Ventilatory Adaptation Research Articles

Physiological adaptations to exercise in people with spinal cord injury.

The number of patients that suffer some type of spinal cord lesion in recent years are high and have increased because of factors such as traffic accidents. Although their life expectancy has increased, cardiovascular illnesses is one of the main causes of morbidity and mortality. Since the degree of physical fitness is an important factor regarding the risk of cardiovascular disease, the objective of the present study was to examine the global adaptation (cardiorespiratory, metabolic and thermoregulatory response) of the organism to exercise and the application of this data to the habitual practice of physical activity to improve state of health. A group of 42 patients with spinal injury, 85% of whom were paraplegic and the remaining 15% tetraplegic performed 42 exercise tests on a cycloergometer. Body temperature (tympanum, surface of the deltoids and surface of the back), metabolic parameters (plasma uric acid, glycemia, plasma lactate), cardiocirculatory adaptation (heart rate, blood pressure arm, blood pressure leg) and ventilatory adaptation (VO2, VCO2, fr Vt, VE) were monitored. Blood pressure in the arm, blood concentrations of lactate and ventilatory parameters showed an evolution statistically dependent on the work to which the subject was submitted. Heart rate showed a statistically significant correlation with the ventilatory parameters and work load. The proportional response of the cardioventilatory parameters to the increase in the work load allowed us to evaluate the repercussion of a given exercise and thus avoid exercise of an excessive intensity that could produce cardiocirculatory changes that might entail an added risk. Heart rate presents an excellent correlation, shown in this work, with the oxygen consumption and could therefore be used to quantify the cardiorespiratory and metabolic repercussion of the exercise carried out. Furthermore, this quantification may allow for the adaptation of exercise intensity to the patient thus improving the results obtained from the practice of exercise that has been proven so necessary in these patients.

Relationship between feeding‐induced ventilatory activity and bioaccumulation of dissolved and algal‐bound cadmium in the Asiatic clam Corbicula fluminea

The influence of feeding-induced ventilatory adaptation on cadmium accumulation patterns was analyzed in quiescent Asiatic clam Corbicula fluminea studied in steady-state conditions at 15 degrees C and 25 degrees C and in air-equilibrated water. Ventilatory activity, algae inflow rate, amounts of inspired dissolved and algae-bound Cd, and whole-body and tissue-specific metal concentrations were studied during a 15-d exposure period at a low dissolved cadmium concentration of 2 microg/L and various algal concentrations of Scenedesmus subspicatus. Great care was taken not to externally stimulate animals. Four main results were obtained as regard to regulation of ventilatory activity and metal accumulation rate. First, at 25 degrees C, feeding purposes strongly stimulated ventilatory activity, while at 15 degrees C, it was independent of it except at 1 to 2 x 10(5) algae/ml. Second, Cd accumulation rate increased at higher temperature. Third, accumulation rate exhibited a positive correlation with the ventilatory flow rate. Fourth, no correlation was observed with the quantity of ventilated algae-bound Cd but, rather, with the quantity of ventilated dissolved Cd. It is concluded that the physiology of the animals can be fundamental in affecting metal accumulation process.

Defective carotid body function and impaired ventilatory responses to chronic hypoxia in mice partially deficient for hypoxia-inducible factor 1 alpha.

To investigate whether the transcriptional activator hypoxia-inducible factor 1 (HIF-1) is required for ventilatory responses to hypoxia, we analyzed mice that were either wild type or heterozygous for a loss-of-function (knockout) allele at the Hif1a locus, which encodes the O(2)-regulated HIF-1 alpha subunit. Although the ventilatory response to acute hypoxia was not impaired in Hif1a(+/-) mice, the response was primarily mediated via vagal afferents, whereas in wild-type mice, carotid body chemoreceptors played a predominant role. When carotid bodies isolated from wild-type mice were exposed to either cyanide or hypoxia, a marked increase in sinus nerve activity was recorded, whereas carotid bodies from Hif1a(+/-) mice responded to cyanide but not to hypoxia. Histologic analysis revealed no abnormalities of carotid body morphology in Hif1a(+/-) mice. Wild-type mice exposed to hypoxia for 3 days manifested an augmented ventilatory response to a subsequent acute hypoxic challenge. In contrast, prior chronic hypoxia resulted in a diminished ventilatory response to acute hypoxia in Hif1a(+/-) mice. Thus partial HIF-1 alpha deficiency has a dramatic effect on carotid body neural activity and ventilatory adaptation to chronic hypoxia.

