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1.
Thepresent study was a prospective, nonrandomized, observationalexamination of the relationship among hypoproteinemia and electrolyteand acid-base status in a critical care population of patients. A totalof 219 arterial blood samples reviewed from 91 patients was analyzedfor arterial blood gas, electrolytes, lactate, and total protein.Plasma strong-ion difference ([SID]) was calculated from[Na+] + [K+]  [Cl]  [La].Total protein concentration was used to derive the total concentration of weak acid([A]tot).[A]tot encompassed arange of 18.7 to 9.0 meq/l, whereas [SID] varied from 48.1 to 26.6 meq/l and was directly correlated with[A]tot. The decline in[SID] was primarily attributable to an increase in[Cl]. A directcorrelation was also noted betweenPCO2 and [SID], but notbetween PCO2 and[A]tot. The decrease in [SID] and PCO2 wassuch that neither [H+]nor [HCO3] changedsignificantly with[A]tot.

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2.
Assisted ventilation with pressure support (PSV)or proportional assist (PAV) ventilation has the potential to produceperiodic breathing (PB) during sleep. We hypothesized that PB willdevelop when PSV level exceeds the product of spontaneous tidal volume (VT) and elastance(VTsp · E)but that the actual level at which PB will develop[PSV(PB)] will be influenced by thePCO2 (difference between eupneicPCO2 andCO2 apneic threshold) and by RR[response of respiratory rate (RR) to PSV]. We also wishedto determine the PAV level at which PB develops to assess inherentventilatory stability in normal subjects. Twelve normal subjectsunderwent polysomnography while connected to a PSV/PAV ventilatorprototype. Level of assist with either mode was increased in smallsteps (2-5 min each) until PB developed or the subject awakened.End-tidal PCO2,VT, RR, and airway pressure (Paw) were continuously monitored, and the pressure generated byrespiratory muscle (Pmus) was calculated. The pressure amplification factor (PAF) at the highest PAV level was calculated from[(Paw + Pmus)/Pmus], where Paw is peak Paw  continuous positive airway pressure. PB with central apneas developedin 11 of 12 subjects on PSV. PCO2ranged from 1.5 to 5.8 Torr. Changes in RR with PSV were small andbidirectional (+1.1 to 3.5min1). With use ofstepwise regression, PSV(PB) was significantly correlated withVTsp(P = 0.001), E(P = 0.00009),PCO2 (P = 0.007), and RR(P = 0.006). The final regressionmodel was as follows: PSV(PB) = 11.1 VTsp + 0.3E  0.4 PCO2  0.34 RR  3.4 (r = 0.98). PBdeveloped in five subjects on PAV at amplification factors of1.5-3.4. It failed to occur in seven subjects, despite PAF of upto 7.6. We conclude that 1) aPCO2 apneic threshold exists duringsleep at 1.5-5.8 Torr below eupneicPCO2,2) the development of PB during PSVis entirely predictable during sleep, and3) the inherent susceptibility to PBvaries considerably among normal subjects.

