Breathing pattern and occlusion pressure during exercise in pre- and peripubertal swimmers

In two groups of young swimmers (prepubertal stage: group A; peripubertal stage: group B), the ventilatory response to graded exercise work with a cycle ergometer was studied. Ventilatory variables (ventilation, VE, tidal volume, VT, respiratory frequency,f, ratio between inspiratory period and total breath duration, TI/TTOT, and mean inspiratory flow, VT/TI) as well as mouth occlusion pressure measured at 100 msec (P0.1), effective impedance of the respiratory system (P0.1/VT/TI), inspiratory power for breathing (W) and O2 uptake (VO2) were measured during the third minute of each work load. At the same level of exercise both groups showed identical values of VT/TI, but VE was higher in group A individuals. This resulted from higher values of respiratory frequency with higher TI/TTOT ratios. P0.1, P0.1(VT/TI) and W were also much higher during work load in group A than in peripubertal subjects. When the above results were related to the same percentage of VO2 max, P0.1, W, respiratory frequency and duty cycle did not differ within both groups. However, VE, VT and VT/TI were lower in group A subjects with a higher P0.1/(VT/TI) ratio. Further corrections of VT, VT/TI and P0.1/(VT/TI) ratios by body weight cancelled all these differences. In conclusion, our results strongly suggest that biometric factors only determined interindividual differences in ventilatory response to exercise in prepubertal and peripubertal swimmers.     

Breathing pattern and neuromuscular drive during CO2 rebreathing in normal man and in patients with COPD

In 11 normal subjects and in 10 patients with chronic obstructive pulmonary disease we evaluated breathing pattern and mouth occlusion pressure (PO.1), while breathing room air and during reinhalation of a hypercapnic hyperoxic gas mixture. In the breathing pattern we analyzed the time and volume components of the respiratory cycle: tidal volume (VT), inspiratory time (Ti), expiratory time (Te), total time of respiratory cycle (Ttot); mean inspiratory flow (VT/Ti) and Ti/Ttot ratios, respiratory frequency (RF) and instantaneous ventilation (VE). In the normal subjects, increase in VE during rebreathing mainly depended on an increase in both VT and VT/Ti without significant changes in Ti. During CO2 rebreathing the patients exhibited a lesser increase in VE compared to normals, due to a lesser increase in VT. However, expressing VT in percent of resting inspiratory capacity showed that VT attained at the end of rebreathing (VTmax) was similar to that noted in the normal subjects at the same minute of rebreathing. Furthermore, percent increase in VE, VT, VT/Ti and PO.1 between resting value and that at 56 mm Hg (delta %), were significant in both groups with a major increase in the normal subjects for VE and VT/Ti. In comparison, delta % decreases in both Te and Ttot were found to be significant only in the normal subjects. VT/Ti was related to VE in a similar way in the two groups. In contrast, in the normal subjects, Ti/Ttot did not increase with increasing VE. During rebreathing increase in PO.1 was found to be similar in the normal subjects and in patients. However, for a given neuromuscular drive VE and VT/Ti were greater in the normal subjects than in the patients. These data show that in the patients as a whole no significant changes in breath intervals occur during CO2 rebreathing. Furthermore, in patients, in spite of a similar increase in neuromuscular drive, the efficiency by which inspiratory muscle output (PO.1) is converted into VT/Ti was found to be reduced.     

Neural respiratory drive and neuromuscular coupling during CO2 rebreathing in patients with chronic interstitial lung disease

In 12 patients with CILD and 18 age-matched normal subjects we assessed the ventilatory control system at three levels: (a) neural, as assessed by EMGd (XP/Ti) and EMGint muscles via surface electrodes; (b) muscular, as assessed by mouth occlusion pressure (P0.1); and (c) ventilatory, as assessed by both ventilation (VE) and the related parameters, tidal volume (VT) and respiratory frequency (f). Compared with a normal control group, patients exhibited a significant decrease in lung volumes and in MIP; VT and inspiratory time (Ti) were significantly lower, while VT/Ti, P0.1, and both EMGd and EMGint were significantly greater in patients. During a CO2 rebreathing test, patients exhibited significantly greater EMGd, EMGint, and P0.1 responses to increasing PETCO2 than the control group. VE response slopes were similar in the two groups. For a given EMGd response slope (delta XP/Ti/delta PETCO2), the average P0.1 response slope (delta P0.1/delta PETCO2) was found to be significantly lower in patients than in the normal control group. Compared with normal subjects, CILD patients have a normal or increased neural component of respiratory activity and relatively low neuromuscular coupling (delta P0.1/delta XP/Ti). The decreased neuromuscular coupling could be explained in these patients by a reduced inspiratory muscle strength.     

