Effect of prolonged, heavy exercise on pulmonary gas exchange in athletes

During maximalexercise, ventilation-perfusion inequality increases, especially inathletes. The mechanism remains speculative. Wehypothesized that, if interstitial pulmonary edema is involved, prolonged exercise would result in increasing ventilation-perfusion inequality over time by exposing the pulmonary vascular bed to highpressures for a long duration. The response to short-term exercise wasfirst characterized in six male athletes [maximal O₂ uptake(O_{2 max}) = 63 ml · kg¹ · min¹] by using 5 minof cycling exercise at 30, 65, and 90%O_{2 max}. Multiple inert-gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained. Resting log SD of the perfusion distribution (logSD) was normal [0.50 ± 0.03 (SE)] and increased with exercise (logSD = 0.65 ± 0.04, P < 0.005), alveolar-arterialO₂ difference increased (to 24 ± 3 Torr), and end-capillary pulmonary diffusion limitation occurred at 90%O_{2 max}. The subjectsrecovered for 30 min, then, after resting measurements were taken,exercised for 60 min at ~65%O_{2 max}.O₂ uptake, ventilation, cardiacoutput, and alveolar-arterial O₂difference were unchanged after the first 5 min of this test, but logSD increased from0.59 ± 0.03 at 5 min to 0.66 ± 0.05 at 60 min(P < 0.05), without pulmonary diffusion limitation. LogSD was negativelyrelated to total lung capacity normalized for body surface area(r = 0.97,P < 0.005 at 60 min). These data are compatible with interstitial edema as a mechanism and suggest that lungsize is an important determinant of the efficiency of gas exchangeduring exercise.

     

Association of chest wall motion and tidal volume responses during CO2 rebreathing

Yan, Sheng, Pawel Sliwinski, and Peter T. Macklem.Association of chest wall motion and tidal volume responses during CO₂ rebreathing.J. Appl. Physiol. 81(4):1528-1534, 1996.The purpose of this study is to investigate theeffect of chest wall configuration at end expiration on tidal volume(VT) response duringCO₂ rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory andend-inspiratory volume of the rib cage (Vrc,E andVrc,I, respectively) and abdomen (Vab,E and Vab,I, respectively) measured by linearizedmagnetometers were expressed as a function of end-tidalPCO₂(PET_CO2). The changes inend-expiratory and end-inspiratory volumes of the chest wall(Vcw,E and Vcw,I,respectively) were calculated as the sum of the respectiverib cage and abdominal volumes. The magnetometer coils were placed atthe level of the nipples and 1-2 cm above the umbilicus andcalibrated during quiet breathing against theVT measured from apneumotachograph. TheVrc,E/PET_CO2 slope was quite variable among subjects. It was significantly positive (P < 0.05) in fivesubjects, significantly negative in four subjects(P < 0.05), and not different fromzero in the remaining two subjects. TheVab,E/PET_CO2slope was significantly negative in all subjects(P < 0.05) with a much smallerintersubject variation, probably suggesting a relatively more uniformrecruitment of abdominal expiratory muscles and a variable recruitmentof rib cage muscles during CO₂rebreathing in different subjects. As a group, the meanVrc,E/PET_CO2,Vab,E/PET_CO2, andVcw,E/PET_CO2slopes were 0.010 ± 0.034, 0.030 ± 0.007, and0.020 ± 0.032 l / Torr, respectively;only theVab,E/PET_CO2 slope was significantly different from zero. More interestingly, theindividualVT/PET_CO2slope was negatively associated with theVrc,E/PET_CO2(r = 0.68,P = 0.021) and Vcw,E/PET_CO2slopes (r = 0.63,P = 0.037) but was not associated withtheVab,E/PET_CO2slope (r = 0.40, P = 0.223). There was no correlation oftheVrc,E/PET_CO2 andVcw,E/PET_CO2slopes with age, body size, forced expiratory volume in 1 s, orexpiratory time. The groupVab,I/PET_CO2 slope (0.004 ± 0.014 l / Torr) was not significantlydifferent from zero despite theVT nearly being tripled at theend of CO₂ rebreathing. Inconclusion, the individual VTresponse to CO₂, althoughindependent of Vab,E, is a function ofVrc,E to the extent that as theVrc,E/PET_CO2slope increases (more positive) among subjects, theVT response toCO₂ decreases. These results maybe explained on the basis of the respiratory muscle actions andinteractions on the rib cage.

