Hormonal, electrolyte, and renal responses to exercise are intensity dependent

Previous work indicates that the magnitude and direction of renal responses to exercise depend on the exercise intensity. To examine mechanisms responsible for these findings, renal and hormonal responses were studied in eight healthy male subjects (29.6 +/- 1.9 yr) before and immediately after four 20-min bouts of submaximal exercise (cycle ergometry) at work loads representing 25, 40, 60, and 80% of maximal oxygen consumption. Urine flow, osmotic clearance, glomerular filtration rate, and sodium excretion (UNa+V) all tended to rise at the 25% work load but were markedly reduced at the higher work intensities. Changes in urine flow paralleled changes in glomerular filtration rate (r = 0.91). Plasma vasopressin (ADH), aldosterone, and plasma renin activity tended to increase progressively with increases in work load, with the increases for all hormones reaching statistical significance when the level of exercise reached greater than or equal to 60% of maximal oxygen consumption. However, atrial natriuretic peptide was elevated (P less than 0.05) at all work loads from greater than 1.6-fold of control levels at the 25% work load to greater than 7-fold at the 80% work load. The increase in urine flow (6 of 8 subjects) and UNa+V (7 of 8 subjects) may be due to the increase in atrial natriuretic peptide and/or a 10% suppression (P less than 0.05) of ADH at the 25% work load.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ability of man to detect increases in his breathing.

The ability of four normal subjects to detect increases in their ventilation was studied at rest and at two levels of exercise using a raised inspired Pco2 to further increase ventilation. Subjects signaled when the increase in ventilation was recognized. The average tidal volume (VT) at rest was 520 ml with a frequency of 14; these values increased to an average of 3,300 ml and 21 at the highest work load. There was no significant change in frequency with CO2. Detection occurred when the tidal volume increased by 700 ml (varying 550-890 between subjects but constant for any one subject at the three levels of ventilation.) Thus the appreciation of increase is proportionately more sensitive at higher levels of ventilation. Experiments in which the ventilation was increased by hypoxia or by following a visual demand, and observations of other sensations (oral, cerebral) indicate that the increase in vetilation is recognized through increased breathing rather than awareness of ventilatory stimuli.     

Metabolic responses to light arm and leg exercise when sitting

Seven male subjects performed progressive exercises with a light work load on an upper limb or bicycle ergometer in the sitting position. At any comparable work load above zero, arm exercise induced higher oxygen uptake, ventilation, heart rate, oxygen pulse, respiratory rate and tidal volume than leg exercise. At similar levels of VO2 above 0.45 1 X min-1, heart rate and ventilation were higher during arm exercise. A close linear relationship between carbon dioxide output and oxygen uptake was observed during both arm and leg exercises, the slope for arm work being steeper. The ventilatory equivalent for VCO2 (VE/VCO2) gradually decreased during both types of exercise. The ventilatory equivalent for VO2(VE/VO2) remained constant (arm) while it rose (leg) to a peak at 9.8 W and then gradually decreased. Ventilation in relation to tidal volume had a linear relationship with leg exercise, but became curvilinear with arm exercise after tidal volume exceeded 1100 ml. The observed differences in response between arm and leg exercises at a given work load appear to be influenced by differences in sympathetic outflow due to the greater level of static contraction of the relatively small muscle groups required by arm exercise.     

Oxygen uptake/heart rate relationship in leg and arm exercise, sitting and standing.

