0.032 l / Torr, respectively;only theVab,E/PETCO2 slope was significantly different from zero. More interestingly, theindividualVT/PETCO2slope was negatively associated with theVrc,E/PETCO2(r = 0.68,P = 0.021) and Vcw,E/PETCO2slopes (r = 0.63,P = 0.037) but was not associated withtheVab,E/PETCO2slope (r = 0.40, P = 0.223). There was no correlation oftheVrc,E/PETCO2 andVcw,E/PETCO2slopes with age, body size, forced expiratory volume in 1 s, orexpiratory time. The groupVab,I/PETCO2 slope (0.004 ± 0.014 l / Torr) was not significantlydifferent from zero despite theVT nearly being tripled at theend of CO2 rebreathing. Inconclusion, the individual VTresponse to CO2, althoughindependent of Vab,E, is a function ofVrc,E to the extent that as theVrc,E/PETCO2slope increases (more positive) among subjects, theVT response toCO2 decreases. These results maybe explained on the basis of the respiratory muscle actions andinteractions on the rib cage.

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6.
Ventilatory long-term facilitation in unanesthetized rats   总被引:5,自引:0,他引:5  
Wetested the hypothesis that unanesthetized rats exhibit ventilatorylong-term facilitation (LTF) after intermittent, but not continuous,hypoxia. Minute ventilation (E) and carbon dioxide production (CO2) were measured inunanesthetized, unrestrained male Sprague-Dawley rats via barometricplethysmography before, during, and after exposure to continuous orintermittent hypoxia. Hypoxia was either isocapnic [inspiredO2 fraction (FIO2) = 0.08-0.09 and inspired CO2 fraction(FICO2) = 0.04] or poikilocapnic(FIO2 = 0.11 andFICO2 = 0.00). Sixty minutes afterintermittent hypoxia, E orE/CO2 wassignificantly greater than baseline in both isocapnic and poikilocapnicconditions. In contrast, 60 min after continuous hypoxia,E andE/CO2 were notsignificantly different from baseline values. These data demonstrateventilatory LTF after intermittent hypoxia in unanesthetized rats.Ventilatory LTF appeared similar in its magnitude (after accounting forCO2 feedback), time course, and dependence on intermittenthypoxia to phrenic LTF previously observed in anesthetized,vagotomized, paralyzed rats.

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7.
Chilibeck, P. D., D. H. Paterson, D. A. Cunningham, A. W. Taylor, and E. G. Noble. Muscle capillarization,O2 diffusion distance, andO2 kinetics in old andyoung individuals. J. Appl. Physiol.82(1): 63-69, 1997.The relationships between muscle capillarization, estimated O2diffusion distance from capillary to mitochondria, andO2 uptake(O2) kineticswere studied in 11 young (mean age, 25.9 yr) and 9 old (mean age, 66.0 yr) adults. O2kinetics were determined by calculating the time constants () forthe phase 2 O2 adjustment to andrecovery from the average of 12 repeats of a 6-min, moderate-intensityplantar flexion exercise. Muscle capillarization was determined fromcross sections of biopsy material taken from lateral gastrocnemius.Young and old groups had similarO2 kinetics(O2-on = 44 vs. 48 s;O2-off = 33 vs. 44 s, for young and old, respectively), muscle capillarization, andestimated O2 diffusion distances.Muscle capillarization, expressed as capillary density or averagenumber of capillary contacts per fiber/average fiber area, and theestimates of diffusion distance were significantly correlated toO2-off kinetics in theyoung (r = 0.68 to 0.83;P < 0.05). We conclude that1) capillarization andO2 kinetics during exerciseof a muscle group accustomed to everyday activity (e.g., walking) arewell maintained in old individuals, and2) in the young, recovery of O2 after exercise isfaster, with a greater capillary supply over a given muscle fiber areaor shorter O2 diffusion distances.