Comparative human ventilatory adaptation to high altitude

Studies of ventilatory response to high altitudes have occupied an important position in respiratory physiology. This review summarizes recent studies in Tibetan high-altitude residents that collectively challenge the prior consensus that lifelong high-altitude residents ventilate less than acclimatized newcomers do as the result of acquired ‘blunting’ of hypoxic ventilatory responsiveness. These studies indicate that Tibetans ventilate more than Andean high-altitude natives residing at the same or similar altitudes (P et CO 2 in Tibetans=29.6±0.8 vs. Andeans=31.0±1.0, P<0.0002 at ∼4200 m), a difference which approximates the change that occurs between the time of acute hypoxic exposure to once ventilatory acclimatization has been achieved. Tibetans ventilate as much as acclimatized newcomers whereas Andeans ventilate less. However, the extent to which differences in hypoxic ventilatory response (HVR) are responsible is uncertain from existing data. Tibetans have an HVR as high as those of acclimatized newcomers whereas Andeans generally do not, but HVR is not consistently greater in comparisons of Tibetan versus Andean highland residents. Human and experimental animal studies demonstrate that inter-individual and genetic factors affect acute HVR and likely modify acclimatization and hyperventilatory response to high altitude. But the mechanisms responsible for ventilatory roll-off, hyperoxic hyperventilation, and acquired blunting of HVR are poorly understood, especially as they pertain to high-altitude residents. Developmental factors affecting neonatal arterial oxygenation are likely important and may vary between populations. Functional significance has been investigated with respect to the occurrence of chronic mountain sickness and intrauterine growth restriction for which, in both cases, low HVR seems disadvantageous. Additional studies are needed to address the various components of ventilatory control in native Tibetan, Andean and other lifelong high-altitude residents to decide the factors responsible for blunting HVR and diminishing ventilation in some native high-altitude residents.

Ventilatory compensation for inspiratory resistive loads during anaesthesia with halothane or isoflurane

We have analysed the ventilatory response to sustained inspiratory resistive loads in 14 patients, while awake and during halothane (n = 7) or isoflurane (n = 7) anaesthesia. Patients breathed halothane or isoflurane in oxygen at 1.2 minimum alveolar concentration (MAC). Inspiratory resistances of 0, 12 and 37 cm H2O litre-1 s were applied. Tidal volume (VT) was maintained with the greater loads. At the greatest resistance, a significant reduction in minute ventilation occurred in both awake (-18.9%) and anaesthetized states, with both halothane (-10.4%) and isoflurane (-14.5%). Ventilatory frequency decreased significantly from mean 14.6 (SD 4.7) to 12.5 (4.3) bpm in the awake state and during anaesthesia, with increasing inspiratory resistance (29.5 (3.6) to 23.7 (7.2) bpm and 25.8 (3.3) to 23.4 (4.0) bpm, respectively, for halothane and isoflurane) because inspiratory time (TI) was significantly longer (P < 0.01). End-tidal PCO2 increased by 0.3 kPa, on average, from baseline to the highest level of resistance (P < 0.01). Inspiratory occlusion pressure at 100 ms increased significantly with increased loading in all situations (P < 0.001). We found a similar pattern of ventilatory adaptation to sustained inspiratory flow resistive loads both in awake and anaesthetized states. VT was maintained at increased loads because of an increase in inspiratory neuromuscular output and inspiratory duration.

