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PubMed1978

The effect of breath holding, hyperventilation, and exercise on nasal resistance.

A group of 51 patients was studied by a technique of active posterior rhinomanometry that assessed the influence of breath holding, hyperventilation, and exercise on nasal resistance. Breath hodling of 30 seconds or longer produced a decrease in nasal resistance in most of the subjects tested. Hyperventilation had variable effects on nasal resistance, and exercise consistently decreased nasal resistance. These observations are consistent with the proposed effect of chemoreceptor stimulation on nasal airway resistance.

Adolescent↗
PubMedDate not supplied

Breathing out into water during subtotal immersion: a therapy for chronic pulmonary emphysema.

OBJECTIVE: To determine the importance of a breathing out into water exercise during subtotal immersion for emphysematous patients. DESIGN: Results of a respiratory function test and arterial blood gas analysis were examined to compare the programs of breathing exercise with and without the breathing out into water exercise. The breathing exercises in a pool filled with 38 degrees C water were performed 30 min/day, 5 days/wk, for 2 mo in 17 patients with stable chronic emphysema. Patients were randomly assigned to breathing exercise programs including subtotal water immersion with the nose and mouth either immersed (9 patients) or out of the water (8 patients) during exhalation. RESULTS: The ratio of %forced expired volume in 1 sec to forced vital capacity and %forced vital capacity at rest were significantly increased in the program with the breathing out into water exercise, but they did not change in the program without the breathing out into water exercise. A significant increase in peak flow was observed in the former program, although it did not change in the latter program. The maximal expiratory flow at 25% did not change in either program. Pao2 was significantly increased and Paco2 was significantly decreased in the former program, although a trend for a decrease in Paco2 was observed in the latter program. CONCLUSIONS: These results suggest that the breathing out into water exercise enhances the effects of a breathing exercise during immersion and is useful in rehabilitation for chronic pulmonary emphysema.

Aged↗
PubMed1988

Role of CO2 responsiveness and breathing efficiency in determining exercise capacity of patients with chronic airway obstruction.

We examined the role of CO2 responsiveness and breathing efficiency in limiting exercise capacity in 15 patients with chronic airway obstruction (FEV1 = 0.88 +/- 0.25 L, mean +/- SD). Responses of minute ventilation and P0.1 (mouth pressure 0.1 s after the onset of occluded inspiration) to hypercapnia (delta VE/delta PCO2, delta P0.1/delta PCO2) were measured by rebreathing, and the ratio of the two (delta VE/delta P0.1) was defined as an index of breathing efficiency during hyperventilation. Exercise capacity was measured as symptom-limited, maximal oxygen consumption (VO2max/BW) in an incremental treadmill test and also as the 12-min walking distance (TMD). All patients discontinued the treadmill test because of dyspnea, and the exercise capacity correlated with the degree of airway obstruction, although there was a wide variability among patients with comparable FEV1. There were no significant correlations between the responses to CO2 and exercise capacity. However, there was a significant correlation between delta VE/delta P0.1 and VO2max/BW (r = 0.87, p less than 0.001) or TMD (r = 0.78, p less than 0.001), and these correlations remained significant even when the relational effects of FEV1 were taken out. These results support the hypothesis that airway obstruction and breathing efficiency are important, but that CO2 responsiveness is not a major factor in determining the exercise capacity of patients with chronic airway obstruction.

Aged↗
PubMed1997

[Associations between breathing pattern during submaximal exercise and exercise capacity in patients with pulmonary emphysema].

We sought to clarify the factors associated with exercise capacity in patients with pulmonary emphysema. Exercise capacities of 20 men with pulmonary emphysema were evaluated by bicycle ergometery, and the results were used to divide the subjects into two groups: high exercise capacity (n = 10) and low exercise capacity (n = 10). Pulmonary-function tests were done, emphysema scores were computed from CT scans, breathing pattern was recorded during submaximal exercise (up to 20 watts), and index of rapid shallow breathing was computed. Neither FEV1 nor airway resistance differed between the two groups, and patients with lower exercise capacity tended to have lower tidal volumes and higher values of the index of rapid shallow breathing during submaximal exercise. Functional residual capacity measured by body plethysmography and emphysema scores were inversely associated with exercise capacity. We speculate that among patients with pulmonary emphysema and a given degree of airway obstruction, a high functional residual capacity causes breathing during submaxinal exercise to be rapid and shallow, and that this rapid and shallow breathing makes ventilation inefficient, increases the work of breathing, and limits exercise capacity.

