Caffeine effect on respiratory muscle endurance and sense of effort during loaded breathing

The present study examined respiratory muscle endurance and the magnitude of the sense of effort during inspiratory threshold loading following a dose of caffeine (600 mg) previously observed to increase diaphragm strength. Experiments were performed on 12 normal subjects. Respiratory muscle endurance at a given level of load was assessed from the time of exhaustion and from the time course of the change in the power spectrum (centroid frequency) of the diaphragm electromyogram (EMG). The intensity of the sense of effort during loaded breathing was evaluated using a category (Borg) scale. Increasingly severe loads were associated with more rapid onset of fatigue. At a given load, caffeine prolonged the time to exhaustion and decreased the rate of fall of the centroid frequency of the diaphragm EMG. Caffeine also decreased the sense of effort during loaded breathing in 9 of 11 subjects. Changes in respiratory muscle endurance after caffeine administration were not explained by changes in the pressure-time index of the respiratory muscles or the pattern of thoracoabdominal movement. We conclude that caffeine enhances inspiratory muscle endurance, while concomitantly reducing the sense of effort associated with fatiguing inspiratory muscle contractions.     

Breathlessness during exercise with and without resistive loading

The purpose of this study was to quantify the intensity of breathlessness associated with exercise and respiratory resistive loading, with the specific purpose of isolating the quantitative contributions of inspiratory pressure, length, velocity, and frequency of inspiratory muscle shortening and duty cycle to breathlessness. The intensity of inspiratory pressure was quantified by measurement of estimated esophageal pressure (Pes = pressure at the mouth plus lung pressure), the extent of shortening by tidal volume (VT), and the velocity of shortening by inspiratory flow rate (VI). Six normal subjects underwent five incremental (100 kpm X min-1 X min-1) exercise tests on a cycle ergometer to maximum capacity. The first and last test were unloaded and the intervening tests were performed with external added resistances of 33, 57, and 73 cm H2O X l-1 X s in random order. The resistances were selected to provide a range of pressures, tidal volumes, flow rates, and patterns of breathing. At rest and at the end of each minute during exercise the subjects estimated the intensity of breathlessness (psi) by selecting a number ranging from 0 to 10 (Borg rating scale, 0 indicating no appreciable breathlessness and 10 the maximum tolerable sensation). Breathlessness was significantly and independently related to Pes (P less than 0.0001), VI (P less than 0.0001), frequency of breathing (fb) (P less than 0.01), and duty cycle [ratio of inspiratory duration to total breath duration (TI/TT)] (P less than 0.01): psi = 0.11 Pes + 0.61 VI + 1.99 TI/TT + 0.04 fb - 2.60 (r = 0.83). The results suggest that peak pressure (tension), VI (velocity of inspiratory muscle shortening), TI/TT, and fb contribute independently and collectively to breathlessness. The perception of respiratory muscle effort is ideally suited to subserve this sensation. The neurophysiological mechanism purported is a conscious awareness of the intensity of the outgoing motor command by means of corollary discharge within the central nervous system.     

Ventilatory response to fatiguing and nonfatiguing resistive loads in awake sheep

To study the changes in ventilation induced by inspiratory flow-resistive (IFR) loads, we applied moderate and severe IFR loads in chronically instrumented and awake sheep. We measured inspired minute ventilation (VI), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory cycle time (TT), tidal volume (VT), mean inspiratory flow (VT/TI), and respiratory duty cycle (TI/TT)], transdiaphragmatic pressure (Pdi), functional residual capacity (FRC), blood gas tensions, and recorded diaphragmatic electromyogram. With both moderate and severe loads, Pdi, TI, and TI/TT increased, TE, TT, VT, VT/TI, and VI decreased, and hypercapnia ensued. FRC did not change significantly with moderate loads but decreased by 30-40% with severe loads. With severe loads, arterial PCO2 (PaCO2) stabilized at approximately 60 Torr within 10-15 min and rose further to levels exceeding 80 Torr when Pdi dropped. This was associated with a lengthening in TE and a decrease in breathing frequency, VI, and TI/TT. We conclude that 1) timing and volume responses to IFR loads are not sufficient to prevent alveolar hypoventilation, 2) with severe loads the considerable increase in Pdi, TI/TT, and PaCO2 may reduce respiratory muscle endurance, and 3) the changes in ventilation associated with neuromuscular fatigue occur after the drop in Pdi. We believe that these ventilatory changes are dictated by the mechanical capability of the respiratory muscles or induced by a decrease in central neural output to these muscles or both.     

