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Biomedical subjects

B J Whipp

Publications and source records attributed to B J Whipp.

At least 145 records · Page 8Linked to original sources
PubMed1981

Effect of CO2 set point on ventilatory response to exercise.

The ventilatory response to exercise was determined in seven normal adults during induced chronic metabolic acidosis, chronic metabolic alkalosis, and a control state. Incremental and constant-load exercise tests were performed in each condition on a cycle ergometer. Ventilation and gas exchange variables were determined breath by breath, and CO2 partial pressure (PCO2), pH, and HCO3 were determined from arterialized venous blood (Pa-VCO2). During chronic metabolic acidosis PaVCO2 was lower than control (36.3 +/- 2.1 and 43.7 +/- 2.9 Torr, respectively) and during alkalosis it was elevated to 47.1 +/- 1.3 Torr. The new PCO2 levels caused by chronic acid-base alterations were unchanged during moderate exercise. The ventilatory response (VE) to the same metabolic rate increment was therefore larger (delta VE = 20.6 +/- 2.91/min) when PCO2 was lower than the control level (delta VE = 14.5 +/- 2.01/min. VE also increased more steeply in response to incremental exercise tests when PCO2 was reduced. Thus the hyperpnea of moderate exercise reflects the level at which arterial PCO2 is regulated at rest, as well as the metabolic load (VCO2).

Acidosis↗
PubMed1980

The relation of ventilation to metabolic rate during moderate exercise in man.

To characterize more precisely the relationship between ventilation (VE) and CO2 output (VCO2) during incremental exercise, 35 healthy males were studied at rest and during upright cycle ergometry, with the work rate incremented every 4 min up to each subject's anaerobic threshold (Oan). Twenty-one subjects had arterial blood sampled at rest and in the steady state at each work rate to determine the relationship between physiological dead space ventilation (VD) and VCO2. At these work rates arterial PCO2 was regulated at the resting, control value. VE (BTPS) was linearly related to VCO2 from rest Oan with a slope of 24.6. However, the regression had a significant positive intercept of 3.2 L/min-1. This causes the ventilatory equivalent for CO2 (i.e., VE/VCO2) to decrease with increasing work rates. VD also increased linearly with increasing VCO2. However, this was consequent to increased breathing frequency as VD remained constant. Thus, the observed fall in VE/VCO2 with increasing work rates is due to the positive intercept but the inherent relationship between VE and VCO2, reflected by the linear regression slope, remains unchanged from rest through moderate exercise.

Adult↗
PubMed1980

Ventilatory control during exercise with increased external dead space.

Effects of increased external dead space (VD) on ventilatory control in steady-state exercise were determined in three healthy adults. The subjects performed cycle ergometer exercise on six occasions, each with a different VD (range: 0.1--1.0 liter); work rate was incremented every 5 min by 15--20 W. Minute ventilation (VE), CO2 output (VCO2), and mean alveolar PCO2 (PACO2) were measured in the steady state. Without VD, the VE-VCO2 relationship was linear, having a small positive VE intercept, and PACO2 was constant, independent of VCO2. Increased VD was associated with an upward shift of the VE-VCO2 relationship, and an elevated PACO2, again independent of VCO2. At each work rate, the increases in VE accompanying increased VD were no greater than could be expected from a conventional CO2 inhalation study. It is concluded that increasing external dead space does not impair the ability of the human respiratory system to regulate PACO2 during exercise except for resetting the regulated PCO2 level.

Adult↗
PubMed1980

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work.

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.

Adult↗
PubMed1980

Role of neural afferents from working limbs in exercise hyperpnea.

To determine the role of reflex discharge of afferent nerves from the working limbs in the exercise hyperpnea, 1.5- to 2.5-min periods of phasic hindlimb muscle contraction were induced in anesthetized cats by bilateral electrical stimulation of ventral roots L7, S1, and S2. Expired minute ventilation (VE) and end-tidal PCO2 (PETCO2) were computed breath by breath, and mean arterial PCO2 (PaCO2) was determined from discrete blood samples and, also in most animals, by continuous measurement with an indwelling PCO2 electrode. During exercise VE rose progressively with a half time averaging approximately 30 s, but a large abrupt increase in breathing at exercise onset typically did not occur. Mean PaCO2 and PETCO2 remained within approximately 1 Torr of control levels across the work-exercise transition, and PaCO2 was regulated at an isocapnic level after VE had achieved its peak value. Sectioning the spinal cord at L1-L2 did not alter these response characteristics. Thus, reflex discharge of afferent nerves from the exercising limbs was not requisite for the matching of ventilation to metabolic demand during exercise.

Afferent Pathways↗
PubMed1980

Carotid bodies and ventilatory control dynamics in man.

