Effect of weight loss on operational lung volumes and oxygen cost of breathing in obese women.

BACKGROUND: The effects of moderate weight loss on operational lung volumes during exercise and the oxygen (O2) cost of breathing are unknown in obese women but could have important implications regarding exercise endurance. METHODS: In 29 obese women (33±8 years, 97±14 kg, body mass index: 36±4 kg m(-2), body fat: 45.6±4.5%; means±s.d.), body composition, fat distribution (by magnetic resonance imaging), pulmonary function, operational lung volumes during exercise and the O2 cost of breathing during eucapnic voluntary hyperpnea (([Vdot ]O2) vs ([Vdot ]E) slope) were studied before and after a 12-week diet and resistance exercise weight loss program. RESULTS: Participants lost 7.5±3.1 kg or ≈8% of body weight (P<0.001), but fat distribution remained unchanged. After weight loss, lung volume subdivisions at rest were increased (P<0.05) and were moderately associated (P<0.05) with changes in weight. End-expiratory lung volume (percentage of total lung capacity) increased at rest and during constant load exercise (P<0.05). O2 cost of breathing was reduced by 16% (2.52±1.02-2.11±0.72 ml l(-1); P=0.003). As a result, O2 uptake of the respiratory muscles ([Vdot ]O2Resp), estimated as the product of O2 cost of breathing and exercise ([Vdot ]E) during cycling at 60 W, was significantly reduced by 27±31 ml (P<0.001), accounting for 46% of the reduction in total body ([Vdot ]O2) during cycling at 60 W. CONCLUSIONS: Moderate weight loss yields important improvements in respiratory function at rest and during submaximal exercise in otherwise healthy obese women. These changes in breathing load could have positive effects on the exercise endurance and adherence to physical activity.

Heat stress does not augment ventilatory responses to presyncopal limited lower body negative pressure.

Simulated haemorrhage, e.g. lower body negative pressure (LBNP), reduces central blood volume and mean arterial pressure, while ventilation increases. Passive whole-body heat stress likewise increases ventilation. The objective of this project was to test the hypothesis that ventilatory responses to reductions in central blood volume and arterial pressure during simulated haemorrhage are enhanced when individuals are heat stressed rather than normothermic. Eight healthy men (34 ± 9 years old, 176 ± 6 cm tall and 80.2 ± 4.2 kg body weight) underwent a simulated haemorrhagic challenge via LBNP until presyncope on two separate occasions, namely normothermic control and whole-body heat-stress trials. Baseline ventilation and core and mean skin temperatures were not different between trials (all P > 0.05). Prior to LBNP, heat stress increased core (from 36.8 ± 0.2 to 38.2 ± 0.2°C, P < 0.05) and mean skin temperatures (from 33.9 ± 0.5 to 38.1 ± 0.6°C, P < 0.05), as well as minute ventilation (from 8.01 ± 2.63 to 13.68 ± 6.68 l min(-1), P < 0.01). At presyncope, mean arterial pressure and middle cerebral artery blood velocity decreased in both trials (P < 0.05). At presyncope, ventilation increased to 23.22 ± 6.78 (P < 0.01) and 25.88 ± 10.16 l min(-1) (P < 0.01) in the normothermic and hyperthermic trials, respectively; however, neither the increase in ventilation from the pre-LBNP period nor the absolute ventilation was different between normothermic and hyperthermic trials (P > 0.05). These data suggest that the increase in ventilation during simulated haemorrhage induced via LBNP is not altered in heat-stressed humans.

Mild-to-moderate obesity: implications for respiratory mechanics at rest and during exercise in young men.