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8.
Gonzalez, Norberto C., Richard L. Clancy, Yoshihiro Moue,and Jean-Paul Richalet. Increasing maximal heart rate increases maximal O2 uptake in ratsacclimatized to simulated altitude. J. Appl.Physiol. 84(1): 164-168, 1998.Maximal exerciseheart rate (HRmax) is reducedafter acclimatization to hypobaric hypoxia. The lowHRmax contributes to reducemaximal cardiac output(max) andmay limit maximal O2 uptake(O2 max). Theobjective of these experiments was to test the hypothesisthat the reduction inmax afteracclimatization to hypoxia, due, in part, to the lowHRmax, limitsO2 max. Ifthis hypothesis is correct, an increase in max wouldresult in a proportionate increase inO2 max. Rats acclimatized to hypobaric hypoxia [inspiredPO2(PIO2) = 69.8 ± 3 Torr for 3 wk] exercised on a treadmill in hypoxic (PIO2 = 71.7 ± 1.1 Torr) or normoxic conditions(PIO2 = 142.1 ± 1.1 Torr). Each rat ran twice: in one bout the rat was allowed to reach itsspontaneous HRmax, which was 505 ± 7 and 501 ± 5 beats/min in hypoxic and normoxic exercise,respectively; in the other exercise bout,HRmax was increased by 20% to the preacclimatization value of 600 beats/min by atrial pacing. This resulted in an ~10% increase inmax, since theincrease in HRmax was offset by a10% decrease in stroke volume, probably due to shortening of diastolicfilling time. The increase inmax was accompanied by a proportionate increase in maximal rate of convective O2 delivery(max × arterial O2 content), maximal workrate, and O2 max inhypoxic and normoxic exercise. The data show that increasingHRmax topreacclimatization levels increasesO2 max, supportingthe hypothesis that the lowHRmax tends to limitO2 max after acclimatization to hypoxia.

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9.
Dwinell, M. R., P. L. Janssen, J. Pizarro, and G. E. Bisgard. Effects of carotid body hypocapnia during ventilatory acclimatization to hypoxia. J. Appl.Physiol. 82(1): 118-124, 1997.Hypoxicventilatory sensitivity is increased during ventilatory acclimatizationto hypoxia (VAH) in awake goats, resulting in a time-dependent increasein expired ventilation (E). Theobjectives of this study were to determine whether the increasedcarotid body (CB) hypoxic sensitivity is dependent on the level of CB CO2 and whether the CBCO2 gain is changed during VAH.Studies were carried out in adult goats with CB blood gases controlled by an extracorporeal circuit while systemic (central nervous system) blood gases were regulated independently by the level of inhaled gases. Acute E responsesto CB hypoxia (CB PO2 40 Torr) and CBhypercapnia (CB PCO2 50 and 60 Torr)were measured while systemic normoxia and isocapnia were maintained. CBPO2 was then lowered to 40 Torr for 4 h while the systemic blood gases were kept normoxic and normocapnic.During the 4-h CB hypoxia, E increasedin a time-dependent manner. Thirty minutes after return to normoxia,the ventilatory response to CB hypoxia was significantly increasedcompared with the initial response. The slope of the CBCO2 response was also elevatedafter VAH. An additional group of goats(n = 7) was studied with asimilar protocol, except that CB PCO2was lowered throughout the 4-h hypoxic exposure to prevent reflexhyperventilation. CB PCO2 wasprogressively lowered throughout the 4-h CB hypoxic period to maintainE at the control level. After the 4-hCB hypoxic exposure, the ventilatory response to hypoxia was alsosignificantly elevated. However, the slope of the CBCO2 response was not elevatedafter the 4-h hypoxic exposure. These results suggest that CBsensitivity to both O2 andCO2 is increased after 4 h of CBhypoxia with systemic isocapnia. The increase in CB hypoxic sensitivityis not dependent on the level of CBCO2 maintained during the 4-hhypoxic period.

