Journal of applied physiology: respiratory, environmental and exercise physiology最新文献

To assess the role of carotid bodies in modulating the ventilation-CO2 production relationship, steady-state responses to mild exercise were determined in goats following several experimental manipulations that led to chronic changes in resting ventilation and arterial blood gases. The experimental conditions were 1) control, 2) whole body serotonin depletion (induced by p-chlorophenylalanine, 100 mg/kg), 3) carotid body denervation (CBX), and 4) serotonin depletion with CBX. Resting values of arterial CO2 pressure (Pco2) ranged from 32 to 48 Torr. In each condition, arterial Pco2 was regulated to a similar degree in exercise due to changes in the slope of the ventilation-CO2 production relationship (delta Vi/delta Vco2) in accordance with the requirements of gas exchange. delta Vi/delta Vco2 increased with serotonin depletion both before and after CBX. The principal component of ventilation contributing to changes in delta Vi/delta Vco2 was tidal volume. These results suggest a basic property of the ventilatory control system whereby enhanced ventilatory activity at rest is associated with an increased ventilatory response to exercise via a mechanism that does not require peripheral chemoreceptors.

In seven unanesthetized cats, radiolabeled microspheres were used to determine regional brain blood flow (rBBF) to the medulla-pons (M-P), midbrain-thalamus (M-T), cerebellum (Cb), and cortex (Cx) during three conditions: 1) control [arterial O2 tension (PaO2) = 81 Torr, arterial CO2 tension (PaCO2) = 26 Torr]; 2) hypocapnic hypoxia (PaO2 = 39 Torr, PaCO2 = 22 Torr); and 3) isocapnic hypoxia (PaO2 = 47 Torr, PaCO2 = 26 Torr). Hypoxia increased blood flow significantly more in the caudal brain stem (M-P) than in the Cx (P less than 0.05) during both hypocapnic hypoxia (M-P/Cx: +33/ +17 ml X min-1 X 100 g-1) and isocapnic hypoxia (M-P/Cx: +13/ -2 ml X min-1 X 100 g-1). Since sympathetic innervation is greater anatomically to rostral than to caudal vessels, we examined the rBBF response to hypocapnic hypoxia in seven additional cats after unilateral superior cervical gangliectomy. All seven cats had a reduction in the cortical-to-caudal brain stem trend on the denervated side of the brain (M-P/Cx: +27/+28 ml X min-1 X 100 g-1) compared with the intact side of the brain (M-P/Cx: +34/+24 ml X min-1 X 100 g-1) owing to both increases in Cx and decreases in M-P flows. We conclude that in unanesthetized cats hypoxia causes a greater increase in the caudal brain stem compared with cortical blood flow, and this differential response is related to modulation by the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Specific airway conductance (sGaw) was measured during quiet breathing and during panting in 21 normal subjects and 10 patients with obstructive lung disease. The direct method used does not require measuring thoracic gas volume (TGV). Coefficients of variation were 5.5% for panting and 5.1% for quiet breathing. Interobserver variability was 4.7% in the quiet-breathing method and 6.3% in the panting method. The two methods gave equivalent results for sGaw. A slightly greater sGaw was found by the panting method in normal subjects with the highest sGaw values, probably due to widening of the oropharynx-glottis during panting. In six normal subjects studied for intrasubject variability over time, no significant diurnal or day-to-day variability was seen by either method. We conclude that the quiet-breathing method is a simple valid means of determining sGaw and utilizes a physiological respiratory maneuver. Obviation of the need to measure TGV is advantageous. Results are equivalent to those of the panting method and variability is similar.

Enzymes specific for O-2 and H2O2 metabolism [superoxide dismutase (SOD) and catalase] can be delivered to the rat brain following entrapment in liposomes and intravenous injection and will protect against hyperbaric O2-induced convulsions in rats. Liposome-mediated superoxide dismutase and catalase augmentation of brain enzyme activity was 2.7-fold and 1.9-fold, respectively, 15 min after intravenous injection of superoxide dismutase plus catalase-entrapped liposomes. Rats treated with liposomes containing superoxide dismutase plus catalase 2 h before 6 ATA 100% O2 exposure had the time to convulsion extended three times that of controls. This protective effect was dose-dependent and was primarily due to augmentation of catalase activity. These findings show O-2 and H2O2 are important mediators of hyperbaric O2-induced central nervous system toxicity and that liposome-mediated augmentation of brain antioxidant enzymes has a biological effect.

