Voluntary Isocapnic Hyperventilation Research Articles

Downregulation of Cough by Exercise and Voluntary Hyperpnea

No information exists on the effects of hyperpnea on the sensory and cognitive aspects of coughing evoked by inhalation of tussigenic agents. The threshold for the cough reflex induced by inhalation of increasing concentrations of ultrasonically nebulized distilled water (fog), and the index of cough reflex sensitivity, was assessed in 12 healthy humans in control conditions, during exercise, and during voluntary isocapnic hyperventilation (VIH) to the same level as the exercise. The intensity of the urge-to-cough (UTC), a cognitive component of coughing, was also recorded throughout the trials. The log-log relationship between inhaled fog concentrations and the correspondingly evoked UTC values, an index of the perceptual magnitude of the UTC sensitivity, was also calculated. Cough appearance was always assessed audiovisually. At an exercise level of 80% of anaerobic threshold, the mean cough threshold was increased from a control value of 1.03 +/- 0.65 to 2.25 +/- 1.14 ml/min (p < 0.01), i.e., cough sensitivity was downregulated. With VIH, the mean (+/-SD) threshold increased from 1.03 +/- 0.65 to 2.42 +/- 1.16 ml/min (p < 0.01), a similar downregulation. With exercise and VIH compared with control, mean UTC values at cough threshold were not significantly changed: control, 3.83 +/- 1.11 cm; exercise, 3.12 +/- 0.82 cm; VIH, 4.08 +/- 1.67 cm. Since the slopes of the log fog concentration/log UTC value were approximately halved during exercise and VIH compared with control, the UTC sensitivity to fog was depressed (p < 0.01). The results indicate that the adjustments brought into action by exercise-induced or voluntary hyperventilation exert inhibitory influences on the sensory and cognitive components of fog-induced cough.

Thyroarytenoid muscle activity during hypoxia, hypercapnia, and voluntary hyperventilation in humans

Intramuscular electromyographic activity of the thyroarytenoid (TA) muscle, a vocal cord adductor, was recorded in nine normal adult humans during progressive isocapnic hypoxia and hyperoxic hypercapnia. Four of the nine subjects also performed voluntary isocapnic hyperventilation. During quiet breathing of room air, the TA exhibited phasic activity in expiration and often tonic activity throughout the respiratory cycle. Both phasic and tonic TA activity progressively decreased with either increasing hypoxia or hypercapnia. Tonic activity appeared to decrease more rapidly than phasic activity with increasing chemical stimulation. At comparable tidal volume increments, the relative decrease in phasic TA activity appeared to be greater under hypoxic than under hypercapnic conditions. During voluntary isocapnic hyperventilation, phasic TA activity decreased without significant change in tonic activity. At tidal volumes approximately double those of base line, the relative decrease in TA activity was similar during both hypercapnia and voluntary hyperventilation, although differences appeared at higher tidal volumes. The results, in combination with recent findings in humans regarding the posterior cricoarytenoid muscle, a vocal cord abductor, suggest that vocal cord position is dependent on the net balance of counteracting forces not only during quiet breathing but also during involuntary and voluntary hyperpnea.

The effect of voluntary isocapnic hyperventilation on breathlessness during exercise

The effect of voluntary isocapnic hyperventilation on breathlessness during exercise

The response of the nasal airway to exercise.

Exercise causes a fall in nasal resistance that may be due to sympathetic vasoconstriction in the nasal mucosa. Other factors potentially involved in the exercise effect on nasal resistance are: increased alae nasi muscle activity, passive redistribution of blood to exercising muscle and away from the nasal mucosa, increased nasal air flow, and hyperventilation. In order to determine the importance of these factors, 6 healthy adults had nasal pressure/flow data collected at rest and after bicycle exercise at 100 to 160 W. Erect exercise with nose breathing, erect exercise with mouth breathing, voluntary isocapnic hyperventilation at the minute volumes achieved during exercise, and supine exercise were performed. The alae nasi muscles were voluntarily activated during pressure/flow measurements. The pressure/flow data were displayed on a logarithmic plot; parallel rightward shifts of this plot indicate falls in nasal resistance mediated by enlargement of the air passage. The position of the plot was defined by the flow rate at which the slope of the logarithmic plot steepens abruptly (Vtr). Erect exercise with nose breathing caused a fall in nasal resistance in all 6 subjects (mean change in Vtr, +14.4 L/min). Exercise mouth breathing and supine exercise caused similar falls in nasal resistance in all subjects (mean change of Vtr, +14.1 and +14.2 L/min, respectively). Voluntary isocapnic hyperventilation had no effect on nasal pressure/flow properties in any subject (mean change in Vtr, -1.3 L/min).(ABSTRACT TRUNCATED AT 250 WORDS)

The Effect of Voluntary Isocapnic Hyperventilation on Breathlessness during Exercise in Normals