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10.
To test thehypothesis that muscle O2 uptake(O2) on-kinetics islimited, at least in part, by peripheralO2 diffusion, we determined theO2 on-kinetics in1) normoxia (Control);2) hyperoxic gas breathing(Hyperoxia); and 3) hyperoxia andthe administration of a drug (RSR-13, Allos Therapeutics), whichright-shifts the Hb-O2dissociation curve (Hyperoxia+RSR-13). The study was conducted inisolated canine gastrocnemius muscles(n = 5) during transitions from restto 3 min of electrically stimulated isometric tetanic contractions(200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% peakO2). In all conditions,before and during contractions, muscle was pump perfused withconstantly elevated blood flow (), at a levelmeasured at steady state during contractions in preliminary trials withspontaneous . Adenosine was infusedintra-arterially to prevent inordinate pressure increases with theelevated . was measuredcontinuously, arterial and popliteal venousO2 concentrations were determinedat rest and at 5- to 7-s intervals during contractions, andO2 was calculated as · arteriovenous O2 content difference.PO2 at 50%HbO2saturation (P50) was calculated.Mean capillary PO2(cO2)was estimated by numerical integration.P50 was higher in Hyperoxia+RSR-13[40 ± 1 (SE) Torr] than in Control and in Hyperoxia (31 ± 1 Torr). After 15 s of contractions,cO2was higher in Hyperoxia (97 ± 9 Torr) vs. Control (53 ± 3 Torr) and in Hyperoxia+RSR-13 (197 ± 39 Torr) vs. Hyperoxia. Thetime to reach 63% of the difference between baseline and steady-stateO2 during contractions was 24.7 ± 2.7 s in Control, 26.3 ± 0.8 s in Hyperoxia, and 24.7 ± 1.1 s in Hyperoxia+RSR-13 (not significant). Enhancement ofperipheral O2 diffusion (obtainedby increasedcO2at constant O2 delivery) duringthe rest-to-contraction (60-70% of peakO2) transition did notaffect muscle O2on-kinetics.

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11.
Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response toexercise in diabetic subjects with autonomic neuropathy.J. Appl. Physiol. 81(5):1978-1986, 1996.We have used diabetic autonomic neuropathy as amodel of chronic pulmonary denervation to study the ventilatoryresponse to incremental exercise in 20 diabetic subjects, 10 with(Dan+) and 10 without (Dan) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan subjectsachieved lower O2 consumption andCO2 production(CO2) thancontrol subjects at peak of exercise, they attained similar values ofeither minute ventilation(E) oradjusted ventilation (E/maximalvoluntary ventilation). The increment of respiratory rate withincreasing adjusted ventilation was much higher in Dan+ than inDan and control subjects (P < 0.05). The slope of the linearE/CO2relationship was 0.032 ± 0.002, 0.027 ± 0.001 (P < 0.05), and 0.025 ± 0.001 (P < 0.001) ml/min inDan+, Dan, and control subjects, respectively. Bothneuromuscular and ventilatory outputs in relation to increasingCO2 were progressivelyhigher in Dan+ than in Dan and control subjects. At peak ofexercise, end-tidal PCO2 was muchlower in Dan+ (35.9 ± 1.6 Torr) than in Dan (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects.We conclude that pulmonary autonomic denervation affects ventilatoryresponse to stressful exercise by excessively increasing respiratoryrate and alveolar ventilation. Reduced neural inhibitory modulationfrom sympathetic pulmonary afferents and/or increasedchemosensitivity may be responsible for the higher inspiratoryoutput.

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12.
Gautier, Henry, Cristina Murariu, and Monique Bonora.Ventilatory and metabolic responses to ambient hypoxia orhypercapnia in rats exposed to CO hypoxia. J. Appl. Physiol.83(1): 253-261, 1997.We have investigated at ambienttemperatures (Tam) of 25 and5°C the effects of ambient hypoxia(Hxam; fractional inspired O2 = 0.14) and hypercapnia(fractional inspiredCO2 = 0.04) on ventilation (),O2 uptake(O2), andcolonic temperature (Tc) in 12 conscious rats before and after carotid body denervation (CBD). Therats were concomitantly exposed to CO hypoxia (HxCO; fractional inspired CO = 0.03-0.05%), which decreases arterial O2 saturation by ~25-40%.The results demonstrate the following. 1) AtTam of 5°C, in both intact andCBD rats,/O2 islarger when Hxam orCO2 is associated withHxCO than with normoxia. At Tam of 25°C, this is also thecase except for CO2 in CBD rats. 2) AtTam of 5°C, the changes inO2 andTc seem to result from additiveeffects of the separate changes induced byHxam,CO2, andHxCO. It is concluded that, inconscious rats, central hypoxia does not depress respiratory activity.On the contrary, particularly whenO2 is augmented during acold stress, both/O2during HxCO and the ventilatoryresponses to Hxam andCO2 are increased. The mechanismsinvolved in this relative hyperventilation are likely to involvediencephalic integrative structures.

