Control of exercise hyperpnea during hypercapnia in humans

Previous studies have yielded conflicting results on the ventilatory response to CO2 during muscular exercise. To obviate possible experimental errors contributing to such variability, we have examined the CO2-exercise interaction in terms of the ventilatory response to exercise under conditions of controlled hypercapnia. Eight healthy male volunteers underwent a sequence of 5-min incremental treadmill exercise runs from rest up to a maximum CO2 output (VCO2) of approximately 1.5 l . min-1 in four successive steps. The arterial PCO2 (PaCO2) at rest was stabilized at the control level or up to 14 Torr above control by adding 0-6% CO2 to the inspired air. Arterial isocapnia (SD = 1.2 Torr) throughout each exercise run was maintained by continual adjustment of the inspired PCO2. At all PaCO2 levels the response in total ventilation (VE) was linearly related to exercise VCO2. Hypercapnia resulted in corresponding increases in both the slope (S) and zero intercept (V0) of the VE-VCO2 curve; these being directly proportional to the rise in PaCO2 (means +/- SE: delta S/ delta PaCO2, 2.73 +/- 0.28 Torr-1; delta V0/ delta PaCO2, 1.67 +/- 0.18 l . min-1 . Torr-1). Thus the ventilatory response to concomitant hypercapnia and exercise was characterized by a synergistic (additive plus multiplicative) effect, suggesting a positive interaction between these stimuli. The increased exercise sensitivity in hypercapnia is qualitatively consistent with the hypothesis that VE is controlled to minimize the conflicting challenges due to chemical drive and the mechanical work of breathing (Poon, C. S. In: Modelling and Control of Breathing, New York: Elsevier, 1983, p. 189-196).     

Hyperventilation in ponies at the onset of and during steady-state exercise

We studied blood gases in ponies to assess the relationship of alveolar ventilation (VA) to pulmonary CO2 delivery during moderate treadmill exercise. In normal ponies for 1.8, 3, or 6 mph, respectively, partial pressure of CO2 in arterial blood (PaCO2) decreased maximally by 3.1, 4.4, and 5.7 Torr at 30-90 s of exercise and remained below rest by 1.4, 2.3, and 4.5 Torr during steady-state (4-8 min) exercise (P less than 0.01). Partial pressure of O2 in arterial blood (PaO2) and arterial pH, (pHa) also reflected hyperventilation. Mixed venus CO2 partial pressure (PVCO2) decreased 2.3 and 2.9 Torr by 30 s for 3 and 6 mph, respectively (P less than 0.05). In work transitions either from 1.8 to 6 mph or from 6 mph to 1.8 mph, respectively, PaCO2 either decreased 3.8 Torr or increased 3.3 Torr by 45 s of the second work load (P less than 0.01). During exercise in acute (2-4 wk) carotid body denervated (CBD) ponies at 1.8, 3, or 6 mph, respectively, PaCO2 decreased maximally below rest by 9.0, 7.6, and 13.2 Torr at 30-45 s of exercise and remained below rest by 1.3, 2.3, and 7.8 Torr during steady-state (4-8 min) exercise (P less than 0.1). In the chronic (1-2 yr) CBD ponies, the hypocapnia was generally greater than normal but less than in the acute CBD ponies. We conclude that in the pony 1) VA is not tightly matched to pulmonary CO2 delivery during exercise, particularly during transitional states, 2) the exercise hyperpnea is not mediated by PaCO2 or PVCO2, and 3) during transitional states in the normal pony, the carotid bodies attenuate VA drive thereby reducing arterial hypocapnia.     

