Work of breathing during exercise in normal subjects and in patients with obstructive and restrictive lung disease.
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Chronic obstructive lung disease represents the most important field of application for respiratory physiotherapy. The technic comprises two successive stages: inhalation of a bronchospasmolytic and secretolytic aerosol (e.g. Alupent or Ventolin, diluted in tacholiquine or Bisolvon) followed by breathing exercises. These exercises are divided into three parts: respiratory movements such as diaphragmatic or abdominal breathing, drainage of bronchial secretions, and exercises to relax the muscles of the shoulders, the thorax and the skin, all these movements being executed in the rhythm of breathing. The effect of respiratory physiotherapy depends on the cooperation of the patient, the technic and the degree of severity of bronchiolar stenosis. The method is only successful in patients with slight to moderate bronchospasm; in those who suffer from dyspnea at rest it is usually ineffective. The prerequisite for success is longterm treatment. This means that the patient must continue to practice the acquired technique at home at least once a day. A description of the other indications for breathing exercises, such as bronchiectasis, chronic pneumonia, lung abscess, atelectasis, pleural fibrosis etc., is followed by a summary of the contraindications for the method.
BACKGROUND: Previous studies have shown that breathing techniques reduce short acting beta(2) agonist use and improve quality of life (QoL) in asthma. The primary aim of this double blind study was to compare the effects of breathing exercises focusing on shallow nasal breathing with those of non-specific upper body exercises on asthma symptoms, QoL, other measures of disease control, and inhaled corticosteroid (ICS) dose. This study also assessed the effect of peak flow monitoring on outcomes in patients using breathing techniques. METHODS: After a 2 week run in period, 57 subjects were randomised to one of two breathing techniques learned from instructional videos. During the following 30 weeks subjects practised their exercises twice daily and as needed for relief of symptoms. After week 16, two successive ICS downtitration steps were attempted. The primary outcome variables were QoL score and daily symptom score at week 12. RESULTS: Overall there were no clinically important differences between the groups in primary or secondary outcomes at weeks 12 or 28. The QoL score remained unchanged (0.7 at baseline v 0.5 at week 28, p = 0.11 both groups combined), as did lung function and airway responsiveness. However, across both groups, reliever use decreased by 86% (p<0.0001) and ICS dose was reduced by 50% (p<0.0001; p>0.10 between groups). Peak flow monitoring did not have a detrimental effect on asthma outcomes. CONCLUSION: Breathing techniques may be useful in the management of patients with mild asthma symptoms who use a reliever frequently, but there is no evidence to favour shallow nasal breathing over non-specific upper body exercises.
During exercise, large pleural, abdominal, and transdiaphragmatic pressure swings might produce substantial rib cage (RC) distortions. We used a three-compartment chest wall model (J. Appl. Physiol. 72: 1338-1347, 1992) to measure distortions of lung- and diaphragm-apposed RC compartments (RCp and RCa) along with pleural and abdominal pressures in five normal men. RCp and RCa volumes were calculated from three-dimensional locations of 86 markers on the chest wall, and the undistorted (relaxation) RC configuration was measured. Compliances of RCp and RCa measured during phrenic stimulation against a closed airway were 20 and 0%, respectively, of their values during relaxation. There was marked RC distortion. Thus nonuniform distribution of pressures distorts the RC and markedly stiffens it. However, during steady-state ergometer exercise at 0, 30, 50, and 70% of maximum workload, RC distortions were small because of a coordinated action of respiratory muscles, so that net pressures acting on RCp and RCa were nearly the same throughout the respiratory cycle. This maximizes RC compliance and minimizes the work of RC displacement. During quiet breathing, plots of RCa volume vs. abdominal pressure were to the right of the relaxation curve, indicating an expiratory action on RCa. We attribute this to passive stretching of abdominal muscles, which more than counterbalances the insertional component of transdiaphragmatic pressure.
This descriptive study analyzed serial, individual changes in the exercise pattern of breathing (POB) of patients with stable chronic heart failure (CHF). Twenty-two CHF patients underwent maximal, symptom-limited cardiopulmonary exercise test on a treadmill. Minute ventilation (VE), tidal volume (VT), breathing frequency (f), the ventilatory equivalent for carbon dioxide (VE/VCO2) and estimated dead-space to tidal volume ratio (VD/VT) were continuously recorded. The VE/VCO2 slope was calculated in every subject as the slope of the regression line relating VE to VCO2 during exercising testing. Pattern of breathing was investigated by constructing the individual VT-f relationship for each patient separately. In 16 (73%) patients (group 1), the VT-f plot was initially linear, but subsequently exhibited an inflection point at which VT stopped increasing with further increases in f. In six (27%) patients (group 2) no inflection point was evident on the VT-f relation; in four of these patients the VT-f relation remained linear but shifted to the right throughout testing, and two patients decreased VT before peak exercise achieving high breathing frequencies. Comparing group 1 to group 2 patients, they had higher VEmax (68+/-23 vs. 44+/-10 l/min, P=0.02) and VO2max (17+/-5 vs. 12+/-3 ml/min/kg, P=0.01). In contrast, the two groups did not differ in terms of age, weight, height, diagnosis, ejection fraction or VE/VCO2 slope. In conclusion, patients with CHF adopt variable breathing patterns during exercise; specific patterns are associated with greater impairment in functional capacity.