Effect of frequency on perceived magnitude of added loads to breathing

Using open-magnitude scaling, six normal subjects estimated the perceived magnitude of a range of added elastic loads (20-76 cmH2O/l), applied for a sequence of five breaths, at frequencies varying from 5 to 26.4 breaths/min. Two experiments were performed. In the first, frequency was increased by a reduction in expiratory duration (TE), and the duty cycle (ratio of inspiratory duration to total breath duration, TI/TT) ranged between 0.10 and 0.52. The perceived magnitude psi increased significantly with the peak airway pressure (Pm) (P less than 0.0001) but did not reach conventional significance with frequency (fb) (P = 0.15): psi = K0Pm1.23fb0.07 (r = 0.911). However, the sensory magnitude increased significantly as the duty cycle increased (P less than 0.01), but when it was included, the magnitude decreased minimally with frequency (P less than 0.01): psi = K0Pm1.3fb-0.97 TI/TT1.14 (r = 0.92). In the second experiment the duty cycle (TI/TT) was kept constant [(0.43 +/- 0.008 (SE)] and frequency (5-26.4 breaths/min) increased at the expense of shortening both TI and TE. The perceived magnitude of the added elastances decreased with the increase in frequency. However, when the perceived magnitude was corrected for the duration of inspiration, which is known to increase the sensory magnitude, psi = K0Pm1.3TI0.56, the sensory magnitude increased significantly with frequency (P less than 0.001): psi/TI0.56 = K0Pm1.21fb0.28 (r = 0.773). The decrease in inspiratory duration had a greater quantitative effect decreasing sensory magnitude than frequency had on increasing the magnitude. The effect of increasing frequency is complex and depends on the simultaneous intensity, duration of inspiratory pressure, and the duty cycle.     

Critique on application of diaphragmatic time-tension index to spontaneously breathing humans

Bellemare and Grassino (J. Appl. Physiol. 53: 1196-1206, 1982) have reported that the diphragmatic time-tension index (TTdi) (i.e., the product of mean transdiaphragmatic pressure/maximum transdiaphragmatic pressure and the inspiratory duty cycle) can be used as a predictor of diaphragmatic fatigue in humans. However, the publications of these authors do not directly address the question of whether inspiratory flow or transdiaphragmatic pressure should be used to calculate the inspiratory duty cycle. To gather data on this point, we computed TTdi by both methods in spontaneously breathing normal adult males (AMN) and age-matched males with chronic obstructive pulmonary disease (COPD) at rest and during treadmill exercise. During rest and exercise in both AMN and COPD, the fraction of the breathing cycle over which diaphragmatic tension was maintained (Tdi/TT) exceeded the fraction of the breathing cycle over which inspiratory airflow was maintained (TI/TT). Therefore, TTdi calculations using Tdi/TT were greater (P less than 0.05) than TTdi computations using TI/TT. However, this difference in TTdi values was relatively small (approximately 15%).     

Effect of inspiratory muscle fatigue on breathing pattern

Our aim was to determine whether inspiratory muscle fatigue changes breathing pattern and whether any changes seen occur before mechanical fatigue develops. Nine normal subjects breathed through a variable inspiratory resistance with a predetermined mouth pressure (Pm) during inspiration and a fixed ratio of inspiratory time to total breath duration. Breathing pattern after resistive breathing (recovery breathing pattern) was compared with breathing pattern at rest and during CO2 rebreathing (control breathing pattern) for each subject. Relative rapid shallow breathing was seen after mechanical fatigue and also in experiments with electromyogram evidence of diaphragmatic fatigue where Pm was maintained at the predetermined level during the period of resistive breathing. In contrast there was no significant difference between recovery and control breathing patterns when neither mechanical nor electromyogram fatigue was seen. It is suggested that breathing pattern after inspiratory muscle fatigue changes in order to minimize respiratory sensation.     