Ventilatory drive and respiratory muscle function in pregnancy

It has been demonstrated that during pregnancy expiratory reserve volume (ERV) decreases and minute ventilation (VE) increases initially and then stabilizes. In order to determine the role of thoracoabdominal mechanics, control of breathing, and inspiratory muscle function in these alterations, we studied inspiratory pressures, lung volumes, thoracic configuration, and respiratory drive in 18 normal pregnant women at Weeks 13, 21, 30, and 37 of pregnancy. Ten of them were studied 6 months after delivery. Transdiaphragmatic pressure (Pdi) was measured at Week 37 and 3 months after delivery in an additional group of seven women. VE as well as VT/TI increased early during gestation and remained unchanged thereafter. In contrast, mouth occlusion pressure (P0.1) increased progressively during pregnancy, from 1.53 +/- 0.16 (mean +/- SE) to 2.02 +/- 0.18 cm H2O, and fell significantly to 1.1 +/- 0.15 cm H2O after delivery, indicating that effective respiratory impedance increases during pregnancy. Mean P0.1 correlated with progesterone plasma levels (r = 0.918 p less than 0.05). No changes in Plmax, PEmax, and Pdimax, were observed. End-expiratory gastric pressure (Pga) increases significantly during pregnancy: 11.8 +/- 0.8 versus 8.4 +/- 1.12 cm H2O after delivery (p less than 0.012). This increment was correlated with the fall in ERV observed in late pregnancy (r = 0.74 p less than 0.05). Our results demonstrate that during pregnancy ventilatory drive and respiratory impedance increase with the consequent stabilization of VE, but our data do not permit us to differentiate whether the increment in P0.1 is secondary to the increase in impedance or to the rise in progesterone. Respiratory muscle function remains normal despite the alteration of thoracic configuration.     

Differential effects of beta-adrenergic blockade on P0.1 and mean inspiratory flow

To quantitatively examine and compare the effects of beta-adrenergic blockade on ventilation, we studied 20 healthy volunteers during inhalation of room air and at steady state CO2 (2.0, 4.4, 6.0%) following a single oral dose of bupranolol (vs. placebo). During room air breathing, minute ventilation (VE) and mean inspiratory flow (VT/TI) were significantly reduced after beta-blockade with a concomitant increase in blood PaCO2 (p less than 0.01). The timing factor TI/Ttot and mouth occlusion pressure P0.1 remained unchanged. These differences were, as shown from calculated effective alveolar ventilation, mainly attributed to a decrease in physiological dead space ventilation following beta-blockade. With a stepwise increase in FICO2, the difference in PaCO2 between placebo and bupranolol tended to approach zero, whereas VE and VT/TI remained significantly lower during beta-blockade (P less than 0.05). In contrast, no difference existed in P0.1 between bupranolol and placebo. We suggest that (1) respiratory drive assessed by P0.1 is unaffected by beta-blockade and (2) mean inspiratory flow depends also on CO2 elimination characteristics, which are influenced by beta-blockade.     

Respiratory responses to changes in airflow resistance in conscious man.

The time course and magnitude of adjustments in respiratory activity during the application and following the removal of inspiratory resistive loads were determined in conscious men. Changes in airflow resistance were made periodically during rebreathing of a gas mixture of carbon dioxide and oxygen. Ventilation, the ratio of tidal volume to inspiratory duration and the mouth pressure during airway occlusion, 100 ms after the onset of inspiration were used as measures of inspiratory neuromuscular activity. The occlusion pressure was measured during each breath using an electrically activated solenoid shutter which obstructed the airway for only the first 100 ms of each inspiration. During the second breath following the application of the resistive load, there was an increase in inspiratory output which occurred independently of changes in PCO2 and PO2. Further increases in inspiratory activity during successive loaded breaths, however, were due exclusively to changing chemical drive. The level of inspiratory neuromuscular activity remained elevated for a single breath following removal of the added resistance. Adjustments in respiratory activity were greater the more severe the load. The results suggest that non-chemically mediated respiratory compensation in conscious individuals develops rapidly and is important in maintaining ventilation when breathing is encumbered.     

