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1.
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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2.
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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3.
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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4.
Parker, James C., Chris B. Cave, Jeffrey L. Ardell, CharlesR. Hamm, and Susan G. Williams. Vascular treestructure affects lung blood flow heterogeneity simulated in threedimensions. J. Appl. Physiol. 83(4):1370-1382, 1997.Pulmonary arterial tree structures related toblood flow heterogeneity were simulated by using a symmetrical,bifurcating model in three-dimensional space. The branch angle (),daughter-parent length ratio(rL), branchrotation angle (), and branch fraction of parent flow () for asingle bifurcation were defined and repeated sequentially through 11 generations. With  fixed at 90°, tree structures were generatedwith  between 60 and 90°,rL between 0.65 and 0.85, and an initial segment length of 5.6 cm and sectioned into1-cm3 samples for analysis. Bloodflow relative dispersions (RD%) between 52 and 42% and fractaldimensions (Ds)between 1.20 and 1.15 in 1-cm3samples were observed even with equal branch flows. When  0.5, RD% increased, butDs eitherdecreased with gravity bias of higher branch flows or increased withrandom assignment of higher flows. Blood flow gradients along gravityand centripetal vectors increased with biased flow assignment of higherflows, and blood flows correlated negatively with distance only when   0.5. Thus a recursive branching vascular tree structuresimulated Ds andRD% values for blood flow heterogeneity similar to those observedexperimentally in the pulmonary circulation due to differences in thenumber of terminal arterioles per1-cm3 sample, but blood flowgradients and a negative correlation of flows with distance requiredunequal partitioning of blood flows at branchpoints.

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5.
Fitzgerald, Margaret D., Hirofumi Tanaka, Zung V. Tran, andDouglas R. Seals. Age-related declines in maximal aerobic capacityin regularly exercising vs. sedentary women: a meta-analysis. J. Appl. Physiol. 83(1): 160-165, 1997.Our purpose was to determine the relationship between habitualaerobic exercise status and the rate of decline in maximal aerobiccapacity across the adult age range in women. A meta-analytic approachwas used in which mean maximal oxygen consumption(O2 max) values fromfemale subject groups (ages 18-89 yr) were obtained from thepublished literature. A total of 239 subject groups from 109 studiesinvolving 4,884 subjects met the inclusion criteria and werearbitrarily separated into sedentary (groups = 107; subjects = 2,256),active (groups = 69; subjects = 1,717), and endurance-trained (groups = 63; subjects = 911) populations.O2 max averaged 29.7 ± 7.8, 38.7 ± 9.2, and 52.0 ± 10.5 ml · kg1 · min1,respectively, and was inversely related to age within each population (r = 0.82 to 0.87, allP < 0.0001). The rate of decline inO2 max withincreasing subject group age was lowest in sedentary women (3.5ml · kg1 · min1· decade1), greater inactive women (4.4ml · kg1 · min1· decade1), andgreatest in endurance-trained women (6.2ml · kg1 · min1 · decade1)(all P < 0.001 vs. each other). Whenexpressed as percent decrease from mean levels at age ~25 yr, therates of decline inO2 max were similarin the three populations (10.0 to 10.9%/decade). Therewas no obvious relationship between aerobic exercise status and therate of decline in maximal heart rate with age. The results of thiscross-sectional study support the hypothesis that, in contrast to theprevailing view, the rate of decline in maximal aerobic capacity withage is greater, not smaller, in endurance-trained vs. sedentary women.The greater rate of decline inO2 max in endurance-trained populations may be related to their higher values asyoung adults (baseline effect) and/or to greater age-related reductions in exercise volume; however, it does not appear to berelated to a greater rate of decline in maximal heart rate with age.

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6.
To evaluatewhether interferon- (IFN-) is involved in the interaction betweenthe immune and endocrine systems in vivo, we studied six healthysubjects twice in a placebo-controlled trial: once after administrationof recombinant human IFN- and, on another occasion, afteradministration of saline. The rate of appearance of glucose wasdetermined by infusion of[6,6-2H2]glucoseand resting energy expenditure by indirect calorimetry. Human leukocyteantigen-DR gene expression on monocytes and serum neopterin increased after administration of IFN-(P < 0.05 vs. control). IFN-increased serum interleukin-6 levels significantly. Levels of tumornecrosis factor- remained below detection limits. IFN- increasedplasma concentrations of ACTH and cortisol(P < 0.05 vs. control), IFN- didnot alter concentrations of growth hormone,(nor)epinephrine, insulin, C peptide, glucagon, or insulin-like growthfactor I. IFN- did not alter plasma concentrations of glucose andfree fatty acids nor the rate of appearance of glucose. IFN-increased resting energy expenditure significantly. We conclude thatIFN- is a minor stimulator of the endocrine and metabolic pathways.Therefore, IFN- by itself is probably not a major mediator in theinteraction between the immune and the endocrine and metabolic systems.  相似文献   

