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1.
The purpose ofthe present study was to determine the separate and combined effects ofaerobic fitness, short-term heat acclimation, and hypohydration ontolerance during light exercise while wearing nuclear, biological, andchemical protective clothing in the heat (40°C, 30% relativehumidity). Men who were moderately fit [(MF); <50ml · kg1 · min1maximal O2 consumption;n = 7] and highly fit[(HF); >55ml · kg1 · min1maximal O2 consumption;n = 8] were tested while theywere euhydrated or hypohydrated by ~2.5% of body mass throughexercise and fluid restriction the day preceding the trials. Tests wereconducted before and after 2 wk of daily heat acclimation (1-htreadmill exercise at 40°C, 30% relative humidity, while wearingthe nuclear, biological, and chemical protective clothing). Heatacclimation increased sweat rate and decreased skin temperature andrectal temperature (Tre) in HF subjects but had no effecton tolerance time (TT). MF subjects increased sweat rate but did notalter heart rate, Tre, or TT. In both MF and HF groups, hypohydration significantly increased Tre and heart rate and decreasedthe respiratory exchange ratio and the TT regardless of acclimationstate. Overall, the rate of rise of skin temperature was less, whileTre, the rate of rise of Tre, and the TTwere greater in HF than in MF subjects. It was concluded thatexercise-heat tolerance in this uncompensable heat-stress environmentis not influenced by short-term heat acclimation but is significantlyimproved by long-term aerobic fitness.

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2.
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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3.
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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4.
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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5.
Nitric oxide and thermoregulation during exercise in the horse   总被引:1,自引:0,他引:1  
Mills, Paul C., David J. Marlin, Caroline M. Scott, andNicola C. Smith. Nitric oxide and thermoregulation during exercise in the horse. J. Appl. Physiol. 82(4):1035-1039, 1997.The effect of inhibition of nitric oxideproduction on sweating rate (SR) and on core, rectal, and tail skintemperatures was measured in five Thoroughbred horses during exerciseof variable intensity on a high-speed treadmill. A standard exercisetest consisting of three canters [~55% maximumO2 uptake(O2 max)], withwalking (~9%O2 max) and trotting(~22% O2 max)between each canter, was performed twice (control or test), in randomorder, by each horse.NG-nitro-L-arginine methyl ester(L-NAME; 20 mg/kg), acompetitive inhibitor of nitric oxide synthase, was infused into thecentral circulation and induced a significant reduction in the SRmeasured on the neck (31.6 ± 6.4 vs. 9.7 ± 4.2 g · min1 · m2;69%) and rump (14.7 ± 5.2 vs. 4.8 ± 1.6 g · min1 · m2;67%) of the horses during canter (P < 0.05). Significant increases in core, rectal, and tailskin temperatures were also measured (P < 0.05).L-Arginine (200 mg/kg iv)partially reversed the inhibitory effects ofL-NAME on SR, but core, rectal,and tail skin temperatures continued to increase(P < 0.05), suggesting a cumulationof body heat. The results support the contention that nitric oxidesynthase inhibition diminishes SR, resulting in elevated core andperipheral temperatures leading to deranged thermoregulation duringexercise. The inhibition of sweating byL-NAME may be related toperipheral vasoconstriction but may also involve the neurogenic controlof sweating.

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6.
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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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.
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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9.
Kinetics of oxygen uptake at the onset of exercise in boys and men   总被引:3,自引:0,他引:3  
The objective of this study was to compare theO2 uptake(O2) kinetics at the onsetof heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cyclingtask to determine peak O2(O2 peak).On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice bycycling at 50%O2 peak for 3.5 min,once by cycling at 100%O2 peak for 2 min,and once by cycling at 130%O2 peak for 75 s.O2 deficit was not significantlydifferent between boys and men (respectively, 50%O2 peak task: 6.6 ± 11.1 vs. 5.5 ± 7.3 ml · min1 · kg1;100% O2 peak task:28.5 ± 8.1 vs. 31.8 ± 6.3 ml · min1 · kg1;and 130%O2 peaktask: 30.1 ± 5.7 vs. 35.8 ± 5.3 ml · min1 · kg1).To assess the kinetics, phase I was excluded from analysis. Phase IIO2 kinetics could bedescribed in all cases by a monoexponential function. ANOVA revealed nodifferences in time constants between boys and men (respectively, 50%O2 peaktask: 22.8 ± 5.1 vs. 26.4 ± 4.1 s; 100%O2 peak task: 28.0 ± 6.0 vs. 28.1 ± 4.4 s; and 130%O2 peak task: 19.8 ± 4.1 vs. 20.7 ± 5.7 s). In conclusion, O2 deficit and fast-componentO2 on-transientsare similar in boys and men, even at high exercise intensities, whichis in contrast to the findings of other studies employing simplermethods of analysis. The previous interpretation that children relyless on nonoxidative energy pathways at the onset of heavy exercise isnot supported by our findings.

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10.
Katz, Stuart D., Jeannette Yuen, Rachel Bijou, and ThierryH. LeJemtel. Training improves endothelium-dependent vasodilation in resistance vessels of patients with heart failure.J. Appl. Physiol. 82(5):1488-1492, 1997.The effects of physical training onendothelium-dependent vasodilation in skeletal muscle resistance vessels were investigated in patients with heart failure. Forearm bloodflows(ml · min1 · 100 ml1) in response tobrachial arterial administration of acetylcholine (5 × 105 and 5 × 104 M at 1 ml/min) andnitroglycerin (5 × 106 and 5 × 105 M at 1 ml/min) weredetermined by strain-gauge venous occlusion plethysmography before andafter 8 wk of daily handgrip exercise in 12 patients with chronic heartfailure. After 8 wk of daily handgrip exercise, the vasodilatoryresponses to acetylcholine significantly increased from pretrainingvalues, i.e., 16.6 ± 2.0 vs. 8.6 ± 1.3 ml · min1 · 100 ml1(P < 0.05) and 27.5 ± 1.5 vs. 14.6 ± 1.7 ml · min1 · 100 ml1(P < 0.05), respect- ively,whereas the vasodilatory responses to nitroglycerin did notchange. Handgrip exercise training appears to specificallyenhance endothelium-dependent vasodilation in the forearm skeletalmuscle circulation of patients with heart failure.

