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1.
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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2.
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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3.
Grassi, Bruno, Claudio Marconi, Michael Meyer, Michel Rieu,and Paolo Cerretelli. Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients. J. Appl. Physiol. 82(6): 1952-1962, 1997.Metabolicand cardiovascular adjustments to various submaximal exercises wereevaluated in 82 heart transplant recipients (HTR) and in 35 controlsubjects (C). HTR were tested 21.5 ± 25.3 (SD) mo (range1.0-137.1 mo) posttransplantation. Three protocols were used:protocol A consisted of 5 min of rectangular 50-W load repeatedtwice, 5 min apart [5 min rest, 5 min 50 W (Ex 1), 5 minrecovery, 5 min 50 W (Ex 2)]; protocol B consistedof 5 min of rectangular load at 25, 50, or 75 W; protocol Cconsisted of 15 min of rectangular load at 25 W. Breath-by-breathpulmonary ventilation (E),O2 uptake (O2),and CO2 output(CO2) were determined.During protocol A, beat-by-beat cardiacoutput () was estimated by impedance cardiography. The half times (t1/2) of the on- andoff-kinetics of the variables were calculated. In all protocols,t1/2 values forO2 on-,E on-, andCO2 on-kinetics were higher(i.e., the kinetics were slower) in HTR than in C, independently ofworkload and of the time posttransplantation. Also,t1/2 on- was higher in HTRthan in C. In protocol A, no significant difference of t1/2 O2on- was observed in HTR between Ex 1 (48 ± 9 s) and Ex2 (46 ± 8 s), whereas t1/2 on- was higher during Ex 1 (55 ± 24 s)than during Ex 2 (47 ± 15 s). In all protocols and for all variables, the t1/2 off-values were higher in HTRthan in C. In protocol C, no differences of steady-stateE,O2, andCO2 were observed in bothgroups between 5, 10, and 15 min of exercise. We conclude that1) in HTR, a "priming" exercise, while effective inspeeding up the adjustment of convective O2 flow to muscle fibers during a second on-transition, did not affect theO2 on-kinetics, suggestingthat the slower O2 on- inHTR was attributable to peripheral (muscular) factors; 2) thedissociation between on- andO2 on-kinetics in HTRindicates that an inertia of muscle metabolic machinery is the mainfactor dictating theO2 on-kinetics; and 3) theO2 off-kinetics was slowerin HTR than in C, indicating a greater alactic O2 deficitin HTR and, therefore, a sluggish muscleO2 adjustment.

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4.
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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5.
Oxygen transport in conscious newborn dogs during hypoxic hypometabolism   总被引:1,自引:0,他引:1  
We questioned whether the decrease inO2 consumption(O2) during hypoxia innewborns is a regulated response or reflects a limitation inO2 availability. Experiments wereconducted on previously instrumented conscious newborn dogs.O2 was measured at a warmambient temperature (30°C, n = 7)or in the cold (20°C, n = 6),while the animals breathed air or were sequentially exposed to 15 minof fractional inspired O2(FIO2): 21, 18, 15, 12, 10, 8, and 6%. In normoxia,O2 averaged 15 ± 1 (SE)and 25 ± 1 ml · kg1 · min1in warm and cold conditions, respectively. In the warmcondition, hypometabolism (i.e., hypoxicO2 < normoxicO2) occurred at FIO2 10%, whereas in thecold condition, hypometabolism occurred atFIO2 12%. The sameresults were obtained in a separate group(n = 14) of noninstrumented puppies.For all levels of FIO2 withhypometabolism, the relationships between measures ofO2 availability (arterialO2 saturation or content, venousPO2 or saturation,x-axis) vs.O2(y-axis) had lower slopes in warm than in coldconditions. Hence, O2 during hypometabolism in the warm condition was not the maximal attainable for the level of oxygenation. The results do not support thepossibility that the hypoxic drop inO2 in the newborn reflects a limitation in O2availability. The results are compatible with the ideathat the phenomenon is one of "regulated conformism" tohypoxia.

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6.
The purpose ofthis study was to examine the influence of the type of exercise(running vs. cycling) on the O2uptake (O2) slow component.Ten triathletes performed exhaustive exercise on a treadmill and on acycloergometer at a work rate corresponding to 90% of maximalO2 (90% work rate maximalO2). The duration of thetests before exhaustion was superimposable for both type of exercises(10 min 37 s ± 4 min 11 s vs. 10 min 54 s ± 4 min 47 s forrunning and cycling, respectively). TheO2 slow component (difference between O2 atthe last minute and minute 3 ofexercise) was significantly lower during running compared with cycling(20.9 ± 2 vs. 268.8 ± 24 ml/min). Consequently, there was norelationship between the magnitude of theO2 slow component and thetime to fatigue. Finally, because blood lactate levels at the end of the tests were similar for both running (7.2 ± 1.9 mmol/l) and cycling (7.3 ± 2.4 mmol/l), there was a clear dissociation between blood lactate and the O2slow component during running. These data demonstrate that1) theO2 slow component dependson the type of exercise in a group of triathletes and2) the time to fatigue isindependent of the magnitude of theO2 slow component and bloodlactate concentration. It is speculated that the difference in muscularcontraction regimen between running and cycling could account for thedifference in theO2 slow component.