Effects of breathing pattern on inspiratory muscle endurance in humans

Endurance of the inspiratory muscles was measured in normal volunteers using a threshold resistance that produced a relatively constant mouth-pressure load, independent of inspiratory flow rate (VTI). Breathing pattern was controlled by visual feedback from an oscilloscope. Endurance was measured as the length of time (Tlim) a target VTI could be maintained with maximum effort. Effects of changes in breathing pattern on Tlim were compared with control measurements made the same day. Increases in VTI or in duty cycle (inspiratory time/total period) shortened Tlim, whereas decreases lengthened Tlim. However, effects of changes in VTI were less than equivalent changes in tidal volume produced by alterations in duty cycle. Furthermore, when two breathing pattern changes were altered simultaneously to keep the rate of external inspiratory work (Winsp) constant, significant effects due to changes in duty cycle were still observed. In conclusion, 1) both VTI and duty cycle have significant effects on measurements of inspiratory muscle endurance and 2) the effects of VTI are less than the effects of duty cycle for the same Winsp.     

Effect of fatigue on maximal inspiratory pressure-flow capacity.

The inspiratory muscles can be fatigued by repetitive contractions characterized by high force (inspiratory resistive loads) or high velocities of shortening (hyperpnea). The effects of fatigue induced by inspiratory resistive loaded breathing (pressure tasks) or by eucapnic hyperpnea (flow tasks) on maximal inspiratory pressure-flow capacity and rib cage and diaphragm strength were examined in five healthy adult subjects. Tasks consisted of sustaining an assigned breathing frequency, duty cycle, and either a "pressure-time product" of esophageal pressure (for the pressure tasks) or peak inspiratory flow rate (for the flow tasks). Esophageal pressure was measured during maximal inspiratory efforts against a closed glottis (Pesmax), maximal transdiaphragmatic pressure was measured during open-glottis expulsive maneuvers (Pdimax), and maximal inspiratory flow (VImax) was measured during maximal inspiratory efforts with no added external resistance before and after fatiguing pressure and flow tasks. The reduction in Pesmax) with pressure fatigue (-25 +/- 7%) was significantly greater than the change in Pesmax with flow fatigue (-8 +/- 8%, P less than 0.01). In contrast, the reductions in Pdimax (-11 +/- 8%) and VImax (-16 +/- 3%) with flow fatigue were greater than the changes in Pdimax (-0.6 +/- 4%, P less than 0.05) or VImax (-3 +/- 4%, P less than 0.05) with pressure fatigue. We conclude that respiratory muscle performance is dependent not only on the presence of fatigue but whether fatigue was induced by pressure tasks or flow tasks. The specific impairment of Pesmax and not of Pdimax or flow with pressure fatigue may reflect selective fatigue of the rib cage muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pressure-time product, work rate, and endurance during resistive breathing in humans

We examined the effect of increasing work rate, without a corresponding increase in the pressure-time product, on energy cost and inspiratory muscle endurance (Tlim) in five normal subjects during inspiratory resistive breathing. Tidal volume, mean inspiratory mouth pressure, duty cycle, and hence the pressure-time product were kept constant, whereas work rate was varied by changing the frequency of breathing. There was a linear decrease in Tlim of -2.1 +/- 0.5 s.J-1.min-1 (r = 0.87 +/- 0.06) with increasing work rate. The data satisfied a model of energy balance during fatiguing runs (Monod and Scherrer. Ergonomics 8: 329-337, 1965) and were consistent with the hypothesis that the rate of energy supply, or respiratory muscle blood flow, is fixed when the pressure-time product is constant. Our results indicate that during inspiratory resistive breathing against fatiguing loads, work rate determines endurance independently of the pressure-time product. On the basis of the model, our results lead to estimates of respiratory muscle blood flow and available energy stores under the conditions of our experiment.     

