Exercise tolerance at 4 and 6 ATA

Seven normal male subjects performed 5-min bicycle exercise ranging from 50-100% maximum oxygen uptake at 4 ATA and three were also studied at 6 ATA. At all pressures, the subjects breathed 0.2 ATA O2 plus nitrogen. All subjects were able to perform maximum work at all pressures. No pressure-dependent variations in heart rate, O2 uptake, or CO2 output were noted. At both 4 and 6 ATA, ventilation was decreased at exercise levels greater than 80% maximum O2 uptake. The magnitude of the decrease was not great, however, and signified only minor CO2 retention. In some instances exercise ventilation closely approached the 15-S maximum breathing capacity and these subjects noted severe dyspnea, possibly due to dynamic compression of large airways. In three subjects, respiratory frequency was measured as well as minute ventilation; this relationship did not change with depth. Subjects performing heavy exercise at 6 ATA noted disturbances of consciousness, presumably due to N2 narcosis.     

Problems of immuno- and mesenchyma-suppressive therapy of inflammatory liver diseases

We have studied maximal oxygen uptake, maximal heart rate, maximal exercise ventilation and the ventilatory response to exercise in 24 male and 14 female Scottish athletes. The values for maximal oxygen uptake are similar to those reported in other international studies. In eight athletes repeat measurements of maximal oxygen uptake 7-11 months after the initial study showed no change from the initial values. The values for the ventilatory response to exercise in our athletes were normal. The relationship is discussed between maximal oxygen uptake and ventilatory responses to exercise, hypoxia and hypercapnia and it is suggested that these may be related to athletic event.     

Effects of head-out water immersion on cardiorespiratory responses to maximal cycling exercise

Our objectives were to determine effects of head-out immersion (HOI), scuba breathing, and water temperature on cardiorespiratory responses to maximal aerobic work. Measurements of VO2, VE, and heart rate (HR) were obtained on seven men (27 yr, 177 cm, 67 kg) as they performed the same upright bicycling exercise to exhaustion (4-5 min) in 23 degrees C air and 30 degrees C water. Maximal oxygen uptake (VO2 max) during HOI was 3.18 liters - min-1, which was not statistically different from the mean of 3.29 liters- min-1 in air. When compressed air was breathed via scuba during HOI, VO2 max was 3.12 liters- min-1 and not significantly different from that when room air was breathed and a low-resistance valve in water was used. HOI decreased VE by 15.7 liters - min-1 and HR by 10 beats (b) - min-1. Scuba breathing further reduced VE by 22.0 liters - min-1. Similar measurements were made on four of the subjects after 18 min of HOI in water temperatures of 35,30, and 25 degrees C. Water temperature had no significant affect on VO2 max, although HR was 8 b- min-1 lower in 30 degrees C and 15 b - min-1 lower in 25 degrees C as compared to 35 degrees C water. The results show that VO2 max was not significantly changed by HOI, scuba breathing, or brief exposures to 25, 30, and 35 degrees C water, despite significant reductions that occurred for VE and HR.     

Ventilatory responses in man to hypoxia and hypercapnia under conditions of decreased respiratory resistance

In young healthy male adults, a decrease in the mechanical load of the ventilatory apparatus was followed by readjustment in the respiratory cycle. During hyperventilation due to an enhanced hypercapnic stimulus, a reduction of resistance against breathing tells on the value of ventilatory response, the latter being greater than when breathing with mixtures of ordinary density. The data obtained confirm the significance of value of the mechanical load of respiratory apparatus for formation of ventilatory response to hypoxia and hypercapnia.     

Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans

Sixteen healthy volunteers breathed 100% O2 or room air for 10 min in random order, then their ventilatory response to sustained normocapnic hypoxia (80% arterial O2 saturation, as measured with a pulse oximeter) was studied for 20 min. In addition, to detect agents possibly responsible for the respiratory changes, blood plasma of 10 of the 16 subjects was chemically analyzed. 1) Preliminary O2 breathing uniformly and substantially augmented hypoxic ventilatory responses. 2) However, the profile of ventilatory response in terms of relative magnitude, i.e., biphasic hypoxic ventilatory depression, remained nearly unchanged. 3) Augmented ventilatory increment by prior O2 breathing was significantly correlated with increment in the plasma glutamine level. We conclude that preliminary O2 administration enhances hypoxic ventilatory response without affecting the biphasic response pattern and speculate that the excitatory amino acid neurotransmitter glutamate, possibly derived from augmented glutamine, may, at least in part, play a role in this ventilatory enhancement.     

Regulation of breathing in hyperthyroidism: relationship to hormonal and metabolic changes

We sought to examine the breathing pattern, inspiratory drive and chemosensitivity of hyperthyroid patients and to explore the interactions between their thyroid hormones, basal metabolism and chemosensitivity. We studied 15 hyperthyroid patients and 15 sex- and age-matched controls. Thyroid hormone levels, arterial blood gas tensions, lung volumes, diffusing capacity for CO, maximal respiratory pressures and oxygen uptake measurements were performed. Breathing pattern and mouth occlusion pressure (P0.1), as well as ventilatory and P0.1 responses to hyperoxic progressive hypercapnia and isocapnic progressive hypoxia, were also evaluated. Compared with the control subjects, the hyperthyroid patients showed significantly lower resting arterial CO2 tension, tidal volume and significantly higher mean inspiratory flow and P0.1. Ventilatory and P0.1 responses to CO2 and hypoxia were also greater in the hyperthyroid patients than in the control group. All these changes returned to normal after treatment. In the patients, significant relationships between tri-iodothyronine and P0.1, P0.1 response to hypoxia, and P0.1 response to hypercapnia were found. In contrast, in hyperthyroidism there was no relationship between oxygen uptake and P0.1 response to hypoxia. We conclude that hyperthyroid patients exhibit a significant relationship between their thyroid hormone levels and their increased inspiratory drive and chemosensitivity.     

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.     

Regulation of ventilatory capacity during exercise in asthmatics

In asthmatic and control subjects, we examined the changes in ventilatory capacity (VECap), end-expiratory lung volume (EELV), and degree of flow limitation during three types of exercise: 1) incremental, 2) constant load (50% of maximal exercise capacity; 36 min), and 3) interval (alternating between 60 and 40% of maximal exercise capacity; 6-min workloads for 36 min). The VECap and degree of flow limitation at rest and during the various stages of exercise were estimated by aligning the tidal breathing flow-volume (F-V) loops within the maximal expiratory F-V (MEFV) envelope using the measured EELV. In contrast to more usual estimates of VECap (i.e., maximal voluntary ventilation and forced expiratory volume in 1 s x 40), the calculated VECap depended on the existing bronchomotor tone, the lung volume at which the subjects breathed (i.e., EELV), and the tidal volume. During interval and constant-load exercise, asthmatic subjects experienced reduced ventilatory reserve, higher degrees of flow limitation, and had higher EELVs compared with nonasthmatic subjects. During interval exercise, the VECap of the asthmatic subjects increased and decreased with variations in minute ventilation, due in part to alterations in their MEFV curve as exercise intensity varied between 60 and 49% of maximal capacity. In conclusion, asthmatic subjects have a more variable VECap and reduced ventilatory reserve during exercise compared with nonasthmatic subjects. The variations in VECap are due in part to a more labile MEFV curve secondary to changes in bronchomotor tone. Asthmatics defend VECap and minimize flow limitation by increasing EELV.     