OBJECTIVE: To investigate the effect of mild-to-moderate obesity on respiratory mechanics at rest and during exercise in obese men. We hypothesized that the simple mass loading of obesity would alter both end-expiratory lung volume (EELV) and respiratory pressures (gastric, P(ga) and transpulmonary, P(TP)) in resting body positions and during graded cycle ergometry to exhaustion. SUBJECTS: A total of 10 obese (38+/-5% body fat; mean+/-s.d.) and nine lean (18+/-4%) men were studied. METHODS: Body composition (by body circumferences and hydrostatic weighing) and pulmonary function were measured at rest. Breathing mechanics were measured at rest in the upright-seated position, supine, and during cycling exercise. Data were analyzed by independent t-test. RESULTS: EELV was significantly lower in the obese men in the supine (30+/-4 vs 37+/-6% total lung capacity (TLC)) and seated (39+/-6 vs 47+/-5%TLC) positions and at ventilatory threshold (35+/-5 vs 45+/-7%TLC) (P<0.01). In contrast, at peak exercise, EELV was not different between groups. Respiratory pressures (P(ga) and P(TP)) were elevated (P<0.05) during one or more phases of the breathing cycle at rest and during exercise in obese men. CONCLUSION: These data demonstrate that mild-to-moderate obesity in young men results in reduced lung volumes and alterations in respiratory mechanics when supine, seated at rest, and during exercise. During moderate exercise, obesity does not appear to limit changes in EELV; however, the regulation of EELV during heavy exercise appears to be affected.

Exaggerated respiratory chemosensitivity and association with SaO2 level at 3568 m in obesity.

To investigate whether obesity is associated with alterations in respiratory chemosensitivity, we compared the ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) in 9 obese men (BMI: 37.0+/-4.3 kg m(-2)) and 10 lean men (BMI: 25.8+/-4.8 kg m(-2)). HVR (DeltaVE, L min(-1) per DeltaSaO2, %) was measured by a progressive isocapnic hypoxia technique, and HCVR (DeltaVE/DeltaPETCO2, L min(-1)Torr(-1)) was measured by a progressive hypercapnic method. HCVR, was greater (p<0.001) in the obese men (2.68+/-0.78) than in the lean men (1.4+/-0.45) as was HVR (p<0.05) (1.26+/-0.65 versus 0.71+/-0.43, respectively). The difference (DeltaSaO2, 4.30+/-3.69 and 10.54+/-3.45 in the lean and obese men, respectively, p<0.01) between daytime (86+/-1 and 86+/-1%) and nighttime SaO2 (81+/-3 and 76+/-4%) at a simulated altitude of 3658 m was significantly (p<0.05) correlated with both HVR (r=0.51) and HCVR (r=0.48). These results suggest that chemosensitivity in mildly obese men is increased, not blunted. Furthermore, otherwise healthy, obese individuals have the potential for significant desaturation during sleep at high altitude possibly due to exaggerated sleep-disordered breathing.

Ventilatory response to exercise in aged runners breathing He-O2 or inspired CO2.

The ventilatory response to exercise below ventilatory threshold (VTh) increases with aging, whereas above VTh the ventilatory response declines only slightly. We wondered whether this same ventilatory response would be observed in older runners. We also wondered whether their ventilatory response to exercise while breathing He-O(2) or inspired CO(2) would be different. To investigate, we studied 12 seniors (63 +/- 4 yr; 10 men, 2 women) who exercised regularly (5 +/- 1 days/wk, 29 +/- 11 mi/wk, 16 +/- 6 yr). Each subject performed graded cycle ergometry to exhaustion on 3 separate days, breathing either room air, 3% inspired CO(2), or a heliox mixture (79% He and 21% O(2)). The ventilatory response to exercise below VTh was 0.35 +/- 0.06 l x min(-1) x W(-1) and above VTh was 0.66 +/- 0.10 l x min(-1) x W(-1). He-O(2) breathing increased (P < 0.05) the ventilatory response to exercise both below (0.40 +/- 0.12 l x min(-1) x W(-1)) and above VTh (0.81 +/- 0.10 l x min(-1) x W(-1)). Inspired CO(2) increased (P < 0.001) the ventilatory response to exercise only below VTh (0.44 +/- 0.10 l x min(-1) x W(-1)). The ventilatory responses to exercise with room air, He-O(2), and CO(2) breathing of these fit runners were similar to those observed earlier in older sedentary individuals. These data suggest that the ventilatory response to exercise of these senior runners is adequate to support their greater exercise capacity and that exercise training does not alter the ventilatory response to exercise with He-O(2) or inspired CO(2) breathing.

Hyperventilation with He-O2 breathing is not decreased by superimposed external resistance.