The modern living lifestyle is known to produce various physical and psychological stresses and subject the individual to produce oxidative stresses as well. The aim of this study has been to assess the effect of yogic breathing exercises (pranayama) on the oxidatives stress. The study group consisted of 30 young male volunteers, trained for the purpose of this study and an equal number of controls were used. The free radicals and Super oxide dismutase levels were measured before the study and at the end of the study. The free radicals were decreased significantly in the study group but the SOD was increased insignificantly as compared to the control group. Yogic breathing exercises not only help in relieving the stresses of life but also improve the antioxidant status of the individual. An improvement in the antioxidant status is helpful in preventing many pathological processes that are known with impaired antioxidant system of body.
Neuroendrocrine and substrate responses were investigated in eight male athletes during inhalation of either 100% O2 (HE), 14% O2 (HO) or normoxio gas (NO) before, during and after 60 min of cycle ergometry at the same absolute work rate. Concentrations of prolactin (PRL), growth hormone (GH), testosterone (T), adrenocorticotropic hormone (ACTH), cortisol (COR), adrenalin (A), noradrenalin (NA), insulin (INS), ammonia (NH3), free fatty acids, serotonin (5-HT), total protein, branched-chain amino acids (BCAA) and free tryptophan (free TRP) were determined in venous blood and lactate concentration [LA-], partial pressure of oxygen (PO2), oxygen saturation (SO2), partial pressure of carbon dioxide and pH in capillary blood. The PO2 and SO2 were augmented in HE and decreased in HO (P < or = 0.01). In HO and NO no significant changes were found for any other parameter during 30 min of rest prior to exercise. In HE, PRL increased by about 400% during this time, while NA declined (P < or = 0.01). Heart rate (HR) and [LA-] were higher during exercise in HO (P < or = 0.01). In all trials, NH3, NA, A, T, GH and ACTH increased during exercise (P < or = 0.01), while BCAA and INS declined. In comparison to NO and HE, increases of NA, A, GH, COR and ACTH were higher in HO (P < or = 0.01). The PRL in NO and COR in NO and HE did not change significantly. In HE, after the initial increase at rest, PRL declined during exercise but remained higher than in HO. Higher values for NA, A, GH, COR and ACTH in HO were likely to have reflected an augmented relative exercise intensity. Our results showed that PRL but no other hormone increased during acute exposure to hyperoxia. This PRL release was independent of exercise stress and greater than PRL augmentation during hypoxia, which was related to a higher relative exercise intensity as indicated by [LA-] and HR. Responses of plasma NH3, BCAA, free TRP and 5-HT could not explain PRL augmentation induced by the increment in blood SO2 during hyperoxia.
OBJECTIVES: We hypothesized that exercise-related periodic breathing (EPB) would be associated with poor prognosis in advanced chronic heart failure (CHF). BACKGROUND: Patients with CHF might present instability of the ventilatory control system characterized by cyclic waxing and waning of tidal volume (periodic breathing [PB]). This condition is associated with several deleterious circulatory and neuro-endocrine responses; in fact, PB in awake and asleep patients has been identified as an independent risk factor for cardiac death. During exercise, however, the prognostic value of PB is still unknown in CHF patients awaiting heart transplantation. METHODS: Eighty-four patients with established CHF (65 male, 19 female) were submitted to clinical evaluation, echocardiogram, ventricular scintigraphy, determination of resting serum norepinephrine levels, and an incremental cardiopulmonary exercise test on cycle ergometer. Patients were followed for up to 49.7 months (median = 15.3), and 26 patients (30.9%) died during this period. RESULTS: Twenty-five of 84 patients presented EPB (29.7%). The following variables were related to mortality according to Kaplan-Meier and univariate Cox regression analysis: EPB (p = 0.004), New York Heart Association class (p = 0.04), serum norepinephrine (p = 0.06), peak oxygen uptake (ml.min(-1).kg(-1) and % predicted; p = 0.085 and p = 0.10, respectively), slope of the ratio of change in minute ventilation to change in carbon dioxide output during exercise (p = 0.10), and scintigraphic left ventricular ejection fraction (p = 0.10). Cox multivariate analysis identified EPB as the only independent variable for cardiac death prediction (p = 0.007). Therefore, EPB alone was associated with a 2.97-fold increase in risk of death in this population (95% confidence interval = 1.34 to 6.54). CONCLUSIONS: Exercise-related periodic breathing independently predicts cardiac mortality in CHF patients considered for heart transplantation.