7.
Repetitiveisometric tetanic contractions (1/s) of the caninegastrocnemius-plantaris muscle were studied either at optimal length(Lo) or shortlength (Ls;~0.9 · Lo),to determine the effects of initial length on mechanical and metabolicperformance in situ. Respective averages of mechanical and metabolicvariables were(Lo vs.Ls, allP < 0.05) passive tension (preload) = 55 vs. 6 g/g, maximal active tetanic tension(Po) = 544 vs. 174 (0.38 · Po)g/g, maximal blood flow () = 2.0 vs. 1.4 ml · min1 · g1,and maximal oxygen uptake(O2) = 12 vs. 9 µmol · min1 · g1.Tension at Lodecreased to0.64 · Po over20 min of repetitive contractions, demonstrating fatigue; there were nosignificant changes in tension atLs. In separatemuscles contracting atLo, was set to that measured atLs (1.1 ml · min1 · g1),resulting in decreased O2(7 µmol · min1 · g1),and rapid fatigue, to0.44 · Po. Thesedata demonstrate that 1)muscles at Lohave higher andO2 values than those at Ls;2) fatigue occurs atLo with highO2, adjusting metabolic demand (tension output) to match supply; and3) the lack of fatigue atLs with lowertension, , andO2 suggestsadequate matching of metabolic demand, set low by shortmuscle length, with supply optimized by low preload. Thesedifferences in tension andO2 betweenLo andLs groupsindicate that muscles contracting isometrically at initial lengthsshorter than Loare working under submaximal conditions.

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8.
Tyler, Catherine M., Lorraine C. Golland, David L. Evans,David R. Hodgson, and Reuben J. Rose. Changes in maximum oxygenuptake during prolonged training, overtraining, and detraining inhorses. J. Appl. Physiol. 81(5):2244-2249, 1996.Thirteen standardbred horses were trained asfollows: phase 1 (endurance training, 7 wk),phase 2 (high-intensity training, 9 wk),phase 3 (overload training, 18 wk), andphase 4 (detraining, 12 wk). Inphase 3, the horses were divided intotwo groups: overload training (OLT) and control (C). The OLT groupexercised at greater intensities, frequencies, and durations than groupC. Overtraining occurred after 31 wk of training and was defined as asignificant decrease in treadmill run time in response to astandardized exercise test. In the OLT group, there was a significantdecrease in body weight (P < 0.05).From pretraining values of 117 ± 2 (SE)ml · kg1 · min1,maximal O2 uptake(O2 max) increased by15% at the end of phase 1, and when signs of overtraining werefirst seen in the OLT group,O2 max was 29%higher (151 ± 2 ml · kg1 · min1in both C and OLT groups) than pretraining values. There was nosignificant reduction inO2 max until after 6 wk detraining whenO2 max was 137 ± 2 ml · kg1 · min1.By 12 wk detraining, meanO2 max was134 ± 2 ml · kg1 · min1,still 15% above pretraining values. When overtraining developed, O2 max was notdifferent between C and OLT groups, but maximal values forCO2 production (147 vs. 159 ml · kg1 · min1)and respiratory exchange ratio (1.04 vs. 1.11) were lower in the OLTgroup. Overtraining was not associated with a decrease inO2 max and, afterprolonged training, decreases inO2 max occurredslowly during detraining.

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9.
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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10.
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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11.
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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12.
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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13.
Tanaka, Hirofumi, Christopher A. DeSouza, Pamela P. Jones,Edith T. Stevenson, Kevin P. Davy, and Douglas R. Seals. Greater rate of decline in maximal aerobic capacity with age in physically active vs. sedentary healthy women. J. Appl.Physiol. 83(6): 1947-1953, 1997.Using ameta-analytic approach, we recently reported that the rate of declinein maximal oxygen uptake(O2 max) with age inhealthy women is greatest in the most physically active and smallest inthe least active when expressed in milliliters per kilogram per minuteper decade. We tested this hypothesis prospectively underwell-controlled laboratory conditions by studying 156 healthy, nonobesewomen (age 20-75 yr): 84 endurance-trained runners (ET) and 72 sedentary subjects (S). ET were matched across the age range forage-adjusted 10-km running performance. Body mass was positivelyrelated with age in S but not in ET. Fat-free mass was not differentwith age in ET or S. Maximal respiratory exchange ratio and rating ofperceived exertion were similar across age in ET and S, suggestingequivalent voluntary maximal efforts. There was a significant butmodest decline in running mileage, frequency, and speed with advancingage in ET.O2 max(ml · kg1 · min1)was inversely related to age (P < 0.001) in ET (r = 0.82) and S(r = 0.71) and was higher atany age in ET. Consistent with our meta-analysic findings,the absolute rate of decline inO2 max was greater inET (5.7ml · kg1 · min1 · decade1)compared with S (3.2 ml · kg1 · min1 · decade1;P < 0.01), but the relative (%)rate of decline was similar (9.7 vs 9.1%/decade; notsignificant). The greater absolute rate of decline inO2 max in ET comparedwith S was not associated with a greater rate of decline in maximalheart rate (5.6 vs. 6.2beats · min1 · decade1),nor was it related to training factors. The present cross-sectional findings provide additional evidence that the absolute, but not therelative, rate of decline in maximal aerobic capacity with age may begreater in highly physically active women compared with theirsedentary healthy peers. This difference does not appear to be relatedto age-associated changes in maximal heart rate, bodycomposition, or training factors.