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7.
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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8.
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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9.
Persons with type II diabetes mellitus(DM), even without cardiovascular complications have a decreasedmaximal oxygen consumption (O2 max) andsubmaximal oxygen consumption(O2) duringgraded exercise compared with healthy controls. Weevaluated the hypothesis that change in the rate ofO2 in response to the onsetof constant-load exercise (measured byO2-uptakekinetics) was slowed in persons with type II DM. Ten premenopausalwomen with uncomplicated type II DM, 10 overweight, nondiabeticwomen, and 10 lean, nondiabetic women had aO2 max test. On twoseparate occasions, subjects performed 7-min bouts of constant-loadbicycle exercise at workloads below and above the lactate threshold toenable measurements of O2kinetics and heart rate kinetics (measuring rate of heart rate rise).O2 maxwas reduced in subjects with type II DM compared with both lean andoverweight controls (P < 0.05).Subjects with type II DM had slowerO2 and heart rate kineticsthan did controls at constant workloads below the lactate threshold.The data suggest a notable abnormality in the cardiopulmonary responseat the onset of exercise in people with type II DM. The findings mayreflect impaired cardiac responses to exercise, although an additional defect in skeletal muscle oxygen diffusion or mitochondrial oxygen utilization is also possible.

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10.
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   

11.
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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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.
The accumulation ofvisceral fat is independently associated with an increased risk forcardiovascular disease. The aim of this study was to determine whetherthe loss of visceral adipose tissue area (VAT; computed tomography) isrelated to improvements in maximal O2 uptake(O2 max) during a weight loss(250-350 kcal/day deficit) and walking (3 days/wk, 30-40 min)intervention. Forty obese [body fat 47 ± 1 (SE) %], sedentary(O2 max 19 ± 1 ml · kg1 · min1)postmenopausal women (age 62 ± 1 yr) participated in the study. The intervention resulted in significant declines in body weight (8%), total fat mass (dual-energy X-ray absorptiometry; 17%), VAT(17%), and subcutaneous adipose tissue area (17%) with no changein lean body mass (all P < 0.001). Women with anaverage 10% increase in O2 max reducedVAT by an average of 20%, whereas those who did not increaseO2 max decreased VAT by only 10%,despite comparable reductions in body fat, fat mass, and subcutaneousadipose tissue area. The decrease in VAT was independently related tothe change in O2 max(r2 = 0.22; P < 0.01) andfat mass (r2 = 0.08; P = 0.05). These data indicate that greater improvements inO2 max with weight loss and walking areassociated with greater reductions in visceral adiposity in obesepostmenopausal women.

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14.
To test thehypothesis that muscle O2 uptake(O2) on-kinetics islimited, at least in part, by peripheralO2 diffusion, we determined theO2 on-kinetics in1) normoxia (Control);2) hyperoxic gas breathing(Hyperoxia); and 3) hyperoxia andthe administration of a drug (RSR-13, Allos Therapeutics), whichright-shifts the Hb-O2dissociation curve (Hyperoxia+RSR-13). The study was conducted inisolated canine gastrocnemius muscles(n = 5) during transitions from restto 3 min of electrically stimulated isometric tetanic contractions(200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% peakO2). In all conditions,before and during contractions, muscle was pump perfused withconstantly elevated blood flow (), at a levelmeasured at steady state during contractions in preliminary trials withspontaneous . Adenosine was infusedintra-arterially to prevent inordinate pressure increases with theelevated . was measuredcontinuously, arterial and popliteal venousO2 concentrations were determinedat rest and at 5- to 7-s intervals during contractions, andO2 was calculated as · arteriovenous O2 content difference.PO2 at 50%HbO2saturation (P50) was calculated.Mean capillary PO2(cO2)was estimated by numerical integration.P50 was higher in Hyperoxia+RSR-13[40 ± 1 (SE) Torr] than in Control and in Hyperoxia (31 ± 1 Torr). After 15 s of contractions,cO2was higher in Hyperoxia (97 ± 9 Torr) vs. Control (53 ± 3 Torr) and in Hyperoxia+RSR-13 (197 ± 39 Torr) vs. Hyperoxia. Thetime to reach 63% of the difference between baseline and steady-stateO2 during contractions was 24.7 ± 2.7 s in Control, 26.3 ± 0.8 s in Hyperoxia, and 24.7 ± 1.1 s in Hyperoxia+RSR-13 (not significant). Enhancement ofperipheral O2 diffusion (obtainedby increasedcO2at constant O2 delivery) duringthe rest-to-contraction (60-70% of peakO2) transition did notaffect muscle O2on-kinetics.