Hypoxia causes severe disruption of both rapid-eye-movement (REM) and non-REM (NREM) sleep. Experiments were performed on rats to determine if hypoxic insomnia is mediated by peripheral chemoreceptors and if normal sleep is restored during acclimatization to low O2. Novel methods were devised to measure distribution of amplitudes of cortical slow waves during NREM sleep and to detect REM sleep from the ratio of amplitudes of theta-to delta-frequency bands in the hippocampal electroencephalogram (EEG). Acute exposure of rats to 10.5% O2 (5,030 m altitude equivalent) during daylight hours virtually abolished REM sleep and shifted the distribution of amplitudes of slow-wave sleep EEG toward awake values. Similar disruption of sleep occurred during inhalation of 0.05% CO with steady-state carboxyhemoglobin of approximately 35%. Respiratory rate and alveolar ventilation were greatly increased by 10.5% O2 but were unaffected by CO. Therefore, hypoxic disruption of sleep was not mediated by peripheral chemoreceptors regulating breathing. Partial recovery of sleep occurred after 1-2 wk of hypoxia, but both REM and NREM were still subnormal after 1 mo. Decreased intensity of NREM sleep during hypoxia, measured by amplitude of cortical slow waves, may explain the disparity between subjective complaints of insomnia at altitude and evaluations of sleep by direct observation or by conventional EEG. Loss of appetite, loss of weight, irritability, and other symptoms of altitude sickness may be related to hypoxic insomnia.

During dynamic exercise cardiac output (Q) normally increases approximately 5 liters per liter of increase in O2 uptake (Vo2) (i.e., delta Q/delta Vo2 approximately equal to 5), indicative of a tight coupling between systemic O2 transport and utilization. We studied four patients with muscle phosphorylase deficiency (McArdle's disease) in whom Q was normal at rest, but delta Q/delta Vo2 was 14.1 +/- 1.3 during bicycle exercise. Procedures designed to alter the availability of substrates were employed to test the hypothesis that the increased delta Q/delta Vo2 is linked to the abnormal metabolic state of skeletal muscle. Fasting plus prolonged moderate exercise was used to increase the availability of plasma free fatty acid (FFA) and resulted in a normalization of delta Q/delta Vo2 (5.3 +/- 0.4). Hyperglycemia (70% above control levels) partially normalized delta Q/delta Vo2. Nicotinic acid lowered plasma FFA concentration and dramatically increased delta Q/delta Vo2 (4.6 to 13.7) when administered after fasting plus prolonged exercise in one patient. Glucose infusion after nicotinic acid administration markedly lowered delta Q/delta Vo2. The results support the hypothesis and suggest that the metabolic state of skeletal muscle, possibly via activation of muscle afferents, participates in the regulation of systemic O2 transport.

Eight well-trained male rowers exercised as hard as possible on a bicycle ergometer for 60 min at an ambient temperature of 18 degrees C. On 1 day (precooling test, PRET) exercise was preceded by a double cold exposure that caused starting body temperatures to be approximately 4.5, 1.0, 0.8, and 0.4 degrees C (mean skin, mean body, tympanic, and esophageal temperatures, respectively) lower than in the control test (CONT). In PRET the mean 1-h work rate (172 W) was 6.8% larger than in CONT (161 W), O2 uptake (Vo2) was 9.6% higher (2.86 vs. 2.61 1 X min-1), and O2 pulse was increased by 5.6% (18.8 vs. 17.8 ml), whereas the sweat rate was 20.3% lower in PRET (1.06 vs. 1.33 mg X cm-2.min-1). No differences in heart rate, efficiency, postexercise blood values of lactate, or acid-base status were demonstrated. It appears that the improved performance in PRET was related to an increased O2 supply to the working muscles. Although plasma levels of total beta H-endorphin immunoreactivity were in the same range under both test conditions, different components of beta H-endorphin immunoreactivity were indicated to exist in PRET and CONT.

Dogs with indwelling catheters in the jugular vein and in the carotid artery ran on the treadmill (slope: 15%, speed: 133 m/min). Lactate turnover and glucose turnover were measured using [U-14C]lactate and [3-3H]glucose as tracers, according to the primed constant-rate infusion method. In addition, the participation of plasma glucose in lactate production (Ra-L) was measured with [U-14C]glucose. Propranolol was given either (A) before exercise (250 micrograms/kg, iv) or (B) in form of a primed infusion administered to the dog running at a steady rate. Measurements of plasma propranolol concentration showed that in type A experiments plasma propranolol fell in 45 min below the lower limit of the complete beta-blockade. In the first 15 min of work Ra-L rose rapidly; then it fell below that of the control (exercise) values. During steady exercise, the elevated Ra-L was decreased by propranolol infusion close to resting values. beta-Blockade doubled the response of glucose production, utilization, and metabolic clearance rate to exercise. In exercising dogs approximately 40-50% of Ra-L arises from plasma glucose. This value was increased by the blockade to 85-90%. It is concluded that glycogenolysis in the working muscle has a dual control: 1) an intracellular control operating at the beginning of exercise, and 2) a hormonal control involving epinephrine and the beta-adrenergic receptors.