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

4.
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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5.
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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6.
Gosselin, Luc E., David Megirian, Joshua Rodman, DonnaMueller, and Gaspar A. Farkas. Respiratory muscle reserve in ratsduring heavy exercise. J. Appl.Physiol. 83(4): 1405-1409, 1997.The extent towhich the respiratory pump muscles limit maximal aerobic capacity inquadrupeds is not entirely clear. To examine the effect of reducedrespiratory muscle reserve on aerobic capacity, whole bodypeak oxygen consumption(O2 peak) wasmeasured in healthy Sprague-Dawley rats before and after Sham,unilateral, or bilateral hemidiaphragm denervation (Dnv) surgery.O2 peak wasdetermined by using a graded treadmill running test.Hemidiaphragm paralysis was verified after testing byrecording the absence of electromyographic activity duringinspiration. Before surgery, O2 peak averaged 86, 87, and 92 ml · kg1 · min1for the Sham, unilateral, and bilateral Dnv groups, respectively. Twoweeks after surgery, there was no significant change inO2 peak foreither the Sham or unilateral Dnv group. However,O2 peak decreased~19% in the bilateral Dnv group 2 wk after surgery. These findingsstrongly suggest that the pulmonary system in rats is designed suchthat during heavy exercise, the remaining respiratory pump muscles areable to compensate for the loss of one hemidiaphragm, but not of both.

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7.
VO2 max is associated with ACE genotype in postmenopausal women   总被引:6,自引:0,他引:6  
Relationships have frequently been found betweenangiotensin-converting enzyme (ACE) genotype and various pathologicaland physiological cardiovascular outcomes and functions. Thuswe sought to determine whether ACE genotype affected maximalO2 consumption (O2 max) and maximalexercise hemodynamics in postmenopausal women with different habitualphysical activity levels. Age, body composition, and habitual physicalactivity levels did not differ among ACE genotype groups. However, ACEinsertion/insertion (II) genotype carriers had a 6.3 ml · kg1 · min1higher O2 max(P < 0.05) than the ACEdeletion/deletion (DD) genotype group after accounting for the effectof physical activity levels. The ACE II genotype group also had a 3.3 ml · kg1 · min1higher O2 max(P < 0.05) than the ACEinsertion/deletion (ID) genotype group. The ACE ID group tended to havea higher O2 max thanthe DD genotype group, but the difference was not significant. ACEgenotype accounted for 12% of the variation inO2 max among womenafter accounting for the effect of habitual physical activity levels.The entire difference inO2 max among ACEgenotype groups was the result of differences in maximal arteriovenousO2 difference (a-vDO2).ACE genotype accounted for 17% of the variation in maximal a-vDO2 inthese women. Maximal cardiac output index did not differ whatsoeveramong ACE genotype groups. Thus it appears that ACE genotype accountsfor a significant portion of the interindividual differences inO2 max among thesewomen. However, this difference is the result of genotype-dependentdifferences in maximala-vDO2 andnot of maximal stroke volume and maximal cardiac output.

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8.
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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9.
Chilibeck, P. D., D. H. Paterson, D. A. Cunningham, A. W. Taylor, and E. G. Noble. Muscle capillarization,O2 diffusion distance, andO2 kinetics in old andyoung individuals. J. Appl. Physiol.82(1): 63-69, 1997.The relationships between muscle capillarization, estimated O2diffusion distance from capillary to mitochondria, andO2 uptake(O2) kineticswere studied in 11 young (mean age, 25.9 yr) and 9 old (mean age, 66.0 yr) adults. O2kinetics were determined by calculating the time constants () forthe phase 2 O2 adjustment to andrecovery from the average of 12 repeats of a 6-min, moderate-intensityplantar flexion exercise. Muscle capillarization was determined fromcross sections of biopsy material taken from lateral gastrocnemius.Young and old groups had similarO2 kinetics(O2-on = 44 vs. 48 s;O2-off = 33 vs. 44 s, for young and old, respectively), muscle capillarization, andestimated O2 diffusion distances.Muscle capillarization, expressed as capillary density or averagenumber of capillary contacts per fiber/average fiber area, and theestimates of diffusion distance were significantly correlated toO2-off kinetics in theyoung (r = 0.68 to 0.83;P < 0.05). We conclude that1) capillarization andO2 kinetics during exerciseof a muscle group accustomed to everyday activity (e.g., walking) arewell maintained in old individuals, and2) in the young, recovery of O2 after exercise isfaster, with a greater capillary supply over a given muscle fiber areaor shorter O2 diffusion distances.