Arterial blood gases and acid-base status of dogs during graded dynamic exercise

The objective of this study was to determine whether arterial PCO2 (PaCO2) decreases or remains unchanged from resting levels during mild to moderate steady-state exercise in the dog. To accomplish this, O2 consumption (VO2) arterial blood gases and acid-base status, arterial lactate concentration ([LA-]a), and rectal temperature (Tr) were measured in 27 chronically instrumented dogs at rest, during different levels of submaximal exercise, and during maximal exercise on a motor-driven treadmill. During mild exercise [35% of maximal O2 consumption (VO2 max)], PaCO2 decreased 5.3 +/- 0.4 Torr and resulted in a respiratory alkalosis (delta pHa = +0.029 +/- 0.005). Arterial PO2 (PaO2) increased 5.9 +/- 1.5 Torr and Tr increased 0.5 +/- 0.1 degree C. As the exercise levels progressed from mild to moderate exercise (64% of VO2 max) the magnitude of the hypocapnia and the resultant respiratory alkalosis remained unchanged as PaCO2 remained 5.9 +/- 0.7 Torr below and delta pHa remained 0.029 +/- 0.008 above resting values. When the exercise work rate was increased to elicit VO2 max (96 +/- 2 ml X kg-1 X min-1) the amount of hypocapnia again remained unchanged from submaximal exercise levels and PaCO2 remained 6.0 +/- 0.6 Torr below resting values; however, this response occurred despite continued increases in Tr (delta Tr = 1.7 +/- 0.1 degree C), significant increases in [LA-]a (delta [LA-]a = 2.5 +/- 0.4), and a resultant metabolic acidosis (delta pHa = -0.031 +/- 0.011). The dog, like other nonhuman vertebrates, responded to mild and moderate steady-state exercise with a significant hyperventilation and respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arterial-alveolar CO2 equilibration in exercising dogs during prolonged rebreathing

Arterial-alveolar equilibration of CO2 during exercise was studied by normoxic CO2 rebreathing in six dogs prepared with a chronic tracheostomy and exteriorized carotid loop and trained to run on a treadmill. In 153 simultaneous measurements of PCO2 in arterial blood (PaCO2) and end-tidal gas (PE'CO2) obtained in 46 rebreathing periods at three levels of mild-to-moderate steady-state exercise, the mean PCO2 difference (PaCO2-PE'CO2) was -1.0 +/- 1.0 (SD) Torr and was not related to O2 uptake or to the level of PaCO2 (30-68 Torr). The small negative PaCO2-PE'CO2 is attributed to the lung-to-carotid artery transit time delay which must be taken into account when both PaCO2 and PE'CO2 are continuously rising during rebreathing (average rate 0.22 Torr/s). Assuming that blood-gas equilibrium for CO2 was complete, a lung-to-carotid artery circulation time of 4.6 s accounts for the observed uncorrected PaCO2-PE'CO2 of -1.0 Torr. The results are interpreted to indicate that in rebreathing equilibrium PCO2 in arterial blood and alveolar gas are essentially identical. This conclusion is at variance with previous studies in exercising humans during rebreathing but is in full agreement with our recent findings in resting dogs.     

Ventilatory compensation for lactacidosis in ponies: role of carotid chemoreceptors and lung afferents

We investigated changes in arterial PCO2 (PaCO2) and pulmonary ventilation (VE) in normal, carotid chemoreceptor-denervated, and hilar nerve-denervated ponies during intravenous lactic acid infusion at rest and treadmill exercise at 1.8 mph-5% grade (mild) and 1.8 mph-15% grade (moderate). Lactic acid, (0.5 M) infusion of 0.10, 0.13, and 0.20 ml.min-1.kg-1 at rest and mild and moderate exercise increased arterial [H+] linearly throughout the 10 min of acid infusion. At 10 min of infusion, arterial [H+] had increased approximately 20 nmol/l (0.2 pH units) for each condition and group. Under most conditions, the temporal pattern of PaCO2 during acid infusion was biphasic. At rest and during mild exercise in all groups, and in carotid chemoreceptor-denervated ponies during moderate exercise, PaCO2 increased approximately 2 Torr (P less than 0.05) during the first 2 min of acid infusion. However, in normal ponies during moderate exercise, PaCO2 was not changed from control in the first 2 min of infusion. Between 2 and 10 min of infusion at rest and mild and moderate exercise in all groups, there was a 5-Torr significant decrease in PaCO2, which did not differ (P greater than 0.10) between groups. VE increased between 15-30 s and 2 min of infusion, but VE changed minimally between 2 and 10 min of infusion at rest and exercise in all groups of ponies. We conclude that lactacidosis does increase VE at rest and submaximal exercise in the pony.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventilatory and blood gas dynamics at onset and offset of exercise in the pony