The effect of leg exercise and of arm exercise in sitting and standing body positions on energy output and on some cardiorespiratory parameters was studied in seven male subjects. Oxygen uptake (VO2), heart rate (fH), pulmonary ventilation (VE) and respiratory frequency were measured at rest, in the 7-8th min of submaximal work (300, 600, 900 kpm/min), and at maximal effort. Significantly higher Vo2, fH, and VE in arm cranking than in cycling were found at submaximal work loads above 300 kpm/min. Though the maximal work load in arm exercise was 50-60% of that in cycling, Vo2 in arm work was at maximal effort only 22% lower than in leg exercise while the difference in fH was insignificant. No differences were found in arm work between the results obtained at any work level in sitting and standing body positions. The only postural difference in arm work was a 13% higher work load achieved at maximal effort when standing than when sitting. Differences in fH between arm and leg exercise were much smaller for the same Vo2 than for the same work load and were time dependent. While fH quickly leveled off in leg exercise, fH in arm cranking rose steadily during the first 6 min of work which created the fH differences observed in the 7-8 min of submaximal arm arm and leg exercise. At submaximal work levels a tendency to synchronize the respiratory frequency with the frequency of the rotatory movements was more apparent in arm cranking than in cycling.     

Effect of respiratory alkalosis during exercise on blood lactate

A biofeedback model of hyperventilation during exercise was used to assess the independent effects of pH, arterial CO2 partial pressure (PaCO2), and minute ventilation on blood lactate during exercise. Eight normal subjects were studied with progressive upright bicycle exercise (2-min intervals, 25-W increments) under three experimental conditions in random order. Arterialized venous blood was drawn at each work load for measurement of blood lactate, pH, and PaCO2. Results were compared with those from reproducible control tests. Experimental conditions were 1) biofeedback hyperventilation (to increase pH by 0.08-0.10 at each work load); 2) hyperventilation following acetazolamide (which returned pH to control values despite ventilation and PaCO2 identical to condition 1); and 3) metabolic acidosis induced by acetazolamide (with spontaneous ventilation). The results showed an increase in blood lactate during hyperventilation. Blood lactate was similar to control with hyperventilation after acetazolamide, suggesting that the change was due to pH and not to PaCO2 or total ventilation. Exercise during metabolic acidosis (acetazolamide alone) was associated with blood lactate lower than control values. Respiratory alkalosis during exercise increases blood lactate. This is due to the increase in pH and not to the increase in ventilation or the decrease in PaCO2.     

Effect of elastic loading on ventilatory pattern during progressive exercise

Ventilatory responses to progressive exercise, with and without an inspiratory elastic load (14.0 cmH2O/l), were measured in eight healthy subjects. Mean values for unloaded ventilatory responses were 24.41 +/- 1.35 (SE) l/l CO2 and 22.17 +/- 1.07 l/l O2 and for loaded responses were 24.15 +/- 1.93 l/l CO2 and 20.41 +/- 1.66 l/l O2 (P greater than 0.10, loaded vs. unloaded). At levels of exercise up to 80% of maximum O2 consumption (VO2max), minute ventilation (VE) during inspiratory elastic loading was associated with smaller tidal volume (mean change = 0.74 +/- 0.06 ml; P less than 0.05) and higher breathing frequency (mean increase = 10.2 +/- 0.98 breaths/min; P less than 0.05). At levels of exercise greater than 80% of VO2max and at exhaustion, VE was decreased significantly by the elastic load (P less than 0.05). Increases in respiratory rate at these levels of exercise were inadequate to maintain VE at control levels. The reduction in VE at exhaustion was accompanied by significant decreases in O2 consumption and CO2 production. The changes in ventilatory pattern during extrinsic elastic loading support the notion that, in patients with fibrotic lung disease, mechanical factors may play a role in determining ventilatory pattern.     

Effect of inspiratory resistive loading on control of ventilation during progressive exercise

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.     

Exercise hyperventilation in patients with McArdle's disease

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.     