The purpose of this study was to determine the effect of imposed external resistance on the ventilatory response to He-O(2) breathing during peak exercise. To accomplish this purpose, separate inspiratory and expiratory external resistances were applied to offset for the decrease in intrapulmonary airway resistance with He-O(2) breathing. Seven men and three women (69+/-3 years, mean+/-S.D.) with normal pulmonary function performed graded cycle ergometry to exhaustion breathing room air, He-O(2) (79% He, 21% O(2)), He-O(2) with imposed expiratory resistance, and He-O(2) with imposed inspiratory resistance. Ventilation (VE), lung mechanics, and PET(CO(2)) were measured during each 1 min increment in work rate and were analyzed by one-way ANOVA for repeated measures at rest, ventilatory threshold (VTh), and peak exercise. In response, VE was increased and PET(CO(2)) was decreased at VTh (P<0.01) and peak exercise (P<0.01) whenever breathing He-O(2). Thus, VE was increased during exercise above VTh with He-O(2) breathing regardless of increases in inspiratory or expiratory external resistance. In conclusion, these data suggest that inspiratory resistive unloading is no more important than expiratory resistive unloading to the increase in VE with He-O(2) breathing during heavy and peak exercise.

Mild obesity does not limit change in end-expiratory lung volume during cycling in young women.

To investigate the effects of obesity on the regulation of end-expiratory lung volume (EELV) during exercise we studied nine obese (41 +/- 6% body fat and 35 +/- 7 yr, mean +/- SD) and eight lean (18 +/- 3% body fat and 34 +/- 4 yr) women. We hypothesized that the simple mass loading of obesity would constrain the decrease in EELV in the supine position and during exercise. All subjects underwent respiratory mechanics measurements in the supine and seated positions, and during graded cycle ergometry to exhaustion. Data were analyzed between groups by independent t-test in the supine and seated postures, and during exercise at ventilatory threshold and peak. Total lung capacity (TLC) was reduced in the obese women (P < 0.05). EELV was significantly lower in the obese subjects in the supine (37 +/- 6 vs. 45 +/- 5% TLC) and seated (45 +/- 6 vs. 53 +/- 5% TLC) positions and at ventilatory threshold (41 +/- 4 vs. 49 +/- 5% TLC) (P < 0.01). In conclusion, despite reduced resting lung volumes and alterations in respiratory mechanics during exercise, mild obesity in women does not appear to constrain EELV during cycling nor does it limit exercise capacity. Also, these data suggest that other nonmechanical factors also regulate the level of EELV during exercise.

Breathing He-O2 increases ventilation but does not decrease the work of breathing during exercise.

We previously observed an increase in minute ventilation (V E) with resistive unloading (He-O2 breathing) in healthy elderly subjects with normal pulmonary function. To investigate the effects of resistive unloading in elderly subjects with mild chronic airflow limitation (FEV(1)/FVC: 61 +/- 4%), we studied 10 elderly men and women 70 +/- 3 yr of age. These subjects performed graded cycle ergometry to exhaustion, once breathing room air and once breathing a He-O2 gas mixture (79% He, 21% O2). V E, pulmonary mechanics, and PET(CO2) were measured during each 1-min increment in work rate. Data were analyzed by paired t test at rest, at ventilatory threshold (VTh), and during maximal exercise. V E was significantly (p < 0.05) increased at VTh (3.4 +/- 4.0 L/min or 12 +/- 15% increase) and maximal exercise (15.2 +/- 9.7 L/min or 22 +/- 13% increase) while breathing He-O2. Concomitant to the increase in V E, PET(CO2) was decreased at all levels (p < 0.01), whereas total work of breathing against the lung was not different. We concluded that V E is increased during He-O2 breathing because of resistive unloading of the airways and the maintenance of the relationship between the work of breathing and exercise work rate.

Mechanism of reduced maximal expiratory flow with aging.

To investigate the determinants of maximal expiratory flow (MEF) with aging, 17 younger (7 men and 10 women, 39 +/- 4 yr, mean +/- SD) and 19 older (11 men and 8 women, 69 +/- 3 yr) subjects with normal pulmonary function were studied. For further comparison, we also studied 10 middle-aged men with normal lung function (54 +/- 6 yr) and 15 middle-aged men (54 +/- 7 yr) with mild chronic airflow limitation (CAL; i.e., forced expiratory volume in 1 s/forced vital capacity = 63 +/- 8%). MEF, static lung elastic recoil pressure (Pst), and the minimal pressure for maximal flow (Pcrit) were determined in a pressure-compensated, volume-displacement body plethysmograph. Values were compared at 60, 70, and 80% of total lung capacity. In the older subjects, decreases in MEF (P < 0.01) and Pcrit (P < 0.05), compared with the younger subjects, were explained mainly by loss of Pst (P < 0.05). In the CAL subjects, MEF and Pcrit were lower (P < 0.05) than in the older subjects, but Pst was similar. Thus decreases in MEF and Pcrit were greater than could be explained by the loss of Pst and appeared to be related to increased upstream resistance. These data indicate that the loss of lung recoil explains the decrease in MEF with aging subjects, but not in the mild CAL patients that we studied.