Physiological response to emersion in the amphibious crab Chasmagnathus granulata Dana (Decapoda Grapsidae): biochemical and ventilatory adaptations

The adaptation of Chasmagnathus granulata to air breathing depends on two types of physiological mechanisms: (1) Biochemical adjustments, comprising the achievement of new steady state values for partial pressure of carbon dioxide ( P CO 2 ) and total carbon dioxide concentration ( C CO 2 ). The initial increase in hemolymph bicarbonate is stabilized by dehydration to CO 2 presumably catalyzed by carbonic anhydrase (CA) at the basolateral side of the gill epithelium. Thus, an adequate transbranchial gradient of P CO 2 is restored. Inhibition of CA with acetazolamide (Az) reduces the rate of CO 2 excretion and elevates P CO 2 . The respiratory acidosis caused by increased P CO 2 is compensated by increase in the difference between Na + and Cl − concentrations. Az does not affect hemolymph ionic concentrations. (2) Ventilatory control: untreated animals show a significant decrease in scaphognathite frequency ( F SC) during emersion, while Az treated crabs show a slight increase of this variable. F SC of Az crabs tends to decrease with hemolymphatic CO 2, presumably by clearance of the CA inhibitor from hemolymph. These results suggest that C. granulata possess a ventilatory control based on a primary oxygen-dependent stimulus and a secondary one dependent on CO 2.

Endogenous carbon monoxide in control of respiration

It is being increasingly appreciated that gas molecules such as nitric oxide (NO) function as chemical messengers in the nervous system. Recent studies suggest that carbon monoxide (CO) is another gas molecule that has similar biological actions as NO. The purpose of this article is to highlight the current information on the significance of endogenously generated CO in control of breathing. In mammalian cells, CO is generated during oxidative cleavage of heme by heme oxygenases (HO) and molecular oxygen is essential for this reaction. Two forms of HO have been identified including an inducible HO-1, that resembles stress-inducible protein HSP-32, and a constitutively expressed HO-2. HO-2 is expressed in many respiratory related neural structures including airway ganglion, carotid body, petrosal and nodose ganglia., nucleus of the tractus solitarius (nTS), and neurons of the rostral ventrolateral medulla (RVLM). Basal expression of HO-1 is either very low or even absent, but can be elevated during oxidative stress and hypoxia. Physiological studies have shown that CO might be of importance in vagally mediated contractions of airways. Several lines of evidence indicate that endogenously generated CO is a physiological modulator of the ventilatory response to hypoxia via its actions on carotid bodies and perhaps at brainstem neurons. In addition, CO might play a role in ventilatory adaptation to hypoxia, as low oxygen is a potent inducer of HO-1. Many of the neuronal structures that express HO also contain NOS, the enzyme that generates NO. Much remains to be studied on regulatory interactions between CO and NO and their impact on breathing.

Effect of chronic hyperoxia on young and old rat carotid body ultrastructure.

Morphologic, physiological, and biochemical changes occur in the carotid body (CB) during postnatal development in relation to physiological requirements. Chronic normobaric hyperoxia attenuates the carotid chemosensory response to hypoxia. During aging there is less of a CB response to hypoxia, which results in a reduced ventilatory adaptation and chemosensory discharge. To test if the oxygen-sensitive mechanism is affected by chronic hyperoxia in an age-dependent fashion, we have studied structural and ultrastructural aspects of young and old rat CBs. Four groups of six male Wistar rats were used. One group of two-month-old rats and another of 25-month-old rats were kept at room air. The other two groups, age matched, were exposed to 98-100% O2, for 60-65 h, in a large Plexiglas chamber. The rats were anesthetized, CBs were fixed in situ with glutaraldehyde (2.5% in phosphate buffer. pH 7.4, 320 mOsm), and were prepared for electron microscopy. Young hyperoxic rats showed focal necrosis in type I cells, along with an increase of endoplasmic reticulum, Golgi apparatus, and of mitochondria volume, with loss of cristae. These changes were less pronounced in the older rat CBs compared with the young rats. In conclusion, hyperoxia seems to affect the oxygen-sensitive mechanism in the carotid body cells, and the reduced effects shown in the old rat CBs suggest an age-related decreased sensitivity to oxygen.

Does chronic hypoxia increase rat carotid body nitric oxide?

The carotid body plays an important role in ventilatory adaptation during chronic hypoxia. Nitric oxide (NO) may act as a regulator in neurotransmission, influencing the carotid body chemosensory discharge. The aim of the study was to understand if NO could contribute to the adaptation process during chronic hypoxia. The rats were kept in chronic hypoxia (10–11% inspired oxygen) for 12 days, while the controls were kept in room air (21% O 2). The distribution for diaphorase activity and immunohistochemistry for nitric oxide synthase (NOS) showed that chronic hypoxia induces an increase in NOS activity in the carotid body. It was concluded that NO release increased during chronic hypoxia and causes an inhibitory effect on carotid chemosensory discharge of the rat carotid body.