The normal role of the carotid bodies in ventilatory dynamics in man has been inferred from studies comparing the responses of a group of control subjects to: a) hypoxic-hyperoxic transitions, b) steady-state hypercapnia, c) constant-load and incremental exercise, and d) breath holding with various inspired O2 levels, with the responses of subjects who had had both carotid bodies surgically resected (CBR). Ventilation, metabolic rate, and alveolar gas tensions were computed breath by breath and blood was sampled from a brachial artery catheter. With eucapnia, hypoxic ventilatory drive is subserved entirely by the carotid bodies, both at rest and during exercise, whereas only approximatly equal to 30% of the hyercapnic response in euoxia is attributable to these structures. CBR resulted in appreciable slowing of the ventilatory dynamics during exercise, causing a transient respiratory acidosis. In the steady state of moderate exercise, ventilation was normal in the CBR group, as other receptors provide the approximately equal to 15% of the drive attributable to the carotid bodies. The respiratory compensation for the acute metabolic acidosis of exercise appears to be exclusively mediated by the carotid bodies. Breath-holding time is significantly prolonged following CBR, especially under hypoxic conditions. The carotid bodies therefore provide important information to respiratory control in man, most notably under hypoxia, metabolic acidosis, and dynamic states of muscular exercise.

Acid-Base Equilibrium↗
PubMed1979

Ventilation and gas exchange during phasic hindlimb exercise in the dog.

To investigate the importance of the major neural afferent component from the exercising extremities in exercise hyperpnea, rhythmic contraction of hindlimb muscles was produced in the dog, by electrically stimulating the peripheral cut ends of the sciatic and femoral nerves, bilaterally, for 4- to 5-min periods. VE, VCO2, and VO2 were computed breath-by-breath and PaCO2 was monitored continuously with an indwelling arterial electrode. During exercise, VO2 and VCO2 were approximately doubled in the steady state, rising with t1/2 of 25 +/- 2 and 35 +/- 4 s, respectively. VE increased within five breaths after exercise onset, and thereafter rose to a steady state with a t1/2 of 37 +/- 5 s. Mean PaCO2 increased transiently within the 1st min of stimulation but was not significantly different from control in the steady state. We conclude that the major neural afferent component from the contracting muscles is not an obligatory requirement for normal ventilatory response in the steady state of phasic exercise.

Afferent Pathways↗
PubMed1979

Anaerobic threshold alterations caused by endurance training in middle-aged men.

Nine previously sedentary middle-aged males underwent cycle endurance training 45 min/day for 9 wk with an average attendance of 4.1 days/wk. Seven males served as controls. Before and after the training period, the subjects performed three cycle ergometer tests. Work rate was incremented by 15 W/min, to the limit of the subjects' tolerance, in the first two tests; the third test consisted of contant-load cycling at an O2 uptake (VO2) just below the pretraining anaerobic threshold (AT). After training, the AT increased significantly by 44%, expressed as absolute VO2, and by 15%, expressed relative to VO2 max. Significant increases were also noted in VO2max (25%), maximal minute ventilation (19%), and maximal work rate (28%). The test-retest correlation coefficients for the AT (%VO2max) were 0.91, pre- and posttraining. Training did not alter steady-state VO2 during the submaximal exercise test whereas significant decreases occurred in CO2 output, VE, respiratory quotient, and VE/VO2. No changes occurred in the control subjects during this period. These results demonstrate that the AT is profoundly influenced by endurance training in previously sedentary middle-aged males.

Adult↗
PubMed1979

Determinants of gas exchange kinetics during exercise in the dog.

Following exercise onset, CO2 output (VCO2) and O2 uptake (VO2) increase exponentially, but with appreciably different time constants. To determine the sensitivity of the time courses of these variables to altered ventilatory kinetics, rhythmic exercise was induced abruptly in anesthetized dogs by bilateral stimulation of the peripheral ends of the cut sciatic and femoral nerves. This increased the metabolic rate by 83 +/- 25 (SD) %. The dogs were ventilated with a constant-volume pump, the frequency of which was changed exponentially from the start of the exercise up to the ventilation that returned arterial CO2 and O2 pressure (PCO2 and PO2) in the steady state to resting levels. The time constant (tau) of the increase in ventilation (VE) was varied among trials. VCO2, VO2, end-tidal PCO2 and PO2, and arterial PCO2 were measured breath by breath. tauVO2 was constant at approximately 18 s regardless of alterations in tauVE. In contrast, tauVCO2 was strongly dependent on tauVE, apparently due to the larger body stores for CO2; the transitions were isocapnic when tau VE was approximately 40 s. We conclude that ventilatory dynamics can markedly influence the dynamics of CO2 exchange during exercise, but has no appreciable effect on O2 uptake dynamics.