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3.
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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4.
Griffin, M. Pamela. Role for anions in pulmonaryendothelial permeability. J. Appl.Physiol. 83(2): 615-622, 1997.-Adrenergic stimulation reduces albumin permeation across pulmonary artery endothelial monolayers and induces changes in cell morphology that aremediated by Cl flux. Wetested the hypothesis that anion-mediated changes in endothelial cellsresult in changes in endothelial permeability. We measured permeationof radiolabeled albumin across bovine pulmonary arterial endothelialmonolayers when the extracellular anion was Cl,Br,I,F, acetate(Ac), gluconate(G), and propionate(Pr). Permeability toalbumin (Palbumin)was calculated before and after addition of 0.2 mM of thephosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), whichreduces permeability. InCl, thePalbumin was 3.05 ± 0.86 × 106 cm/s andfell by 70% with the addition of IBMX. The initialPalbumin was lowest forPr andAc. InitialPalbumin was higher inBr,I,G, andF than inCl. A permeability ratiowas calculated to examine the IBMX effect. The greatest IBMX effect wasseen when Cl was theextracellular anion, and the order among halide anions wasCl > Br > I > F. Although the level ofextracellular Ca2+ concentration([Ca2+]o)varied over a wide range in the anion solutions,[Ca2+]odid not systematically affect endothelial permeability in this system.When Cl was theextracellular anion, varying[Ca2+]ofrom 0.2 to 2.8 mM caused a change in initialPalbumin but no changein the IBMX effect. The anion channel blockers4-acetamido-4-isothiocyanotostilbene-2,2-disulfonic acid(0.25 mM) and anthracene-9-carboxylic acid (0.5 mM) significantly altered initialPalbumin and the IBMXeffect. The anion transport blockers bumetanide (0.2 mM) and furosemide(1 mM) had no such effects. We conclude that extracellular anionsinfluence bovine pulmonary arterial endothelial permeability and thatthe pharmacological profile fits better with the activity of anionchannels than with other anion transport processes.

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5.
Hardarson, Thorir, Jon O. Skarphedinsson, and TorarinnSveinsson. Importance of the lactate anion in control ofbreathing. J. Appl. Physiol. 84(2):411-416, 1998.The purpose of this study was to examine theeffects of raising the arterialLa andK+ levels on minute ventilation(E) in rats. EitherLa or KCl solutions wereinfused in anesthetized spontaneously breathing Wistar rats to raisethe respective ion arterial concentration ([La] and[K+]) gradually tolevels similar to those observed during strenuous exercise.E, blood pressure, and heart rate wererecorded continuously, and arterial[La],[K+], pH, and bloodgases were repeatedly measured from blood samples. To prevent changesin pH during the Lainfusions, a solution of sodium lactate and lactic acid was used. Raising [La] to13.2 ± 0.6 (SE) mM induced a 47.0 ± 4.0% increase inE without any concomitant changes ineither pH or PCO2. Raising[K+] to 7.8 ± 0.11 mM resulted in a 20.3 ± 5.28% increase inE without changes in pH. Thus ourresults show that Laitself, apart from lactic acidosis, may be important in increasing E during strenuous exercise, and weconfirm earlier results regarding the role of arterial[K+] in the control ofE during exercise.

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6.
The redistributionof blood flow (BF) in the abdominal viscera during right-legged kneeextension-flexion exercise at very low intensity [peak heart rate(HR), 76 beats/min] was examined by using Doppler ultrasound.While sitting, subjects performed a right-legged knee extension-flexionexercise every 6 s for 20 min. BF was measured in the upper abdominalaorta (Ao), right common femoral artery (RCFA), and left common femoralartery (LCFA). Visceral BF(BFVis) was determined by theequation [BFAo  (BFRCFA + BFLCFA)]. A comparisonwith the change in BF (BF) preexercise showed a greater increase inBFRCFA than inBFAo during exercise. Thisresulted in a reduction of BFVisto 56% of its preexercise value or a decrease in flow by 1,147 ± 293 (±SE) ml/min at the peak workload. Oxygen consumptioncorrelated positively withBFAo, BFRCFA, andBFLCFA but inversely withBFVis during exercise andrecovery. Furthermore, BFVis (% of preexercise value) correlated inversely with both an increase in HR(r = 0.89), and percent peakoxygen consumption (r = 0.99).This study demonstrated that, even during very-low-intensity exercise(HR <90 beats/min), there was a significant shift in BF from theviscera to the exercising muscles.  相似文献   