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10.
Men with chronic heart failure (CHF) have alterationsin their skeletal muscle that are partially responsible for a decreased exercise tolerance. The purpose of this study was to investigate whether skeletal muscle alterations in women with CHF are similar tothose observed in men and if these alterations are related to exerciseintolerance. Twenty-five men and thirteen women with CHFperformed a maximal exercise test for evaluation of peak oxygen consumption (O2) and resting leftventricular ejection fraction, after which a biopsy of the vastuslateralis was performed. Twenty-one normal subjects (11 women, 10 men)were also studied. The relationship between muscle markers and peakO2 was consistent for CHF men and women.When controlling for gender, analysis showed that oxidative enzymes andcapillary density are the best predictors of peak O2. These results indicatethat aerobically matched CHF men and women have no differences inskeletal muscle biochemistry and histology. However, when CHF groupswere separated by peak exercise capacity of 4.5 metabolic equivalents(METs), CHF men with peak O2 >4.5METs had increased citrate synthase and 3-hydroxyacyl-CoA dehydrogenasecompared with CHF men with peak O2 <4.5METs. CHF men with a lower peak O2 hadincreased capillary density compared with men with higher peakO2. These observations were notreproduced in CHF women. This suggests that differences may existin how skeletal muscle adapts to decreasing peakO2 in patients with CHF.

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11.
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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12.
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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13.
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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14.
Barstow, Thomas J., Andrew M. Jones, Paul H. Nguyen, andRichard Casaburi. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.J. Appl. Physiol. 81(4):1642-1650, 1996.We tested the hypothesis that the amplitude ofthe additional slow component ofO2 uptake(O2) during heavy exerciseis correlated with the percentage of type II (fast-twitch) fibers inthe contracting muscles. Ten subjects performed transitions to a workrate calculated to require aO2 equal to 50% betweenthe estimated lactate (Lac) threshold and maximalO2 (50%).Nine subjects consented to a muscle biopsy of the vastus lateralis. Toenhance the influence of differences in fiber type among subjects,transitions were made while subjects were pedaling at 45, 60, 75, and90 rpm in different trials. Baseline O2 was designed to besimilar at the different pedal rates by adjusting baseline work ratewhile the absolute increase in work rate above the baseline was thesame. The O2 response after the onset of exercise was described by a three-exponential model. Therelative magnitude of the slow component at the end of 8-min exercisewas significantly negatively correlated with %type I fibers at everypedal rate (r = 0.64 to 0.83, P < 0.05-0.01). Furthermore,the gain of the fast component forO2 (asml · min1 · W1)was positively correlated with the %type I fibers across pedal rates(r = 0.69-0.83). Increase inpedal rate was associated with decreased relative stress of theexercise but did not affect the relationships between%fiber type and O2parameters. The relative contribution of the slow component was alsosignificantly negatively correlated with maximalO2(r = 0.65), whereas the gainfor the fast component was positively associated(r = 0.68-0.71 across rpm). Theamplitude of the slow component was significantly correlated with netend-exercise Lac at all four pedal rates(r = 0.64-0.84), but Lac was notcorrelated with %type I (P > 0.05).We conclude that fiber type distribution significantly affects both thefast and slow components ofO2 during heavy exerciseand that fiber type and fitness may have both codependent andindependent influences on the metabolic and gas-exchange responses toheavy exercise.

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15.
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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16.
Hepple, R. T., S. L. M. Mackinnon, J. M. Goodman, S. G. Thomas, and M. J. Plyley. Resistance and aerobic training in oldermen: effects onO2 peak and thecapillary supply to skeletal muscle. J. Appl.Physiol. 82(4): 1305-1310, 1997.Both aerobic training (AT) and resistance training (RT) may increase aerobic power(O2 peak) in theolder population; however, the role of changes in the capillary supplyin this response has not been evaluated. Twenty healthymen (age 65-74 yr) engaged in either 9 wk of lower body RTfollowed by 9 wk of AT on a cycle ergometer (RTAT group) or 18 wk of AT on a cycle ergometer (ATAT group). RT was performedthree times per week and consisted of three sets of four exercises at6-12 repetitions maximum. AT was performed threetimes per week for 30 min at 60-70% heart ratereserve. O2 peak was increasedafter both RT and AT (P < 0.05).Biopsies (vastus lateralis) revealed that the number of capillaries per fiber perimeter length was increased after both AT and RT(P < 0.05), paralleling the changesin O2 peak, whereascapillary density was increased only after AT(P < 0.01). These results, and thefinding of a significant correlation between the change in capillarysupply and O2 peak(r = 0.52), suggest the possibility that similar mechanisms may be involved in the increase ofO2 peak afterhigh-intensity RT and AT in the older population.