Aged↗
PubMed1995

Validity of breathing frequency to monitor exercise intensity in trained cyclists.

This study compared breathing frequency (fB) during a ventilation threshold (VT) test with fB during a simulated 40 km time trial (40TT) to assess whether fB can be used to monitor exercise intensity. Twenty-six male cyclists (mean +/- SD VO2max = 4.42 +/- 0274 l.min-1) performed an incremental VT ergometer test and a simulated 40TT on a set of wind-loaded rollers. During the 40TT, expired gas was collected for 3 min using open circuit spirometry at 10 km intervals. A significant correlation (r = 0.89; p < or = 0.05) was found between the fB threshold (VTf) and the gas exchange VT (VTg) (3.42 +/- 0.08 and 3.31 +/- 0.09 l.min-1, respectively). No differences were found in VO2 at the VTf vs. X VO2 (3.48 +/- 0.08 l.min-1) during the simulated 40TT. However, when fB in br.min-1 calculated from the VT test (32.5 br.min-1), was compared with fB during the 40TT (45.6 br.min-1), there was a significant difference. Ventilation, heart rate and the respiratory exchange ratio were all significantly higher during the 40TT. Although a significant relationship was found between the VT test and the 40TT for VTf measured in l.min-1 of VO2 (r = 0.66; p < or = 0.05), fB in br.min-1 obtained from the incremental test should not be used to identify exercise training intensity. These data suggest that during competition, trained athletes exercise at a higher fB than that determined when being tested, implying that fB in br.min-1 may not be a valid measurement of exercise intensity.

Adult↗
PubMed1997

Ventilation and respiratory mechanics during exercise in younger subjects breathing CO2 or HeO2.

To determine if ventilation (VE) during maximal exercise would be increased as much by 3% CO2 loading as by resistive unloading of the airways, we studied seven subjects (39 +/- 5 years; mean +/- S.D.) during graded-cycle ergometry to exhaustion while breathing: (1) room air (RA); (2) 3% CO2, 21% O2, and 76% N2; or (3) 79% He and 21% O2). VE and respiratory mechanics were measured during each 1-min increment (20 or 30 W) in work rate. VE during maximal exercise was increased 21 +/- 17% when breathing 3% CO2 and 23 +/- 16% when breathing HeO2 (P < 0.01). Further, the ventilatory response to exercise above ventilatory threshold (VTh) was increased (P < 0.05) when breathing HeO2 (0.89 +/- 0.26 L/min/W) as compared with breathing RA (0.65 +/- 0.12). When breathing HeO2, end-expiratory lung volume (% total lung capacity, TLC) was lower during maximal exercise (46 +/- 7) when compared with RA (53 +/- 6, P < 0.01). In conclusion, VE during maximal exercise can be augmented equally by 3% CO2 loading as by resistive unloading of the airways in younger subjects. This suggests that in younger subjects with normal lung function there are minimal mechanical ventilatory constraints on VE during maximal exercise.

Adult↗
PubMed1987

Effects of reduced frequency breathing on arterial hypoxemia during exercise.

It is uncertain that exercise with reduced frequency breathing (RFB) results in arterial hypoxemia. This study was designed to investigate whether RFB during exercise creates a true hypoxic condition in arterial blood by examining arterial oxygen saturation (SaO2) directly. Six subjects performed ten 30 s periods of exercise on a Monark bicycle ergometer at a work rate of 210 W alternating with 30 s rest intervals. The breath was controlled to use 1 s each for inspiration and expiration, and two trials with different breathing patterns were used; a continuous breathing (CB) trial and an RFB trial consisting of four seconds of breath-holding at functional residual capacity (FRC). Alveolar oxygen pressure during exercise showed a slight but significant (p less than 0.05) reduction with RFB as compared to CB. However, a marked increase in alveolar-arterial pressure difference for oxygen (A-aDO2) (p less than 0.05) with RFB over CB resulted in a marked (p less than 0.05) reduction in arterial oxygen pressure. Consequently, SaO2 fell as low as 88.8% on average. Additional examination of RFB with breath-holding at total lung capacity showed no increases in A-aDO2 in spite of the same amount of hypoventilation as compared with that at FRC. These results indicate that RFB during exercise can result in arterial hypoxemia if RFB is performed with breath-holding at FRC, this mechanism being closely related to the mechanical responses due to lung volume restriction.