Active inspiratory impedance and neuromuscular respiratory output during halothane anaesthesia in humans

The aim of this study was to measure, in 11 patients with healthy lungs, active inspiratory impedance during anaesthesia. In addition, we recorded changes in inspiratory occlusion pressure at 100 ms (P0.1) and ventilatory pattern while awake and during anaesthesia with a mean inspiratory fraction (FI) of 0.017 halothane in O2. The total active inspiratory resistance and elastance values were 5.4 +/- 3.3 hPa.l.1.s and 29.9 +/- 6.2 hPa.l.1, respectively. P0.1 and the ratio between P0.1 and mean inspiratory flow (P0.1/(VT/TI)) increased 124% (p less than 0.001) and 68% (p less than 0.001), respectively, during anaesthesia. Respiratory frequency rose significantly from 12.2 +/- 1.5 (mean +/- SD) to 24.6 +/- 4.6 cycles.min-1, while tidal volume and inspiratory duty cycle lowered significantly from 0.599 +/- 0.195 l and 0.44 +/- 0.04 to 0.372 +/- 0.088 l (p less than 0.001) and 0.40 +/- 0.04 (p less than 0.05), respectively. Minute ventilation (VE) and VT/TI did not change significantly. During halothane anaesthesia with an FI:0.017, the increase in neuromuscular respiratory output appears to compensate for the increased mechanical load, thus resulting in maintenance of VE at levels similar to those of an awake state.     

Ventilatory responses to chemosensory stimuli in quadriplegic subjects

We tested the hypothesis that interruption of motor traffic running down the spinal cord to respiratory muscle motoneurons suppresses the ventilatory response to increased chemical drive. We compared the hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses, based on the rebreathing technique, before and during inspiratory flow-resistive loading in 17 quadriplegic patients with low cervical spinal cord transection and in 17 normal subjects. The ventilatory response was evaluated from minute ventilation (VE) and mouth occlusion pressure (P0.2) slopes on arterial oxygen saturation (SaO2) or on end-tidal PCO2 (PACO2), and from absolute VE values at SaO2 80% or at PACO2 55 mmHg. We found no difference in the unloaded HVR or HCVR between the quadriplegic and normal subjects. In the loaded HVR, the delta VE/delta SaO2 slope tended to decrease similarly in both groups of subjects. The delta P0.2/delta SaO2 slope was shifted upwards in normal subjects, yielding a significantly higher P0.2 at a given SaO2. In contrast, this rise in the P0.2 level during loaded HVR was absent in quadriplegics. Loaded HCVR yielded qualitatively similar results in both groups of subjects; delta VE/delta PACO2 decreased and delta P0.2/delta PACO2 increased significantly. The results show that the ventilatory chemosensory responses were unsuppressed in quadriplegics, although they displayed a disturbance in load-compensation, as reflected by occlusion pressure, in hypoxia. We conclude that the descending drive to respiratory muscle motoneurons is not germane to the operation of the chemosensory reflexes.     

Ventilatory regulation in eucapnic morbid obesity

In morbid obesity, there is an increased hindrance to breathing caused by the effects of the increased mass on the chest wall and abdomen; subjects with morbid obesity can maintain eucapnia by increasing inspiratory neuromuscular drive and/or by altering central breath timing. We studied 23 eucapnic, obese subjects (greater than 190% predicted ideal weight), 7 males and 16 females with a mean age of 36.6 +/- 9.2 yr and 18 healthy, normal male subjects. Total lung capacity, functional residual capacity, and total thoracic compliance were significantly (p less than 0.05) reduced in the obese subjects. At rest, minute ventilation was significantly increased because of an increase in respiratory frequency, which in turn was due to a significant decrease in the expiratory time (TE) per breath; the ratio of inspiratory to expiratory time (TI/TE) was thus significantly altered, indicating an alteration in central breath timing. Resting inspiratory neuromuscular drive (as represented by mouth occlusion pressure) was significantly increased in the obese subjects, but tidal volume was not significantly altered. There was an increased ventilatory responsiveness to hypoxia and relatively decreased ventilatory responsiveness to hypercapnia in the obese subjects. These results indicate that morbidly obese subjects maintain eucapnia primarily by an alteration in central breath timing. Although these subjects have decreased responsiveness to CO2, putting them at some risk of developing respiratory failure under conditions of hypercapnic/hypoxic stress, it is possible that this is counteracted by the increased responsiveness to hypoxia.     