Critical behavior of random walks

Cardiopulmonary exercise testing is commonly used to assess patients with heart failure. Analysis of expired gases during exercise requires the use of either a facemask or mouthpiece with nose clip. The authors sought to determine if the method of expired gas collection during exercise testing (facemask or mouthpiece) influences gas exchange measurements in patients with heart failure. Nine patients with heart failure performed two maximal treadmill tests. Expired gases were collected with a facemask in one exercise test and a mouthpiece in the other. There were no significant differences in exercise test duration, peak oxygen uptake, heart rate, respiratory exchange ratio, or perceived exertion during maximal exercise performed with the facemask when compared to the mouthpiece. Test subjects reported that the overall comfort of the facemask was significantly greater than that of the mouthpiece (P < .02). The method of expired gas collection during cardiopulmonary exercise testing does not significantly affect measures of gas exchange or exercise performance in patients with heart failure. Heart failure patients find the overall comfort of the facemask superior to that of the mouthpiece, but this comfort preference does not affect exercise performance.     

Effect of step duration during incremental exercise on breathing pattern and mouth occlusion pressure

We compared the effects of two step durations on breathing pattern, mouth occlusion pressure and "effective" impedance of the respiratory system during incremental exercise. Nine normal subjects (mean age: 27.8+/-1.21 years) performed two incremental exercise tests in randomized order: one test with step increments every 1 min 30s and the other, every 4 min. After a warm-up at 25 W for the 1 min 30 s test, the power was increased by 50 W from 50 W to exhaustion. During the last minute at each power, we measured ventilation (VE), tidal volume (VT), breathing frequency (fR), inspiratory and expiratory time (TI and TE), total time of the respiratory cycle (TTOT), TI/TTOT, mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1), "effective" impedance of the respiratory system (P0.1/(VT/ TI)) and venous blood lactate concentration ([La]). Our result showed that at maximal exercise the power was significantly higher (p < 0.01) and [La] lower (p < 0.01) in the 1 min 30 s test. At 100, 150 and 200 W, the 4 min test showed significantly higher oxygen uptake (VO2), carbon dioxide output (VCO2), VE, P0.1, fR, VT/TI and HR (p <0.001) and significantly lower TI, TE and TTOT (p<0.01). [La] was significantly higher at 150 W (p<0.05) and 200 W (p<0.001). At the same VCO2, P0.1 was not significantly different between the two tests, whereas VE showed a tendency to be higher (p = 0.08) and P0.1/(VT/TI) was significantly lower during the 4 min test. In conclusion, this study allowed us to quantify the difference in inspiratory neuromuscular output and ventilatory response between 1 min 30s and 4 min tests and showed that different step durations alter the relationship between inspiratory neuromuscular output and mean inspiratory flow.     

Function of the diaphragm during exercise]

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30%, 60%, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Respiratory pressures, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. The respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.     

Assessment of ventilatory neuromuscular drive in patients with obstructive sleep apnea

The presence of abnormalities of the respiratory center in obstructive sleep apnea (OSA) patients and their correlation with polysomnographic data are still a matter of controversy. Moderately obese, sleep-deprived OSA patients presenting daytime hypersomnolence, with normocapnia and no clinical or spirometric evidence of pulmonary disease, were selected. We assessed the ventilatory control and correlated it with polysomnographic data. Ventilatory neuromuscular drive was evaluated in these patients by measuring the ventilatory response (VE), the inspiratory occlusion pressure (P.1) and the ventilatory pattern (VT/TI, TI/TTOT) at rest and during submaximal exercise, breathing room air. These analyses were also performed after inhalation of a hypercapnic mixture of CO2 (delta P.1/delta PETCO2, delta VE/delta PETCO2). Average rest and exercise ventilatory response (VE: 12.2 and 32.6 l/min, respectively), inspiratory occlusion pressure (P.1: 1.5 and 4.7 cmH2O, respectively), and ventilatory pattern (VT/TI: 0.42 and 1.09 l/s; TI/TTOT: 0.47 and 0.46 l/s, respectively) were within the normal range. In response to hypercapnia, the values of ventilatory response (delta VE/delta PETCO2: 1.51 l min-1 mmHg-1) and inspiratory occlusion pressure (delta P.1/delta PETCO2: 0.22 cmH2O) were normal or slightly reduced in the normocapnic OSA patients. No association or correlation between ventilatory neuromuscular drive and ventilatory pattern, hypersomnolence score and polysomnographic data was found; however a significant positive correlation was observed between P.1 and weight. Our results indicate the existence of a group of normocapnic OSA patients who have a normal awake neuromuscular ventilatory drive at rest or during exercise that is partially influenced by obesity.     