The Effect of Voluntary Isocapnic Hyperventilation on Breathlessness during Exercise in Normals

Exercise-induced Bronchodilation in Asthma

Of 34 symptomatic adult asthmatic patients (23 men) aged 51 +/- 13 years (mean +/- 1 SD) with moderately severe airways obstruction who underwent maximal exercise testing at room temperature (22 degrees C) and humidity (44 percent RH) using a bicycle ergometer, we identified seven male patients aged 56 +/- 9 years in whom forced expired volume in one second (FEV1) increased greater than or equal to 20 percent over the baseline pre-exercise value (exercise-induced bronchodilation). At maximal exercise, these patients achieved an O2 consumption of 1.4 +/- 0.4 L/min and a minute ventilation of 56 +/- 9 L/min. Baseline FEV1 was 1.3 +/- 0.5 L (SD) (43 +/- 12 percent predicted) and increased to 2.1 +/- 0.5 L at five minutes after exercise and persisted at least 20 minutes. Exercise was repeated in all seven patients on a separate day one to six months later, and results were similar in six. In these seven patients, three minutes of voluntary isocapnic hyperventilation achieving a minute ventilation comparable to that during maximal exercise led to an increase in FEV1 of 20 +/- 18 percent (range 0 to 54 percent). The Vmax50 was 22 +/- 30 percent before, and 10 +/- 21 percent after maximal exercise and 25 +/- 37 percent before, and 11 +/- 22 percent after isocapnic hyperventilation. Pre-treatment with acetylsalicylic acid (mean serum concentration 120 +/- 64 micrograms/ml) in the six patients with reproducible bronchodilation completely blocked exercise bronchodilation in one patient and blunted it in four others. Findings suggest that a subset of adult patients with symptomatic asthma may develop bronchodilation after six to eight minutes of exercise, that exercise-induced bronchodilation may in part be reproduced with isocapnic hyperventilation, and that it may be blocked completely or partially by acetylsalicylic acid, implying mediation by prostaglandins.

Time course of posthyperventilation breathing in humans depends on alveolar CO2 tension.

The time course of the decrease in ventilation immediately after 1 min of voluntary isocapnic hyperventilation was studied in eight healthy subjects. The hyperventilation tests were done at three different levels of alveolar CO2 tension (PACO2), and at each PACO2 level with a fixed respiratory frequency and with a freely chosen (increased) frequency. The time constant of the decrease in ventilation after free-frequency hyperventilation was inversely related to the PACO2, with a regression equation of tau 1 (s) = 78.6 - 1.2 PACO2. After the fixed-frequency hyperventilation, the time constant of the decrease in ventilation was virtually zero and independent of PACO2. These results do not agree with earlier findings in anesthetized animals. The fact that hypocapnia increases the excitability of neurons might explain the findings. The extreme respiratory afterdischarge phenomenon in hypocapnic patients suffering from the hyperventilation syndrome is consistent with the outcome of this study.

Venous plasma histamine in exercise- and hyperventilation-induced asthma in man.

1. Venous plasma histamine was measured by a specific and sensitive radioenzymatic assay in seven male extrinsic asthmatic and six age-matched non-atopic non-asthmatic male subjects during exercise and voluntary isocapnic hyperventilation. 2. There was no change in peak expiratory flow in normal subjects with exercise or hyperventilation, but asthmatic subjects showed a 29.4 +/- SEM 5.8% fall after exercise and a 29.0 +/- 5.4% fall after matched hyperventilation. 3. Plasma histamine was significantly higher (P less than 0.05) in asthmatic (6.2 +/- 0.95 nmol/l) than that in normal subjects (3.4 +/- 0.61 mol/l) and showed a significant (P less than 0.01) rise (to 14.4 +/- 1.83 nmol/l) during exercise in asthmatic, but not in normal subjects. This suggests that discharge of mast-cell mediators may occur during exercise in asthmatic subjects who develop exercise-induced asthma. 4. With hyperventilation there was no change in plasma histamine in either asthmatic or normal subjects, but this does not exclude the possibility that mediators may be released locally in the airways.

The role of hyperventilation in exercise-induced bronchoconstriction.

Significant bronchoconstriction, comparable in severity to that observed after moderate treadmill exercise, was induced in asthmatic children by voluntary isocapnic hyperventilation of 3-min and 10-min duration. In both hyperventilation and exercise, nasal breathing inhibited the bronchoconstrictive responses, whereas mouth breathing potentiated the bronchoconstrictive response. In the asthmatic children, 10 min of voluntary isocapnic hyperventilation did not represent a greater bronchoconstrictive stimulus than did 10 min of exercise or 3 min of isocapnic hyperventilation. This study also showed that in normal children there was no measurable airway response after either voluntary isocapnic hyperventilation or moderate exercise. Finally, this study indicates that it is the stimulation of upper airway receptors by relatively cold and dry air, rather than hyperventilation per se, that provokes exercise-induced bronchoconstriction.