7.
We examined the hypothesis that glucose flux wasdirectly related to relative exercise intensity both beforeand after a 12-wk cycle ergometer training program [5days/wk, 1-h duration, 75% peakO2 consumption(O2 peak)] inhealthy female subjects (n = 17; age23.8 ± 2.0 yr). Two pretraining trials (45 and 65% of O2 peak)and two posttraining trials [same absolute workload (65% of oldO2 peak)and same relative workload (65% of new O2 peak)] wereperformed on nine subjects by using a primed-continuous infusion of[1-13C]- and[6,6-2H]glucose.Eight additional subjects were studied by using[6,6-2H]glucose.Subjects were studied postabsorption for 90 min of rest and 1 h ofcycling exercise. After training, subjects increased O2 peak by 25.2 ± 2.4%. Pretraining, the intensity effect on glucose kinetics wasevident between 45 and 65% ofO2 peak with rates ofappearance (Ra: 4.52 ± 0.25 vs. 5.53 ± 0.33 mg · kg1 · min1),disappearance (Rd: 4.46 ± 0.25 vs. 5.54 ± 0.33 mg · kg1 · min1),and oxidation (Rox: 2.45 ± 0.16 vs. 4.35 ± 0.26 mg · kg1 · min1)of glucose being significantly greater(P  0.05) in the 65% thanin the 45% trial. Training reducedRa (4.7 ± 0.30 mg · kg1 · min1),Rd (4.69 ± 0.20 mg · kg1 · min1),and Rox (3.54 ± 0.50 mg · kg1 · min1)at the same absolute workload (P  0.05). When subjects were tested at the same relative workload,Ra,Rd, andRox were not significantlydifferent after training. However, at both workloads after training,there was a significant decrease in total carbohydrate oxidation asdetermined by the respiratory exchange ratio. These results show thefollowing in young women: 1)glucose use is directly related to exercise intensity;2) training decreasesglucose flux for a given power output;3) when expressed asrelative exercise intensity, training does not affect the magnitude ofblood glucose flux during exercise; but4) training does reduce totalcarbohydrate oxidation.

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8.
Inhibition of carbonic anhydrase (CA) isassociated with a lower plasma lactate concentration([La]pl)during fatiguing exercise. We hypothesized that a lower[La]plmay be associated with faster O2uptake (O2) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz,10 mg/kg body wt iv). On 6 separate days, each subject performed 6-minstep transitions in work rate from 0 to 100 W (below ventilatory threshold,<ET)or to a O2 corresponding to~50% of the difference between the work rate atET and peakO2(>ET).Gas exchange was measured breath by breath. Trials were interpolated at1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (<ET) or athree-component exponential model(>ET).Arterialized venous blood was sampled from a dorsal hand vein andanalyzed for[La]pl.MRT was similar during Con (31.2 ± 2.6 and 32.7 ± 1.2 s for onand off, respectively) and Acz (30.9 ± 3.0 and 31.4 ± 1.5 s for on and off, respectively) for work rates<ET. Atwork rates >ET, MRTwas similar between Con (69.1 ± 6.1 and 50.4 ± 3.5 s for on andoff, respectively) and Acz (69.7 ± 5.9 and 53.8 ± 3.8 s for on and off, respectively). On- and off-MRTs were slower for>ET thanfor <ETexercise.[La]plincreased above 0-W cycling values during<ET and>ET exercise but was lower at the end of the transition during Acz (1.4 ± 0.2 and 7.1 ± 0.5 mmol/l for<ET and>ET,respectively) than during Con (2.0 ± 0.2 and 9.8 ± 0.9 mmol/lfor <ETand >ET,respectively). CA inhibition does not affectO2 utilization at the onset of<ET or>ETexercise, suggesting that the contribution of oxidative phosphorylationto the energy demand is not affected by acute CA inhibition with Acz.