The purpose of these experiments was to examine the temporal pattern of arterial carbon dioxide tension (PaCO2) to assess the relationship between alveolar ventilation (VA) and CO2 return to the lung at the onset and offset of submaximal treadmill exercise. Five healthy ponies exercised for 8 min at two work rates: 50 m/min 6% grade and 70 m/min 12% grade. PaCO2 decreased (P less than 0.05) below resting values within 1 min after commencement of exercise at both work rates and reached a nadir at 90 s. PaCO2 decreased maximally by 2.5 and 3.5 Torr at the low and moderate rate, respectively. After the nadir, PaCO2 increased across time during both work rates and reached values that were not significantly different (P greater than 0.05) from rest at minute 4 of exercise. Partial pressure of O2 in arterial blood and arterial pH reflected hyperventilation during the first 3 min of exercise. At the termination of exercise PaCO2 increased (1.5 Torr) above rest (P less than 0.05), reaching a zenith at 2-3 min of recovery. These data suggest that VA and CO2 flow to the lung are not tightly matched at the onset and offset of exercise in the pony and thus challenges the traditional concept of blood gas homeostasis during muscular exercise.     

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.     

Ventilatory control during exercise with peripheral chemoreceptor stimulation: hypoxia vs. domperidone

Hypoxia potentiates the ventilatory response to exercise, eliciting a greater decrease in arterial PCO2 (PaCO2) from rest to exercise than in normoxia. The mechanism of this hypoxia-exercise interaction requires intact carotid chemoreceptors. To determine whether carotid chemoreceptor stimulation alone is sufficient to elicit the mechanism without whole body hypoxia, ventilatory responses to treadmill exercise were compared in goats during hyperoxic control conditions, moderate hypoxia (PaO2 = 38-44 Torr), and peripheral chemoreceptor stimulation with the peripheral dopamine D2-receptor antagonist, domperidone (Dom; 0.5 mg/kg iv). Measurements with Dom were made in both hyperoxia (Dom) and hypoxia (Dom/hypoxia). Finally, ventilatory responses to inspired CO2 at rest were compared in each experimental condition because enhanced CO2 chemoreception might be expected to blunt the PaCO2 decrease during exercise. At rest, PaCO2 decreased from control with Dom (-5.0 +/- 0.9 Torr), hypoxia (-4.1 +/- 0.5 Torr), and Dom/hypoxia (-11.1 +/- 1.2 Torr). The PaCO2 decrease from rest to exercise was not significantly different between control (-1.7 +/- 0.6 Torr) and Dom (-1.4 +/- 0.8 Torr) but was significantly greater in hypoxia (-4.3 +/- 0.7 Torr) and Dom/hypoxia (-3.5 +/- 0.9 Torr). The slope of the ventilation vs. CO2 production relationship in exercise increased with Dom (16%), hypoxia (18%), and Dom/hypoxia (68%). Ventilatory responses to inspired CO2 at rest increased from control to Dom (236%) and Dom/hypoxia (295%) and increased in four of five goats in hypoxia (mean 317%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Independence of exercise hyperpnea and acidosis during high-intensity exercise in ponies

We investigated arterial PCO2 (PaCO2) and pH (pHa) responses in ponies during 6-min periods of high-intensity treadmill exercise. Seven normal, seven carotid body-denervated (2 wk-4 yr) (CBD), and five chronic (1-2 yr) lung (hilar nerve)-denervated (HND) ponies were studied during three levels of constant load exercise (7 mph-11%, 7 mph-16%, and 7 mph-22% grade). Mean pHa for each group of ponies became alkaline in the first 60 s (between 7.45 and 7.52) (P less than 0.05) at all work loads. At 6 min pHa was at or above rest at 7 mph-11%, moderately acidic at 7 mph-16% (7.32-7.35), and markedly acidic at 7 mph-22% (7.20-7.27) for all groups of ponies. Yet with no arterial acidosis at 7 mph 11%, normal ponies decreased PaCO2 below rest (delta PaCO2) by 5.9 Torr at 90 s and 7.8 Torr by 6 min of exercise (P less than 0.05). With a progressively more acid pHa at the two higher work loads in normal ponies, delta PaCO2 was 7.3 and 7.8 Torr by 90 s and 9.9 and 11.4 Torr by 6 min, respectively (P less than 0.05). CBD ponies became more hypocapnic than the normal group at 90 s (P less than 0.01) and tended to have greater delta PaCO2 at 6 min. The delta PaCO2 responses in normal and HND ponies were not significantly different (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of altered CSF [H+] on ventilatory responses to exercise in the awake goat

