Biomedical subjects

J A Dempsey

Publications and source records attributed to J A Dempsey.

At least 145 records · Page 8Linked to original sources

PubMed1987

Exercise-induced changes in functional residual capacity.

We used a helium-rebreathe technique in nine healthy subjects to determine the effects of exercise intensity and duration on end-expiratory lung volume (EELV). The rebreathe functional residual capacity (FRC) technique was shown: (a) to be similar to that measured in the body plethysmograph, at rest; (b) to agree closely with volitionally induced changes in EELV as determined by inductance plethysmography, at rest; (c) to be reproducible within subjects between trials conducted at rest or exercise on different days (r = 0.96, coefficient of variation +/- 3%); (d) to correlate significantly with coincident changes in end-expiratory esophageal pressure from rest to exercise, with increasing exercise intensity and over time at a constant exercise load. Exercise-induced reductions in EELV occurred in all subjects, averaging 0.3 L (-0.1 to -0.7 L) in light exercise and 0.79 L (-0.5 to -1.2 L) in heavy or maximum exercise. This reduction in EELV accounted for slightly more than one-half of the increase in VT during light exercise and slightly less than one-half of the increased VT in heavy exercise. In heavy prolonged exercise lasting 8-15 min, EELV fell in the initial 2 min and was either sustained at this reduced level or fell further with exercise duration to exhaustion. We found that FRC was reduced even in very light exercise when changes in TE and VE from rest were minimal; further reductions in EELV occurred as end-inspiratory lung volume increased and expiratory time shortened with increasing exercise intensity and duration. Based on these types of changes we speculate that active expiration during exercise in humans may be controlled by a combination of locomotor-related feed-forward and lung volume related feed-back mechanisms.

Adult↗

PubMed1987

Ventilatory compensation for changes in functional residual capacity during sleep.

The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2-3 min at a constant level (range of increase 160-1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35-50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.

Adult↗

PubMed1987

Effect of hypoxia-induced periodic breathing on upper airway obstruction during sleep.

We studied the effect of hypoxia-induced unstable and periodic breathing on the incidence of obstructed breaths in nine subjects who varied widely in their increase in total pulmonary resistance (RL) during non-rapid-eye-movement (NREM) sleep. During normoxic NREM sleep, all subjects showed hypoventilation, augmented diaphragmatic electromyogram (EMGdi), and increased RL. This response varied: two subjects doubled their mean RL (range 6-9 cmH2O X l-1 X s); four moderate snorers increased RL four- to eightfold (RL = 16-48 cmH2O X l-1 X s); three heavy snorers showed high RL (31-89 cmH2O X l-1 X s) plus cyclical obstructive hypopnea as their predominant breathing pattern. In seven of nine subjects, hypoxia and coincident hypocapnia initially caused an irregular cyclical breathing pattern with obstructed breaths (RL greater than 50 cmH2O X l-1 X s). The incidence of obstructed breaths induced by unstable breathing was closely correlated with the level of RL experienced in the control condition of normoxic sleep (r = 0.91). The obstructed breaths had relatively high O2 saturation (90-96%) and markedly reduced EMGdi activity and peak flow rate (less than 0.2 l/s) compared with breaths immediately after the obstructed breaths, which showed lower O2 saturation (81-93%) and markedly augmented EMGdi and flow rates. After 3-6 cycles of obstructive hypopnea, periodic breathing occurred in most subjects. During periodic breathing in six of seven subjects, the incidence of obstructed or high-resistance breaths was decreased or eliminated since each central apneic period was followed by breath clusters characterized by very high EMGdi, very low RL, and high flow rates. The remaining subject showed a high incidence of obstructed breaths during all phases of normoxic and hypoxic sleep. These data show that hypoxia-induced instability in breathing pattern can cause obstructed breaths during sleep coincident with reduced motor output to inspiratory muscles. However, this obstruction is only manifested in subjects susceptible to upper airway atonicity and narrowing (such as snorers) and can be prevented in most cases if respiratory drive is permitted to reach sufficiently high levels (as during central apnea).

Adult↗

PubMed1987

NHLBI workshop summary. Respiratory disorders of sleep. Pathophysiology, clinical implications, and therapeutic approaches.