The dynamic influences of end-tidal CO2 and exercise on ventilation are compared when CO2 and exercise are imposed separately and when they are imposed simultaneously. Five human subjects are studied. The subjects performed three trials: random work rate forcing, random CO2 inhalation and their simultaneous loading. The work rate was varied between 20 and 80 W as a pseudorandom binary sequence. The concentration of inspired CO2 was varied randomly between 0 and 7 per cent, adjusted so that it produced approximately the same amount of ventilatory fluctuations as the random work load. The relative contribution of each variable was analysed using multivariate autoregressive analysis at frequencies ranging from 0.1 to 1 cycle min-1. The results show that the dynamics of the response to CO2 inhalation, exercise and their combination are nonlinear and that the combination of CO2 inhalation and exercise magnifies the nonlinear behaviour. Ventilation is largely unaffected by either work rate or end-tidal CO2 at 1 cycle min-1. During simultaneous CO2 and work rate forcing, ventilation tends to follow the change in the end-tidal CO2.
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The purpose of this study was to determine the effect of a reduced ventilatory frequency (Vf) on blood gases and acid-base changes during three intensities of cycling exercise. VO2max and lactate threshold workload (LaT) of six subjects were assessed on a Monark ergometer. Experimental rides were performed 1) with no restriction on Vf (NB) and 2) with a prescribed Vf of 10/min (CFB). Each exercise period consisted of 8 min at 10% of VO2max below the LaT (WI), followed immediately by 8 min at LaT (WII), followed immediately by 8 min at 10% of VO2max above LaT (WIII). Blood was taken from a heated fingertip at the end of each load and analyzed for lactate concentration, pH, PO2, and PCO2. Respiratory exchange was monitored continuously using open circuit indirect calorimetry. Minute ventilation (VE) was significantly reduced by CFB at all three workloads. The reduced VE resulted in lower (p less than 0.05) blood PO2 at each workload (p less than 0.05), however, neither blood lactate nor VO2 were significantly different between CFB and NB for the three loads. Blood [H+] was significantly higher in CFB than NB at all three loads with the greatest difference between trials at WIII (NB: 37.93 +/- 0.68 nM: CFB: 44.77 +/- 1.02 nM). This was accounted for by a significantly higher PCO2 during CFB in WII and WIII (WII, NB: 33.0 +/- 1.4 mmHg, CFB: 35.7 +/- 2.7 mmHg; WIII, NB: 31.2 +/- 1.7 mmHg, CFB: 38.9 +/- 2.4 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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Recipients of heart-lung transplants represent an unusual opportunity to study the regulation of ventilation, because the neural pathways between the lungs and the central nervous system are disrupted in these patients. We compared the ventilation response in seven recipients of heart-lung transplants who had normal pulmonary function and seven recipients of heart transplants, all of whom performed incremental bicycle ergometry. The level of ventilation in recipients of heart-lung transplants was similar to that in heart-transplant recipients for equivalent levels of carbon dioxide production. Arterial pH and partial pressure of carbon dioxide at maximal exercise were normal and not significantly different in the two groups, also suggesting that levels of ventilation were appropriate in both groups. However, the rate of the rise in respiratory rate for increasing levels of ventilation was significantly lower in recipients of heart-lung transplants than in heart-transplant recipients, and the initial increase in tidal volume was more rapid in the former group than in the latter. Thus, recipients of heart-lung transplants have an appropriate level of ventilation during exercise as the result of a disproportionate increase in tidal volume at a reduced respiratory rate. We speculate that intrapulmonary receptors are important in regulating the pattern, but not the absolute level, of ventilation during exercise.
Ventilation minute volume, tidal volume and cardiac frequency during submaximal exercise have been measured in healthy young soldier volunteers exposed to O-chlorobenzylidene malononitrile (CS) and ammonia gas in concentrations respectively of 0.16 to 4.4 mg.m(-3) and 50 to 344 mg.m(-3). The response of ventilation minute volume to the two gases is apparently similar; both gases cause a reduction of, on average 6%. With low doses this reflects a diminution in respiratory frequency whereas with higher doses it is due to a reduction in tidal volume which is accompanied by tachypnoea. The findings may result from stimulation successively of receptors in the larynx and of irritant receptors in the large airways of the lung. The pain which is a feature of exposure to CS but not to ammonia is due to stimulation of other so far unidentified receptors. Neither gas has a direct effect upon the exercise cardiac frequency.
The mechanisms mediating the exercise hyperpnea remain controversial; there is no unequivocal evidence that any of numerous proposed mechanisms mediates the hyperpnea. However, a great deal has been learned including the potential role of changes in PCO2, [H+], strong ion differences (SID), weak acids, or any other acid-base component. The contribution of acid-base changes to the hyperpnea during exercise is likely through known or postulated chemoreceptors. Two of these, pulmonary and intracranial chemoreceptors, do not appear critical for the ventilatory adjustments to meet the metabolic demands of exercise. A third, the carotid chemoreceptors, appear to fine-tune alveolar ventilation during exercise to minimize disruptions in arterial blood gases. The role of the fourth chemoreceptors, those within skeletal muscles, is least clear. However, there is evidence that they do contribute to the hyperpnea, and it is quite clear that a muscle chemoreflex contributes to the exercise muscle pressor reflex; thus the contribution of these chemoreceptors to the exercise hyperpnea requires additional study.