Blood lactate responses in incremental exercise as predictors of constant load performance

Seven trained male cyclists (VO2max = 4.42 +/- 0.23 l.min-1; weight 71.7 +/- 2.7 kg, mean +/- SE) completed two incremental cycling tests on the cycle ergometer for the estimation of the "individual anaerobic threshold" (IAT). The cyclists completed three more exercises in which the work rate incremented by the same protocol, but upon reaching selected work rates of approximately 40, 60 and 80% VO2max, the subjects cycled for 60 min or until exhaustion. In these constant load studies, blood lactate concentration was determined on arterialized venous ([La-]av) and deep venous blood ([La-]v) of the resting forearm. The av-v lactate gradient across the inactive forearm muscle was -0.08 mmol.l-1 at rest. After 3 min at each of the constant load work rates, the gradients were +0.05, +0.65* and +1.60* mmol.l-1 (*P less than 0.05). The gradients after 10 min at these same work rates were -0.09, +0.24 and +1.03* mmol.l-1. For the two highest work rates taken together, the lactate gradient was less at 10 min than 3 min constant load exercise (P less than 0.05). The [La-]av was consistently higher during prolonged exercise at both 60 and 80% VO2max than that observed at the same work rate during progressive exercise. At the highest work rate (at or above the IAT), time to exhaustion ranged from 3 to 36 min in the different subjects. These data showed that [La-] uptake across resting muscle continued to increase to work rates above the IAT. Further, the greater av-v lactate gradient at 3 min than 10 min constant load exercise supports the concept that inactive muscle might act as a passive sink for lactate in addition to a metabolic site.     

Modulation of cytokine profiles by malaria pigment--hemozoin: role of IL-10 in suppression of proliferative responses of mitogen stimulated human PBMC

The malaria parasite pigment hemozoin (Hz) is internalized by circulating and resident phagocytes and modulates their functions. We report here that Hz from Plasmodium falciparum inhibits proliferative responses of PHA stimulated human peripheral blood mononuclear cells (PBMC) in a dose dependent manner. Hz phagocytosed monocyte/macrophages (MO/MQ) secreted high levels of IL-10, IL-1beta and TNF-alpha, but inhibition of proliferation was mediated by IL-10 alone which was reversed by neutralization of the cytokine. Drastic decrease in the levels of IL-2, IL-12 and IFN-gamma were observed in supernatants from PBMC stimulated in the presence of Hz loaded MO/MQ cells. Exogenous addition of these cytokines did not abrogate immunosuppression indicating the inability of these cytokines to enhance proliferation in the presence of IL-10. We provide additional data that the IL-10 levels correlated positively with the load of Hz in the MO/MQ. Kinetics of IL-10 secretion analyzed up to day 6 in MO/MQ cultures fed with Hz revealed that high levels of IL-10 were secreted during the first 48 h after ingestion and decreased drastically at later time points.     

Sinoaortic contribution to ventilatory control in exercising dogs

The role of the sinoaortic reflexes in the regulation of ventilation during exercise was evaluated in seven awake dogs prepared with chronic tracheostomies and arterial catheters. Each dog ran on a treadmill at several work loads before and after sinoaortic denervation and served as its own control. Minute ventilation in the sinoaortic denervated state was significantly reduced from intact values by 10-40% at the mild and moderate levels of exercise [O2 uptake (VO2) = 30-50 ml . kg-1 . min-1] mainly as a result of a lowering respiratory frequency. At higher work loads (VO2 = 70-80 ml . kg-1 . min-1) minute ventilation was similar in the intact and denervated states, but the pattern of ventilation was altered with a higher frequency and a lower tidal volume in the denervated state. The rise in ventilation toward a stable plateau was slower at all work loads in the denervated than in the intact state. After sinoaortic denervation, arterial PCO2(PaCO2) levels were significantly elevated above intact PaCO2 levels during both the preexercise period and the steady state at all exercise levels. These results suggest that the sinoaortic reflexes contribute to both the control of ventilation and the pattern of breathing during mild and heavy levels of exercise in the conscious dog.     

Continuous measurement of breathlessness during exercise: validity, reliability, and responsiveness.