Exercise training in COPD patients: the basic questions

Pulmonary rehabilitation programmes aim at improving exercise capacity, activities of daily living, quality of life and perhaps survival in patients with chronic obstructive pulmonary disease (COPD). Recently, well-designed studies investigated and confirmed the efficacy of comprehensive pulmonary rehabilitation programmes, including exercise training, breathing exercises, optimal medical treatment, psychosocial support and health education. In the present overview, the contribution of exercise training in clinical practice to the demonstrated effects of pulmonary rehabilitation is discussed by means of six basic questions. These include: 1) the significance of exercise training; 2) the optimal intensity for exercise training; 3) prescribing training modalities; 4) the effects of exercise training combined with medication, nutrition or oxygen; 5) how training effects should be maintained; and 6) where the rehabilitation programme should be performed: in-patient, out-patient or homecare? First, exercise training has been proven to be an essential component of pulmonary rehabilitation. Training intensity is of key importance. High-intensity training (>70% maximal workload) is feasible even in patients with more advanced COPD. In addition, the effects on peripheral muscle function and ventilatory adaptations are superior to low-intensity training. There is, however, no consensus on the optimal training modalities. Both walking and cycling improved exercise performance. Since peripheral muscle function has been recognized as an important contributor to exercise performance, specific peripheral muscle training recently gained interest. Improved submaximal exercise performance and increased quality of life were found after muscle training. The optimal training regimen (strength or endurance) and the muscle groups to be trained, remain to be determined. Training of respiratory muscles is recommended in patients with ventilatory limitation during exercise. The additional effects of anabolic-androgenic drugs, oxygen and nutrition are not well-established in COPD patients and need further research. In order to maintain training effects, close attention of the rehabilitation team is required. The continuous training frequency necessary to maintain training effects remains to be defined. At this point in time, out-patient-based programmes show the best results and guarantee the best supervision and a multidisciplinary approach. Future research should focus on the role of homecare programmes to maintain improvements.

Ventilatory Adaptation to Exercise in Hypertensive Left Ventricular Hypertrophy with Associated Diastolic Dysfunction

Ventilatory Adaptation to Exercise in Hypertensive Left Ventricular Hypertrophy with Associated Diastolic Dysfunction

Regulation of neuronal nitric oxide synthase gene expression by hypoxia. Role of nitric oxide in respiratory adaptation to low pO2.

Nitric oxide synthase (NOS) catalyzes the formation of nitric oxide (NO) in mammalian cells. Three isoforms of NOS have been isolated that include inducible (i), endothelial (e) and neuronal (n) NOS. We have previously reported the distribution of nNOS in carotid bodies as well as in brain stem neurons that process peripheral chemoreceptor inputs (Prabhakar et al 1993, 1995a). Physiological studies have further shown that endogenous NO modulates the ventilatory response to hypoxia by acting both at peripheral chemoreceptors and central neurons. Chronic hypoxia is known to trigger expression of several genes including erythropoietin (Goldberg et al, 1988); tyrosine hydroxylase (Czyzyk-Krzeska et al, 1994), c-fos protoncogene (Prabhakar et al, 1995b). The objective of the present study is to examine whether chronic hypoxia also regulates nNOS gene expression, and if so to assess the role of NO in ventilatory adaptations to hypoxia.

Noninvasive Nasal Mask Ventilation Beyond the ICU for an Exacerbation of Chronic Respiratory Insufficiency