Animals↗
PubMed1979

Hypopnea consequent to reduced pulmonary blood flow in the dog.

The ventilatory responses to diminished pulmonary blood flow (Qc), as a result of partial cardiopulmonary bypass (PCB), were studied in chloralose-urethan-anesthetized dogs. Qc was reduced by diverting vena caval blood through a membrane gas exchanger and returning it to the ascending aorta. PCB flows of 400--1,600 ml/min were utilized for durations of 2--3 min. Decreasing Qc, while maintaining systemic arterial blood gases and perfusion, results in a significant (P less than 0.05) decrease in expiratory ventilation (VE) (15.9%) and alveolar ventilation (VA) (31.0%). The ventilatory decreases demonstrated for this intact group persist after bilateral cervical vagotomy (Vx), carotid body and carotid sinus denervation (Cx), and combined Vx and Cx. The changes in VE and VA were significantly (P less than 0.001) correlated with VCO2 changes, r = 0.80 and r = 0.93, respectively. These ventilatory changes were associated with an overall average decrease in left ventricular PCO2 of 2.1 Torr; this decrease was significant (P less than 0.05) only in the intact and Cx groups. Decreasing pulmonary blood flow results in a decrease in ventilation that may be CO2 related; however, the exact mechanism remains obscure but must have a component that is independent of vagally mediated cardiac and pulmonary afferents and peripheral baroreceptor and chemoreceptor afferents.

Animals↗
PubMed1979

Hyperoxic attenuation of exercise-induced bronchospasm in asthmatics.

To investigate the mechanism of exercise-induced bronchospasm, we measured specific airway conductance before and after exercise in 7 healthy normals, 12 asthmatics with intact carotid bodies, and 5 asthmatics who had had bilateral carotid body resection. The subjects breathed either air or oxygen (randomly assigned) during cycle ergometer exercise. Post-exercise bronchodilation was the usual pattern in normals, whereas post-exercise bronchospasm occurred in all asthmatics who breathed air during exercise. Oxygen breathing during exercise markedly attenuated the post-exercise bronchospasm in those asthmatics with intact carotid bodies, but had no significant effect in those without effect in those without carotid bodies. The attenuation of the bronchospasm with oxygen occurred with either incremental or constant load exercise of high intensity. The degree of attenuation did not correlate significantly with changes in end-tidal PCO2, maximum work rate, maximum exercise ventilation, or maximum heart rate. These studies indicate that oxygen attenuates exercise-induced bronchospasm in asthmatics through its action on the carotid bodies.

Adolescent↗
PubMed1979

Doxapram hydrochloride: a respiratory stimulant for patients with primary alveolar hypoventilation.

Four patients (ages 43 to 51) with primary alveolar hypoventilation (PAH) syndrome were studied to characterize the pharmacologic augmentation of ventilation with intravenous doxapram hydrochloride. Doxapram hydrochloride evoked a rapid ventilatory increase of 50 to 100 percent in all four subjects with a consequent decrease in arterial CO2 tension. Blood pressure and heart rate measurements showed small increases during the doxapram infusion. These responses, however, were only sustained during the infusion, decreasing to their predoxapram level when the drug was discontinued. The ventilatory response to the drug was more marked in the pressence of hypoxia than during high O2 breathing, suggesting that the carotid bodies are a site of action for this drug in man. Doxapram hydrochloride can be an effective respiratory stimulant in patients with PAH.

Doxapram↗
PubMed1979

Peripheral chemoreceptors and exercise hyperpnea.

The carotid bodies appear to be the only peripheral chemoreceptors mediating ventilatory control during exercise in man. While little is known about the mechanism of stimulation, much is known about the effects of carotid body stimulation upon pulmonary ventilation (VE). These effects have been produced by hypercapnia, hypoxia, metabolic acidosis, arterial blood pressure, temperature, and catecholamines. A signal from CO2 flow is attractive because of the strong correlation between CO2 output and VE during exercise. The carotid body's role in the hyperpnea depends on the intensity of exercise. During heavy exercise, pH falls and hyperventilation ensues. The carotid bodies appear to be the exclusive mediators of the ventilatory compensation for the acidosis at this exercise intensity. For moderate exercise, mean arterial PCO2 does not change. Therefore, how is the CO2 signal transmitted to the respiratory center? Two current theories are: (1) since arterial PCO2 and pH oscillate with each breath, the amplitude and period of these oscillations may change during exercise and may be of sufficient magnitude to stimulate the carotid bodies, and (2) there exists a disequilibrium between hydrogen ion activity within the red blood cell and in the plasma because carbonic anhydrase is found in the former but not the latter. This theory assumes that the enzyme is not accessible to the plasma.

Aortic Bodies↗