The extensive investigation into complex interactions of breathing and sleep have produced answers to numerous important questions, but it is clear that many of the most important questions in this area remain unanswered. Our understanding of the mechanisms through which sleep alters breathing and how disordered breathing can, in turn, effect sleep is rudimentary. Although a large body of recent work has done much to elucidate the factors that act to maintain the patency of the upper airway during sleep, our understanding of such mechanisms and the relative importance of structure and function in this context remains primitive. A better understanding of these issues will be critical in elucidating the pathophysiology of respiratory disorders of sleep. Although some progress has been made in this area, new insights will be critically important to the design of novel, potentially more effective approaches to treatment. Therapeutic decisions are greatly hampered by major uncertainties regarding respiratory disorders of sleep and the clinical significance of symptoms, signs, and laboratory findings, and their relationship to morbidity and mortality. It seems clear that new information regarding the pathophysiology and natural history of these disorders will be important in the development of new, more effective strategies for therapeutic intervention, and this together with rigorous, systematic evaluation of new and future therapeutic approaches will be critical to clinical progress in this field.

Airway Resistance↗

PubMed1986

Anesthetic effects on [H+]a and muscle metabolites at rest and following exercise.

We determined the effects of ether, intra-arterial Na+ pentobarbital (SP) and decapitation on arterial [H+] and labile metabolites in plantaris, diaphragm and intercostal muscles of rats at rest and following exhaustive treadmill exercise. 30-60 sec post-analgesia arterial [Lactate] ([LA]a) increased with both anesthetics. SP rats retained CO2 resulting in mixed acidosis, while ether anesthetized rats hyperventilated and maintained pH. During recovery from exercise ether anesthesia had no effect but SP anesthesia caused CO2 retention. Decapitation of resting rats markedly decreased [CP] and elevated [LA] and [G6P] in all three muscles, thereby negating any subsequent exercise effects. The effects of ether differed from those of SP in that with ether anesthesia: [CP]/[Total Creatine] fell and [LA] rose significantly with exercise; resting [LA] was lower and increased with exercise; and metabolite variability was less with ether than with SP. We conclude that: anesthesia obscured the true effects of exercise on acid-base status by increasing [LA]a in the resting state; decapitation is unsuitable for the study of exercise effects on most muscle metabolites; ether anesthesia is most suitable for use in studies aimed at detecting exercise effects on muscle metabolites and for preserving arterial acid-base status closest to the unanesthetized state.

Acid-Base Equilibrium↗

PubMed1986

Carotid bodies are required for ventilatory acclimatization to chronic hypoxia.

We have compared the ventilatory responses of intact and carotid body-denervated (CBD) goats to moderate [partial pressure of O2 in arterial blood; (Pao2) approximately 44 Torr] and severe (Pao2 approximately 33 Torr) many time points for up to 7 days of hypobaria. In the intact group there were significant time-dependent decreases in partial pressure of CO2 in arterial blood (PaCO2) in both moderate and severe hypoxemia (approximately-7 and -11 Torr) that were largely complete by 8 h of hypoxemia and maintained throughout. Acute restoration of normoxia in chronically hypoxic intact animals produced time-dependent increases in Paco2 over 2 h, but hypocapnia persisted relative to sea-level control. Arterial plasma [HCO3-] and [H+] decreased, and [Cl-] increased with a time course and magnitude consistent with developing hypocapnia. Chronic CBD, per se, resulted in a sustained, partially compensated respiratory acidosis, as PaCO2 rose 6 Torr and base excess rose 3 mEq/1, [Cl-] fell 1 mEq/1, and pHa fell 0.01 units. During exposure to identical levels of arterial hypoxemia as in the intact group. CBD animals showed no significant changes in PaCO2, [H+]a, or [HCO3-]a at any time during moderate or severe hypoxemia. Plasma [C1-] remained within the normal range throughout exposure to moderate hypoxia and increased in severe hypoxia. In a few instances some hypocapnia was observed, but this was highly inconsistent and was always less than one-third of that observed in intact goats. In contrast to intact goats, acute restorations of normoxia in the chronically hypoxic CBD goats always caused hyperventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1986

Effects of exercise in normoxia and acute hypoxia on respiratory muscle metabolites.