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13.
Grassi, Bruno, Claudio Marconi, Michael Meyer, Michel Rieu,and Paolo Cerretelli. Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients. J. Appl. Physiol. 82(6): 1952-1962, 1997.Metabolicand cardiovascular adjustments to various submaximal exercises wereevaluated in 82 heart transplant recipients (HTR) and in 35 controlsubjects (C). HTR were tested 21.5 ± 25.3 (SD) mo (range1.0-137.1 mo) posttransplantation. Three protocols were used:protocol A consisted of 5 min of rectangular 50-W load repeatedtwice, 5 min apart [5 min rest, 5 min 50 W (Ex 1), 5 minrecovery, 5 min 50 W (Ex 2)]; protocol B consistedof 5 min of rectangular load at 25, 50, or 75 W; protocol Cconsisted of 15 min of rectangular load at 25 W. Breath-by-breathpulmonary ventilation (E),O2 uptake (O2),and CO2 output(CO2) were determined.During protocol A, beat-by-beat cardiacoutput () was estimated by impedance cardiography. The half times (t1/2) of the on- andoff-kinetics of the variables were calculated. In all protocols,t1/2 values forO2 on-,E on-, andCO2 on-kinetics were higher(i.e., the kinetics were slower) in HTR than in C, independently ofworkload and of the time posttransplantation. Also,t1/2 on- was higher in HTRthan in C. In protocol A, no significant difference of t1/2 O2on- was observed in HTR between Ex 1 (48 ± 9 s) and Ex2 (46 ± 8 s), whereas t1/2 on- was higher during Ex 1 (55 ± 24 s)than during Ex 2 (47 ± 15 s). In all protocols and for all variables, the t1/2 off-values were higher in HTRthan in C. In protocol C, no differences of steady-stateE,O2, andCO2 were observed in bothgroups between 5, 10, and 15 min of exercise. We conclude that1) in HTR, a "priming" exercise, while effective inspeeding up the adjustment of convective O2 flow to muscle fibers during a second on-transition, did not affect theO2 on-kinetics, suggestingthat the slower O2 on- inHTR was attributable to peripheral (muscular) factors; 2) thedissociation between on- andO2 on-kinetics in HTRindicates that an inertia of muscle metabolic machinery is the mainfactor dictating theO2 on-kinetics; and 3) theO2 off-kinetics was slowerin HTR than in C, indicating a greater alactic O2 deficitin HTR and, therefore, a sluggish muscleO2 adjustment.