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9.
Dysoxia canbe defined as ATP flux decreasing in proportion toO2 availability with preserved ATPdemand. Hepatic venous -hydroxybutyrate-to-acetoacetate ratio(-OHB/AcAc) estimates liver mitochondrial NADH/NAD and may detectthe onset of dysoxia. During partial dysoxia (as opposed to anoxia),however, flow may be adequate in some liver regions, diluting effluentfrom dysoxic regions, thereby rendering venous -OHB/AcAc unreliable.To address this concern, we estimated tissue ATP whilegradually reducing liver blood flow of swine to zero in a nuclearmagnetic resonance spectrometer. ATP flux decreasing withO2 availability was taken asO2 uptake(O2) decreasing inproportion to O2 delivery(O2);and preserved ATP demand was taken as increasingPi/ATP.O2, tissuePi/ATP, and venous -OHB/AcAcwere plotted againstO2to identify critical inflection points. Tissue dysoxia required meanO2for the group to be critical for bothO2 and forPi/ATP. CriticalO2values for O2 andPi/ATP of 4.07 ± 1.07 and 2.39 ± 1.18 (SE) ml · 100 g1 · min1,respectively, were not statistically significantly different but notclearly the same, suggesting the possibility that dysoxia might havecommenced after O2 begandecreasing, i.e., that there could have been"O2 conformity." CriticalO2for venous -OHB/AcAc was 2.44 ± 0.46 ml · 100 g1 · min1(P = NS), nearly the same as that forPi/ATP, supporting venous -OHB/AcAc as a detector of dysoxia. All issues considered, tissue mitochondrial redox state seems to be an appropriate detector ofdysoxia in liver.

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10.
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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11.
During short-term maximal exercise,horses have impaired pulmonary gas exchange, manifested by diffusionlimitation and arterial hypoxemia, without marked ventilation-perfusion(A/)inequality. Whether gas exchange deteriorates progressively duringprolonged submaximal exercise has not been investigated. Sixthoroughbred horses performed treadmill exercise at ~60% of maximaloxygen uptake until exhaustion (28-39 min). Multipleinert gas, blood-gas, hemodynamic, metabolic rate, and ventilatory datawere obtained at rest and 5-min intervals during exercise. Oxygenuptake, cardiac output, and alveolar-arterialPO2 gradient were unchanged after thefirst 5 min of exercise. Alveolar ventilation increased progressivelyduring exercise, from increased tidal volume and respiratory frequency,resulting in an increase in arterialPO2 and decrease in arterialPCO2. At rest there was minimal A/inequality, log SD of the perfusion distribution (logSD) = 0.20. This doubled by 5 min of exercise (logSD = 0.40) butdid not increase further. There was no evidence of alveolar-end-capillary diffusion limitation during exercise. However, there was evidence for gas-phase diffusion limitation at all time points, and enflurane was preferentially overretained. Horses maintainexcellent pulmonary gas exchange during exhaustive, submaximal exercise. AlthoughA/inequality is greater than at rest, it is less than observed in mostmammals and the effect on gas exchange is minimal.

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12.
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   

13.
Increased ventilation-perfusion(A/)inequality is observed in ~50% of humans during heavy exercise andcontributes to the widening of the alveolar-arterialO2 difference(A-aDO2). Despite extensive investigation, the cause remains unknown. As a firststep to more direct examination of this problem, we developed an animalmodel. Eight Yucatan miniswine were studied at rest and duringtreadmill exercise at ~30, 50, and 85% of maximalO2 consumption (O2 max). Multipleinert-gas, blood-gas, and metabolic data were obtained. TheA-aDO2increased from 0 ± 3 (SE) Torr at rest to 14 ± 2 Torr duringthe heaviest exercise level, but arterialPO2(PaO2) remained at resting levels during exercise. There was normalA/inequality [log SD of the perfusion distribution(log) = 0.42 ± 0.04] at rest, and moderate increases(log = 0.68 ± 0.04, P < 0.0001) wereobserved with exercise. This result was reproducible on a separate day.TheA/inequality changes are similar to those reported in highly trainedhumans. However, in swine, unlike in humans, there was no inert gasevidence for pulmonary end-capillary diffusion limitation during heavyexercise; there was no systematic difference in the measuredPaO2 and the PaO2 as predicted from the inertgases. These data suggest that the pig animal model iswell suited for studying the mechanism of exercise-inducedA/ inequality.