     

New in situ mouse model to quantify alveolar epithelial fluid clearance

Because the availability of transgenic micemakes it possible to examine the contribution of single genes to invivo function, we developed a simple in situ mouse model that can beused to quantify isosmolar alveolar epithelial fluid clearance (AFC). Mice were killed, a tracheostomy was done, and then a test solution ofa 5% isosmolar albumin solution with 0.1 µCi of¹²⁵I-labeled albumin was instilledvia the trachea into the distal air spaces of both lungs. Afterinstillation, the lungs were inflated to 7 cmH₂O with 100%O₂ and maintained at 37°C byplacing the animals under an infrared lamp. AFC was measured by theprogressive increase in concentration of labeled and unlabeled proteinover 1 h. The results indicated the following.1) Basal, unstimulated AFC in mouselungs was significantly faster than in ex vivo rat lungs (27 ± 5%in in situ mice vs. 11 ± 3% in ex vivo rat lungs; P < 0.05).2) Comparison of equivalent doses(10⁴ M) of -adrenergicagonist (isoproterenol) and₂-adrenergic agonists(terbutaline and salmeterol) indicated that stimulated clearanceoccurred only in presence of isoproterenol.3) Because atenolol, a specific₁-antagonist, abolished theeffect of isoproterenol, the -adrenergic stimulation appears to bemediated by ₁-receptors. Therate of AFC in nonperfused mouse lungs was significantly faster than inprior studies of nonperfused lungs in rats and sheep. Interestingly,the stimulated clearance rate in mice was similar to the fast rates ofAFC that we recently reported in patients recovering from hydrostaticpulmonary edema. This in situ model is a unique experimentalpreparation that can be readily used to quantify isosmolar epithelialfluid clearance in mice.

     

Ragweed sensitization alters pulmonary vascular responses to bronchoprovocation in beagle dogs

Theodorou, Andreas, Natalie Weger, Kathleen Kunke, KyooRhee, David Bice, Bruce Muggenberg, and Richard Lemen. Ragweed sensitization alters pulmonary vascular responses to bronchoprovocation in beagle dogs. J. Appl. Physiol.83(3): 912-917, 1997.In ragweed (RW)-sensitized beagle dogs, wetested the hypothesis that reactivity of the pulmonary vasculature wasenhanced with aerosolized histamine (Hist) and RW. Seven dogs wereneonatally sensitized with repeated intraperitoneal RW injections, and12 dogs were controls (Con). The dogs were anesthetizedwith intravenous chloralose, mechanically ventilated, and instrumentedwith femoral arterial and pulmonary artery catheters. Specific lungcompliance(CL_sp),specific lung conductance (G_sp),systemic vascular resistance index, and pulmonary vascular resistanceindex (PVRI) were measured before and after bronchoprovocation withHist and RW. After Hist inhalation (5 breaths of 30 mg/ml), both Conand RW dogs had significant (P < 0.05) decreases inCL_sp(51 ± 4 and 53 ± 5%, respectively) andG_sp (65 ± 5 and69 ± 3%, respectively), but only RW-sensitized dogs had asignificant increase in PVRI (38 ± 10%). After RW inhalation (60 breaths of 0.8 mg/ml), only RW-sensitized dogs had significant increases (62 ± 20%) in PVRI and decreases inG_sp (77 ± 4%) and CL_sp(65 ± 7%). We conclude that, compared with Con,RW-sensitized beagle dogs have increased pulmonary vasoconstrictiveresponses with Hist or RW inhalation.