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14.
Barstow, Thomas J., Andrew M. Jones, Paul H. Nguyen, andRichard Casaburi. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.J. Appl. Physiol. 81(4):1642-1650, 1996.We tested the hypothesis that the amplitude ofthe additional slow component ofO2 uptake(O2) during heavy exerciseis correlated with the percentage of type II (fast-twitch) fibers inthe contracting muscles. Ten subjects performed transitions to a workrate calculated to require aO2 equal to 50% betweenthe estimated lactate (Lac) threshold and maximalO2 (50%).Nine subjects consented to a muscle biopsy of the vastus lateralis. Toenhance the influence of differences in fiber type among subjects,transitions were made while subjects were pedaling at 45, 60, 75, and90 rpm in different trials. Baseline O2 was designed to besimilar at the different pedal rates by adjusting baseline work ratewhile the absolute increase in work rate above the baseline was thesame. The O2 response after the onset of exercise was described by a three-exponential model. Therelative magnitude of the slow component at the end of 8-min exercisewas significantly negatively correlated with %type I fibers at everypedal rate (r = 0.64 to 0.83, P < 0.05-0.01). Furthermore,the gain of the fast component forO2 (asml · min1 · W1)was positively correlated with the %type I fibers across pedal rates(r = 0.69-0.83). Increase inpedal rate was associated with decreased relative stress of theexercise but did not affect the relationships between%fiber type and O2parameters. The relative contribution of the slow component was alsosignificantly negatively correlated with maximalO2(r = 0.65), whereas the gainfor the fast component was positively associated(r = 0.68-0.71 across rpm). Theamplitude of the slow component was significantly correlated with netend-exercise Lac at all four pedal rates(r = 0.64-0.84), but Lac was notcorrelated with %type I (P > 0.05).We conclude that fiber type distribution significantly affects both thefast and slow components ofO2 during heavy exerciseand that fiber type and fitness may have both codependent andindependent influences on the metabolic and gas-exchange responses toheavy exercise.

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15.
Li, M. H., J. Hildebrandt, and M. P. Hlastala.Quantitative analysis of transpleural flux in the isolated lung.J. Appl. Physiol. 82(2): 545-551, 1997.In this study, the loss of inert gas through the pleura of anisolated ventilated and perfused rabbit lung was assessed theoreticallyand experimentally. A mathematical model was used to represent an idealhomogeneous lung placed within a box with gas flow(box) surrounding the lung. Thealveoli are assumed to be ventilated with room air(A) andperfused at constant flow () containinginert gases (x) with various perfusate-air partition coefficients(p,x).The ratio of transpleural flux of gas(plx)to its total delivery to the lung via pulmonary artery( ),representing fractional losses across the pleura, can be shown todepend on four dimensionless ratios:1)p,x,2) the ratio of alveolar ventilation to perfusion(A/), 3) the ratioof the pleural diffusing capacity(Dplx) to the conductance ofthe alveolar ventilation (Dplx /Ag,where g is the capacitancecoefficient of gas), and 4) theratio of extrapleural (box) ventilation to alveolar ventilation(box/A).Experiments were performed in isolated perfused and ventilated rabbitlungs. The perfusate was a buffer solution containing six dissolvedinert gases covering the entire 105-fold range ofp,x usedin the multiple inert gas elimination technique. Steady-state inert gasconcentrations were measured in the pulmonary arterial perfusate,pulmonary venous effluent, exhaled gas, and box effluent gas. Theexperimental data could be described satisfactorily by thesingle-compartment model. It is concluded that a simple theoreticalmodel is a useful tool for predicting transpleural flux from isolatedlung preparations, with known ventilation and perfusion, for inertgases within a wide range of .

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16.
We evaluated the hypotheses that endurance training increasesrelative lipid oxidation over a wide range of relative exercise intensities in fed and fasted states and that carbohydrate nutrition causes carbohydrate-derived fuels to predominate as energy sources during exercise. Pulmonary respiratory gas-exchange ratios [(RER) = CO2production/O2 consumption(O2)] were determinedduring four relative, graded exercise intensities in both fed andfasted states. Seven untrained (UT) men and seven category 2 and 3 US Cycling Federation cyclists (T) exercised in the morning in random order, with target power outputs of 20 and 40% peakO2(O2 peak) for 2 h,60% O2 peak for 1.5 h, and 80%O2 peak fora minimum of 30 min after either a 12-h overnight fast or 3 h after astandardized breakfast. Actual metabolic responses were 22 ± 0.33, 40 ± 0.31, 59 ± 0.32, and 75 ± 0.39%O2 peak. T subjectsshowed significantly (P < 0.05)decreased RER compared with UT subjects at absolute workloads when fedand fasted. Fasting significantly decreased RER values compared withthe fed state at 22, 40, and 59%O2 peak inT and at 40 and 59%O2 peak in UTsubjects. Training decreased (P < 0.05) mean RER values compared with UT subjects at 22%O2 peak when theyfasted, and at 40%O2 peak when fed orfasted, but not at higher relative exercise intensities in eithernutritional state. Our results support the hypothesis that endurancetraining enhances lipid oxidation in men after a 12-h overnight fast at low relative exercise intensities (22 and 40%O2 peak). However, atraining effect on RER was not apparent at high relative exercise intensities (59 and 75%O2 peak). Becausemost athletes train and compete at exercise intensities >40% maximalO2, they will not oxidize agreater proportion of lipids compared with untrained subjects,regardless of nutritional state.  相似文献   