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17.
Proctor, David N., Kenneth C. Beck, Peter H. Shen, Tamara J. Eickhoff, John R. Halliwill, and Michael J. Joyner. Influence ofage and gender on cardiacoutput-O2 relationshipsduring submaximal cycle ergometry. J. Appl.Physiol. 84(2): 599-605, 1998.It is presentlyunclear how gender, aging, and physical activity status interact todetermine the magnitude of the rise in cardiac output(c) during dynamic exercise. To clarify this issue,the present study examined thec-O2 uptake(O2) relationship duringgraded leg cycle ergometry in 30 chronically endurance-trained subjects from four groups (n = 6-8/group): younger men (20-30 yr), older men (56-72yr), younger women (24-31 yr), and older women(51-72 yr). c (acetylene rebreathing), strokevolume (c/heart rate), and whole bodyO2 were measured at restand during submaximal exercise intensities (40, 70, and ~90% of peakO2). Baseline restinglevels of c were 0.6-1.2 l/min less in theolder groups. However, the slopes of thec-O2relationship across submaximal levels of cycling were similar among allfour groups (5.4-5.9 l/l). The absolute cassociated with a given O2(1.0-2.0 l/min) was also similar among groups. Resting andexercise stroke volumes (ml/beat) were lower in women than in men butdid not differ among age groups. However, older men and women showed areduced ability, relative to their younger counterparts, to maintainstroke volume at exercise intensities above 70% of peakO2. This latter effect wasmost prominent in the oldest women. These findings suggest that neitherage nor gender has a significant impact on thec-O2 relationships during submaximal cycle ergometry among chronically endurance-trained individuals.

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18.
The mechanism(s)limiting muscle O2 uptake(O2) kinetics wasinvestigated in isolated canine gastrocnemius muscles(n = 7) during transitions from restto 3 min of electrically stimulated isometric tetanic contractions(200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% of peakO2). Two conditions weremainly compared: 1) spontaneousadjustment of blood flow () [control, spontaneous (C Spont)]; and2) pump-perfused, adjusted ~15 s before contractions at aconstant level corresponding to the steady-state value duringcontractions in C Spont [faster adjustment ofO2 delivery (FastO2 Delivery)]. During FastO2 Delivery, 1-2 ml/min of102 M adenosine wereinfused intra-arterially to prevent inordinate pressure increases withthe elevated . The purpose of the study was todetermine whether a faster adjustment ofO2 delivery would affectO2 kinetics. was measured continuously; arterial(CaO2) and popliteal venous(CvO2)O2 contents were determined atrest and at 5- to 7-s intervals during contractions;O2 delivery was calculated as · CaO2,and O2 was calculated as · arteriovenous O2 content difference. Times toreach 63% of the difference between baseline and steady-stateO2 during contractions were23.8 ± 2.0 (SE) s in C Spont and 21.8 ± 0.9 s in FastO2 Delivery (not significant). Inthe present experimental model, elimination of any delay inO2 delivery during therest-to-contraction transition did not affect muscleO2 kinetics, which suggeststhat this kinetics was mainly set by an intrinsic inertia of oxidativemetabolism.

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19.
Langsetmo, I., G. E. Weigle, M. R. Fedde, H. H. Erickson, T. J. Barstow, and D. C. Poole.O2 kinetics in thehorse during moderate and heavy exercise. J. Appl.Physiol. 83(4): 1235-1241, 1997.The horse is asuperb athlete, achieving a maximalO2 uptake (~160ml · min1 · kg1)approaching twice that of the fittest humans. Although equine O2 uptake(O2) kinetics arereportedly fast, they have not been precisely characterized, nor hastheir exercise intensity dependence been elucidated. To addressthese issues, adult male horses underwent incremental treadmill testingto determine their lactate threshold (Tlac) and peakO2(O2 peak),and kinetic features of their O2 response to"square-wave" work forcings were resolved using exercisetransitions from 3 m/s to abelow-Tlac speed of 7 m/s or anabove-Tlac speed of 12.3 ± 0.7 m/s (i.e., between Tlac and O2 peak) sustainedfor 6 min. O2 andCO2 output were measured using anopen-flow system: pulmonary artery temperature was monitored, and mixedvenous blood was sampled for plasma lactate.O2 kinetics at work levelsbelow Tlac were well fit by atwo-phase exponential model, with a phase2 time constant(1 = 10.0 ± 0.9 s) thatfollowed a time delay (TD1 = 18.9 ± 1.9 s). TD1 was similar tothat found in humans performing leg cycling exercise, but the timeconstant was substantially faster. For speeds aboveTlac,TD1 was unchanged (20.3 ± 1.2 s); however, the phase 2 time constantwas significantly slower (1 = 20.7 ± 3.4 s, P < 0.05) than for exercise belowTlac. Furthermore, in four of fivehorses, a secondary, delayed increase inO2 became evident135.7 ± 28.5 s after the exercise transition. This "slowcomponent" accounted for ~12% (5.8 ± 2.7 l/min) of the netincrease in exercise O2. Weconclude that, at exercise intensities below and aboveTlac, qualitative features ofO2 kinetics in the horseare similar to those in humans. However, at speeds belowTlac the fast component of theresponse is more rapid than that reported for humans, likely reflectingdifferent energetics of O2utilization within equine muscle fibers.

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20.
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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