Airflow limitation and control of end-expiratory lung volume during exercise.

To test the hypothesis that the presence of airflow limitation (AFL) influences the control of end-expiratory lung volume (EELV) during exercise, 11 subjects with normal lung function, performed submaximal exercise (SM) on a cycle ergometer, with and without AFL. AFL was achieved during exercise by increasing the density of the air via a hyperbaric chamber, compressed to a depth of 3 atm (3 ATA; with AFL). Five subjects achieved AFL during SM exercise at 3 ATA while the remaining six subjects did not achieve AFL. SM exercise was performed with the same apparatus in the hyperbaric chamber at sea level pressure with none of the subjects achieving AFL (SL; no-AFL). EELV (% of TLC, BTPS), was significantly larger during exercise at 3 ATA than during exercise at SL for the AFL group (SL = 44 +/- 6%; 3 ATA-AFL = 51 +/- 9%, P < 0.05; but, was not for the no-AFL group (SL = 46 +/- 6%; 3 ATA-no AFL = 46 +/- 7%). End inspiratory lung volume was significantly elevated during exercise at 3 ATA compared with SL in the AFL group (SL = 80 +/- 6%; 3 ATA-AFL = 86 +/- 6%; P = 0.01) but not in the no-AFL group (SL = 82 +/- 4%; 3 ATA-no AFL = 84 +/- 4%). Tidal volume and ventilation were not different for any condition. These data suggest that the occurrence of AFL influences the control of EELV.

Progressive mechanical ventilatory constraints with aging.

To investigate the progressive nature of mechanical ventilatory constraints with aging, we studied 20 young (age 39 +/- 3 yr), 14 senior (70 +/- 2 yr), and 11 elderly (88 +/- 2 yr) men and women during exercise. All subjects had normal pulmonary function and performed graded cycle ergometry to exhaustion. Minute ventilation (V E), lung volume, and expiratory airflow limitation (EAFL) were measured during each 1-min increment in work rate. Data were analyzed by two-way analysis of variance (ANOVA; age x gender) at rest, ventilatory threshold (VTh), and peak exercise. If an interaction was present, each gender was analyzed with a one-way ANOVA. Aging resulted in an increased V E for a given submaximal work rate, although V E during peak exercise was lowest in the elderly group (p < 0.01). End-expiratory lung volume (EELV, % of TLC) in men increased progressively with age and all groups were different at VTh (p < 0.01) and peak exercise (p < 0.01). In women, EELV (% of TLC) also increased with aging, the senior and elderly subjects had a greater EELV at VTh (p < 0.01) and peak exercise (p < 0.01) than the young group. Additionally, the normal decrease in EELV during the early stages of exercise was not observed in elderly subjects. End-inspiratory lung volume (EILV) also progressively increased with aging; senior and elderly subjects had a higher EILV at rest (p < 0.05), VTh (p < 0.01), and peak exercise (p < 0.01) than young subjects. EAFL (% of VT) increased with aging; elderly subjects experienced greater EAFL at rest (p < 0.05), VTh (p < 0.01), and peak exercise (p < 0.01) than both young and senior subjects. We conclude that mechanical ventilatory constraints are progressive with aging, elderly subjects demonstrating marked mechanical ventilatory constraints during exercise. The impact of these constraints on exercise tolerance cannot be determined from this investigation and remains unclear.

Mechanical ventilatory constraints in aging, lung disease, and obesity: perspectives and brief review.