     

Changes in maximum oxygen uptake during prolonged training, overtraining, and detraining in horses

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 ^· kg^{1 ·} min¹,maximal O₂ uptake(O_{2 max}) increased by15% at the end of phase 1, and when signs of overtraining werefirst seen in the OLT group,O_{2 max} was 29%higher (151 ± 2 ml ^· kg^{1 ·} min¹in both C and OLT groups) than pretraining values. There was nosignificant reduction inO_{2 max} until after 6 wk detraining whenO_{2 max} was 137 ± 2 ml ^· kg^{1 ·} min¹.By 12 wk detraining, meanO_{2 max} was134 ± 2 ml ^· kg^{1 ·} min¹,still 15% above pretraining values. When overtraining developed, O_{2 max} was notdifferent between C and OLT groups, but maximal values forCO₂ production (147 vs. 159 ml ^· kg^{1 ·} min¹)and respiratory exchange ratio (1.04 vs. 1.11) were lower in the OLTgroup. Overtraining was not associated with a decrease inO_{2 max} and, afterprolonged training, decreases inO_{2 max} occurredslowly during detraining.

     

Skeletal muscle mass and the reduction of VO2 max in trained older subjects

Proctor, David N., and Michael J. Joyner. Skeletalmuscle mass and the reduction ofO_{2 max} in trainedolder subjects. J. Appl. Physiol.82(5): 1411-1415, 1997.The role of skeletal muscle mass in theage-associated decline in maximalO₂ uptake (O_{2 max}) is poorlydefined because of confounding changes in muscle oxidative capacity andin body fat and the difficulty of quantifying active muscle mass duringexercise. We attempted to clarify these issues byexamining the relationship between several indexes of muscle mass, asestimated by using dual-energy X-ray absorptiometry and treadmillO_{2 max} in 32 chronically endurance-trained subjects from four groups(n = 8/group): young men(20-30 yr), older men (56-72 yr), young women(19-31 yr), and older women (51-72 yr).O_{2 max} per kilogrambody mass was 26 and 22% lower in the older men (45.9 vs. 62.0 ml · kg¹ · min¹)and older women (40.0 vs. 51.5 ml · kg¹ · min¹).These age differences were reduced to 14 and 13%, respectively, whenO_{2 max} was expressedper kilogram of appendicular muscle. When appropriately adjusted forage and gender differences in appendicular muscle mass by analysis ofcovariance, whole body O_{2 max} was 0.50 ± 0.09 l/min less (P < 0.001) in theolder subjects. This effect was similar in both genders.These findings suggest that the reducedO_{2 max} seen in highlytrained older men and women relative to their younger counterparts isdue, in part, to a reduced aerobic capacity per kilogram of activemuscle independent of age-associated changes in body composition, i.e.,replacement of muscle tissue by fat. Because skeletal muscleadaptations to endurance training can be well maintained in oldersubjects, the reduced aerobic capacity per kilogram of muscle likelyresults from age-associated reductions in maximalO₂ delivery (cardiac outputand/or muscle blood flow).

     

Effects of endurance training on the cardiovascular system and water compartments in elderly subjects

Pickering, Gisèle P., Nicole Fellmann, BéatriceMorio, Patrick Ritz, Aimé Amonchot, Michel Vermorel, and JeanCoudert. Effects of endurance training on the cardiovascularsystem and water compartments in elderly subjects. J. Appl. Physiol. 83(4): 1300-1306, 1997.Theeffects of endurance training on the water compartments and thecardiovascular system were determined in 10 elderly subjects [age62 ± 2 yr, pretraining maximal oxygen consumption(O_{2 max})/kg = 25 ± 2 ml · min¹ · kg¹body wt]. They trained on a cycloergometer 3 times/wk for 16 wk(50-80%O_{2 max},then 80-85%O_{2 max}). They werechecked at 8 wk, 16 wk, and 4 mo after detraining. Training improvedO_{2 max} (+16%) andinduced plasma volume expansion (+11%). No change in total body water,extracellular fluid, interstitial and intracellular fluid volumes,fat-free mass, and body weight was detected in this small sample withtraining. Body fat mass decreased (2.1 ± 2.2 kg).Echocardiography at rest showed increased fractional shortening andejection fraction and decreased left ventricular end-systolic dimension(P < 0.05). Blood volume expansioncorrelates with cardiac contractility and has an impact on cardiacfunction. These improvements are precarious, however, and arecompletely lost after 4 mo of detraining, when elderly subjects losethe constraints and the social stimulation of the imposed protocol.