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14.
Wells, U. M., S. Duneclift, and J. G. Widdicombe.H2O2increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin. J. Appl.Physiol. 82(2): 621-631, 1997.Exogenous hydrogenperoxide(H2O2)causes airway epithelial damage in vitro. We have studied the effectsof luminalH2O2in the sheep trachea in vivo on tracheal permeability tolow-molecular-weight hydrophilic (technetium-99m-labeleddiethylenetriamine pentaacetic acid;99mTc-DTPA) and lipophilic([14C]antipyrine;[14C]AP) tracers andon the tracheal vascular response to luminal capsaicin, whichstimulates afferent nerve endings. A tracheal artery was perfused, andtracheal venous blood was collected. H2O2exposure (10 mM) reduced tracheal potential difference(42.0 ± 6.4 mV) to zero. It increased arterial andvenous flows (56.7 ± 6.1 and 57.3 ± 10.0%,respectively; n = 5, P < 0.01, paired t-test) but not tracheal lymph flow(unstimulated flow 5.0 ± 1.2 µl · min1 · cm1,n = 4). DuringH2O2exposure, permeability to 99mTc-DTPA increased from2.6 to 89.7 × 107 cm/s(n = 5, P < 0.05), whereas permeability to[14C]AP (3,312.6 × 107 cm/s,n = 4) was not altered significantly(2,565 × 107cm/s). Luminal capsaicin (10 µM) increased tracheal blood flow (10.1 ± 4.1%, n = 5)and decreased venous 99mTc-DTPAconcentration (19.7 ± 4.0, P < 0.01), and these effects weresignificantly greater after epithelial damage (28.1 ± 6.0 and45.7 ± 4.3%, respectively,P < 0.05, unpairedt-test). Thus H2O2increases the penetration of a hydrophilic tracer into tracheal bloodand lymph but has less effect on a lipophilic tracer. It also enhancesthe effects of luminal capsaicin on blood flow and tracer uptake.

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15.
Cardenas, Victor, Jr., Thomas A. Heming, and Akhil Bidani.Kinetics of CO2 excretion andintravascular pH disequilibria during carbonic anhydrase inhibition.J. Appl. Physiol. 84(2): 683-694, 1998.Inhibition of carbonic anhydrase (CA) activity (activity in redblood cells and activity available on capillary endothelium) results indecrements in CO2 excretion(CO2) and plasma-erythrocyteCO2--H+disequilibrium as blood travels around the circulation. To investigate the kinetics of changes in blood PCO2and pH during progressive CA inhibition, we used our previouslydetailed mathematical model of capillary gas exchange to analyzeexperimental data of CO2 and blood-gas/pH parameters obtained from anesthetized, paralyzed, andmechanically ventilated dogs after treatment with acetazolamide (Actz,0-100 mg/kg iv). Arterial and mixed venous blood samples werecollected via indwelling femoral and pulmonary arterial catheters, respectively. Cardiac output was measured by thermodilution. End-tidal PCO2, as a measure of alveolarPCO2, was obtained from continuousrecords of airway PCO2 above thecarina. Experimental results were analyzed with the aid of amathematical model of lung and tissue-gas exchange. Progressive CAinhibition was associated with stepwise increments in the equilibratedmixed venous-alveolar PCO2 gradient(9, 19, and 26 Torr at 5, 20, and 100 mg/kg Actz, respectively). Themaximum decrements in CO2were 10, 24, and 26% with 5, 20, and 100 mg/kg Actz, respectively,without full recovery ofCO2 at 1 h postinfusion. Equilibrated arterial PCO2overestimated alveolar PCO2, andtissue PCO2 was underestimated by themeasured equilibrated mixed venous bloodPCO2. Mathematical model computations predicted hysteresis loops of the instantaneousCO2--H+relationship and in vivo bloodPCO2-pH relationship due to thefinite reaction times forCO2--H+reactions. The shape of the hysteresis loops was affected by the extentof Actz inhibition of CA in red blood cells and plasma.