To assess the usefulness of noninvasive nasal mask ventilation (NMV) in the treatment of an exacerbation of chronic respiratory insufficiency in patients stable enough to be admitted to a non-ICU ward. A prospective study in which the beneficial effect of NMV was compared with conservative treatment. A ward of respiratory medicine of a tertiary-referral teaching hospital. The study group included 15 patients with acute respiratory acidosis. These patients had pH less than 7.35 and PaCO2 more than 60 mm Hg, respiratory rate of 30 breaths or less per minute, hemodynamic stability, and alertness and willingness of cooperation with the NMV treatment. The control group consisted of 16 patients who fulfilled the same arterial blood gas requirements, retrospectively selected from the discharge forms of the ward of respiratory medicine for the year 1993. Patients underwent NMV for two sessions per day (one in the morning and one in the afternoon), each session lasting 4 h. A volumetric respirator (Monnal D; Taema; Paris, France) was used in four patients with restrictive disease. A positive-pressure ventilator (DP90; Taema; Paris, France) was used in 11 patients with obstructive disease. Control patients received standard medical, oxygen, and chest physical therapy. As compared with pre-NMV values, mean pH was significantly higher at 4 h of NMV after the patient's ventilatory adaptation (t = 8.814, p < 0.001) and at the end of NMV (t = 12.06, p < 0.001). Ventilatory support also produced a significant improvement in hypercapnia (pre-NMV vs NMV after the patient's ventilatory adaptation, t = 6.675, p < 0.001; pre-NMV vs post-NMV, t = 6.976, p < 0.001). Posttreatment pH and PaCO2 values were significantly higher and lower, respectively, in NMV-treated patients than in controls. At the end of treatment, a significantly higher PaO2/FIO2 ratio was documented in the study group than in controls (post-NMV vs posttreatment, t = 2.846, p < 0.01). NMV associated with standard treatment may be more beneficial than conservative treatment alone for improving blood gas exchange in patients with chronic respiratory insufficiency admitted to the hospital (but not the ICU) for an episode of acute decompensation and respiratory acidosis.

Effect of Alcohol on Acute Ventilatory Adaptation to Mild Hypoxia at Moderate Altitude

To evaluate the influence of alcohol on acute adaptation to mild hypoxia at moderate altitude. Randomized, double-blind, placebo-controlled crossover trial. University clinic and mountaineering resort at altitudes of 171 m and 3000 m, respectively, in the Austrian Alps. 10 healthy male alpinists, 22 to 24 years of age. Single dose of 50 g of alcohol or placebo at altitudes of 171 m and 3000 m. Arterial oxygen pressure (Pao2) and arterial carbon dioxide pressure (Paco2) before and 1 hour after consumption of alcohol or placebo. At an altitude of 171 m, 50 g of alcohol caused no statistical change in Pao2 and Paco2 (median Pao2, 91.5 compared with 90.5 mm Hg [P = 0.89]; median Paco2, 37.5 compared with 36.0 mm Hg [P = 0.41]). At an altitude of 3000 m, the median Pao2 decreased from 69.0 to 64.0 mm Hg, a median decrease in the paired difference of 4.0 mm Hg (95.1% CI, 1.5 to 6.5 mm Hg; P < 0.01), and the median Paco2 increased from 32.5 to 34.0 mm Hg, a median increase in the paired difference of 3.0 mm Hg (95.1% CI, 2.0 to 4.0 mm Hg; P < 0.01) 1 hour after drinking 50 g of alcohol. Placebo did not influence Pao2 or Paco2 at either altitude. Alcohol inhibits the initial stages of adequate acute ventilatory adaptation to mild hypoxia at moderate altitude. Caution in the use of alcoholic beverages at moderate altitude is therefore necessary.

981-53 Impaired Ventilatory Adaptations to Submaximal Exercise in Patients with Chronic Heart Failure

The physiologic determinants limiting maximal exercise performance in patients with congestive heart failure (CHF) have not been completely characterized. Cardiac, peripheral, and ventilatory responses to exercise are attenuated in patients with CHF. While ventilatory factors are not believed to limit maximal exercise, several abnormalities of pulmonary function have been documented. Maximal voluntary ventilation (MVV) is a brief hyperventilatory maneuver that is usually performed at rest. We hypothesized that this maneuver performed during exercise could further elucidate exercise-induced pulmonary abnormalities in patients with CHF. Accordingly, MVV (in L/min, determined by a 12-second maximal hyperventilatory effort) was measured at rest and during 10 minutes of submaximal bicycle exercise (at 55% of a previously determined maximal effort) in 9 normal subjects (NL) and 9 patients with CHF (mean EF 0.23). VO 2 max Peak V E Rest MVV Exercise MVV NL 38.3 ± 7.1 132 ± 32 175 ± 42 193 ± 36 CHF 15.4 ± 1.9 * 73 ± 13 * 143 ± 28 143 ± 25 * Peak V E = peak ventilation during maximal exercise * P &lt; 0.05. CHF vs normals Although ventilatory factors did not appear to limit exercise (since MVV &gt;&gt; peak V E in both NL and CHF), MVV increased during submaximal exercise only in normal subjects but not in patients with CHF (+ 11% vs +0%, P &lt; 0.05). The exercise-induced increase in MW in normal subjects may represent an adaptive response to exercise related to exercise-induced bronchodilation or sympathetic stimulation of the diaphragm. These mechanisms may be attenuated in CHF secondary to bronchial edema from high left ventricular filling pressures, or due to intrinsic diaphragmatic muscle abnormalities. The absence of normal ventilatory adaptations to exercise may contribute to exercise intolerance in patients with CHF