Ventilation response and drive during hypoxia in adult patients with asthma.

We studied ventilation and inspiratory muscle activity during progressive isocapnic hypoxia in adult asthmatic patients to determine whether the decreased hypoxic ventilatory response previously identified is due to the mechanical abnormalities of the respiratory system or to low respiratory center output. The mouth pressure produced by inspiratory muscle activity, a reflection of respiratory center output, was measured at 100 msec of inspiration against an occluded airway at functional residual capacity. At end-tidal oxygen tension (PETO2) of 80 mm Hg, inspiratory muscle activity was greater in asthmatic patients than in normal subjects for the same level of ventilation, but at PETO2 of 40 mm Hg, both inspiratory muscle activity and ventilation were lower in asthmatic patients. Consequently, the changes in inspiratory muscle activity and ventilation per mm Hg change in PETO2 were lower in the asthmatic patients. To generate the same ventilation during progressive hypoxia, more inspiratory muscle activity was needed by asthmatic patients. We concluded that the decreased hypoxic ventilation in asthmatic patients resulted from both decreased respiratory center output and from mechanical abnormalities of the respiratory system.     

Volume-assured pressure support ventilation (VAPSV). A new approach for reducing muscle workload during acute respiratory failure.

This study reports the preliminary clinical evaluation of a new mode of ventilation--volume-assured pressure support ventilation (VAPSV)--which incorporates inspiratory pressure support (PSV) with conventional volume-assisted cycles (VAV). This combination optimizes the inspiratory flow during assisted/controlled cycles, reducing the patient's respiratory burden commonly observed during VAV. Different from conventional PSV, VAPSV assures precise control of tidal volume (VT) in unstable patients. Eight patients with acute respiratory failure (ARF) were submitted to assisted ventilation under VAV and VAPSV. Patient's ventilatory workload (evaluated through the pressure-time product, mechanical work per liter of ventilation, and work per minute) and patient's ventilatory drive (occlusion pressure--P0.1) were significantly reduced during VAPSV. This "relief" was more evident among the most distressed patients (p < 0.001), allowing a reduction of more than 60 percent in muscle load, without the need of increasing peak tracheal pressure. Mean inspiratory flow (VT/TI), VT, and effective dynamic compliance were significantly increased during VAPSV, whereas the effective inspiratory impedance decreased. These mechanical advantages of VAPSV allowed a reduction of intrinsic PEEP, whenever it was present. Blood gas values were similar in both periods. We concluded that VAPSV is a promising form of ventilatory support. At the same time that it was able to safely assure a minimum preset VT, VAPSV reduced patient workload and improved synchrony between the patient and the ventilator during ARF.     

Hypnosis effect on carbon dioxide chemosensitivity

Hypnosis is an induced state of heightened suggestibility during which certain physiologic variables can be altered. To investigate if carbon dioxide (CO2) chemosensitivity could be blunted during this suggestible state, we measured hypercapnic ventilatory response (HCVR, delta VE/delta PaCO2), oxygen consumption (VO2), breathing pattern (VT and f), inspiratory flow rate (VT/Ti), and inspiratory timing (Ti/Ttot) in 20 healthy subjects. Mouth occlusion pressures (P0.1) were measured in the last nine subjects. Resting oxygen consumption and minute ventilation were measured during awake and hypnotic control states. The HCVR was measured spontaneously and with the suggestion to maintain normal ventilation during both awake and hypnotic conditions. It was found that without a change in metabolism, ventilatory responses to CO2 could be blunted both voluntarily, and to a greater degree, with hypnotic suggestion. These findings may have important implications in clinical settings in which patients suffer from marked dyspnea secondary to increased ventilatory chemosensitivity.     

Awake inspiratory airway occlusion in normal humans is followed by hyperpnea and hypocapnia