We investigated the effects of selective large changes in the acid-base environment of medullary chemoreceptors on the control of exercise hyperpnea in unanesthetized goats. Four intact and two carotid body-denervated goats underwent cisternal perfusion with mock cerebrospinal fluid (CSF) of markedly varying [HCO-3] (CSF [H+] = 21-95 neq/l; pH 7.68-7.02) until a new steady state of alveolar hypo- or hyperventilation was reached [arterial PCO2 (PaCO2) = 31-54 Torr]. Perfusion continued as the goats completed two levels of steady-state treadmill walking [2 to 4-fold increase in CO2 production (VCO2)]. With normal acid-base status in CSF, goats usually hyperventilated slightly from rest through exercise (-3 Torr PaCO2, rest to VCO2 = 1.1 l/min). Changing CSF perfusate [H+] changed the level of resting PaCO2 (+6 and -4 Torr), but with few exceptions, the regulation of PaCO2 during exercise (delta PaCO2/delta VCO2) remained similar regardless of the new ventilatory steady state imposed by changing CSF [H+]. Thus the gain (slope) of the ventilatory response to exercise (ratio of change in alveolar ventilation to change in VCO2) must have increased approximately 15% with decreased resting PaCO2 (acidic CSF) and decreased approximately 9% with increased resting PaCO2 (alkaline CSF). A similar effect of CSF [H+] on resting PaCO2 and on delta PaCO2/VCO2 during exercise also occurred in two carotid body-denervated goats. Our results show that alteration of the gain of the ventilatory response to exercise occurs on acute alterations in resting PaCO2 set point (via changing CSF [H+]) and that the primary stimuli to exercise hyperpnea can operate independently of central or peripheral chemoreception.     

Exercise-induced hypercapnia in the horse

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.     

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)     

Changes in breathing when switching from nares to tracheostomy breathing in awake ponies

We assessed the consequences of respiratory unloading associated with tracheostomy breathing (TBr). Three normal and three carotid body-denervated (CBD) ponies were prepared with chronic tracheostomies that at rest reduced physiological dead space (VD) from 483 +/- 60 to 255 +/- 30 ml and lung resistance from 1.5 +/- 0.14 to 0.5 +/- 0.07 cmH2O . l-1 . s. At rest and during steady-state mild-to-heavy exercise arterial PCO2 (PaCO2) was approximately 1 Torr higher during nares breathing (NBr) than during TBr. Pulmonary ventilation and tidal volume (VT) were greater and alveolar ventilation was less during NBr than TBr. Breathing frequency (f) did not differ between NBr and TBr at rest, but f during exercise was greater during TBr than during NBr. These responses did not differ between normal and CBD ponies. We also assessed the consequences of increasing external VD (300 ml) and resistance (R, 0.3 cmH2O . l-1 . s) by breathing through a tube. At rest and during mild exercise tube breathing caused PaCO2 to transiently increase 2-3 Torr, but 3-5 min later PaCO2 usually was within 1 Torr of control. Tube breathing did not cause f to change. When external R was increased 1 cmH2O . l-1 . s by breathing through a conventional air collection system, f did not change at rest, but during exercise f was lower than during unencumbered breathing. These responses did not differ between normal, CBD, and hilar nerve-denervated ponies, and they did not differ when external VD or R were added at either the nares or tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of high-intensity exercise on the VE-VCO2 relationship