We determined changes in rat plantaris, diaphragm, and intercostal muscle metabolites following exercise of various intensities and durations, in normoxia and hypoxia (FIO2 = 0.12). Marked alveolar hyperventilation occurred during all exercise conditions, suggesting that respiratory muscle motor activity was high. [ATP] was maintained at rest levels in all muscles during all normoxic and hypoxic exercise bouts, but at the expense of creatine phosphate (CP) in plantaris muscle and diaphragm muscle following brief exercise at maximum O2 uptake (VO2max) in normoxia. In normoxic exercise plantaris [glycogen] fell as exercise exceeded 60% VO2max, and was reduced to less than 50% control during exhaustive endurance exercise (68% VO2max for 54 min and 84% for 38 min). Respiratory muscle [glycogen] was unchanged at VO2max as well as during either type of endurance exercise. Glucose 6-phosphate (G6P) rose consistently during heavy exercise in diaphragm but not in plantaris. With all types of exercise greater than 84% VO2max, lactate concentration ([LA]) in all three muscles rose to the same extent as arterial [LA], except at VO2max, where respiratory muscle [LA] rose to less than half that in arterial blood or plantaris. Exhaustive exercise in hypoxia caused marked hyperventilation and reduced arterial O2 content; glycogen fell in plantaris (20% of control) and in diaphragm (58%) and intercostals (44%). We conclude that respiratory muscle glycogen stores are spared during exhaustive exercise in the face of substantial glycogen utilization in plantaris, even under conditions of extreme hyperventilation and reduced O2 transport. This sparing effect is due primarily to G6P inhibition of glycogen phosphorylase in diaphragm muscle. The presence of elevated [LA] in the absence of glycogen utilization suggests that increased lactate uptake, rather than lactate production, occurred in the respiratory muscles during exhaustive exercise.

Animals↗

PubMed1986

A sleep-induced apneic threshold and its consequences.

We have emphasized the mechanisms and consequences of sleep state effects on the manifestation of a sensitive apneic threshold. In the absence of the stabilizing influences of wakefulness, even the healthy person is vulnerable to instabilities and ventilatory control as maintenance of a rhythmic breathing pattern becomes overwhelmingly dependent on CO2. This sleep-induced unmasking of the depressant effects of hypocapnia contrasts with the relatively minor effects of sleep on the ventilatory response to a wide variety of other acute or chronic ventilatory stimuli or inhibitors. This combination of an apneic threshold with a maintained hypoxic (and asphyxic) responsiveness during non-REM sleep probably explains much of the periodic breathing in hypoxic sleep in adults and in newborns. Furthermore, applying acute hypoxia to persons with upper airways that are susceptible to collapse, i.e., snorers, showed that fluctuating chemical stimuli and the accompanying instability in ventilatory control during sleep can cause obstructive apnea, at least under conditions where chemoreceptor stimuli are sufficient to initiate some inspiratory effort but insufficient to insure a completely patent upper airway. We emphasize that chemoreceptor-induced instability and/or apnea probably plays little or no role in the induction of many other varieties of sleep apnea including most obstructive sleep apneas and perhaps even in some types of nonobstructive apnea. The consequences of these chemoreceptor-induced instabilities are, of course, substantial in terms of impairment of pulmonary gas exchange and the precipitation of events that contribute significantly to the development of chronic cor pulmonale.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemoreceptor Cells↗

PubMed1986

J.B. Wolffe memorial lecture. Is the lung built for exercise?

In summary, we have shown that the design of the pulmonary system from the architectural capacities of the lung parenchyma and respiratory muscles to the remarkable, multi-level neural integration of breathing pattern and respiratory muscle recruitment is clearly intended for the exercising state. Furthermore, the system shows remarkable capability for true adaptation, both phylogenetically and even within only a few generations within a species, when preservation of the organism's ability to survive and function is at stake. At the same time there are limits to the system's homeostatic capabilities, and these appear in instances other than the "usual" ones, where the capabilities for gas transport and utilization beyond the lung (i.e., by the cardiovascular and musculo-skeletal systems) surpass those of the lung and chest wall, such as during exercise in certain pulmonary disease states or in alien environments or in the highly trained. Exercise-induced hypoxemia in the thoroughbred horse is a different type of dominance of the superior locomotor control system, because their extraordinary capability to produce and sustain a very high limb velocity dictates requirements for airway flow rates which may surpass the mechanical capabilities of the lung and perhaps even the chest wall. So this hypothesis does indeed suggest that the healthy pulmonary system may become a so-called "limiting" factor to oxygen transport and utilization and to CO2 transport and elimination, at least during short-term maximum exercise in the highly trained. On the one hand, the idea is especially appealing in a philosophical sense because of its conceptual tidiness and its confirmation of the premise that no organ system has limitless functional capacity; on the other hand, given the long list of our still untested speculations, we could use a bit more data.

