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1.
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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2.
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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3.
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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4.
Diffusional permeability (P) to sucrose(Psuc) andNa+(PNa+)was determined in specimens of rabbit sternal parietal pericardium,which may be obtained without stripping. Specimens were mounted in anUssing apparatus with 3H-labeledsucrose and22Na+in a luminal (L) or interstitial (I) chamber.Psuc was 2.16 ± 0.44 for LI and 2.63 ± 0.45 (SE) × 105 cm/s for IL,i.e., ~10 times smaller than that previously obtained in strippedspecimens of pleura despite the similarity of intercellular junctionsin pericardium and pleural mesothelium of various species. Thesefindings suggest that previousPsuc wasoverestimated because stripping damages the mesothelium.PNa+ (×105 cm/s) was 7.07 ± 0.71 for LI and 7.37 ± 0.69 × 105 cm/s for IL.Measurements were also done with phospholipids, which are adsorbed onthe luminal side of mesothelium in vivo. With phospholipids in L,Psuc was 0.75 ± 0.10 and 0.65 ± 0.08 andPNa+was 3.80 ± 0.32 and 3.76 ± 0.15 × 105 cm/s for LI andIL, respectively, i.e., smaller than without phospholipids.With phospholipids in I (where they are not adsorbed), Psuc (2.33 ± 0.42 × 105 cm/s) andPNa+(7.01 ± 0.45 × 105 cm/s) were similar tothose values without phospholipids. Hence, adsorbed phospholipidsdecrease P of mesothelium. If themesothelium were scraped away from the specimen,Psuc of theconnective tissue would be 13.2 ± 0.76 × 105 cm/s.Psuc of themesothelium, computed fromPsuc of theunscraped and scraped specimens, corrected for the effect of unstirredlayers (2.54 and 19.4 × 105 cm/s, respectively),was 2.92 and 0.74 × 105 cm/s without and withphospholipids, respectively. Hence, most of the resistance to diffusionof the pericardium is provided by the mesothelium.

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5.
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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6.
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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7.
Smaller lungs in women affect exercise hyperpnea   总被引:2,自引:0,他引:2  
We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygenuptake (O2 max): 57 ± 6 ml · kg1 · min1;35-70ml · kg1 · min1]to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age-and height-matched men. The higher maximal workload in highly fit(O2 max > 57 ml · kg1 · min1,n = 14) vs. less-fit(O2 max < 56 ml · kg1 · min1,n = 15) women caused a higher maximalventilation (E) with increased tidal volume (VT)and breathing frequency (fb) atcomparable maximal VT/vitalcapacity (VC). More expiratory flow limitation (EFL; 22 ± 4% ofVT) was also observed duringheavy exercise in highly fit vs. less-fit women, causing higherend-expiratory and end-inspiratory lung volumes and greater usage oftheir maximum available ventilatory reserves.HeO2 (79% He-21%O2) vs. room air exercise trialswere compared (with screens added to equalize external apparatusresistance). HeO2 increasedmaximal expiratory flow rates (20-38%) throughout the range ofVC, which significantly reduced EFL during heavy exercise. When EFL wasreduced with HeO2, VT,fb, andE (+16 ± 2 l/min) weresignificantly increased during maximal exercise. However, in theabsence of EFL (during room air exercise),HeO2 had no effect onE. We conclude that smaller lungvolumes and maximal flow rates for women in general, and especiallyhighly fit women, caused increased prevalence of EFL during heavyexercise, a relative hyperinflation, an increased reliance onfb, and a greater encroachment onthe ventilatory "reserve." Consequently,VT andE are mechanically constrained duringmaximal exercise in many fit women because the demand for highexpiratory flow rates encroaches on the airways' maximum flow-volumeenvelope.

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8.
Zhang, Haibo, Peter Rogiers, Nadia Smail, Ana Cabral,Jean-Charles Preiser, Marie-Odile Peny, and Jean-Louis Vincent.Effects of nitric oxide on blood flow distribution andO2 extraction capabilities duringendotoxic shock. J. Appl. Physiol.83(4): 1164-1173, 1997.The effects of the nitric oxide (NO)synthase inhibitorNG-monomethyl-L-arginine(L-NMMA) and the NO donor3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. L-NMMA infusion(10 mg · kg1 · h1)increased arterial and pulmonary artery pressures and systemic andpulmonary vascular resistances but decreased cardiac index, leftventricular stroke work index, and blood flow to the hepatic, portal,mesenteric, and renal beds. SIN-1 infusion (2 µg · kg1 · min1)increased cardiac index; left ventricular stroke work index; andhepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renalblood flow. The critical O2delivery was similar in the L-NMMA group and in the controlgroup (13.3 ± 1.6 vs. 12.8 ± 3.3 ml · kg1 · min1)but lower in the SIN-1 group (9.1 ± 1.8 ml · kg1 · min1,both P < 0.05). The criticalO2 extraction ratio was alsohigher in the SIN-1 group than in the other groups (58.7 ± 10.6 vs.42.2 ± 7.6% in controls, P < 0.05; 43.0 ± 15.5% inL-NMMA group,P = not significant). We conclude thatNO is not implicated in the alterations inO2 extraction capabilitiesobserved early after endotoxin administration.