The intrinsic relationship between ventilation (VE) and carbon dioxide output (VCO2) is described by the modified alveolar ventilation equation VE = VCO2 k/PaCO2(1-VD/VT) where PaCO2 is the partial pressure of CO2 in the arterial blood and VD/VT is the dead space fraction of the tidal volume. Previous investigators have reported that high-intensity exercise uncouples VE from VCO2; however, they did not measure the PaCO2 and VD/VT components of the overall relationship. In an attempt to provide a more complete analysis of the effects of high-intensity exercise on the VE-VCO2 relationship, we undertook an investigation where five subjects volunteered to perform three steady-state tests (SS1, SS2, SS3) at 60 W. One week after SS1 each subject was required to perform repeated 1-min bouts of exercise corresponding to a work rate of approximately 140% of maximal oxygen uptake (VO2max). Two and 24 h later the subjects performed SS2 and SS3, respectively. This exercise intervention caused PaCO2 during SS2 and SS3 to be regulated (P less than 0.01) approximately 4 Torr below the control (SS1) value of 38.8 Torr. Additionally, significant alterations were noted for VCO2 with corresponding values of 1.15 (SS1), 1.10 (SS2), and 1.04 (SS3) l/min. No changes were noted in either VD/VT or VE. In summary, it seems reasonable to suggest that the disproportionate increase in VE with respect to VCO2 noted in earlier work does not reflect an uncoupling. Rather the slope of the VE-VCO2 relationship is increased in a predictable manner as described by the modified alveolar ventilation equation.     

Somatostatin inhibits the ventilatory response to hypoxia in humans

The effects of a 90-min infusion of somatostatin (1 mg/h) on ventilation and the ventilatory responses to hypoxia and hypercapnia were studied in six normal adult males. Minute ventilation (VE) was measured with inductance plethysmography, arterial 02 saturation (SaO2) was measured with ear oximetry, and arterial PCO2 (Paco2) was estimated with a transcutaneous CO2 electrode. The steady-state ventilatory response to hypoxia (delta VE/delta SaO2) was measured in subjects breathing 10.5% O2 in an open circuit while isocapnia was maintained by the addition of CO2. The hypercapnic response (delta VE/delta PaCO2) was measured in subjects breathing first 5% and then 7.5% CO2 (in 52-55% O2). Somatostatin greatly attenuated the hypoxic response (control mean -790 ml x min-1.%SaO2 -1, somatostatin mean -120 ml x min-1.%SaO2 -1; P less than 0.01), caused a small fall in resting ventilation (mean % fall - 11%), but did not affect the hypercapnic response. In three of the subjects progressive ventilatory responses (using rebreathing techniques, dry gas meter, and end-tidal Pco2 analysis) and overall metabolism were measured. Somatostatin caused similar changes (mean fall in hypoxic response -73%; no change in hypercapnic response) and did not alter overall O2 consumption nor CO2 production. These results show an hitherto-unsuspected inhibitory potential of this neuropeptide on the control of breathing; the sparing of the hypercapnic response is suggestive of an action on the carotid body but does not exclude a central effect.     

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.     

Potentiation of exercise ventilatory response by airway CO2 and dead space loading.

We examined the effects of different modes of airway CO2 load on the ventilation-CO2 output (VE-VCO2) relationship during mild to moderate exercise. Four young and three older male subjects underwent incremental steady-state treadmill exercise while breathing a mixture of CO2 in O2 (CO2 loading) or 100% O2 with and without a large external dead space [DS loading and control (C), respectively]. During DS loading, the elevated arterial PCO2 (PaCO2) remained constant from rest to mild exercise and began to increase only at higher work rates. To achieve similar chemical drive, the same PaCO2 levels were established during CO2 loading by external PCO2 forcing. In the young group, CO2 loading resulted in a steepening of the VE-VCO2 relationship compared with C, whereas in the older group the reverse pattern was found. DS loading resulted in a consistent increase in the VE-VCO2 slope compared with C and CO2 loading [39.1 +/- 5.6 (mean +/- SD) vs. 24.9 +/- 5.0 and 26.7 +/- 4.4, respectively] in all subjects. The difference in potentiation of VE-VCO2 by CO2 and DS loading was not due to differences in mean chemical drive or changes in breathing pattern. Thus changes in the profile of airway CO2 influx may have an independent influence on ventilatory CO2-exercise interaction. Peripheral chemoreceptors mediation, although important, is not obligatory for this behavior.     