Adaptation, Physiological↗

PubMed1985

Adaptability of the pulmonary system to changing metabolic requirements.

The conventional view of the healthy pulmonary system during exercise is of a very precise and mechanically efficient homeostatic regulator of ventilation and gas exchange occurring within the reserves of a near ideal architecture of the lung and chest wall. These regulatory and architectural limits may be exceeded in the healthy pulmonary system when extremely high levels of metabolic demand are needed. For example, arterial hypoxemia will often occur at exercise intensities demanding greater than 25 liters/min cardiac output. This may be due to inadequate red cell transit time in the pulmonary capillary bed whose blood volume has been maximally recruited, thereby resulting in alveolar-end-capillary oxygen disequilibrium. At these extreme levels of exercise the hyperventilatory response may be minimal (and clearly inadequate in terms of alveolar oxygenation) despite substantial and progressive metabolic acidosis or hypoxemia or both. This evidence of compromised ventilatory response and inadequate gas exchange in the highly fit human suggests that the pulmonary system may not be reasonably designed or adaptable (with long-term physical training) to the extreme demands imposed on gas transport by a truly adapted cardiovascular system.

Adaptation, Physiological↗

PubMed1985

Airway resistance and respiratory muscle function in snorers during NREM sleep.

The effect of non-rapid-eye-movement (NREM) sleep on total pulmonary resistance (RL) and respiratory muscle function was determined in four snorers and four nonsnorers. RL at peak flow increased progressively from wakefulness through the stages of NREM sleep in all snorers (3.7 +/- 0.4 vs. 13.0 +/- 4.0 cmH2O X 0.1(-1) X s) and nonsnorers (4.8 +/- 0.4 vs. 7.5 +/- 1.1 cmH2O X 1(-1) X s). Snorers developed inspiratory flow limitation and progressive increase in RL within a breath. The increased RL placed an increased resistive load on the inspiratory muscles, increasing the pressure-time product for the diaphragm between wakefulness and NREM sleep. Tidal volume and minute ventilation decreased in all subjects. The three snorers who showed the greatest increase in within-breath RL demonstrated an increase in the contribution of the lateral rib cage to tidal volume, a contraction of the abdominal muscles during a substantial part of expiration, and an abrupt relaxation of abdominal muscles at the onset of inspiration. We concluded that the magnitude of increase in RL leads to dynamic compression of the upper airway during inspiration, marked distortion of the rib cage, recruitment of the intercostal muscles, and an increased contribution of expiratory muscles to inspiration. This increased RL acts as an internal resistive load that probably contributes to hypoventilation and CO2 retention in NREM sleep.

Abdomen↗

PubMed1985

Mechanical impedance as determinant of inspiratory neural drive during exercise in humans.

Five healthy males exercised progressively with small 2-min increments in work load. We measured inspiratory drive (occlusion pressure, P0.1), pulmonary resistance (RL), dynamic pulmonary compliance (Cdyn), transdiaphragmatic pressure (Pdi), and diaphragmatic electromyogram (EMGdi). Minute ventilation (VE), mean inspiratory flow rate (VT/TI), and P0.1 all increased exponentially with increased work load, but P0.1 increased at a faster rate than did VT/TI or VE. Thus effective impedance (P0.1/VT/TI) rose throughout exercise. The increasing P0.1 was mostly due to augmented Pdi and coincided with increased EMGdi during this initial portion of inspiration. We found no consistent change in RL or Cdyn throughout exercise. With He breathing (80% He-20% O2), RL was reduced at all work loads; P0.1 fell in comparison with air-breathing values and VE, VT, and VT/TI rose in moderate and heavy work; and P0.1/VT/TI was unchanged with increasing exercise loads. Step reductions in gas density at a constant work load of any intensity showed an immediate reduction in the rate of rise of EMGdi and Pdi followed by increased VT/TI, breathing frequency, and hypocapnia. These changes were maintained during prolonged periods of unloading and were immediately reversible on return to air breathing. These data are consistent with the existence of a reflex effect on the magnitude of inspiratory neural drive during exercise that is sensitive to the load presented by the normal mechanical time constant of the respiratory system. This "load" is a significant determinant of the hyperpneic response and thus of the maintenance of normocapnia during exercise.

Abdomen↗

PubMed1985

Pulmonary control systems in exercise: update.