Adult↗
PubMed1981

Respiratory alkalemia during exercise reduces angina threshold.

The effect of hyperventilation-induced alkalemia on angina threshold was evaluated in nine subjects who had a consistent pattern of chest pain and ST segment depression during exercise. For this study, the subjects performed graded bicycle exercise to angina during normal breathing and during hyperventilation. The maximum workload achieved was not significantly different between normal breathing and hyperventilation exercise. However, in five subjects who had arterial alkalemia during hyperventilation exercise (mean pH = 7.52), the heart rate X blood pressure product (HR X BP) at angina was 224 X 10(2) compared with 240 X 10(2) during normal breathing exercise (P less than 0.05). Four subjects appeared to hyperventilate, but were not alkalemic (mean pH = 7.40). Their HR X BP at angina was not significantly different between the two exercise periods (288 X 10(2) vs 284 X 10(2). In conclusion, the threshold for angina during exercise fell in the five patients in whom hyperventilation caused alkalemia. This finding suggests that the alkalemia interfered with myocardial oxygen supply.

Alkalosis↗
PubMed1994

Oxygen improves maximal exercise performance in interstitial lung disease.

We examined whether arterial hypoxemia impairs incremental exercise performance in subjects with interstitial lung disease (ILD). Seven subjects underwent two incremental exercise tests on a bicycle ergometer in random order; one while breathing room air (RA), and the other while breathing 60% O2. Maximal exercise performance was impaired in all subjects: maximal oxygen uptake (peak VO2) was 56 +/- 4% predicted (+/- SEM); and all subjects demonstrated significant arterial oxygen desaturation during exercise breathing RA (mean 11 +/- 1%). Breathing 60% O2 during exercise resulted in a significant increase in peak VO2 (RA: 1.32 +/- 0.05 L/min; O2: 1.58 +/- 0.08 L/min; p < 0.05), exercise duration (RA: 390 +/- 21 s; O2: 458 +/- 24 s; p < 0.01) and maximal work load (RA: 112 +/- 6 watts; O2: 129 +/- 6 watts; p < 0.005). There was no significant difference in maximal minute ventilation (VI) achieved at the end of both tests. At matched ventilation (90% peak VI from the RA test), respiratory frequency (f) was significantly higher (RA: 33 +/- 2 breaths/min; O2: 35 +/- 2 breaths/min; p < 0.05), and tidal volume (VT) significantly lower (RA: 1.72 +/- 0.15 L; O2: 1.64 +/- 0.12; p < 0.05) when subjects exercised breathing oxygen. We conclude that arterial hypoxemia significantly impairs incremental exercise performance in subjects with ILD, but that mechanisms other than arterial oxygen desaturation are responsible for the rapid, shallow breathing pattern these subjects adopt during exercise.

Adult↗
PubMed2003

Acute hemodynamic effects of abdominal exercise with and without breath holding.