Ventilatory response to sustained eucapnic hypoxia in the adult conscious dog

The ventilatory response to 20 min sustained isocapnic hypoxia ( Sa O2 , 80 ± 2% ) was examined in 5 trained unanesthetized adult dogs breathing through an endotracheal tube. End tidal P CO 2 was maintained at the resting levels. The dogs' conscious status was monitored by recording EEG and EOG on a chart recorder. The room temperature was kept between 19 and 21 °C. All tests were repeated in each dog on 2 occasions: (1) unloaded tracheal breathing or (2) resistive loaded breathing. During unloaded tracheal breathing, the average ventilation in response to sustained hypoxia rose from a control of 5.1 ± 0.3 L/min ( mean ± within-dog SE) to 9.2 ± 1.1 L/min at the initial stage of hypoxia. Ventilation remained at 20.7 ± 1.3 L/min at 10 min, and then 19.7 ± 1.4 L/min at the completion of the 20 min hypoxic exposure. There was no ventilatory adaptation observed (P > 0.05). After release from hypoxia, the ventilation fell abruptly to 7.6 ± 0.8 L/min , which was higher than the resting baseline level (P < 0.05), and then gradually returned to the resting baseline within 10 min. Experiments exposing the dogs to 40 min sustained hypoxia also failed to elicit significant adaptation. During resistive loading, the pattern of average ventilation in response to sustained hypoxia was similar to that observed in unloaded breathing tests. But the ventilatory recovery was longer than unloaded breathing, returning to the resting baseline within 20 min. Again, there was no ventilatory adaptation observed. These findings indicate that ventilatory adaptation in the awake dog does not occur during exposure to a sustained hypoxia ( 80 ± 2% saturation) over 40 min.

Exercise and Heart Transplantation

Results of heart transplantation as therapy for end-stage cardiac diseases are encouraging not only because of actuarial survival curves but also because of the recovered quality of life for the heart transplant recipient. Although heart transplantation drastically improves the physical capacity of the patients, heart recipients still have a reduced maximal aerobic capacity compared to healthy people. Altered resting and exercise haemodynamics, due to cardiac denervation, are a common finding after orthotopic heart transplantation: increases in heart rate and stroke volume at exercise are first linked with the augmented venous return and later with the increased plasmatic nor-adrenaline level. Maximal heart rate and stroke volume are both reduced when compared to innervated heart. Reduced cardiac output response to exercise therefore results in early anaerobic metabolism, acidosis, hyperventilation and diminished physical capacity. In spite of an altered ventilatory adaptation to exercise, characterised by hyperpnoea in most transplant patients, ventilation is not the limiting factor for exercise in heart recipients without associated obstructive pulmonary disease. Endurance training restores lean tissue, decreases submaximal minute ventilation, increases peak work output, maximal ventilation and peak heart rate. Guidelines for prescribing exercise are not yet standardised due to the limited number of studies on a sufficient cohort of heart recipients. Nevertheless, recommendations similar to those used for persons with coronary heart disease, with modifications due to the denervated heart, seem to be used. The cardiocirculatory and pulmonary capacity of heart transplant recipients allow them to undertake endurance sports activities such as walking, jogging, cycling and swimming, and these should be encouraged.