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11.
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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12.
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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13.
To analyze the effect of hyperthermia on thevascular response, the isometric response of isolated rabbit femoralartery segments was recorded at 37°C and hyperthermia (41 and44°C). Contraction to potassium (5 × 103-5 × 102 M) was significantlygreater at 41 and 44 than at 37°C and increased by inhibition ofnitric oxide (NO) synthesis withN-nitro-L-arginine(L-NNA;104 M) or endotheliumremoval at 37°C but not at 41 or 44°C. Norepinephrine (109-104M) produced a concentration-dependent contraction greater at 41 or 44 than at 37°C and not modified by endothelium removal orL-NNA at either temperature.Phenylephrine(109-104M) produced a contraction increased by warming to 44°C but not to41°C. The specific2-adrenoceptor agonist BHT-920produced a weak contraction, reduced by the1-adrenoceptor antagonist prazosin (106 M) andincreased at 44°C but not at 41°C. The concentration-dependent contraction to endothelin-1 (ET-1;1011-107M) was increased by warming to 41 and 44°C and by endothelium removal or L-NNA at 37°C butnot at 41 or 44°C. Response to ET-1 was reduced by endothelinETA-receptor antagonist BQ-123(105 M) andETB-receptor antagonist BQ-788(105 M). In arteriesprecontracted with ET-1(108-3 × 108 M), relaxation tosodium nitroprusside(108-104M) was increased at 41 and 44°C vs. at 37°C, but that of ACh (108-104M) or adenosine(108-104M) was not different at all temperatures studied. Relaxation to ACh,but not adenosine, was reduced similarly byL-NNA at all temperaturesstudied. These results suggest hyperthermia in muscular arteries mayinhibit production of, and increase dilatation to, NO, resulting inunchanged relaxation to ACh and increased constriction to KCl and ET-1,and may increase constriction to stimulation of1-adrenoceptors byNO-independent mechanisms.

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14.
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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15.
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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16.
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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17.
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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18.
Volek, Jeff S., William J. Kraemer, Jill A. Bush, ThomasIncledon, and Mark Boetes. Testosterone and cortisol inrelationship to dietary nutrients and resistance exercise.J. Appl. Physiol. 82(1): 49-54, 1997.Manipulation of resistance exercise variables (i.e., intensity,volume, and rest periods) affects the endocrine response to exercise;however, the influence of dietary nutrients on basal andexercise-induced concentrations of hormones is less understood. Thepresent study examined the relationship between dietary nutrients andresting and exercise-induced blood concentrations of testosterone (T)and cortisol (C). Twelve men performed a bench press exercise protocol(5 sets to failure using a 10-repetitions maximum load) and a jumpsquat protocol (5 sets of 10 repetitions using 30% of each subject's1-repetition maximum squat) with 2 min of rest between all sets. Ablood sample was obtained at preexercise and 5 min postexercise fordetermination of serum T and C. Subjects also completed detaileddietary food records for a total of 17 days. There was a significant(P  0.05) increase in postexercise Tcompared with preexercise values for both the bench press (7.4%) andjump squat (15.1%) protocols; however, C was not significantly different from preexercise concentrations. Significantcorrelations were observed between preexercise T and percent energyprotein (r = 0.71), percentenergy fat (r = 0.72), saturated fattyacids (g · 1,000 kcal1 · day1;r = 0.77), monounsaturated fatty acids(g · 1,000 kcal1 · day1;r = 0.79), the polyunsaturatedfat-to-saturated fat ratio (r = 0.63), and the protein-to-carbohydrate ratio (r = 0.59). There were nosignificant correlations observed between any nutritional variables andpreexercise C or the absolute increase in T and C after exercise. Thesedata confirm that high-intensity resistance exercise results inelevated postexercise T concentrations. A more impressive finding wasthat dietary nutrients may be capable of modulating restingconcentrations of T.

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19.
The effects of exercise training on hepaticfunction in horses were determined by studying the plasma clearance ofantipyrine (20 mg/kg iv) in adult mares that either underwent treadmilltraining for 5 wk (n = 7) or remainedin box stalls for the same time period (n = 6). Training consisted oftreadmill exercise at 60% (12 min/day) and 90% (3 min/day) ofpretraining maximal oxygen consumption (O2 max) for 6 days/wk for 5 wk.O2 max andvelocity to obtain a blood lactate concentration of 4 mmol/l weresignificantly increased (from 129 to 149 ml · min1 · kg1and from 5.6 to 6.1 m/s, respectively) as a result of training. Theplasma clearance and volume of distribution of antipyrine increasedsignificantly in the trained group (from 5.5 to 6.4 ml · min1 · kg1and from 813 to 881 ml/kg, respectively) and decreased significantly inthe untrained group. Elimination half-lives did not change as a resultof training or box rest. Increases in plasma antipyrine clearance wereindicative of an increase in hepatic metabolism of antipyrine.Increases in the volume of distribution of antipyrine suggest thattotal body water increases as a result of exercise training.

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20.
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   

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