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9.
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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10.
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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11.
Absorption from different intestinal segments during exercise   总被引:2,自引:0,他引:2  
Lambert, G. P., R. T. Chang, T. Xia, R. W. Summers, and C. V. Gisolfi. Absorption from different intestinal segments duringexercise. J. Appl. Physiol. 83(1):204-212, 1997.This study evaluated intestinal absorption fromthe first 75 cm of the proximal small intestine during 85 min of cycleexercise [63.6 ± 0.7% peakO2 consumption(O2 peak)]while subjects ingested either an isotonic carbohydrate-electrolytebeverage (CHO-E) or a water placebo (WP). The CHO-E beverage contained117 mM (4%) sucrose, 111 mM (2%) glucose, 18 meqNa+, and 3 meqK+. The two experiments wereperformed a week apart by seven subjects (6 men and 1 woman; meanO2 peak = 53.5 ± 6.5 ml · kg1 · min1).Nasogastric and multilumen tubes were fluoroscopically positioned inthe gastric antrum and duodenojejunum, respectively. Subjects ingested23 ml/kg body weight of the test solution, 20% (383 ± 11 ml) ofthis volume 5 min before exercise and 10% (191 ± 5 ml) every 10 min thereafter. By using the rate of gastric emptying (18.1 ± 1.1 vs. 19.2 ± 0.7 ml/min for WP and CHO-E, respectively) as the rateof intestinal perfusion, intestinal absorption was determined bysegmental perfusion from the duodenum (0-25 cm) and jejunum(25-50 and 50-75 cm). Water flux was different(P < 0.05) between solutions in the0- to 25- and 25- to 50-cm segments for WP vs. CHO-E (30.7 ± 2.7 vs. 15.0 ± 2.9 and 3.8 ± 1.1 vs. 11.9 ± 3.3 ml · cm1 · h1,respectively). Furthermore, water flux differed(P < 0.05) for WP in a comparison ofthe 0- to 25- to the 25- to 50-cm segment. Total solute flux (TSF) wasnot significantly different among segments for a given solution orbetween solutions for a given segment. There was no difference betweentrials for percent change in plasma volume. These results indicate that1) fluid absorption in the proximalsmall intestine depends on the segment studied and2) solution composition cansignificantly effect water absorption rate in differentintestinal segments.

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12.
The purpose ofthis study was to examine the bioenergetics and regulation ofO2 uptake(O2) and force productionin contracting muscle when blood flow was moderately reduced during asteady-state contractile period. Canine gastrocnemius muscle(n = 5) was isolated, and 3-minstimulation periods of isometric, tetanic contractions were elicitedsequentially at rates of 0.25, 0.33, and 0.5 contractions/s (Hz)immediately followed by a reduction of blood flow [ischemic (I)condition] to 46 ± 3% of the value obtained at 0.5 Hz with normal blood flow. TheO2 of thecontracting muscle was significantly (P < 0.05) reduced during the Icondition [6.5 ± 0.8 (SE) ml · 100 g1 · min1]compared with the same stimulation frequency with normal flow (11.2 ± 1.5 ml · 100 g1 · min1),as was the tension-time index (79 ± 12 vs. 123 ± 22 N · g1 · min1,respectively). The ratio ofO2 to tension-time indexremained constant throughout all contraction periods. Musclephosphocreatine concentration, ATP concentration, and lactate effluxwere not significantly different during the I condition compared withthe 0.5-Hz condition with normal blood flow. However, at comparable rates of O2 andtension-time index, muscle phosphocreatine concentration and ATPconcentration were significantly less during the I condition comparedwith normal-flow conditions. These results demonstrate that, in thishighly oxidative muscle, the normal balance ofO2 supply to force output wasmaintained during moderate ischemia by downregulation of forceproduction. In addition,1) the minimal disruption inintracellular homeostasis after the initiation of ischemia waslikely a result of steady-state metabolic conditions having alreadybeen activated, and 2) thedifference in intracellular conditions at comparable rates ofO2 and tension-time index between the normal flow and I condition may have been due to altered intracellular O2 tension.