Mechanical ventilatory constraints in aging, lung disease, and obesity; perspectives and brief review. Med. Sci. Sports Exerc., Vol. 31, No. 1 (Suppl.), pp. S12-S22, 1999. One of the most difficult tasks of cardiopulmonary exercise testing is to determine the influence of ventilatory limitations on the ventilatory response to exercise. Currently there is no generally accepted method in which to quantify the magnitude of mechanical ventilatory constraints during exercise. Nor is there agreement on how to quantify maximal ventilatory capacity. To address these issues, this article focuses on the evaluation of mechanical ventilatory constraints during exercise and provides an overview of the mechanical ventilatory constraints that are encountered with aging, lung disease, and obesity.

The relationship between maximal expiratory flow and increases of maximal exercise capacity with exercise training.

We previously reported that patients with mild to moderate airflow limitation have a lower exercise capacity than age-matched controls with normal lung function, but the mechanism of this reduction remains unclear (1). Although the reduced exercise capacity appeared consistent with deconditioning, the patients had altered breathing mechanics during exercise, which raised the possibility that the reduced exercise capacity and the altered breathing mechanics may have been causally related. Reversal of reduced exercise capacity by an adequate exercise training program is generally accepted as evidence of deconditioning as the cause of the reduced exercise capacity. We studied 11 asymptomatic volunteer subjects (58 +/- 8 yr of age [mean +/- SD]) selected to have a range of lung function (FEV1 from 61 to 114% predicted, with a mean of 90 +/- 18% predicted). Only one subject had an FEV1 of less than 70% predicted. Gas exchange and lung mechanics were measured during both steady-state and maximal exercise before and after training for 30 min/d on 3 d/wk for 10 wk, beginning at the steady-state workload previously determined to be the maximum steady-state exercise level that subjects could sustain for 30 min without exceeding 90% of their observed maximal heart rate (HR). The training workload was increased if the subject's HR decreased during the training period. After 10 wk, subjects performed another steady-state exercise test at the initial pretraining level, and another maximal exercise test. HR decreased significantly between the first and second steady-state exercise tests (p < 0.05), and maximal oxygen uptake (VO2max) and ventilation increased significantly (p < 0.05) during the incremental test, indicating a training effect. However, the training effect did not occur in all subjects. Relationships between exercise parameters and lung function were examined by regression against FEV1 expressed as percent predicted. There was a significant positive correlation between VO2max percent predicted and FEV1 percent predicted (p < 0.02), and a negative correlation between FEV1 and end-expiratory lung volume (EELV) at maximal exercise (p < 0.03). There was no significant correlation between FEV1 and maximal HR achieved during exercise; moreover, all subjects achieved a maximal HR in excess of 80% predicted, suggesting a cardiovascular limitation to exercise. These data do not support the hypothesis that the lower initial VO2max in the subjects with a reduced FEV1 was due to deconditioning. Although increased EELV at maximal exercise, reduced VO2max and a reduced VO2max response with training are all statistically associated with a reduced FEV1, there is no direct evidence of causality.

Ventilation and respiratory mechanics during exercise in younger subjects breathing CO2 or HeO2.

To determine if ventilation (VE) during maximal exercise would be increased as much by 3% CO2 loading as by resistive unloading of the airways, we studied seven subjects (39 +/- 5 years; mean +/- S.D.) during graded-cycle ergometry to exhaustion while breathing: (1) room air (RA); (2) 3% CO2, 21% O2, and 76% N2; or (3) 79% He and 21% O2). VE and respiratory mechanics were measured during each 1-min increment (20 or 30 W) in work rate. VE during maximal exercise was increased 21 +/- 17% when breathing 3% CO2 and 23 +/- 16% when breathing HeO2 (P < 0.01). Further, the ventilatory response to exercise above ventilatory threshold (VTh) was increased (P < 0.05) when breathing HeO2 (0.89 +/- 0.26 L/min/W) as compared with breathing RA (0.65 +/- 0.12). When breathing HeO2, end-expiratory lung volume (% total lung capacity, TLC) was lower during maximal exercise (46 +/- 7) when compared with RA (53 +/- 6, P < 0.01). In conclusion, VE during maximal exercise can be augmented equally by 3% CO2 loading as by resistive unloading of the airways in younger subjects. This suggests that in younger subjects with normal lung function there are minimal mechanical ventilatory constraints on VE during maximal exercise.

Differences between estimates and measured PaCO2 during rest and exercise in older subjects.