A continuous method for recording changes in breathlessness (dyspnea) during exercise is introduced and compared with the traditional discrete method. In study 1, a category-rating scale was presented on a computer screen, and 14 healthy, young female subjects exercised on a cycle ergometer until exhaustion. Two approaches were used to obtain ratings of breathlessness: a discrete method, in which subjects gave single judgments every minute, and a continuous method, in which subjects throughout exercise moved the mouse so that a bar on the screen extended to the desired location along the scale. Psychophysical results relating measures of breathlessness and the variables of work, oxygen consumption, and minute ventilation were statistically indistinguishable with the two methods, and both methods were highly reliable across test sessions. In study 2, both measurement methods were employed, and the subjects were 14 healthy, young males. In each of two sessions (discrete or continuous method), subjects first rated their breathlessness during an incremental test in which the workload was increased over time and levels of work, and minute ventilation were recorded. Subjects then exercised for 10 min at 60% of the maximal oxygen consumption achieved during the incremental test. At two points during steady-state exercise, a respiratory load was introduced that lasted for 1 min. It was possible to determine the responsiveness of subjects to onset and offset of the respiratory load for the continuous method but not for the discrete method. In study 3, patients with chronic obstructive pulmonary disease employed both methods, and it was found that the continuous method was better at determining whether subjects showed a significant positive slope of the regression line between breathlessness ratings and physiological variables.     

Metabolic and ventilatory responses to hypoxia in two altitudinal populations of the toad, Bufo bankorensis

Effects of hypoxia on resting oxygen consumption (MO2), lung ventilation, and heart rate at different ambient PO2 were compared between lowland and high altitude populations of the toad, Bufo bankorensis. Resting MO2 decreased significantly in mild hypoxia (PO2 = 120 mm Hg) at 10 degrees C and in moderate hypoxia (PO2 = 80 mm Hg) at 25 degrees C in both altitudinal populations; however, resting MO2 did not differ significantly between the two populations. Numbers of lung ventilation periods (VP) and total inspired volume (VL) did not change with PO2 at 10 degrees C, but did increase at moderate and severe hypoxia (40 mm Hg), respectively, at 25 degrees C. Resting heart rates did not change during hypoxia and did not differ between altitude populations. The results suggest (1) the effect of PO2 change on MO2 should be considered in future studies involving transfer of anurans to a different altitude; and (2) the metabolic and ventilatory physiology in B. bankorensis does not compensate for the low temperature and PO2 at high altitude.     

Disturbance of sports performance after partial sleep deprivation

The changes in cardiac and ventilatory responses were measured in 7 endurance athletes during physical exercise on a bicycle ergometer, taking place after a control night and after a night with partial sleep deprivation in the middle of the night. The results show that, despite the maximal work load was not modified with control, heart rate, ventilation and VE/VO2 ratio (ERO2) were greater at the submaximal (75% of the VO2 max) and maximal work load and oxygen consumption decreased at maximal work, after the night of partial sleep deprivation as compared to the control. These findings suggest that acute sleep loss may contribute to alter the endurance performance by impairment of aerobic pathways.     

Role of carotid chemoreceptors and pulmonary vagal afferents during helium-oxygen breathing in ponies