     

Smaller lungs in women affect exercise hyperpnea

We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygenuptake (O_{2 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(O_{2 max} > 57 ml · kg¹ · min¹,n = 14) vs. less-fit(O_{2 max} < 56 ml · kg¹ · min¹,n = 15) women caused a higher maximalventilation (E) with increased tidal volume (VT)and breathing frequency (f_b) 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,f_b, 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 onf_b, 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.

     

Respiratory changes associated with rapid eye movements in normo- and hypercapnia during sleep

Rapid eyemovements during rapid-eye-movement (REM) sleep are associated withrapid, shallow breathing. We wanted to know whether thiseffect persisted during increased respiratory drive byCO₂. In eight healthy subjects, werecorded electroencephalographic, electrooculographic, andelectromyographic signals, ventilation, and end-tidalPCO₂ during the night. InspiratoryPCO₂ was changed to increaseend-tidal PCO₂ by 3 and 6 Torr. During normocapnia, rapid eye movements were associated with a decreasein total breath time by 0.71 ± 0.19 (SE) s(P < 0.05) because of shortenedexpiratory time (0.52 ± 0.08 s,P < 0.001) and with a reduced tidalvolume (89 ± 27 ml, P < 0.05) because of decreased rib cage contribution (75 ± 18 ml, P < 0.05). Abdominal (11 ± 16 ml, P = 0.52) and minuteventilation (0.09 ± 0.21 ml/min, P = 0.66) did not change. Inhypercapnia, however, rapid eye movements were associated with afurther shortening of total breath time. Abdominal breathing was alsoinhibited (79 ± 23 ml, P < 0.05), leading to a stronger inhibition of tidal volume and minuteventilation (1.84 ± 0.54 l/min,P < 0.05). We conclude thatREM-associated respiratory changes are even more pronounced duringhypercapnia because of additional inhibition of abdominal breathing.This may contribute to the reduction of the hypercapnic ventilatory response during REM sleep.

     

Ventilatory response to exercise in diabetic subjects with autonomic neuropathy

Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response toexercise in diabetic subjects with autonomic neuropathy.J. Appl. Physiol. 81(5):1978-1986, 1996.We have used diabetic autonomic neuropathy as amodel of chronic pulmonary denervation to study the ventilatoryresponse to incremental exercise in 20 diabetic subjects, 10 with(Dan+) and 10 without (Dan) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan subjectsachieved lower O₂ consumption andCO₂ production(CO₂) thancontrol subjects at peak of exercise, they attained similar values ofeither minute ventilation(E) oradjusted ventilation (E/maximalvoluntary ventilation). The increment of respiratory rate withincreasing adjusted ventilation was much higher in Dan+ than inDan and control subjects (P < 0.05). The slope of the linearE/CO₂relationship was 0.032 ± 0.002, 0.027 ± 0.001 (P < 0.05), and 0.025 ± 0.001 (P < 0.001) ml/min inDan+, Dan, and control subjects, respectively. Bothneuromuscular and ventilatory outputs in relation to increasingCO₂ were progressivelyhigher in Dan+ than in Dan and control subjects. At peak ofexercise, end-tidal PCO₂ was muchlower in Dan+ (35.9 ± 1.6 Torr) than in Dan (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects.We conclude that pulmonary autonomic denervation affects ventilatoryresponse to stressful exercise by excessively increasing respiratoryrate and alveolar ventilation. Reduced neural inhibitory modulationfrom sympathetic pulmonary afferents and/or increasedchemosensitivity may be responsible for the higher inspiratoryoutput.

     

Optical measurement of isolated canine lung filtration coefficients after alloxan infusion