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13.
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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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.
To evaluate the effects of contractions on thekinetics of uptake and oxidation of palmitate in a physiological musclepreparation, rat hindquarters were perfused with glucose (6 mmol/l),albumin-bound [1-14C]palmitate, andvarying amounts of albumin-bound palmitate (200-2,200 µmol/l) atrest and during muscle contractions. When plotted against the unboundpalmitate concentration, palmitate uptake and oxidation displayedsimple Michaelis-Menten kinetics with estimated maximal velocity(Vmax)and Michaelis-Menten constant(Km) values of42.8 ± 3.8 (SE)nmol · min1 · g1and 13.4 ± 3.4 nmol/l for palmitate uptake and 3.8 ± 0.4 nmol · min1 · g1and 8.1 ± 2.9 nmol/l for palmitate oxidation, respectively, at rest.Whereas muscle contractions increased theVmaxfor both palmitate uptake and oxidation to 91.6 ± 10.1 and 16.5 ± 2.3 nmol · min1 · g1,respectively, theKm remainedunchanged.Vmaxand Km estimates obtained from Hanes-Woolf plots (substrate concentration/velocity vs.substrate concentration) were not significantly different. In theresting perfused hindquarter, an increase in palmitate delivery from31.9 ± 0.9 to 48.7 ± 1.2 µmol · g1 · h1by increasing perfusate flow was associated with a decrease in thefractional uptake of palmitate so that the rates of uptake andoxidation of palmitate remained unchanged. It is concluded that therates of uptake and oxidation of long-chain fatty acids (LCFA) saturatewith an increase in the concentration of unbound LCFA in perfusedskeletal muscle and that muscle contractions, but not an increase inplasma flow, increase theVmaxfor LCFA uptake and oxidation. The data are consistent with the notion that uptake of LCFA in muscle may be mediated in part by a transport system.

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16.
Ward, Michael E. Effect of inhibition of nitric oxidesynthesis on the diaphragmatic microvascular response to hypoxia. J. Appl. Physiol. 81(4):1633-1641, 1996.The purpose of this study was to determine theeffect of inhibition of nitric oxide (NO) release on the diaphragmaticmicrovascular responses to hypoxia. In -chloralose-anesthetizedmongrel dogs, the microcirculation of the vascularly isolated ex vivoleft hemidiaphragm was studied by intravital microscopy. The diaphragmwas pump perfused with blood diverted from the femoral artery through aseries of membrane oxygenators. The responses to supramaximalconcentrations of sodium nitroprusside, moderate hypoxia (phrenicvenous PO2 27 Torr), andsevere hypoxia (phrenic venous PO2 15 Torr) were recorded before and after an infusion ofNG-nitro-L-arginine(L-NNA; 6 × 104 M) into the phreniccirculation for 20 min. Under control conditions, diaphragmatic bloodflow was 12.4 ± 1.1 ml · min1 · 100 g1. Diaphragmatic bloodflows recorded during moderate and severe hypoxia were 15.6 ± 1.2 and 24.3 ± 1.5 ml · min1 · 100 g1, respectively(P < 0.05 for both compared withcontrol values). Treatment withL-NNA reduced diaphragmaticblood flow to 9.6 ± 0.8 ml · min1 · 100 g1 under control conditions(P < 0.05) and caused arteriolarvasoconstriction to a degree that was dependent on vessel size (i.e.,larger vessels constricted more than smaller vessels).L-NNA eliminated the increase inblood flow during moderate hypoxia and inhibited arteriolar dilation byan amount that was related to vessel size (i.e., dilation of largervessels was inhibited more than that of smaller vessels). Inhibition ofNO synthesis had no effect on the increase in diaphragmatic blood flow(23.6 ± 1.9 ml · min1 · 100 g1;P > 0.05 compared with that duringsevere hypoxia before treatment withL-NNA) or arteriolar diametersduring severe hypoxia. NO release plays a role in the diaphragmaticvascular response to hypoxia, but this role is limited to dilation oflarger arterioles during hypoxia of moderate severity.