Enhancement of exercise-induced asthma by cold air

To study the possibility that the inhalation of cold air accentuates the bronchoconstrictor response to exercise in asthma, eight subjects exercised while breathing air at ambient or subfreezing temperatures. On a separate day, cold air was breathed at rest so as to isolate the effects of this stimulus. Pulmonary mechanics were measured before and after each experiment. In all subjects acute bronchoconstriction followed the control exercise challenge. With cold-air breathing, however, the magnitude of the response was markedly enhanced. Residual volume increased 158 per cent more than it did previously, and specific conductance and one-second forced expiratory volumes changed an additional 85 and 100 per cent, respectively. The effects of cold air at rest were very small. The results demonstrate a positive interaction of two common naturally occurring stimuli in the induction of asthmatic attacks, and constitute objective verification of a frequent clinical complaint.     

Cardiac role in exercise limitation in asthmatic subjects with special reference to disease severity

We wanted to assess limitations in cardiorespiratory fitness of asthmatic subjects, acclimatized to 1,300 m altitude and in a clinically stable state. We therefore studied 16 young asthmatic and 8 normal young subjects during an incremental bicycle exercise test. The asthmatics were divided into two groups, according to the Aas classification: a moderate asthma group (degree 2 and 3, no pulmonary impairment during symptom-free intervals), and a severe asthma group (degree 4 and 5, with persistent airway obstruction). The results showed that cardiorespiratory fitness is limited in severe asthmatic subjects acclimatized to an altitude of 1,300 m, due to decreased cardiac output and stroke volume. At submaximal exercise, the lower stroke volume is compensated by an increased arteriovenous oxygen content difference, but this compensation no longer exists at maximal exercise, which explains the lower maximal oxygen uptake in the severe asthma group. The hypothesis that the high tidal volume in the severe asthma group could lead to a decrease in left ventricular performance is considered. In conclusion, with respect to cardiorespiratory response to exercise, asthmatics should not be considered as a homogeneous group. Furthermore, relationship between ventilatory requirement and its consequences upon cardiac stroke volume provides a strong argument for the physical rehabilitation of asthmatics. Indeed, aerobic training can decrease the ventilation level for a given workload, and thus reduce inappropriate adaptations to exercise.     

Contribution of peripheral chemoreceptor drive in exercise hyperpnea in humans

The peripheral chemoreceptors play a dominant role in the respiratory compensation of lactic acidosis during heavy exercise of humans. Our object was to determine the contribution of peripheral chemoreceptors to exercise hyperpnea during mild to moderate and heavy exercise above the anaerobic threshold. We used a hyperoxic suppression test in six normal male subjects. Inspired gas was abruptly changed without the subject's knowledge from air to pure oxygen for 5 to 6 breaths. The maximal ventilatory depression after O2 breathing was 5.5 +/- 1.7 L/min (BTPS) at mild exercise, and the depression increased with increasing exercise intensity up to 12.8 +/- 4.1 L/min (BTPS). The relative contribution of the peripheral chemoreceptors to ventilation in terms of percentage of the maximal ventilatory depression was maintained, being 20% throughout the entire work ranges studied. The contribution of the peripheral chemoreceptors to total ventilation is hardly altered by lactic acidosis caused by heavy exercise above the anaerobic threshold according to our data. These results suggested that the peripheral chemoreceptors may not be solely responsible for excessive hyperventilation, or residual activities of peripheral chemoreceptors still exist after O2 breathing especially during heavy exercise above the anaerobic threshold.     