In this study, lung filtration coefficient(K_fc) wasmeasured in eight isolated canine lung preparations by using threemethods: standard gravimetric (Std), blood-corrected gravimetric (BC), and optical. The lungs were held in zone III conditions and were subjected to an average venous pressure increase of 8.79 ± 0.93 (mean ± SD) cmH₂O. Thepermeability of the lungs was increased with an infusion of alloxan (75 mg/kg). The resultingK_fc values (inmilliliters · min¹ · cmH₂O¹ · 100 g dry lung weight¹)measured by using Std and BC gravimetric techniques before vs. afteralloxan infusion were statistically different: Std, 0.527 ± 0.290 vs. 1.966 ± 0.283; BC, 0.313 ± 0.290 vs. 1.384 ± 0.290. However, the optical technique did not show any statisticaldifference between pre- and postinjury with alloxan, 0.280 ± 0.305 vs. 0.483 ± 0.297, respectively. The alloxan injury, quantified byusing multiple-indicator techniques, showed an increase in permeability and a corresponding decrease in reflection coefficient for albumin (_f). Because the opticalmethod measures the product ofK_fc and _f, this study shows thatalbumin should not be used as an intravascular optical filtrationmarker when permeability is elevated. However, the optical technique,along with another means of measuringK_fc (such as BC),can be used to calculate the _fof a tracer (in this study, _fof 0.894 at baseline and 0.348 after injury). Another important findingof this study was that the ratio of baseline-to-injury K_fc values wasnot statistically different for Std and BC techniques, indicating thatthe percent contribution of slow blood-volume increases does not changebecause of injury.

     

Lactate and epinephrine during exercise in altitude natives

Kayser, Bengt, Roland Favier, Guido Ferretti, DominiqueDesplanches, Hilde Spielvogel, Harry Koubi, Brigitte Sempore, and HansHoppeler. Lactate and epinephrine during exercise in altitudenatives. J. Appl. Physiol. 81(6):2488-2494, 1996.We tested the hypothesis that the reported lowblood lactate accumulation ([La]) during exercise inaltitude-native humans is refractory to hypoxia-normoxia transitions byinvestigating whether acute changes in inspiredO₂ fraction(FI_O2) affect the[La] vs. power output ()relationship or, alternatively, as reported for lowlanders, whetherchanges in [La] vs. on changes inFI_O2 are related tochanges in blood epinephrine concentration ([Epi]). Altitude natives [n = 8, age 24 ± 1 (SE) yr, body mass 62 ± 3 kg, height 167 ± 2 cm]in La Paz, Bolivia (3,600 m) performed incremental exercise with twolegs and one leg in chronic hypoxia and acute normoxia (AN). Submaximalone- and two-leg O₂ uptake (O₂) vs. relationships were not altered byFI_O2. AN increased two-legpeak O₂ by 10% and peak by 7%. AN paradoxically decreasedone-leg peak O₂ by 7%,whereas peak remained the same. The[La] vs. relationships were similar tothose reported in unacclimatized lowlanders. There was a shift to theright on AN, and maximum [La] was reduced by 7 and 8% forone- and two-leg exercises, respectively. [Epi] and[La] were tightly related (mean r = 0.81) independently ofFI_O2. Thus normoxiaattenuated the increment in both [La] and [Epi]as a function of , whereas the correlation between[La] and [Epi] was unaffected. These data suggest loose linkage of glycolysis to oxidative phosphorylation under influence from [Epi]. In conclusion, high-altitudenatives appear to be not fundamentally different from lowlanders with regard to the effect of acute changes inFI_O2 on [La] during exercise.

     

Improved oxygenation with prostaglandin F2alpha with and without inhaled nitric oxide in dogs

Dogs of mixedbreed (n = 7) were anesthetized, rightlung atelectasis was established, and the cyclooxygenase pathway was blocked with ibuprofen. Measurements of pulmonary gas exchange wereperformed (fractional concentration of inspiredO₂ = 0.95) after infusions ofprostaglandin F₂(PGF₂; 2 µg · kg¹ · min¹),ventilation with nitric oxide (NO; 40 ppm), or both(PGF₂ + NO) in random order.The arterial PO₂(Pa_O2) under control conditions was 117 ± 16 Torr (shunt = 33 ± 2.5%), was unchanged with NO alone(Pa_O2 = 114 ± 17 Torr; shunt = 35.7 ± 3.1%), but was significantlyimproved with PGF₂ alone(Pa_O2 = 180 ± 28 Torr; shunt = 23.2 ± 2.8%) and with the combination ofPGF₂ + NO(Pa_O2 = 202 ± 30 Torr; shunt = 20.9 ± 2.5%). The addition of NO didnot significantly enhance the effectiveness of thePGF₂ onPa_O2.Simulation of these data in a computer model, combining pulmonary gasexchange and pulmonary blood flow, reproduced the results on the basisthat vasoconstriction with PGF₂was maximal under hypoxia in the atelectatic lung and reduced byhyperoxia in the ventilated lung, consistent with the hypothesis ofO₂ dependence ofPGF₂ vasoconstriction.