17.
Treppo, Steven, Srboljub M. Mijailovich, and José G. Venegas. Contributions of pulmonary perfusion and ventilation toheterogeneity in A/measured by PET. J. Appl. Physiol. 82(4): 1163-1176, 1997. To estimate the contributions of the heterogeneity in regionalperfusion () and alveolar ventilation(A) to that of ventilation-perfusionratio (A/), we haverefined positron emission tomography (PET) techniques to image localdistributions of andA per unit of gas volume content(s and sA,respectively) and VA/ indogs. sA was assessed in two ways:1) the washout of 13NN tracer after equilibrationby rebreathing (sAi), and2) the ratio of an apneic image after a bolus intravenousinfusion of 13NN-saline solution to an image collectedduring a steady-state intravenous infusion of the same solution(sAp).sAp was systematically higher than sAi in allanimals, and there was a high spatial correlation betweens andsAp in both body positions(mean correlation was 0.69 prone and 0.81 supine) suggesting thatventilation to well-perfused units was higher than to those poorlyperfused. In the prone position, the spatial distributions ofs, sAp, and A/ were fairlyuniform with no significant gravitational gradients; however, in thesupine position, these variables were significantly more heterogeneous,mostly because of significant gravitational gradients (15, 5.5, and10%/cm, respectively) accounting for 73, 33, and 66% of thecorresponding coefficient of variation (CV)2 values. Weconclude that, in the prone position, gravitational forces in blood andlung tissues are largely balanced out by dorsoventral differences inlung structure. In the supine position, effects of gravity andstructure become additive, resulting in substantial gravitationalgradients in s andsAp, with the higherheterogeneity inA/ caused by agravitational gradient in s, only partially compensated by that in sA.

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18.
Oxygen transport in conscious newborn dogs during hypoxic hypometabolism   总被引:1,自引:0,他引:1  
We questioned whether the decrease inO2 consumption(O2) during hypoxia innewborns is a regulated response or reflects a limitation inO2 availability. Experiments wereconducted on previously instrumented conscious newborn dogs.O2 was measured at a warmambient temperature (30°C, n = 7)or in the cold (20°C, n = 6),while the animals breathed air or were sequentially exposed to 15 minof fractional inspired O2(FIO2): 21, 18, 15, 12, 10, 8, and 6%. In normoxia,O2 averaged 15 ± 1 (SE)and 25 ± 1 ml · kg1 · min1in warm and cold conditions, respectively. In the warmcondition, hypometabolism (i.e., hypoxicO2 < normoxicO2) occurred at FIO2 10%, whereas in thecold condition, hypometabolism occurred atFIO2 12%. The sameresults were obtained in a separate group(n = 14) of noninstrumented puppies.For all levels of FIO2 withhypometabolism, the relationships between measures ofO2 availability (arterialO2 saturation or content, venousPO2 or saturation,x-axis) vs.O2(y-axis) had lower slopes in warm than in coldconditions. Hence, O2 during hypometabolism in the warm condition was not the maximal attainable for the level of oxygenation. The results do not support thepossibility that the hypoxic drop inO2 in the newborn reflects a limitation in O2availability. The results are compatible with the ideathat the phenomenon is one of "regulated conformism" tohypoxia.