The ventilatory response following 15 seconds of inspiratory airway occlusion at functional residual capacity (FRC) was studied in nine normal supine awake subjects. Expired minute ventilation (VE), CO2 output (VCO2), tidal volume (VT), and end-tidal PCO2 (PETCO2) were measured on a breath-by-breath basis. Alveolar PCO2 rose 5.6 mm Hg during the apnea (P less than 0.001). Ventilation rose 10.8 L/min on the first breath following apnea and remained elevated above control measurements for five breaths (P less than 0.05). The persistent hyperpnea was due to an increase in tidal volume and was associated with alveolar hypocapnia for 6 breaths or 30 sec (P less than 0.05) and an increase in CO2 output for 4 breaths (P less than 0.05). Changes in end-tidal PCO2 correlated with excess CO2 output relative to control measurements immediately prior to airway occlusion (P less than 0.03). After 15 sec airway occlusion at FRC, there is alveolar hypercapnia with a 2.6-fold first breath rise in ventilation. Persistent alveolar hyperventilation lasting 30 sec following airway occlusion may be due to delays in central chemoreceptor response or an afterdischarge phenomenon. This overshoot hypercapnia following airway occlusion may have some relevance to the development of central apneas following obstructive apnea episodes.     

Physiologic evaluation of pressure support ventilation by nasal mask in patients with stable COPD.

We evaluated the physiologic effects of pressure support ventilation by nasal route (NPSV) in eight patients with severe stable COPD and chronic hypercapnia who were randomly submitted to 2-h sessions of NPSV both with a portable ventilator (Respironics BIPAP device) and with a standard ventilator (Bird 6400ST device) at an inspiratory airway pressure of 22 cm H2O. Two sessions with each ventilator were performed using an FIO2 of 0.21 in each patient on two consecutive days. One patient did not tolerate either form of ventilation. Comparison of spontaneous with BIPAP ventilation showed a significant improvement in pH, PaCO2, and PaO2. Ventilatory pattern assessed by a respiratory inductive plethysmograph showed a significant increase in minute ventilation (VE), VT, and Ttot. Integrated surface diaphragmatic EMG activity measured only during BIPAP device ventilation decreased from that measured during spontaneous breathing. Similar changes in blood gases and ventilatory pattern were observed during ventilation by the Bird 6400ST except for VT/Ti ratio, which significantly increased. Comparison of baseline with measurements performed 12 h after the whole cycle of treatment showed a significant increase in pH and VE and a decrease in PaCO2. We conclude that short-term NPSV may be useful in improving respiratory pattern and blood gases in stable COPD patients with chronic hypercapnia.     

Respiratory control in presenile dementia

To evaluate the role of the cerebral cortex in the response to externally added inspiratory flow-resistive load, we studied 7 patients manifesting clinical presenile dementia of the Alzheimer's type. All subjects exhibited diffuse cerebral cortical atrophy on computerized tomography of the brain. The mean age of the group was 45.6 yr. The rebreathing technique was used to assess minute ventilation (VE) and occlusion pressure (P100) responses to progressive hypercapnia. Rebreathing runs were performed before and during the addition of an inspiratory flow-resistive load of 18 cm H2O.L-1.s. The respiratory control data of these patients were compared with data obtained by similar techniques in a matched normal volunteer control group. In the patient group, with the addition of load, the VE/PCO2 response slope decreased (p less than 0.005), whereas the P100/PCO2 response slope did not significantly change. In the control group, P100/PCO2 response slope increased with load to maintain ventilation. These results suggest that in presenile dementia, during added inspiratory load, the drop in VE is associated with an inadequate increase in respiratory neuromuscular output. This lack of load compensation in patients with presenile dementia suggests a role for the cerebral cortex in the response to externally added load.     

Ventilatory control after pulmonary resection

Because pulmonary resection decreases pulmonary compliance, the effects of resection on ventilation might be similar to the known effects of elastic loading. We evaluated the breathing pattern and ventilatory drive in 12 patients before and after pulmonary resection with mean tissue loss of 4 segments. During resting ventilation, the only significant change after resection was a decrease in inspiratory time (Tl). At a higher level of minute ventilation (VE), induced by CO2 rebreathing, significant changes included increased respiratory frequency, decreased tidal volume and Tl, and increased occlusion pressure (P0.1). Both ventilation and occlusion pressure responses to CO2 (delta VE/delta PACO2, delta P0.1/delta PACO2) were unchanged after resection. We conclude that increased ventilation induced by CO2 rebreathing unmasks a breathing pattern after pulmonary resection which is similar to that seen with breathing against an external elastic load.     