     

Interaction of cross-sectional area, driving pressure, and airflow of passive velopharynx

Isono, Shiroh, Thom R. Feroah, Eric A. Hajduk, Rollin Brant,William A. Whitelaw, and John E. Remmers. Interaction ofcross-sectional area, driving pressure, and airflow of passive velopharynx. J. Appl. Physiol. 83(3):851-859, 1997.Previous studies have shown that, when thepharyngeal muscles are relaxed, the velopharynx is a highly compliantsegment of the pharynx. Thus, under these circumstances,cross-sectional area of the velopharynx (A_VP), drivingpressure across the velopharynx (P), and inspiratory airflow(I) willbe mutually interdependent variables. The purpose of the presentinvestigation was to describe the interrelation among these threevariables during inspiration. We studied 15 sleeping patients withobstructive sleep apnea/hypopnea when the pharyngeal muscles wererendered hypotonic by applying continuous positive airway pressure tothe nasal airway.A_VP, determined by endoscopic imaging, was significantly greater at onset ofI limitationthan at minimum oropharyngeal pressure(P < 0.01). Snoring was neverobserved duringIlimitation. In a subgroup of six patients, values for P,I, andA_VP were obtainedat 0.1-s intervals at various levels of mask pressure. For these sixpatients, the mathematical expressionI = 0.657(A_VP/A_max) · P^0.332,where A_max ismaximal A_VP,described the relationship among the three variables(R² = 0.962) forflow-limited and non-flow-limited inspirations. The impedance of thepassive velopharynx, defined asP^0.33/,was inversely related toA_VP and increaseddramatically when A_VP was <0.3cm². In summary, we observed aprogressive decrease inA_VP during flow-limited inspiration in patients with obstructive sleep apnea. Thisconstriction of the velopharynx contributes to an increase invelopharyngeal impedance that, in turn, counterbalances the increase inP during flow limitation.

     

Kinetics of oxygen uptake at the onset of exercise in boys and men

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(O_{2 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%O_{2 peak} for 3.5 min,once by cycling at 100%O_{2 peak} for 2 min,and once by cycling at 130%O_{2 peak} for 75 s.O₂ deficit was not significantlydifferent between boys and men (respectively, 50%O_{2 peak} task: 6.6 ± 11.1 vs. 5.5 ± 7.3 ml · min¹ · kg¹;100% O_{2 peak} task:28.5 ± 8.1 vs. 31.8 ± 6.3 ml · min¹ · kg¹;and 130%O_{2 peak}task: 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%O_{2 peak}task: 22.8 ± 5.1 vs. 26.4 ± 4.1 s; 100%O_{2 peak} task: 28.0 ± 6.0 vs. 28.1 ± 4.4 s; and 130%O_{2 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.

     

Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans

We tested the hypothesis that the slowerincrease in alveolar oxygen uptake(O₂) at the onset ofsupine, compared with upright, exercise would be accompanied by aslower rate of increase in leg blood flow (LBF). Seven healthy subjectsperformed transitions from rest to 40-W knee extension exercise in theupright and supine positions. LBF was measured continuously with pulsedand echo Doppler methods, andO₂ was measured breath bybreath at the mouth. At rest, a smaller diameter of thefemoral artery in the supine position(P < 0.05) was compensated by agreater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of6 min of exercise, femoral artery diameter was larger in the uprightposition and there were no differences inO₂, MBV, or LBF betweenupright and supine positions. The rates of increase ofO₂ and LBF in thetransition between rest and 40 W exercise, as evaluated by the meanresponse time (time to 63% of the increase), were slower in the supine[O₂ = 39.7 ± 3.8 (SE) s, LBF = 27.6 ± 3.9 s] than in the uprightpositions (O₂ = 29.3 ± 3.0 s, LBF = 17.3 ± 4.0 s;P < 0.05). These data support ourhypothesis that slower increases in alveolarO₂ at the onset of exercisein the supine position are accompanied by a slower increase in LBF.