Arterial PCO2 (PaCO2) has been estimated during exercise with good accuracy in younger individuals by using the Jones equation (PJCO2) (J. Appl. Physiol. 47: 954-960, 1979). The purpose of this project was to determine the utility of estimating PaCO2 from end-tidal PCO2 (PETCO2) or PJCO2 at rest, ventilatory threshold (VTh), and maximal exercise (Max) in older subjects. PETCO2 was determined from respired gases simultaneously (MGA 1100) with arterial blood gases (radial arterial catheter) in 12 older and 11 younger subjects at rest and during exercise. Mean differences were analyzed with paired t-tests, and relationships between the estimated PaCO2 values and the actual values of PaCO2 were determined with correlation coefficients. In the older subjects, PETCO2 was not significantly different from PaCO2 at rest (-1.2 +/- 4.3 Torr), VTh (0.4 +/- 2.5), or Max (-0.8 +/- 2.7), and the two were significantly (P < 0.05) correlated at Vth (r = 0.84) and Max (r = 0.87) but not at rest (r = 0.47). PJCO2 was similar to PaCO2 at rest (-1.0 +/- 3.9) and Vth (-1. 3 +/- 2.3) but significantly lower at Max (-3.0 +/- 2.6), and the two were significantly correlated at Vth (r = 0.86) and Max (r = 0. 80) but not at rest (r = 0.54). PETCO2 was significantly higher than PaCO2 during exercise in the younger subjects but similar to PaCO2 at rest. PJCO2 was similar to PaCO2 at rest and Vth but significantly lower at Max in younger subjects. In conclusion, our data demonstrate that PaCO2 during exercise is better estimated by PETCO2 than by PJCO2 in older subjects, contrary to what is observed in younger subjects. This appears to be related to the finding that PETCO2 does not exceed PaCO2 during exercise in older subjects, as occurs in the younger subjects. However, PaCO2 at rest is best estimated by PJCO2 in both younger and older subjects.

Ventilatory response to exercise in subjects breathing CO2 or HeO2.

To investigate the effects of mechanical ventilatory limitation on the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycle ergometry to exhaustion once while breathing room air; once while breathing 3% CO2-21% O2-balance N2; and once while breathing HeO2 (79% He and 21% O2). Minute ventilation (VE) and respiratory mechanics were measured continuously during each 1-min increment in work rate (10 or 20 W). Data were analyzed at rest, at ventilatory threshold (VTh), and at maximal exercise. When the subjects were breathing 3% CO2, there was an increase (P < 0.001) in VE at rest and at VTh but not during maximal exercise. When the subjects were breathing HeO2, VE was increased (P < 0.05) only during maximal exercise (24 +/- 11%). The ventilatory response to exercise below VTh was greater only when the subjects were breathing 3% CO2 (P < 0.05). Above VTh, the ventilatory response when the subjects were breathing HeO2 was greater than when breathing 3% CO2 (P < 0.01). Flow limitation, as percent of tidal volume, during maximal exercise was greater (P < 0.01) when the subjects were breathing CO2 (22 +/- 12%) than when breathing room air (12 +/- 9%) or when breathing HeO2 (10 +/- 7%) (n = 7). End-expiratory lung volume during maximal exercise was lower when the subjects were breathing HeO2 than when breathing room air or when breathing CO2 (P < 0.01). These data indicate that older subjects have little reserve for accommodating an increase in ventilatory demand and suggest that mechanical ventilatory constraints influence both the magnitude of VE during maximal exercise and the regulation of VE and respiratory mechanics during heavy-to-maximal exercise.

Expiratory flow limitation and regulation of end-expiratory lung volume during exercise.

To investigate the impact of expiratory flow limitation (FL) on breathing pattern and end-expiratory lung volume (EELV), we imposed a small expiratory threshold load for a few breaths during exercise in nine volunteers (29-62 yr): six were healthy and three had mild-to-moderate airflow obstruction (67-71% predicted forced expiratory volume in 1 s). Six subjects showed evidence of FL, i.e., tidal expiratory flow impinging on maximal forced expiratory flow, at one or more exercise levels. Whenever an expiratory threshold load was imposed, mean expiratory flow decreased (P < 0.02) in association with an increased expiratory time (TE; P < 0.05). When the load was imposed during non-FL conditions, TE increased less than expiratory flow decreased and EELV tended to increase. In contrast, during FL, with the load, TE increased more than expiratory flow decreased, subjects did not achieve maximal expiratory flow until a lower volume, and EELV decreased (P < 0.001). Under both FL and no-FL conditions, unloading reversed the changes associated with loading. These data indicate that the increase in EELV during exercise is linked to the occurrence of FL. We suggest that compression of airways downstream from the flow-limiting segment may elicit a reflex mechanism that influences breathing pattern by terminating expiration prematurely, thus increasing EELV.