Our purpose was to assess compensatory breathing responses to airway resistance unloading in ponies. We hypothesized that the carotid bodies and hilar nerve afferents, respectively, sense chemical and mechanical changes caused by unloading, hence carotid body-denervated (CBD) and hilar nerve-denervated ponies (HND) might demonstrate greater ventilatory responses when decreasing resistance. At rest and during treadmill exercise, resistance was transiently reduced approximately 40% in five normal, seven CBD, and five HND ponies by breathing gas of 79% He-21% O2 (He-O2). In all groups at rest, He-O2 breathing did not consistently change ventilation (VE), breathing frequency (f), tidal volume (VT), or arterial PCO2 (PaCO2) from room air-breathing levels. During treadmill exercise at 1.8 mph-5% grade in normal and HND ponies, He-O2 breathing did not change PaCO2 but at moderate (6 mph-5% grade), and heavy (8 mph-8% grade) work loads, absolute PaCO2 tended to decrease by 1 min of resistance unloading. delta PaCO2 calculated as room air minus He-O2 breathing levels at 1 min demonstrated significant changes in PaCO2 during exercise resistance unloading (P less than 0.05). No difference between normal and HND ponies was found in exercise delta PaCO2 responses (P greater than 0.10); however, in CBD ponies, the delta PaCO2 during unloading was greater at any given work load (P less than 0.05), suggesting finer regulation of PaCO2 in ponies with intact carotid bodies. During heavy exercise VE and f increased during He-O2 breathing in all three groups of ponies (P less than 0.05), although there were no significant differences between groups (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiopulmonary control during exercise in the duck

To determine the importance of nonhumoral drives to exercise hyperpnea in birds, we exercised adult White Pekin ducks on a treadmill (3 degrees incline) at 1.44 km X h-1 for 15 min during unidirectional artificial ventilation. Intrapulmonary gas concentrations and arterial blood gases could be regulated with this ventilation procedure while allowing ventilatory effort to be measured during both rest and exercise. Ducks were ventilated with gases containing either 4.0 or 5.0% CO2 in 19% O2 (balance N2) at a flow rate of 12 l X min-1. At that flow rate, arterial CO2 partial pressure (PaCO2) could be maintained within +/- 2 Torr of resting values throughout exercise. Arterial O2 partial pressure did not change significantly with exercise. Heart rate, mean arterial blood pressure, and mean right ventricular pressure increased significantly during exercise. On the average, minute ventilation (used as an indicator of the output from the central nervous system) increased approximately 400% over resting levels because of an increase in both tidal volume and respiratory frequency. CO2-sensitivity curves were obtained for each bird during rest. If the CO2 sensitivity remained unchanged during exercise, then the observed 1.5 Torr increase in PaCO2 during exercise would account for only about 6% of the total increase in ventilation over resting levels. During exercise, arterial [H+] increased approximately 4 nmol X l-1; this increase could account for about 18% of the total rise in ventilation. We conclude that only a minor component of the exercise hyperpnea in birds can be accounted for by a humoral mechanism; other factors, possibly from muscle afferents, appear responsible for most of the hyperpnea observed in the running duck.     

Plasma norepinephrine and muscle sympathetic discharge during rhythmic exercise in humans

The purpose of this study was to examine the relationship between plasma norepinephrine concentrations (PNE) and efferent muscle sympathetic nerve activity to noncontracting muscle (MSNA) during graded, rhythmic exercise in humans. In the initial study, six healthy men (ages 20-30 yr) performed 2-min bouts of two-arm cycling exercise at power outputs of 0, 10, 20, 40, 60 (n = 6), and 80 (n = 3) W. Heart rate (HR) was recorded and intraneural measurements of MSNA (right peroneal nerve) were made continuously for 2 min before (control) and during exercise at each work load. At least 2 wk later, subjects performed the same exercise bouts at which time HR was measured and a venous (forearm) blood sample was obtained for the subsequent determination of PNE by high-performance liquid chromatography. During exercise, HR increased progressively from 0 to 80 W. Neither MSNA nor PNE increased above control in response to arm cycling at 0, 10, and 20 W [0-16 +/- 1% (SE) of peak work load], but both variables increased progressively at the 40-, 60-, and 80-W (33 +/- 1 to 67 +/- 2% of peak work load) levels (all P less than 0.05). The individual MSNA and PNE responses (% change from control) over the six work loads were directly related (r = 0.80, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hormonal and growth factor responses to heavy resistance exercise protocols