     

Esophageal temperature threshold for sweating decreases before ovulation in premenopausal women

The purpose ofthis study was to test the hypothesis that regulated body temperatureis decreased in the preovulatory phase in eumenorrheic women. Six womenwere studied in both the preovulatory phase (Preov-2;days 9-12), which was 1-2days before predicted ovulation when 17-estradiol(E₂) was estimated to peak, andin the follicular phase (F; days2-6). The subjects walked on a treadmill (~225W · m²)in a warm chamber (ambient temperature = 30°C; dew-pointtemperature = 11.5°C) while heavily clothed.E₂, esophageal temperature(T_es), local skin temperatures,and local sweating rate were measured. The estimate of when theE₂ surge would occur was correctfor four of six subjects. In these four subjects,E₂ increased(P  0.05) from 42.0 ± 24.5 pg/mlduring F to 123.2 ± 31.3 pg/ml during Preov-2. RestingT_es was 37.02 ± 0.20°Cduring F and 36.76 ± 0.28°C during Preov-2(P  0.05). TheT_es threshold for sweating wasdecreased (P  0.05) from 36.88 ± 0.27°C during F to 36.64 ± 0.35°C during Preov-2. Both meanskin and mean body temperatures were decreased during rest in Preov-2group. The hypothesis that regulated body temperature is decreasedduring the preovulatory phase is supported.

     

Respiratory muscle reserve in rats during heavy exercise

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(O_{2 peak}) wasmeasured in healthy Sprague-Dawley rats before and after Sham,unilateral, or bilateral hemidiaphragm denervation (Dnv) surgery.O_{2 peak} wasdetermined by using a graded treadmill running test.Hemidiaphragm paralysis was verified after testing byrecording the absence of electromyographic activity duringinspiration. Before surgery, O_{2 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 inO_{2 peak} foreither the Sham or unilateral Dnv group. However,O_{2 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.

     

Optical measurement of isolated canine lung filtration coefficients at normal hematocrits

Klaesner, Joseph W., N. Adrienne Pou, Richard E. Parker,Charlene Finney, and Robert J. Roselli. Optical measurement ofisolated canine lung filtration coefficients at normal hematocrits. J. Appl. Physiol. 83(6):1976-1985, 1997.In this study, lung filtration coefficient(K_fc) valueswere measured in eight isolated canine lung preparations at normalhematocrit values using three methods: gravimetric, blood-correctedgravimetric, and optical. The lungs were kept in zone 3 conditions andsubjected to an average venous pressure increase of 10.24 ± 0.27 (SE) cmH₂O. The resulting K_fc(ml · min¹ · cmH₂O¹ · 100 g dry lung wt¹) measuredwith the gravimetric technique was 0.420 ± 0.017, which wasstatistically different from theK_fc measured bythe blood-corrected gravimetric method (0.273 ± 0.018) or theproduct of the reflection coefficient(_f) andK_fc measuredoptically (0.272 ± 0.018). The optical method involved the use of aCellco filter cartridge to separate red blood cells from plasma, whichallowed measurement of the concentration of the tracer in plasma atnormal hematocrits (34 ± 1.5). The permeability-surface areaproduct was measured using radioactive multiple indicator-dilutionmethods before, during, and after venous pressure elevations. Resultsshowed that the surface area of the lung did not change significantlyduring the measurement ofK_fc. Thesestudies suggest that_fK_fccan be measured optically at normal hematocrits, that this measurement is not influenced by blood volume changes that occur during the measurement, and that the optical_fK_fcagrees with theK_fc obtained viathe blood-corrected gravimetric method.

     

Resistance and aerobic training in older men: effects on VO2 peak and the capillary supply to skeletal muscle

Hepple, R. T., S. L. M. Mackinnon, J. M. Goodman, S. G. Thomas, and M. J. Plyley. Resistance and aerobic training in oldermen: effects onO_{2 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(O_{2 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. O_{2 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 O_{2 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 O_{2 peak}(r = 0.52), suggest the possibility that similar mechanisms may be involved in the increase ofO_{2 peak} afterhigh-intensity RT and AT in the older population.