Postnatal maturation of ventilation and breathing pattern in kittens: influence of sleep

Ventilation and breathing pattern were studied in kittens at 1, 2, 3, 4, and 8 wk of life during quiet wakefulness (W), quiet sleep (QS), and active sleep (AS) with the barometric method. Tidal volume (VT), respiratory frequency (f), ventilation (VE), inspiratory time (TI), expiratory time (TE), mean inspiratory flow (VT/TI), and respiratory "duty cycle" (TI/TT) were measured. VT, VE, TI, TE, and VT/TI increased; f decreased and TI/TT remained constant during postnatal development in wakefulness and in both sleep states. No significant difference was observed between AS and QS for all the ventilatory parameters except TI/TT, which was greater in QS than in AS at 2 wk. VE was larger in W than in both AS and QS at all ages. This was mainly due to a greater f, TI/TT remaining constant. VT/TI, which represents an index of the central inspiratory activity, was larger in W than in sleep, VT not being significantly different whatever the stage of consciousness. The results of this study show that in the kitten 1) unlike in the adult cat, ventilation and breathing pattern are similar in QS and in AS; 2) in sleep, the central inspiratory drive appears to be independent of the type of sleep; and 3) in wakefulness, the increase of the central inspiratory activity could be related to important excitatory inputs.     

Influence of inspiratory flow rate and frequency on O2 cost of resistive breathing in humans

We examined the combined effect of an increase in inspiratory flow rate and frequency on the O2 cost of inspiratory resistive breathing (VO2 resp). In each of three to six pairs of runs we measured VO2 resp in six normal subjects breathing through an inspiratory resistance with a constant tidal volume (VT). One of each pair of runs was performed at an inspiratory muscle contraction frequency of approximately 10/min and the other at approximately 30/min. Inspiratory mouth pressure was 45 +/- 2% (SE) of maximum at the lower contraction frequency and 43 +/- 2% at the higher frequency. Duty cycle (the ratio of contraction time to total cycle time) was constant at 0.51 +/- 0.01. However, during the higher frequency runs, two of every three contractions were against an occluded airway. Because VT and duty cycle were kept constant, mean inspiratory flow rate increased with frequency. Careful selection of appropriate parameters allowed the pairs of runs to be matched both for work rate and pressure-time product. The VO2 resp did not increase, despite approximately threefold increases in both inspiratory flow rate and contraction frequency. On the contrary, there was a trend toward lower values for VO2 resp during the higher frequency runs. Because these were performed at a slightly lower mean lung volume, a second study was designed to measure the VO2 resp of generating the same inspiratory pressure (45% maximum static inspiratory mouth pressure at functional residual capacity) at the same frequency but at two different lung volumes. This was achieved with a negligibly small work rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of expiratory resistive loading on the noninvasive tension-time index in COPD.

Expiratory resistive loading (ERL) is used by chronic obstructive pulmonary disease (COPD) patients to improve respiratory function. We, therefore, used a noninvasive tension-time index of the inspiratory muscles (TT(mus) = I/PI(max) x TI/TT, where I is mean inspiratory pressure estimated from the mouth occlusion pressure, PI(max) is maximal inspiratory pressure, TI is inspiratory time, and TT is total respiratory cycle time) to better define the effect of ERL on COPD patients. To accomplish this, we measured airway pressures, mouth occlusion pressure, respiratory cycle flow rates, and functional residual capacity (FRC) in 14 COPD patients and 10 normal subjects with and without the application of ERL. TT(mus) was then calculated and found to drop in both COPD and normal subjects (P<0.05). The decline in TT(mus) in both groups resulted solely from a prolongation of expiratory time with ERL (P<0.001 for COPD, P<0.05 for normal subjects). In contrast to the COPD patients, normal subjects had an elevation in I and FRC, thus minimizing the decline in TT(mus). In conclusion, ERL reduces the potential for inspiratory muscle fatigue in COPD by reducing TI/TT without affecting FRC and I.     