Steady-state breathing pattern responses to small inspiratory resistive loads in COPD patients. Application to weaning from mechanical ventilation

We investigated the effect of small inspiratory resistive loads on the breathing patterns of patients with COPD admitted to the ICU for acute respiratory failure. Patients were in stable clinical condition three days after weaning from the acute-phase ventilation. Healthy nonsmokers served as controls. Breathing patterns were recorded for 20-min periods during unloaded breathing (R0), then with small inspiratory resistive loads (R1 = 2.5 cmH2O L/s and R2 = 5.2 cmH2O L/s) applied in random order. Respiratory parameters were memorized in real time and blood gases measured continuously with a transcutaneous PO2/PCO2 monitor and compared periodically with arterial blood gases. Minute volume (VE) and respiratory rate decreased with no modification in blood gas values. In the COPD patients, R1 was too small to be perceived; when R2 was applied, no increase in TI was observed, and VT and VT/TI decreased. The VE could not be maintained despite a shortening of expiratory time. The COPD patients did not have significant increase of occlusion pressure (P0.1). Mean blood gas values did not change during the testing, but the coefficient of variation of tcPCO2 increased. During the critical period following weaning from artificial ventilation, COPD patients did not respond in the same manner as normal subjects to inspiratory resistive loads, but did not have modified gas exchange during the 20-min period.     

Naloxone does not alter response to hypercapnia or resistive loading in chronic obstructive pulmonary disease

To assess the role of endogenous opioid peptides in ventilatory control in patients with chronic obstructive lung disease, we measured the ventilatory and mouth occlusion pressure responses to hypercapnia and the compensatory response to an inspiratory resistive load in 11 male patients with COPD before and after intravenous administration of naloxone or placebo on 2 separate days. There were no statistically significant differences between naloxone and placebo administration in any index of ventilatory response to CO2 or resistive loading. When an inspiratory resistive load was added during CO2 rebreathing, minute ventilation at PETCO2 = 50 mm Hg in all 11 patients decreased significantly (p less than 0.05) with placebo and naloxone. In response to the inspiratory resistive load, in eight of the 11 patients mouth occlusion pressure (P0.1) did not increase; these eight subjects were classified as noncompensators. Naloxone did not affect the P0.1 response to inspiratory resistive loading, either in the group as a whole or in the subgroup of eight patients classified as noncompensators. Our study was unable to demonstrate that increased activity of endogenous opioid peptides suppresses the ventilatory response to CO2 or resistive loading in patients with chronic obstructive lung disease.     

Mechanical load on the inspiratory muscles during exercise hyperpnea in patients with Type 1 (insulin-dependent) diabetes mellitus

Summary The aim of this study was to evaluate the difference between Type 1 (insulin-dependent) diabetic patients and healthy control subjects regarding inspiratory muscle load during exercise hyperpnea. For this purpose an incremental progressive exercise test on a cycle ergometer was performed by 36 Type 1 diabetic patients and 40 healthy subjects. In order to determine the mechanical load on the inspiratory muscles breath by breath, we selected the following two parameters, which represent the pressure generated by the inspiratory muscles as well as the duration and velocity of their contraction: (1) the oesophageal tension time index, which is the product of the duty cycle (ratio of inspiratory time to total breath cycle duration) and the mean oesophageal pressure expressed as a percentage of the maximal oesophageal pressure and (2) the mean oesophageal pressure change per time unit during the inspiratory phase of each breathing manoeuver, which is expressed as a fraction of the subject's maximal oesophageal pressure. Comparison of the two groups revealed that at similar levels of ventilation the mechanical load on the inspiratory muscles was significantly higher in the Type 1 diabetic patients than in the control subjects. When the loading was stopped the maximal ventilation was lower in the patients. Nevertheless, they reported a degree of respiratory effort sensation comparable to the control group, which seems to have been caused by an increase of the mechanical load on the ventilatory muscles.     

Amino acids and respiration

Parenteral nutrition containing glucose and amino acids may stimulate respiration. To ascertain the effects of these solutions on respiration, eight normal subjects received an infusion of 5% dextrose (100 mL/h) for 7 days followed by an infusion of 3.5% amino acids (125 mL/h) for 24 hours. Minute ventilation (VE), tidal volume, mean inspiratory flow (VT/VI), oxygen consumption, and carbon dioxide production were significantly depressed after 7 days of 5% dextrose infusion. Ventilation and metabolic rate increased within 4 hours after initiation of the amino acid infusion and returned to normal 24 hours after the infusion. The effects of the amino acids on (VE) was secondary to an increase in (VT/VI), which is an indicator of neuromuscular ventilatory drive. Thus, within 4 hours amino acids will restore depressed metabolic rate, minute ventilation, and ventilatory drive after prolonged infusion of 5% dextrose.