To examine endogenous anabolic hormone and growth factor responses to various heavy resistance exercise protocols (HREPs), nine male subjects performed each of six randomly assigned HREPs, which consisted of identically ordered exercises carefully designed to control for load [5 vs. 10 repetitions maximum (RM)], rest period length (1 vs. 3 min), and total work effects. Serum human growth hormone (hGH), testosterone (T), somatomedin-C (SM-C), glucose, and whole blood lactate (HLa) concentrations were determined preexercise, midexercise (i.e., after 4 of 8 exercises), and at 0, 5, 15, 30, 60, 90, and 120 min postexercise. All HREPs produced significant (P less than 0.05) temporal increases in serum T concentrations, although the magnitude and time point of occurrence above resting values varied across HREPs. No differences were observed for T when integrated areas under the curve (AUCs) were compared. Although not all HREPs produced increases in serum hGH, the highest responses were observed consequent to the H10/1 exercise protocol (high total work, 1 min rest, 10-RM load) for both temporal and time integrated (AUC) responses. The pattern of SM-C increases varied among HREPs and did not consistently follow hGH changes. Whereas temporal changes were observed, no integrated time (AUC) differences between exercise protocols occurred. These data indicate that the release patterns (temporal or time integrated) observed are complex functions of the type of HREPs utilized and the physiological mechanisms involved with determining peripheral circulatory concentrations (e.g., clearance rates, transport, receptor binding). All HREPs may not affect muscle and connective tissue growth in the same manner because of possible differences in hormonal and growth factor release.     

Relationship between hypercapnic and hypoxic stimuli of respiration during muscular activity]

Pulmonary ventilation (V) and alveolar gas composition (PACO2, PAO2) were studied in 12 healthy men who performed gradual muscular work under conditions of controlled hypercapnia, hypoxia, hyperoxia or their combinations. The respiratory response was estimated by absolute values of ventilation at the given PACO2 value and by its rise by 1 mm Hg of increased PACO2 (delta V/delta PACO2) under rest and under transitional and steady-state exercise. The exercise on-switch was accompanied by displacement to the top and an increased slope of the response curve (delta V/delta PACO2) not related to the work load. These changes suggest multiplicative interaction of the neurogenic and hypercapnic drives in the load switch-on. During steady-state exercise an important role of the hypoxic drive was revealed: hypoxemia induced a shift of the delta V/delta PACO2 response curve to a higher level, especially with the great work load. Thus the positive interaction between the hypercapnic and hypoxic respiratory drive augments with muscular exercise.     

Gas exchange abnormalities after pneumonectomy in conditioned foxhounds

Loss of a major portion of lung tissue has been associated with impaired exercise capacity, but the underlying mechanisms are not well defined. We studied the alterations in gas exchange during exercise before and after left pneumonectomy in three conditioned foxhounds. After pneumonectomy, minute ventilation and O2 consumption at comparable submaximal work loads were unchanged but arterial PCO2 at any work load was higher, implying that ventilatory response to CO2 was impaired. Arterial hypoxemia and an elevated alveolar-arterial O2 tension difference (AaDO2) developed during heavy exercise. Using the multiple inert gas elimination technique, we determined the distributions of ventilation-perfusion (VA/Q) ratios postpneumonectomy. Significant increase in VA/Q inequality developed during exercise while the foxhounds were breathing room air, accounting for an average of 42% of the total increase in AaDO2 while diffusion limitation accounted for 58%. While the animals were breathing hypoxic gas mixture, diffusion limitation accounted for an average of 88% of the total increase AaDO2. Cardiac output and O2 delivery were reduced at a given O2 consumption after pneumonectomy. After pneumonectomy, the animals reached O2 consumptions close to the maximum expected for normal dogs. Compensation for the impairment in O2 delivery post-pneumonectomy occurred mainly by an increase in hemoglobin concentration. Training probably played an important role in returning exercise capacity toward prepneumonectomy levels. We conclude that significant abnormalities in gas exchange develop during exercise after loss of 42% of lung tissue, but the animals demonstrate a remarkable ability to compensate for these changes.