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17.
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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18.
Fee, Lawrence L., Richard M. Smith, and Michael B. English.Enhanced ventilatory and exercise performance in athletes withslight expiratory resistive loading. J. Appl.Physiol. 83(2): 503-510, 1997.We determined thecardiorespiratory and performance effects of slight (1.5-3.0cmH2O) expiratory resistiveloading (ERL). Twenty-eight highly fit [peakO2 uptake(O2 peak) = 63.6 ± 1.3 ml · kg1 · min1]athletes (age = 33.5 ± 1.3 yr) performed pairedO2 peak cycle ergometer tests (control vs. ERL). End-expiratory lung volume wasseparately determined in a subset of subjects(n = 12) at steady-state 75% maximumpower output (POmax) and wasfound to increase (0.67 ± 0.29 liter) with ERL. In theO2 peaktests, peak expiratory pressure at the mouth, mean inspiratory flow, minute ventilation, and O2 pulsewere greater with ERL at every intensity level (i.e., 75, 80, 85, and90% POmax). Increased minute ventilation was largely due to a trend toward increased tidal volume(P < 0.05 at 80%POmax).O2 uptake was greater at 90%POmax with ERL. IncreasedO2 pulse with ERL at comparativeworkloads suggests that stroke volume was augmented with ERL. Also,with ERL, athletes attained higherO2 peak (63.0 ± 1.4 vs. 60.1 ± 1.3 ml · kg1 · min1)and greater POmax (352.0 ± 9.9 vs. 345.7 ± 9.5 W). We conclude that elevated end-expiratory lungvolume in response to slight ERL during strenuous exercise served toattenuate both airflow and blood flow limitations, which enhancedexercise capacity.

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19.
Henke, Kathe G. Upper airway muscle activity and upperairway resistance in young adults during sleep. J. Appl. Physiol. 84(2): 486-491, 1998.To determinethe relationship between upper airway muscle activity and upper airwayresistance in nonsnoring and snoring young adults, 17 subjects werestudied during sleep. Genioglossus and alae nasi electromyogramactivity were recorded. Inspiratory and expiratory supraglotticresistance (Rinsp and Rexp, respectively) were measured at peak flow,and the coefficients of resistance(Kinsp andKexp,respectively) were calculated. Data were recorded during control,with continuous positive airway pressure (CPAP), and on the breathimmediately after termination of CPAP. Rinsp during control averaged 7 ± 1 and 10 ± 2 cmH2O · l1 · sand Kinspaveraged 26 ± 5 and 80 ± 27 cmH2O · l1 · s2in the nonsnorers and snorers, respectively(P = not significant). Onthe breath immediately after CPAP,Kinsp did notincrease over control in snorers (80 ± 27 for control vs. 46 ± 6 cmH2O · l1 · s2for the breath after CPAP) or nonsnorers (26 ± 5 vs. 29 ± 6 cmH2O · l1 · s2).These findings held true for Rinsp.Kexp did notincrease in either group on the breath immediately after termination ofCPAP. Therefore, 1) increases inupper airway resistance do not occur, despite reductions inelectromyogram activity in young snorers and nonsnorers, and2) increases in Rexp and expiratoryflow limitation are not observed in young snorers.

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20.
Dehydration and hyperthermia may impair gastricemptying (GE) during exercise; the effect of these alterations onintestinal water flux (WF) is unknown. Thus the purpose of this studywas to determine the effect of hypohydration (~2.7% body weight) on GE and WF of a water placebo (WP) during cycling exercise (85 min, 65%maximal oxygen uptake) in a cool environment (22°C) and to alsocompare GE and WF of three carbohydrate-electrolyte solutions (CES)while the subjects were hypohydrated. GE and WF were determined simultaneously by a nasogastric tube placed in the gastric antrum andvia a multilumen tube that spanned the duodenum and the first 25 cm ofjejunum. Hypohydration was attained 12-16 h before experiments bylow-intensity exercise in a hot (45°C), humid (relative humidity 50%) environment. Seven healthy subjects (age 26.7 ± 1.7 yr,maximal oxygen uptake 55.9 ± 8.2 ml · kg1 · min1)ingested either WP or a 6% (330 mosmol), 8% (400 mosmol), or a 9%(590 mosmol) CES the morning following hypohydration. For comparison,subjects ingested WP after a euhydration protocol. Solutions (~2.0liters total) were ingested as a large bolus (4.6 ml/kg body wt) 5 minbefore exercise and as small serial feedings (2.3 ml/kg body wt) every10 min of exercise. Average GE rates were not different amongconditions (P > 0.05). Mean(±SE) values for WF were also similar(P > 0.05) for the euhydration (15.3 ± 1.7 ml · cm1 · h1)and hypohydration (18.3 ± 2.6 ml · cm1 · h1)experiments. During exercise after hypohydration, waterabsorption was greater (P < 0.05)with ingestion of WP (18.3 ± 2.6) and the 6% CES (16.5 ± 3.7),compared with the 8% CES (6.9 ± 1.5) and the 9% CES (1.8 ± 1.7). Mean values for final core temperature (38.6 ± 0.1°C),heart rate (152 ± 1 beats/min), and change in plasma volume(5.7 ± 0.7%) were similar among experimental trials. Weconclude that 1) hypohydration to~3% body weight does not impair GE or fluid absorption duringmoderate exercise when ingesting WP, and2) hyperosmolality (>400 mosmol)reduced WF in the proximal intestine.

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