Threshold effects of respiratory muscle work on limb vascular resistance

The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (Q(L)) and utilized the changes in mouth twitch pressure (DeltaP(M)T) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 +/- 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1-3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and Q(L), limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control (P > 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 +/- 12% reduction in P(M)T with bilateral phrenic nerve stimulation. During the fatigue trial, Q(L) and LVR were unchanged from baseline at minute 1, but LVR rose 36% and Q(L) fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and Q(L) returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and Q(L), whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in Q(L). We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions.     

Effects of inspiratory resistive load on respiratory control in hypercapnia and exercise

Eight healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with an inspiratory resistive load (IRL) of approximately 12 cmH2O.1-1.s. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0-5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE - VCO2) relationship in NL and IRL. Compared with NL, the VE - VCO2 slope was depressed by IRL, more so in hypercapnic [-19.0 +/- 3.4 (SE) %] than in eucapnic exercise (-6.0 +/- 2.0%), despite a similar increase in the slope of the occlusion pressure at 100 ms - VCO2 (P100 - VCO2) relationship under both conditions. The steady-state hypercapnic ventilatory response at rest was markedly depressed by IRL (-22.6 +/- 7.5%), with little increase in P100 response. For a given inspiratory load, breathing pattern responses to separate or combined hypercapnia and exercise were similar. During IRL, VE was achieved by a greater tidal volume (VT) and inspiratory duty cycle (TI/TT) along with a lower mean inspiratory flow (VT/TI). The increase in TI/TT was solely because of a prolongation of inspiratory time (TI) with little change in expiratory duration for any given VT. The ventilatory and breathing pattern responses to IRL during CO2 inhalation and exercise are in favor of conservation of respiratory work.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accelerated decay of inspiratory pressure during hypercapnic endurance trials in humans

Seven normal human subjects inspired a CO2-O2 mixture from a constant-flow generator while performing maximal inspiratory maneuvers from functional residual capacity. End-tidal CO2 (ETCO2) was maintained at either 5.5 (normocapnia), 3.5 (hypocapnia), or 7% (hypercapnia) on separate testing days. Subjects attained maximal mouth pressure (Pm) while breathing at either 1.25 or 1 l/s, utilizing a fixed breathing pattern (duty cycle 0.43) with an inspiratory time of 1.5 s. Maximal Pm was measured at rest and then during a 10-min endurance trial in which subjects repeated maximal voluntary inspirations with constant flow and breathing pattern. The endurance Pm data were fit to nonlinear exponential regression. The results indicated that 1) maximal Pm at rest was unaffected by changing ETCO2; 2) the rate of Pm decay over time was accelerated by hypercapnia, whereas hypocapnia showed no consistent effects; and 3) "sustainable" Pm, attained toward the end of the endurance trial, was not decreased; therefore sustainable force output was preserved in response to changing ETCO2.     

Effect of inspiratory muscle fatigue on breathing pattern during inspiratory resistive loading

The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.     

Effects of hypercapnia and hypoxemia on fetal breathing after decortication

The effects of hypercapnia and hypoxemia on breathing movements were studied in 12 chronically decorticated fetal sheep, 127-140 days gestation. The fetal state of consciousness was defined in terms of activity of the lateral rectus and nuchal muscles. Arterial blood pressure was monitored. Fetal breathing was determined by integrated diaphragmatic electromyogram (EMG) and analyzed in terms of inspiratory time (TI), expiratory time (TE), electrical equivalent of tidal volume (EVT), breath interval (TT), duty cycle (TI/TT), mean inspiratory flow equivalent (EVT/TI), and instantaneous ventilation equivalent (EVT/TT). Fetal breathing occurred only during episodes of rapid-eye movements, and the response to hypercapnia consisted of an increase in EVT, TI, EVE, and EVT/TI and a decrease in the coefficient of variation of all measured parameters. Induction of hypoxia during episodes of spontaneous fetal breathing produced a decrease in the rate of breathing and an increase in EVT and TI with no change in the variability of all parameters studied. Since similar responses to hypercapnia and hypoxemia are seen in the intact fetus, we conclude that the cerebral cortex has no obvious effect on the chemical control of fetal breathing.     