We examined recent ideas and findings concerned with the regulation of ventilation and gas transport in moderate and heavy exercise. The primary mediation of exercise hyperpnea remains unknown and highly controversial, but two unique approaches to the problem have advanced our understanding of this neurohumoral regulatory scheme. On the one hand, experimental separation of the pulmonary and systemic circulations was used to reveal a vagally mediated ventilatory response that is clearly attributable to CO2 flow to the lung. This mechanism seems to be most effective as a homeostatic regulator of ventilatory control near resting levels of metabolic rate. On the other hand, a descending neurogenic drive to hyperpnea from the locomotor regions of the central nervous system was also demonstrated experimentally. The importance of regulatory feedback by conventional chemoreceptors in determining the precision of the hyperpneic response was emphasized in explaining the wide spectrum of arterial acid-base regulation during exercise in humans and non-human species. Two commonly accepted homeostatic regulators believed to be operative during heavy exercise were questioned, i.e., the compensatory hyperventilatory response and the maintenance of arterial oxygenation. For example, the hyperventilatory response was shown not to require metabolic acidosis; hyperventilation was not always observed at high work rates despite an abundance of chemical stimuli; and arterial hypoxemia occurred at very high metabolic rates in a significant number of highly fit athletes. These data implied that the capabilities of some aspects of even the healthy pulmonary system may be approached-or even exceeded-during heavy exercise.

Animals↗

PubMed1984

Effects of slow wave sleep on ventilatory compensation to inspiratory elastic loading.

We determined the effects of slow wave sleep on ventilatory compensation to inspiratory elastic loads (18 cm H2O/L). Multiple loading trials of variable duration were applied in three healthy adult humans in wakefulness and during NREM sleep. During wakefulness, ventilatory response over 5 loaded breaths were highly variable. Tidal volume (VT), mean inspiratory flow (VT/TI), and minute ventilation (VE) were preserved or increased in 2 of the 3 subjects in whom mouth occlusion pressure (P0.1) was augmented in the immediate (second breath) response to the load. In the third subject who showed no change in P0.1, VE was not preserved during loading. During NREM sleep, the loading response was highly consistent in all trials and in all 3 subjects. P0.1 on the second loaded breath was not increased; thus VE, VT and VT/TI were reduced over five loaded breaths. This absence of immediate load compensation during NREM sleep was similar during normoxia, hyperoxia, and hypercapnia. During sustained loading in NREM sleep VE and VT returned toward control levels coincident with an increase in end tidal CO2. We conclude that augmentation of inspiratory neural drive sufficient for immediate compensation to elastic loads requires wakefulness. Compensatory responses to loading do not occur during NREM sleep until inspiratory effort is augmented by chemical stimuli.

Adult↗

PubMed1984

Exercise-induced arterial hypoxaemia in healthy human subjects at sea level.

We determined the incidence of exercise-induced arterial hypoxaemia and its determinants in sixteen highly trained, healthy runners who were capable of achieving and sustaining very high metabolic rates (maximal O2 uptake = 72 +/- 2 ml kg-1 min-1 or 4.81 +/- 0.13 l min-1). Arterial blood gases and acid-base status were determined at each load of a progressive short-term exercise test and repeatedly during constant-load treadmill running while breathing air and during inhalation of mildly hypoxic, hyperoxic, and helium-enriched gases. Three types of responses to heavy and maximum exercise were evident and highly reproducible within subjects. Four runners maintained arterial PO2 (Pa, O2) within 10 mmHg of resting values, another four showed 10-15 mmHg reductions in Pa, O2, and the remaining eight showed reductions of 21-35 mmHg, i.e. in all cases to a Pa, O2 of less than 75 mmHg and to less than 60 mmHg in two cases. During constant-load exercise, Pa, O2 was often maintained during the initial 30 s when hyperventilation was greatest; then hypoxaemia occurred and in most cases was either maintained or worsened over the ensuing 3-4 min. The most severe hypoxaemia during heavy exercise was associated with no or little alveolar hyperventilation (Pa, CO2 greater than 35 mmHg and PA, O2 less than 110 mmHg) and an alveolar to arterial PO2 difference [(A-a)DO2] in excess of 40 mmHg. During 3-4 min of heavy exercise alveolar PO2 (PA, O2) decreased by 20 mmHg in mild hypoxia (0.17 FI, O2; inspired % O2) and increased by 20 mmHg during mild hyperoxia (0.24 FI, O2) and 10 mmHg during the hyperventilation which accompanied normoxic helium breathing. In all cases Pa, O2 changed in proportion to PA, O2 with no consistent change in the alveolar to arterial PO2 difference [(A-a)DO2]. In view of the correction of hypoxaemia with mild hyperoxia and the very high ratios of alveolar ventilation to pulmonary blood flow (VA/QC = 4-6) achieved during heavy exercise, we think it unlikely that non-uniformity of the VA/QC distribution or veno-arterial shunt could explain the hypoxaemia observed in most of our subjects. By exclusion, we suggest that hypoxaemia may be attributed to a diffusion limitation secondary to very short red cell transit times in at least a portion of the pulmonary circulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1984

Central-peripheral chemoreceptor interaction in awake cerebrospinal fluid-perfused goats.