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14.
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   

15.
Training-induced alterations of glucose flux in men   总被引:5,自引:0,他引:5  
Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl.Physiol. 82(4): 1360-1369, 1997.We examined thehypothesis that glucose flux was directly related to relative exerciseintensity both before and after a 10-wk cycle ergometer trainingprogram in 19 healthy male subjects. Two pretraining trials [45and 65% of peak O2 consumption(O2 peak)] andtwo posttraining trials (same absolute and relative intensities as 65%pretraining) were performed for 90 min of rest and 1 h of cyclingexercise. After training, subjects increasedO2 peak by9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance(Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg · kg1 · min1),disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg · kg1 · min1),oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg · kg1 · min1),and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml · kg1 · min1)of glucose being significantly greater(P  0.05) in the 65% than the 45%O2 peak trial. WhenRd was expressed as a percentage of total energy expended per minute(Rd E), there was nodifference between the 45 and 65% intensities. Training did reduceRa (4.63 ± 0.25),Rd (4.65 ± 0.24),Rox (3.77 ± 0.43), andRd E (15.30 ± 0.40 to12.85 ± 0.81) when subjects were tested at the same absolute workload (P  0.05). However, whenthey were tested at the same relative workload,Ra,Rd, andRd E were not different,although Rox was lowerposttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P  0.05). These results show1) glucose use is directly relatedto exercise intensity; 2) trainingdecreases glucose flux for a given power output;3) when expressed as relativeexercise intensity, training does not affect the magnitude of bloodglucose use during exercise; 4)training alters the pathways of glucose disposal.

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16.
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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17.
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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18.
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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19.
Isono, Shiroh, Thom R. Feroah, Eric A. Hajduk, Rollin Brant,William A. Whitelaw, and John E. Remmers. Interaction ofcross-sectional area, driving pressure, and airflow of passive velopharynx. J. Appl. Physiol. 83(3):851-859, 1997.Previous studies have shown that, when thepharyngeal muscles are relaxed, the velopharynx is a highly compliantsegment of the pharynx. Thus, under these circumstances,cross-sectional area of the velopharynx (AVP), drivingpressure across the velopharynx (P), and inspiratory airflow(I) willbe mutually interdependent variables. The purpose of the presentinvestigation was to describe the interrelation among these threevariables during inspiration. We studied 15 sleeping patients withobstructive sleep apnea/hypopnea when the pharyngeal muscles wererendered hypotonic by applying continuous positive airway pressure tothe nasal airway.AVP, determined by endoscopic imaging, was significantly greater at onset ofI limitationthan at minimum oropharyngeal pressure(P < 0.01). Snoring was neverobserved duringIlimitation. In a subgroup of six patients, values for P,I, andAVP were obtainedat 0.1-s intervals at various levels of mask pressure. For these sixpatients, the mathematical expressionI = 0.657(AVP/Amax) · P0.332,where Amax ismaximal AVP,described the relationship among the three variables(R2 = 0.962) forflow-limited and non-flow-limited inspirations. The impedance of thepassive velopharynx, defined asP0.33/,was inversely related toAVP and increaseddramatically when AVP was <0.3cm2. In summary, we observed aprogressive decrease inAVP during flow-limited inspiration in patients with obstructive sleep apnea. Thisconstriction of the velopharynx contributes to an increase invelopharyngeal impedance that, in turn, counterbalances the increase inP during flow limitation.

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20.
The accumulation ofvisceral fat is independently associated with an increased risk forcardiovascular disease. The aim of this study was to determine whetherthe loss of visceral adipose tissue area (VAT; computed tomography) isrelated to improvements in maximal O2 uptake(O2 max) during a weight loss(250-350 kcal/day deficit) and walking (3 days/wk, 30-40 min)intervention. Forty obese [body fat 47 ± 1 (SE) %], sedentary(O2 max 19 ± 1 ml · kg1 · min1)postmenopausal women (age 62 ± 1 yr) participated in the study. The intervention resulted in significant declines in body weight (8%), total fat mass (dual-energy X-ray absorptiometry; 17%), VAT(17%), and subcutaneous adipose tissue area (17%) with no changein lean body mass (all P < 0.001). Women with anaverage 10% increase in O2 max reducedVAT by an average of 20%, whereas those who did not increaseO2 max decreased VAT by only 10%,despite comparable reductions in body fat, fat mass, and subcutaneousadipose tissue area. The decrease in VAT was independently related tothe change in O2 max(r2 = 0.22; P < 0.01) andfat mass (r2 = 0.08; P = 0.05). These data indicate that greater improvements inO2 max with weight loss and walking areassociated with greater reductions in visceral adiposity in obesepostmenopausal women.

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