Gas exchange during exercise in healthy people II. Venous admixture

1. Venous admixture/cardiac output ratio (Qva/Qt) has been measured in twenty-four healthy volunteer subjects of both sexes aged 20-71 years, at rest and during the steady state of treadmill exercise at two rates of work, and breathing air and breathing oxygen. 2. With oxygen breathing, Qva/Qt was considerably less during exercise than during the time subjects were taking either normal or deep breaths of oxygen at rest, and did not significantly increase with the intensity of exercise. It is postulated that the increase in ventilation during exercise opens most or all of those alveoli which, during oxygen breathing at rest, close because of critically low ventilation/perfusion (V/Q) ratios. 3. With air breathing, Qva/Qt fell from rest to exercise (especially in older subjects), presumably due to improved ventilation of alveoli at the lung bases. With an increase in work rate Qva/Qt increased in all age groups. This increase was not due to increase in the shunt fraction (Qs/Qt), nor to limitation of diffusing capacity; it arose from an increase in V/Q variance. 4. Equations have been derived for the prediction of normal Qva/Qt during exercise, with or without correction for the effects of increasing pulmonary capillary temperature. These effects do not materially influence the accuracy of prediction, but may be relevant to some of the interpretations. In particular, they provide a further indication that Qs/Qt probably cannot be measured by breathing oxygen at rest, even in deep breathing.     

A new oxygen applicator for simultaneous mouth and nose breathing

We have developed a new O2 applicator to try to overcome the problems of long-term oxygen therapy that ensures a sufficient oxygen supply for both nasal and oral breathing and prevents mucosal irritation. Placed on the upper lip, it is unobtrusive. The principle is as follows: due to an enlarged outlet area, turbulence occurs and the oxygen is reduced. Thus, an oxygen cloud is formed that can be inhaled by both mouth or nose. The efficiency of our O2 applicator was compared with a face mask in six healthy subjects and patients with COPD. A similar increase in PO2 was found up to an oxygen flow of 2 L/min for nasal and oral breathing. Mild hypercapnia resulted in three patients with COPD only when a face mask was used and only when patients breathed through the nose. All patients preferred the new applicator.     

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 oxygen uptake (VO2 max): 57 +/- 6 ml . kg-1 . min-1; 35-70 ml . kg-1 . min-1] 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 (VO2 max > 57 ml . kg-1 . min-1, n = 14) vs. less-fit (VO2 max < 56 ml . kg-1 . min-1, n = 15) women caused a higher maximal ventilation (VE) with increased tidal volume (VT) and breathing frequency (fb) at comparable maximal VT/vital capacity (VC). More expiratory flow limitation (EFL; 22 +/- 4% of VT) was also observed during heavy exercise in highly fit vs. less-fit women, causing higher end-expiratory and end-inspiratory lung volumes and greater usage of their maximum available ventilatory reserves. HeO2 (79% He-21% O2) vs. room air exercise trials were compared (with screens added to equalize external apparatus resistance). HeO2 increased maximal expiratory flow rates (20-38%) throughout the range of VC, which significantly reduced EFL during heavy exercise. When EFL was reduced with HeO2, VT, fb, and VE (+16 +/- 2 l/min) were significantly increased during maximal exercise. However, in the absence of EFL (during room air exercise), HeO2 had no effect on VE. We conclude that smaller lung volumes and maximal flow rates for women in general, and especially highly fit women, caused increased prevalence of EFL during heavy exercise, a relative hyperinflation, an increased reliance on fb, and a greater encroachment on the ventilatory "reserve." Consequently, VT and VE are mechanically constrained during maximal exercise in many fit women because the demand for high expiratory flow rates encroaches on the airways' maximum flow-volume envelope.     

Relation between chemosensitivity and the ventilatory response to exercise in chronic heart failure