We assessed the ventilatory interaction between central [central nervous system (CNS)] and peripheral chemoreceptor stimuli in five awake goats. CNS extracellular fluid (ECF) [H+] was altered with cisterna magna perfusion of mock CSF. Peripheral chemoreceptors were stimulated with three doses of NaCN given intravenously. The resulting dose-response curves were used to assess interaction of the central and peripheral stimuli. The observed interaction was hypoadditive; i.e., the average slope of the NaCN-inspired minute ventilation dose-response line was significantly greater during alkaline perfusion than during acidic perfusion. This correlation can be described by slope = -0.24 (CSF [H+]) + 30.7; r = 0.67 (P less than 0.01). Increased ventilatory responses were accompanied by increases in mean inspiratory flow, tidal volume, and breathing frequency and decreases in expiratory time in response to peripheral chemoreceptor stimulation. Unlike previous reports in anesthetized and denervated animals, in our awake intact goats the ventilatory and tidal volume responses showed no significant dependence on the level of control (pre-NaCN stimulus) inspired minute ventilation. We conclude that the level of [H+] in cerebral ECF exerts a significant reflex-mediated hypoadditive effect on the ventilatory responses to peripheral chemoreceptor stimulation.

Animals↗

PubMed1984

Arterial blood acid-base regulation during exercise in rats.

For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (VO2), CO2 production (VCO2), arterial blood gases, arterial lactate concentration ([LA-]a), and rectal temperature (Tre) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in VCO2), PaCO2 fell 5.5 +/- 0.6 Torr, and despite a small but significant increase in [LA-]a, respiratory alkalosis prevailed [change in arterial pH (delta pHa) = 0.034 +/- 0.006]. Arterial PO2 (PaO2) increased 4.1 +/- 1.5 Torr and Tre increased 0.6 +/- 0.1 degrees C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, VO2 increased 3.4-fold (72 +/- 1.50 ml X kg-1 X min-1) and VCO2 increased 4.5-fold (74 +/- 1.90 ml X kg-1 X min-1), resulting in a 9-fold increase in [LA-]a and a severe metabolic acidosis (pHa 7.31 +/- 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 +/- 1.4 Torr] resulted in partial compensation of pHa, but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e., at less than 65% maximum VO2 (VO2max)], and the increased [H+]a with further elevations in VO2 produced no further hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1984

Effects of sleep state on ventilatory acclimatization to hypoxia in humans.

We assessed the influence of sleep state on ventilatory acclimatization to hypoxia. Ventilation, arterial O2 saturation (SaO2), and arterial acid-base status were monitored in healthy adult males during wakefulness, nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep in normoxia [barometric pressure (PB) = 740 Torr] and over 4 continuous days of hypobaric hypoxia (PB = 455 Torr). The relative hypoventilation observed during sleep compared with wakefulness in normoxia was also observed during all stages of hypoxic acclimatization. The characteristic time-dependent changes associated with acclimatization to chronic hypoxia were similar during wakefulness and all sleep states: 1) arterial CO2 partial pressure (PaCO2) decreased 27-31% by night 4 with approximately half of this fall occurring acutely (0.3-3 h hypoxia); 2) minute ventilation increased progressively with duration of hypoxic exposure including increased levels of hyperventilation throughout the initial night of sleep in hypoxia; 3) SaO2 was lowest acutely and gradually increased coincident with the progressive hyperventilation; and 4) pHa increased acutely and remained unchanged despite additional hyperventilation due to a compensatory reduction in [HCO3-]a. In addition, in the acclimatized subject hyperventilation persisted following acute restoration of normoxia, and this continued hyperventilation was similar in magnitude during both wakefulness and NREM sleep. These results indicate that suprapontine influences on ventilatory control associated with the state of wakefulness are not required in the process of ventilatory acclimatization to chronic hypoxia.

Acclimatization↗