Ventilation in Namib Desert Tenebrionid Beetles: Mass Scaling and Evidence of a Novel Quantized Flutter-Phase

The mass scaling of discontinuous ventilation (DV) phenomena in adult motionless insects is currently unknown. I present DV phenomena from 10 species of Namib Desert tenebrionid beetles; four from the dune-sea habitat, five from the river-bed habitat and one from the gravel plain habitat, which is characterized by very low and patchy resource availability. This species differed from the others in many respects. However, all species exhibited a previously undescribed, convective and quantized F phase ventilation (ISP, or intermittent serial pulsation, phase). For dune-sea and river-bed habitat species, all DV characteristics except DV frequency (V phase CO2 emission volume and rate, total and per-burst ISP phase CO2 emission volume, and total rate) scaled tightly with body mass with a scaling exponent close to 1.0 (typical r2&amp;gt;0.95-0.98), as did overall rate of CO2 production and hence metabolic rate (MR). Consequently these parameters were independent of body mass when expressed on a mass-specific basis, explaining the independence of body mass and DV frequency. These findings are compatible with published DV data in other species and orders of insects, suggesting that these scaling phenomena may be widespread. The gravel plain species (Epiphysa arenicola) had an MR of 38%, V phase CO2 volume of 41% and V phase CO2 emission rate of 23% of those predicted on the basis of its body mass, and it emitted a greater proportion of CO2 during its ISP phase (47% vs 24% of total CO2 output per DV cycle in the other species). It is suggested that these discrepancies are respiratory and ventilatory adaptations to scarce and patchy energy and water availability.

Endogenous opiates and ventilatory acclimatization to chronic hypoxia in the cat

The effects of the opiate antagonist naloxone (0.4 mg·kg −1, i.v.) on carotid chemoreceptor and ventilatory responses to graded steady-state levels of hypoxia and hypercapnia were investigated in two groups of cats: chronically normoxic and chronically hypoxic. The cats of the latter group were exposed to P1 o2 of about 70 mm Hg at sea level for 3–4 weeks and showed an attenuated response to hypoxia. All cats were tested under α-chloralose anesthesia. Naloxone treatment did not increase appreciably carotid chemoreceptor activity or its responses to hypoxia and hypercapnia in either cat group. Naloxone caused a small ventilatory stimulation in the chronically hypoxic cats, so that the attenuated response to hypoxia was not relieved. By contrast, the chemoreflex ventilatory response to hypoxia was stimulated by naloxone in the chronically normoxic cats. The findings that the depressed ventilatory chemoreflexes in the chronically hypoxic cat were not ameliorated by the opiate antagonist indicate that an increased elaboration of endogenous opiates does not underlie ventilatory adaptation to chronic hypoxia.

Operation Everest II

To assess the ventilatory adaptation during gradual ascent to extreme altitude, we studied seven healthy males as part of the 40 d simulated ascent of Mt. Everest in a hypobaric chamber. We measured resting ventilation (VE, l.min-1), arterial oxygen saturation (SaO2%), the ventilatory response to oxygen breathing, isocapnic hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) at sea level prior to the ascent (760 torr), 14,000 feet (428 torr), 24,000 feet (305 torr), and within 24 h of descent (765 torr). VE increased from 9.3 +/- 1.1 l.min-1 at 760 torr to 23.4 +/- 1.3 l.min-1 at 305 torr and remained elevated at 14.7 +/- 0.7 l.min-1 after descent. Oxygen breathing decreased VE by 9.6 +/- 1.3 l.min-1 at 305 torr. Isocapnic HVR (expressed as a positive slope of VE/SaO2, l.min-1.%SaO2(-1) increased from 0.18 +/- 0.07 at 760 torr to 0.34 +/- 0.11 and 0.38 +/- 0.5 at 428 torr and 305 torr (P less than 0.05) respectively. HVR was elevated further upon return to sea level (0.8 +/- 0.09, P less than 0.05). HCVR (S = VE/PETCO2, l.min-1.torr-1) increased from sea level (S = 4.4 +/- 0.09) to 305 torr (S = 18.7 +/- 3.5, P less than 0.01) and remained elevated upon return to sea level (S = 10.7 +/- 4.6, P less than 0.001). This study is the first to investigate the ventilatory response to such extreme altitude and so soon after descent and shows that hypoxic and hypercapnic responses increase during prolonged progressive hypoxic exposure and remain significantly elevated from pre-ascent levels immediately upon descent.