OBJECTIVES: To compare the magnitudes of change in heart rate, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure, and rate-pressure product (RPP) during 3 abdominal exercises: straight partial sit-up (SPSU), oblique partial sit-up (OPSU), and the AbSculptor(R) sit-up; and to examine the effect of breath holding on these parameters. DESIGN: Prospective, repeated measures. SETTING: Autonomic research laboratory in a major medical center. PARTICIPANTS: Fourteen normal male and female volunteers (age range, 24-37y; mean, 30.4y). INTERVENTIONS: Hemodynamic parameters were recorded during each abdominal exercise performed with and without breath holding. Mean peak values were calculated for 1 minute before exercise, during exercise, and for 10 minutes after exercise. MAIN OUTCOME MEASURES: Statistical analysis examined for differences in the hemodynamic changes among the 3 exercises under both conditions (with and without breath holding). RESULTS: Heart rate, SBP, DBP, mean blood pressure, and RPP increased during all 3 exercises. The mean peak heart rate and RPP increases were greater for the OPSU than the AbSculptor (heart-rate increase, 21.1+/-6.6bpm vs 17.6+/-5.7bpm, P=.03; RPP increase, 36.9+/-15.5bpm.mmHg vs 29.4+/-10.1bpm.mmHg, P=.05). For all 3 exercises, breath holding significantly increased the hemodynamic parameter elevations during exercise, with the exception of heart rate (SBP, P<.001; DBP, P<.001; mean blood pressure, P<.001; RPP, P=.02). Quantitatively, breath holding during the OPSU resulted in the largest exercise-associated increases in heart rate (21.0+/-8.1bpm), mean blood pressure (22.2+/-16.4mmHg), and RPP (44.9+/-22.3bpm.mmHg). Postexercise, all hemodynamic parameters generally returned to baseline within several minutes. CONCLUSION: When performing the OPSU, SPSU, or the AbSculptor exercises as used in this investigation, normal individuals exercising at low intensities may experience peak heart rate and mean blood pressure increases of 30bpm and 50mmHg, respectively. Voluntary breath holding significantly increased the peak blood pressure elevations and RPP for all 3 exercises, but particularly for the OPSU.

Abdomen↗
PubMed1995

Vasoconstrictor peptides and cold intolerance in patients with stable angina pectoris.

BACKGROUND: The exact mechanism that explains the phenomenon of cold intolerance in patients with angina remains controversial. Although the response to the effects of a cold environment has been examined in these patients, their response to cold air inhalation has produced conflicting results. In addition, the possible role of vasoactive peptides in the pathophysiology has not been explored. OBJECTIVES: The aims of this study were to examine the response of patients with stable angina to the effects of cold air inhalation during exercise testing, and to investigate the possible role played by the vasoconstrictor peptides endothelin-1 (ET-1) and angiotensin-II (AT-II) in the pathophysiology. METHODS: In a randomised order, 12 men with stable angina, whose medication had been stopped, underwent two separate symptom limited treadmill exercise tests. At one visit the patients exercised while breathing room air and at the other visit they exercised while breathing cold air from a specially adapted freezer. Serial peripheral venous blood samples were taken for ET-1 and AT-II estimations during each visit. RESULTS: Cold air inhalation resulted in a significant reduction in the mean time to angina (232.7 (20.4) s v 274.1 (26.9) s, P = 0.04) and the mean total exercise time (299.5 (27.0) s v 350.3 (23.9) s, P = 0.008), but no significant change in the time to 1 mm ST depression (223.3 (29.0) s v 241.3 (29.2) s, P = 0.25). There was no significant difference between the rate-pressure products at the onset of angina (P = 0.13) and the time to 1 mm ST depression (P = 0.85), but at peak exercise the rate-pressure product was significantly lower in patients breathing cold air as opposed to room air (P = 0.049). There was an equivalent significant decrease in ET-1 concentrations at peak exercise compared with that at rest at both visits (room air 5.0 (0.7) pmol/l v 4.3 (0.7) pmol/l, P = 0.03; cold air 4.4 (0.6) pmol/l v 3.8 (0.5) pmol/l, P = 0.02). There was a significant increase in AT-II concentrations 10 min after peak exercise in patients breathing room air (39.2 (6.1) pmol/l v 32.1 (4.8) pmol/l, P = 0.01) which was not repeated during cold air inhalation (36.6 (3.4) pmol/l v 28.3 (3.4) pmol/l, P = 0.07). CONCLUSIONS: Cold air inhalation in patients with stable angina results in an earlier onset of angina and a reduction in exercise capacity. Both peripheral and central reflex mechanisms appear to contribute to the phenomenon of cold intolerance. Peripheral ET-1 and AT-II do not appear to play a significant role in the pathophysiology.

Aged↗