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16.
Attenuation of sympathetic vasoconstriction(sympatholysis) in working muscles during dynamic exercise iscontroversial. A potential mechanism is a reduction in-adrenergic-receptor responsiveness. The purpose of this study wasto examine 1- and 2-adrenergic-receptor-mediated vasoconstriction inresting and exercising skeletal muscle using intra-arterial infusionsof selective agonists. Thirteen mongrel dogs were instrumentedchronically with flow probes on the external iliac arteries of bothhindlimbs and a catheter in one femoral artery. The selective1-adrenergic agonist (phenylephrine) or the selective2-adrenergic agonist (clonidine) was infused as a bolusinto the femoral artery catheter at rest and during mild and heavyexercise. Intra-arterial infusions of phenylephrine elicited reductionsin vascular conductance of 76 ± 4, 71 ± 5, and 31 ± 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively.Intra-arterial clonidine reduced vascular conductance by 81 ± 5, 49 ± 4, and 14 ± 2%, respectively. The response tointra-arterial infusion of clonidine was unaffected by surgicalsympathetic denervation. Agonist infusion did not affect eithersystemic blood pressure, heart rate, or blood flow in the contralateraliliac artery. 1-Adrenergic-receptor responsiveness wasattenuated during heavy exercise. In contrast,2-adrenergic-receptor responsiveness was attenuated evenat a mild exercise intensity. These results suggest that the mechanismof exercise sympatholysis may involve reductions in postsynaptic-adrenergic-receptor responsiveness.

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17.
We have recently demonstrated that changes inthe work of breathing during maximal exercise affect leg blood flow andleg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573-1583,1997). Our present study examined the effects of changesin the work of breathing on cardiac output (CO) during maximalexercise. Eight male cyclists [maximalO2 consumption(O2 max):62 ± 5 ml · kg1 · min1]performed repeated 2.5-min bouts of cycle exercise atO2 max. Inspiratorymuscle work was either 1) at controllevels [inspiratory esophageal pressure (Pes): 27.8 ± 0.6 cmH2O],2) reduced via a proportional-assistventilator (Pes: 16.3 ± 0.5 cmH2O), or 3) increased via resistive loads(Pes: 35.6 ± 0.8 cmH2O).O2 contents measured in arterialand mixed venous blood were used to calculate CO via the direct Fickmethod. Stroke volume, CO, and pulmonaryO2 consumption(O2) were not different(P > 0.05) between control andloaded trials atO2 max but were lower(8, 9, and 7%, respectively) than control withinspiratory muscle unloading atO2 max. Thearterial-mixed venous O2difference was unchanged with unloading or loading. We combined thesefindings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effectson the cardiovascular system: 1) upto 14-16% of the CO is directed to the respiratory muscles; and2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.