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19.
Williams, J. S., and T. G. Babb. Differences betweenestimates and measured PaCO2 during restand exercise in older subjects. J. Appl.Physiol. 83(1): 312-316, 1997.ArterialPCO2 (PaCO2) has been estimated duringexercise with good accuracy in younger individuals by using the Jonesequation(PJCO2)(J. Appl. Physiol. 47: 954-960,1979). The purpose of this project was to determine the utility ofestimating PaCO2 from end-tidal PCO2(PETCO2) orPJCO2at rest, ventilatory threshold (Th), and maximalexercise (Max) in older subjects. PETCO2 was determined fromrespired gases simultaneously (MGA 1100) with arterial blood gases(radial arterial catheter) in 12 older and 11 younger subjects at restand during exercise. Mean differences were analyzed with pairedt-tests, and relationships between theestimated PaCO2 values and the actualvalues of PaCO2 were determined withcorrelation coefficients. In the older subjects, PETCO2 was not significantlydifferent from PaCO2 at rest (1.2 ± 4.3 Torr), Th (0.4 ± 2.5), or Max(0.8 ± 2.7), and the two were significantly(P < 0.05) correlated atth (r = 0.84) andMax (r = 0.87) but not atrest (r = 0.47).PJCO2was similar to PaCO2 at rest (1.0 ± 3.9) and th (1.3 ± 2.3) but significantly lower at Max (3.0 ± 2.6), and the two weresignificantly correlated at th(r = 0.86) and Max(r = 0.80) but not at rest (r = 0.54).PETCO2 was significantlyhigher than PaCO2 during exercise in theyounger subjects but similar to PaCO2 at rest.PJCO2was similar to PaCO2 at rest andth but significantly lower at Max in youngersubjects. In conclusion, our data demonstrate thatPaCO2 during exercise is betterestimated by PETCO2 than byPJCO2in older subjects, contrary to what is observed in younger subjects.This appears to be related to the finding thatPETCO2 does not exceedPaCO2 during exercise in older subjects,as occurs in the younger subjects. However,PaCO2 at rest is best estimated byPJCO2in both younger and older subjects.

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20.
Respiratory muscle work compromises leg blood flow during maximal exercise   总被引:10,自引:0,他引:10  
Harms, Craig A., Mark A. Babcock, Steven R. McClaran, DavidF. Pegelow, Glenn A. Nickele, William B. Nelson, and Jerome A. Dempsey.Respiratory muscle work compromises leg blood flow during maximalexercise. J. Appl. Physiol.82(5): 1573-1583, 1997.We hypothesized that duringexercise at maximal O2 consumption (O2 max),high demand for respiratory muscle blood flow() would elicit locomotor muscle vasoconstrictionand compromise limb . Seven male cyclists(O2 max 64 ± 6 ml · kg1 · min1)each completed 14 exercise bouts of 2.5-min duration atO2 max on a cycleergometer during two testing sessions. Inspiratory muscle work waseither 1) reduced via aproportional-assist ventilator, 2)increased via graded resistive loads, or3) was not manipulated (control).Arterial (brachial) and venous (femoral) blood samples, arterial bloodpressure, leg (legs;thermodilution), esophageal pressure, andO2 consumption(O2) weremeasured. Within each subject and across all subjects, at constantmaximal work rate, significant correlations existed(r = 0.74-0.90;P < 0.05) between work of breathing(Wb) and legs (inverse), leg vascular resistance (LVR), and leg O2(O2 legs;inverse), and between LVR and norepinephrine spillover. Mean arterialpressure did not change with changes in Wb nor did tidal volume orminute ventilation. For a ±50% change from control in Wb,legs changed 2 l/min or 11% of control, LVRchanged 13% of control, and O2extraction did not change; thusO2 legschanged 0.4 l/min or 10% of control. TotalO2 max was unchangedwith loading but fell 9.3% with unloading; thusO2 legsas a percentage of totalO2 max was 81% incontrol, increased to 89% with respiratory muscle unloading, anddecreased to 71% with respiratory muscle loading. We conclude that Wbnormally incurred during maximal exercise causes vasoconstriction inlocomotor muscles and compromises locomotor muscle perfusion andO2.

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