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15.
This study examined the scaling relationships ofnet O2 uptake [O2(net) = O2  restingO2] to body mass(MB) andcombined mass (MC = MB + bicycle)during uphill treadmill bicycling. It was hypothesized thatO2(net)(l/min) would scale proportionally withMC [i.e.,O2(net)  M1.0C] and less than proportionally withMB [i.e.,O2(net)  MB].Twenty-five competitive cyclists [73.9 ± 8.8 and 85.0 ± 9.0 (SD) kg forMB andMC,respectively] rode their bicycles on a treadmill at 3.46 m/s andgrades of 1.7, 3.5, 5.2, and 7.0% whileO2 was measured. Multiplelog-linear regression procedures were applied to the pooledO2(net)data to determine the exponents forMC andMB afterstatistically controlling for differences in treadmill grade anddynamic friction. The regression models were highly significant (R2 = 0.95, P < 0.001). Exponents forMC (0.99, 95%confidence interval = 0.80-1.18) andMB (0.89, 95%confidence interval = 0.72-1.07) did not differ significantly fromeach other or 1.0. It was concluded that the 0.99 MC exponent wasdue to gravitational resistance, whereas theMB exponent was<1.0 because the bicycles were relatively lighter for heaviercyclists.

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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.
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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18.
Swallow, John G., Theodore Garland, Jr., Patrick A. Carter,Wen-Zhi Zhan, and Gary C. Sieck. Effects of voluntary activity andgenetic selection on aerobic capacity in house mice(Mus domesticus). J. Appl. Physiol. 84(1): 69-76, 1998.An animal model was developed to study effects on components ofexercise physiology of both "nature" (10 generations of geneticselection for high voluntary activity on running wheels) and"nurture" (7-8 wk of access or no access to running wheels,beginning at weaning). At the end of the experiment, mice from bothwheel-access groups were significantly lighter in body mass than micefrom sedentary groups. Within the wheel-access group, a statisticallysignificant, negative relationship existed between activity and finalbody mass. In measurements of maximum oxygen consumption during forcedtreadmill exercise (O2 max), mice withwheel access were significantly more cooperative than sedentary mice;however, trial quality was not a significant predictor of individualvariation in O2 max.Nested two-way analysis of covariance demonstrated that both geneticselection history and access to wheels had significant positive effects on O2 max.A 12% difference inO2 max existedbetween wheel-access selected mice, which had the highestmass-correctedO2 max, andsedentary control mice, which had the lowest. The respiratory exchangeratio at O2 max wasalso significantly lower in the wheel-access group. Our results suggestthe existence of a possible genetic correlation between voluntaryactivity levels (behavior) and aerobic capacity (physiology).

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19.
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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20.
Chirpaz-Oddou, M. F., A. Favre-Juvin, P. Flore, J. Eterradossi, M. Delaire, F. Grimbert, and A. Therminarias. Nitric oxide response in exhaled air during an incremental exhaustive exercise. J. Appl. Physiol. 82(4):1311-1318, 1997.This study examines the response of the exhalednitric oxide (NO) concentration (CNO) and the exhaled NOoutput(NO)during incremental exercise and during recovery in six sedentary women,seven sedentary men, and eight trained men. The protocolconsisted of increasing the exercise intensity by 30 W every 3 minuntil exhaustion, followed by 5 min of recovery. Minute ventilation(E), oxygen consumption (O2), carbon dioxideproduction, heart rate, CNO, andNOwere measured continuously. TheCNO in exhaled air decreasedsignificantly provided that the exercise intensity exceeded 65% of thepeak O2. It reached similarvalues, at exhaustion, in all three groups. TheNO increasedproportionally with exercise intensity up to exhaustion and decreasedrapidly during recovery. At exhaustion, the mean values weresignificantly higher for trained men than for sedentary men andsedentary women. During exercise,NOcorrelates well with O2,carbon dioxide production, E, and heartrate. For the same submaximal intensity, and thus a givenO2 and probably a similarcardiac output,NO appearedto be similar in all three groups, even if theE was different. These results suggestthat, during exercise,NO is mainlyrelated to the magnitude of aerobic metabolism and that thisrelationship is not affected by gender differences or by noticeabledifferences in the level of physical training.

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