Laryngeal influences on breathing pattern and posterior cricoarytenoid muscle activity

Receptors responding to transmural pressure, airflow, and contraction of laryngeal muscles have been previously identified in the larynx. To assess the relative contribution of these three types of receptors to the reflex changes in breathing pattern and upper airway patency, we studied diaphragmatic (DIA) and posterior cricoarytenoid muscle (PCA) activity in anesthetized dogs during spontaneous breathing and occluded efforts with and without bypassing the larynx. Inspiratory duration (TI) was longer, mean inspiratory slope (peak DIA/TI) was lower, and PCA activity was greater with upper airway occlusion than with tracheal occlusion (larynx bypassed). Bilateral section of the superior laryngeal nerves eliminated these differences. When respiratory airflow was diverted from the tracheostomy to the upper airway the only change attributable to laryngeal afferents was an increase in PCA activity. These results confirm the importance of the superior laryngeal nerves in the regulation of breathing pattern and upper airway patency and suggest a prevalent role for laryngeal negative pressure receptors.     

Preferential fatigue of the rib cage muscles during inspiratory resistive loaded ventilation

Because the inspiratory rib cage muscles are recruited during inspiratory resistive loaded breathing, we hypothesized that such loading would preferentially fatigue the rib cage muscles. We measured the pressure developed by the inspiratory rib cage muscles during maximal static inspiratory maneuvers (Pinsp) and the pressure developed by the diaphragm during maximal static open-glottis expulsive maneuvers (Pdimax) in four human subjects, both before and after fatigue induced by an inspiratory resistive loaded breathing task. Tasks consisted of maintaining a target esophageal pressure, breathing frequency, and duty cycle for 3-5 min, after which the subjects maintained the highest esophageal pressure possible for an additional 5 min. After loading, Pinsp decreased in all subjects [control, -128 +/- 14 (SD) cmH2O; with fatigue, -102 +/- 18 cmH2O; P less than 0.001, paired t test]. Pdimax was unchanged (control, -192 +/- 23 cmH2O; fatigue, -195 +/- 27 cmH2O). These data suggest that 1) inability to sustain the target during loading resulted from fatigue of the inspiratory rib cage muscles, not diaphragm, and 2) simultaneous measurement of Pinsp and Pdimax may be useful in partitioning muscle fatigue into rib cage and diaphragmatic components.     

Exercise breathing pattern during chronic altitude exposure

Breathing pattern in response to maximal exercise was examined in four subjects during a 7-day acclimatisation to a simulated altitude of 4247 m (barometric pressure, PB = 59.5 kPa). Graded exercise tests to exhaustion were performed during normoxia (day 0), and on days 2 and 7 of hypoxia, respectively. Ventilation was significantly augmented in the hypoxic environment, as were both the mean inspiratory flow (VT/TI) and inspiratory duty cycle (TI/TTOT) components of it. VI/TI was increased due to a significant increase in tidal volume (VT) and a corresponding decrease in inspiratory time duration (TI). Throughout a range of exercise ventilation, TI/TTOT was increased due to an apparently greater decrease in expiratory time duration (TE) with respect to TI. In all cases, the relation between VT and TI displayed a typical range 2 behaviour, with evidence of a range 3 occurring at very high ventilatory rates. There was essentially no difference observed in the VT-TI relation during exercise between the normoxic and hypoxic conditions. No significant changes were observed in the breathing pattern in response to exercise within the exposure period (from day 2 to day 7), although there was a discernible tendency to a higher stage 3 plateau by day 7 of altitude exposure.