Estimation of ventilatory capacity during submaximal exercise.

There is presently no precise way to determine ventilatory capacity for a given individual during exercise; however, this information would be helpful in evaluating ventilatory reserve during exercise. Using schematic representations of maximal expiratory flow-volume curves and individual maximal expiratory flow-volume curves from four subjects, we describe a technique for estimating ventilatory capacity. In these subjects, we measured maximal expiratory flow-volume loops at rest and tidal flow-volume loops and inspiratory capacity (IC) during submaximal cycle ergometry. We also compared minute ventilation (VE) during submaximal exercise with calculated ventilatory maxima (VEmaxCal) and with maximal voluntary ventilation (MVV) to estimate ventilatory reserve. Using the schematic flow-volume curves, we demonstrated the theoretical effect of maximal expiratory flow and lung volume on ventilatory capacity and breathing pattern. In the subjects, we observed that the estimation of ventilatory reserve with use of VE/VEmaxCal was most helpful in indicating when subjects were approaching maximal expiratory flow over a large portion of tidal volume, especially at submaximal exercise levels where VE/VEmaxCal and VE/MVV differed the most. These data suggest that this technique may be useful in estimating ventilatory capacity, which could then be used to evaluate ventilatory reserve during exercise.

Exercise capacity and breathing mechanics in patients with airflow limitation.

To investigate the impact of expiratory airflow limitation on ventilation during exercise, we studied six control subjects with normal lung function (FEV1/FVC = 79 +/- 6%) and eight patients with borderline-to-mild airflow limitation (FEV1/FVC = 68 +/- 4%) during cycle ergometry. VO2, HR, and VE/MVV were not different between the control subjects or patients during maximal or submaximal exercise. In contrast, five of the eight patients achieved maximal expiratory flow over a large portion (37%) of their tidal volume (VT) during submaximal exercise, whereas none of the control subjects achieved maximal expiratory flow. To estimate the fraction of expiratory capacity used by the control subjects and the patients, we calculated a mechanical ventilatory maximum (VEmaxCal) for each level of exercise using the individual's VT, end-expiratory lung volume (EELV), and maximal expiratory flow-volume curve. The patients used a greater fraction of their VEmaxCal at each level of submaximal exercise (P less than 0.03). Despite the flow limitation during submaximal exercise, EELV was similar between the control subjects and patients. In conclusion, even patients with borderline-to-mild airflow limitation achieve maximal expiratory flow during submaximal exercise and these restrictions are not reflected by VE/MVV nor by EELV.

Lung volumes during low-intensity steady-state cycling.

The use of inspiratory capacity (IC) to estimate end-expiratory lung volume (EELV) during exercise has been questioned because of the assumption of constant total lung capacity (TLC). To investigate lung volumes during low-intensity steady-state cycling, we measured EELV by the open-circuit N2 washout method (MR-1, currently Sensormedics 2100) in eight healthy men while at rest and during unloaded and 60-W cycling. TLC was calculated by adding EELV and IC. Measurement variation of TLC was 142 ml at rest, 121 ml during unloaded cycling, and 158 ml during 60-W cycling. TLC did not differ significantly among the three conditions studied. EELV decreased during unloaded (P less than 0.002) and 60-W cycling (P less than 0.001) compared with rest. End-inspiratory lung volume increased only during 60-W cycling (P = 0.03). The decrease in EELV accounted for 100% of the increase in tidal volume during unloaded cycling. Although minute ventilation was similar in the subjects during unloaded cycling, we noted that breathing patterns varied among the subjects. The increase in respiratory frequency was negatively correlated to the change in tidal volume (R2 = 0.54, P = 0.038) and to the change in end-inspiratory lung volume (R2 = 0.68, P = 0.012). We conclude that TLC does not differ significantly during low-intensity steady-state cycling and that use of IC to estimate changes in EELV is appropriate.