OBJECTIVES: This study sought to establish the chemosensitivity of patients with chronic heart failure. BACKGROUND: The ventilatory response to exercise is often increased in patients with chronic heart failure, as characterized by the steeper regression slope relating minute ventilation to carbon dioxide output. We hypothesized that the sensitivity of chemoreceptors may be reset and may in part mediate the exercise hyperpnea seen in this condition. METHODS: Hypoxic and peripheral hypercapnic chemosensitivity were studied in 38 patients with chronic heart failure (35 men, 3 women; mean [+/-SE] age 60.2 +/- 1.3 years; radionuclide left ventricular ejection fraction 25.7 +/- 2.3%) and 15 healthy control subjects (11 men, 4 women; mean age 54.9 +/- 3.0 years) using transient inhalations of pure nitrogen and single breaths of 13% carbon dioxide, respectively. The change in chemosensitivity during mild exercise (25 W) was assessed in the first 15 patients and all control subjects. Central hypercapnic chemosensitivity was also characterized in 25 patients and 10 control subjects by the rebreathing of 7% carbon dioxide in 93% oxygen. Cardiopulmonary exercise testing was performed in all subjects. RESULTS: Maximal oxygen consumption was 16.6 +/- 0.9 versus 29.7 +/- 2.2 mol/kg per min (p < 0.0001), and the ventilation-carbon dioxide output regression slope was 37.2 +/- 1.5 versus 26.5 +/- 1.4 (p < 0.0001) in patients and control subjects, respectively. Hypoxic and central hypercapnic chemosensitivity were enhanced in patients (0.707 +/- 0.076 vs. 0.293 +/- 0.056 liters/min per % arterial oxygen saturation [SaO2], p = 0.0001 and 3.15 +/- 0.41 vs. 2.02 +/- 0.25 liters/min per mm Hg, p = 0.025, respectively) and correlated significantly with the ventilatory response to exercise. Hypoxic chemosensitivity was augmented during exercise in patients and in control subjects but remained higher in the former (1.530 +/- 0.27 vs. 0.685 +/- 0.12 liters/min per %SaO2, p = 0.01). The peripheral hypercapnic chemosensitivity of patients at rest and during exercise was similar to that in control subjects, consistent with its lesser contribution to overall carbon dioxide chemosensitivity. CONCLUSIONS: Enhanced hypoxic and central hypercapnic chemosensitivity may play a role in mediating the increased ventilatory response to exercise in chronic heart failure.     

Unaltered oxygen uptake kinetics at exercise onset with lower-body positive pressure in humans

The purpose of this study was to determine the influence of a reduced skeletal muscle blood flow on oxygen uptake (VO2) kinetics at the onset of cycle ergometer exercise. Seven healthy subjects performed rest-to-exercise transitions with a lower-body positive pressure (LBPP) of 45 Torr. Two work rates were selected for each subject: a moderate intensity (VO2, approximately 1.9 l min-1; delta[lactate], approximately 1 mequiv l-1) below the estimated lactate threshold and a heavy intensity (VO2, approximately 2.6 l min-1; delta[lactate], approximately 3 mequiv l-1) above this threshold. Pulmonary gas exchange variables and ventilatory (VE) responses were computed breath-by-breath from mass spectrometer and turbine volume meter signals, respectively, and mean response times (MRT) calculated. Samples of 'arterialized' venous blood were used for the determination of [lactate], pH and [K+]. While the application of 45 Torr LBPP had no effects on VO2 kinetics during moderate exercise (MRT: 33.5 +/- 1.2 s at 45 Torr vs. 32.8 +/- 1.3 s at 0 Torr; P > 0.05) or on [lactate], pH or [K+], breathing frequency (f) was increased (P < 0.05) and tidal volume (VT) reduced (P < 0.05). The addition of LBPP during heavy exercise did not alter VO2 kinetics (MRT: 35.2 +/- 1.5 s at 45 Torr vs. 34.8 +/- 1.5 s at 0 Torr; P > 0.05), or [lactate], pH or [K+]. Although both the VE (via an increased f) and CO2 output (VCO2) were significantly greater with LBPP by approximately 30 l min-1 and approximately 500 ml min-1, respectively, end-tidal CO2 partial pressure was decreasing, suggesting an additional ventilatory stimulus. These data can be interpreted to suggest that oxygen delivery is not critically dependent upon blood flow to the working muscle at exercise onset, while LBPP-induced increases in VE during suprathreshold exercise may be related to an accumulation of metabolites at the working muscle or the effects of pressure per se.