Ventilatory and PaCO2 responses to voluntary and electrically induced leg exercise

We studied the role of central command mediation of exercise hyperpnea by comparing the ventilatory and arterial CO2 partial pressure (PaCO2) responses to voluntary (ExV) and electrically induced (ExE) muscle contractions in normal, awake human subjects. We hypothesized that if central command signals are critical to a normal ventilatory response, then ExE should cause a slower ventilatory response resulting in hypercapnia at the onset of exercise. ExE was induced through surface electrodes placed over the quadriceps and hamstring muscles. ExE and ExV produced leg extension (40/min) against a spring load that increased CO2 production (VCO2) 100-1,000 ml/min above resting level. PaCO2 and arterial pH during work transitions and in the steady state did not differ significantly from rest (P greater than 0.05) or between ExE and ExV. The temporal pattern of ventilation, tidal volume, breathing frequency, and inspired and expired times, and the ventilation-VCO2 relationship were similar between ExE and ExV. We conclude that since central command was reduced and/or eliminated by ExE, central command is not requisite for the precise matching of alveolar ventilation to increases in VCO2 during low-intensity muscle contractions.     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

To find out whether endurance training influences the kinetics of the increases in heart rate (fc) during exercise driven by the sympathetic nervous system, the changes in the rate of fc adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%-70% of maximal oxygen uptake (VO2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuous fc recording. At the completion of the training programme, the subjects' VO2max had increased significantly (39.2 ml.min-1.kg-1, SD 4.7 vs 46 ml.min-1.kg-1, SD 5.6) and the steady-state fc at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-state fc was found at 150 W (146 beats.min-1, SD 10 vs 169 beats.min-1, SD 9) but the difference between the steady-state fc at 150 W and that at 100 W (delta fc) did not decrease significantly (26 beats.min-1, SD 7 vs 32 beats.min-1, SD 6). The time constant (tau) of the fc increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P less than 0.01) and the acceleration index (A = 0.63.delta fc.tau-1) decreased from 0.20 beats.min-1.s-1, SD 0.05 to 0.14 beats.min-1.s-1, SD 0.04 (P less than 0.02). The major part of the changes in tau and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Effect of tracheal bias flow on gas exchange during high-frequency chest percussion

High-frequency chest percussion (HFP) with constant fresh gas flow (VBF) at the tracheal carina is a variant of high-frequency ventilation (HFV) previously shown to be effective with extremely low tracheal oscillatory volumes (approximately 0.1 ml/kg). We studied the effects of VBF on gas exchange during HFP. In eight anesthetized and paralyzed dogs we measured arterial and alveolar partial pressures of CO2 (PaCO2) and O2 (PaO2) during total body vibration at a frequency of 30 Hz, amplitude of 0.17 +/- 0.019 cm, and tidal volume of 1.56 +/- 0.58 ml. VBF was incrementally varied from 0.1 to 1.2 l.kg-1.min-1. At low flows (0.1-0.4 l.kg-1.min-1), gas exchange was strongly dependent on flow rate but became essentially flow independent with higher VBF (i.e., hyperbolic pattern). At VBF greater than 0.4 l.kg-1.min-1, hyperventilatory blood gas levels were consistently sustained (i.e., PaCO2 less than 20 Torr, PaO2 greater than 90 Torr). The resistance to CO2 transport of the airways was 1.785 +/- 0.657 l-1.kg.min and was independent of VBF. The alveolar-arterial difference of O2 was also independent of the flow. In four of five additional dogs studied as a control group, where constant flow of O2 was used without oscillations, the pattern of PaCO2 vs. VBF was also hyperbolic but at substantially higher levels of PaCO2. It is concluded that, in the range of VBF used, intraairway gas exchange was limited by the 30-Hz vibration. The fresh gas flow was important only to maintain near atmospheric conditions at the tracheal carina.