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18.
Kolka, Margaret A., and Lou A. Stephenson. Effect ofluteal phase elevation in core temperature on forearm blood flow duringexercise. J. Appl. Physiol. 82(4):1079-1083, 1997.Forearm blood flow (FBF) as an index of skinblood flow in the forearm was measured in five healthy women by venousocclusion plethysmography during leg exercise at 80% peak aerobicpower and ambient temperature of 35°C (relative humidity 22%;dew-point temperature 10°C). Resting esophagealtemperature (Tes) was 0.3 ± 0.1°C higher in the midluteal than in the early follicular phase ofthe menstrual cycle (P < 0.05).Resting FBF was not different between menstrual cycle phases. TheTes threshold for onset of skinvasodilation was higher (37.4 ± 0.2°C) in midluteal than inearly follicular phase (37.0 ± 0.1°C; P < 0.05). The slope of the FBF toTes relationship was not different between menstrual cycle phases (14.0 ± 4.2 ml · 100 ml1 · min1 · °C1for early follicular and 16.3 ± 3.2 ml · 100 ml1 · min1 · °C1for midluteal phase). Plateau FBF was higher during exercise inmidluteal (14.6 ± 2.2 ml · 100 ml1 · min1 · °C1)compared with early follicular phase (10.9 ± 2.4 ml · 100 ml1 · min1 · °C1;P < 0.05). The attenuation of theincrease in FBF to Tes occurred when Tes was 0.6°C higher andat higher FBF in midluteal than in early follicular experiments(P < 0.05). In summary, the FBF response is different during exercise in the two menstrual cycle phasesstudied. After the attenuation of the increase in FBF and whileTes was still increasing, thegreater FBF in the midluteal phase may have been due to the effects ofincreased endogenous reproductive endocrines on the cutaneousvasculature.

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19.
VO2 max is associated with ACE genotype in postmenopausal women   总被引:6,自引:0,他引:6  
Relationships have frequently been found betweenangiotensin-converting enzyme (ACE) genotype and various pathologicaland physiological cardiovascular outcomes and functions. Thuswe sought to determine whether ACE genotype affected maximalO2 consumption (O2 max) and maximalexercise hemodynamics in postmenopausal women with different habitualphysical activity levels. Age, body composition, and habitual physicalactivity levels did not differ among ACE genotype groups. However, ACEinsertion/insertion (II) genotype carriers had a 6.3 ml · kg1 · min1higher O2 max(P < 0.05) than the ACEdeletion/deletion (DD) genotype group after accounting for the effectof physical activity levels. The ACE II genotype group also had a 3.3 ml · kg1 · min1higher O2 max(P < 0.05) than the ACEinsertion/deletion (ID) genotype group. The ACE ID group tended to havea higher O2 max thanthe DD genotype group, but the difference was not significant. ACEgenotype accounted for 12% of the variation inO2 max among womenafter accounting for the effect of habitual physical activity levels.The entire difference inO2 max among ACEgenotype groups was the result of differences in maximal arteriovenousO2 difference (a-vDO2).ACE genotype accounted for 17% of the variation in maximal a-vDO2 inthese women. Maximal cardiac output index did not differ whatsoeveramong ACE genotype groups. Thus it appears that ACE genotype accountsfor a significant portion of the interindividual differences inO2 max among thesewomen. However, this difference is the result of genotype-dependentdifferences in maximala-vDO2 andnot of maximal stroke volume and maximal cardiac output.

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20.
The purpose ofthis study was to examine the influence of the type of exercise(running vs. cycling) on the O2uptake (O2) slow component.Ten triathletes performed exhaustive exercise on a treadmill and on acycloergometer at a work rate corresponding to 90% of maximalO2 (90% work rate maximalO2). The duration of thetests before exhaustion was superimposable for both type of exercises(10 min 37 s ± 4 min 11 s vs. 10 min 54 s ± 4 min 47 s forrunning and cycling, respectively). TheO2 slow component (difference between O2 atthe last minute and minute 3 ofexercise) was significantly lower during running compared with cycling(20.9 ± 2 vs. 268.8 ± 24 ml/min). Consequently, there was norelationship between the magnitude of theO2 slow component and thetime to fatigue. Finally, because blood lactate levels at the end of the tests were similar for both running (7.2 ± 1.9 mmol/l) and cycling (7.3 ± 2.4 mmol/l), there was a clear dissociation between blood lactate and the O2slow component during running. These data demonstrate that1) theO2 slow component dependson the type of exercise in a group of triathletes and2) the time to fatigue isindependent of the magnitude of theO2 slow component and bloodlactate concentration. It is speculated that the difference in muscularcontraction regimen between running and cycling could account for thedifference in theO2 slow component.

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