Increase In Occlusion Pressure Research Articles

Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans.

Acute and long-term effects of resistance exercise combined with vascular occlusion on muscular function were investigated. Changes in integrated electromyogram with respect to time (iEMG), vascular resistive index, and plasma lactate concentration were measured in five men either during or after elbow flexion exercises with the proximal end of the arm occluded at 0-100 mmHg. The mean iEMG, postexercise hyperemia, and plasma lactate concentration were all elevated with the increase in occlusion pressure at a low-intensity exercise, whereas they were unchanged with the increase in occlusion pressure at high-intensity exercise. To investigate the long-term effects of low-intensity exercise with occlusion, older women (n = 24) were subjected to a 16-wk exercise training for elbow flexor muscles, in which low-intensity [ approximately 50-30% one repetition maximum (1 RM)] exercise with occlusion at approximately 110 mmHg (LIO), low-intensity exercise without occlusion (LI), and high- to medium-intensity ( approximately 80-50% 1 RM) exercise without occlusion (HI) were performed. Percent increases in both cross-sectional area and isokinetic strength of elbow flexor muscles after LIO were larger than those after LI (P < 0.05) and similar to those after HI. The results suggest that resistance exercise at an intensity even lower than 50% 1 RM is effective in inducing muscular hypertrophy and concomitant increase in strength when combined with vascular occlusion.

Increase in occlusion pressure with ventilation and response to maximal exercise

Fifteen sedentary or mildly active men (low fit group) and 15 trained male athletes (high fit group) performed an incremental exercise bout on a cycle ergometer until exhaustion. At each submaximal load, minute ventilation (VE) and rate of change of mouth pressure (dP/dt) during a brief airway occlusion were computed. The airway was occluded for 40-200 ms and adjusted according to the level of ventilation. Maximal oxygen uptake (VO2peak) and minute ventilation (VEpeak) were measured during the last increment. dP/dt was related to VE in all subjects as dP/dt = a VECURV. The CURV parameter was 0.99-1.95 with a median of 1.49. The subjects were divided into four groups of seven or eight according to their physical fitness and their CURV value. Low and high CURV subjects had a CURV below and above the median, respectively. VE/VO2peak and VE/VCO2peak were significantly higher in the low CURV than in the high CURV group (P < 0.01 and P < 0.05, respectively). Although factors other than the increase in pulmonary impedance with ventilation may influence CURV, the present results indicate the possible influence of mechanical constraint of breathing on the ventilatory output.

Interaction of Hypoxia and Hypercapnia on Respiratory Drive in Patients with COPD

The objective of this study was to compare the response of respiratory drive to progressive hypoxia under eucapnic and hypercapnic conditions in patients with severe COPD. Twenty-five patients with severe COPD and 13 nonsmoking young men were studied. The pressure in the occluded airway measured 0.1 second after the onset of inspiration was used as an index of respiratory drive. The occlusion pressure was measured at levels of SaO2 between 97 and 85 percent while eucapnic. The PETCO2 was then increased 10 mm Hg and the study repeated. The response of respiratory drive to hypoxia as measured by the slope of the regression line relating occlusion pressure to SaO2 was weak and variable in eucapnic hypoxia, and some subjects had no demonstrable response. When mild respiratory acidosis was created by increasing the PETCO2, the response to hypoxia was much greater and occurred in all subjects studied. Respiratory acidosis resulting from acute elevation of the PaCO2 greatly potentiates the increase in respiratory drive in response to hypoxia in normal subjects and in patients with severe COPD. Increase in occlusion pressure may occur with slight degrees of hypoxia when acute hypercapnia is present. These observations suggest that patients with acute respiratory failure complicating COPD, treated with controlled oxygen administration with only partial correction of hypoxia and continued respiratory acidosis, will have high respiratory drive.

The transition between apnoea and spontaneous ventilation in patients with coma due to voluntary intoxication with barbiturates and carbamates

We have investigated the transition from apnoea to spontaneous breathing in five comatose patients self intoxicated with barbiturates and carbamates. All patients were apnoeic on admission, and were studied throughout the course of recovery. The transition between the first respiratory movements and a stable and nearly normal ventilation (stable respiratory activity) ranged from 15 to 105 min, a very short time compared to the duration of the apnoeic state that lasted 6 to 72 h from admission. Minute ventilation and occlusion pressure during the first respiratory movements were 6.3 +/- 2.7 l.min-1 and 1.35 +/- 0.45 kPa, respectively. These values increased by roughly 50 and 100% by the time stable respiratory activity was achieved. The increase in minute ventilation was entirely due to an increased inspiratory flow, in relation to a proportionate increase in occlusion pressure, and without significant changes in the respiratory times or in the effective elastance. We conclude that the transition between apnoea and stable respiratory activity is characterized by its rapidity, by the fact that respiratory times are fixed throughout the recovery process, and by the fact that effective elastance is high.

Effect of aerosolized histamine on occlusion pressure and ventilation in humans.

To define further the mechanism by which inspiratory neural activity is increased in asthma, we studied the effect of aerosolized histamine on occlusion pressure (P100) and ventilation in conscious humans while end-tidal CO2 partial pressure was maintained at a constant, slightly hypercapnic level. The dose of histamine we employed varied from subject to subject but was such that it produced a 70% reduction in specific airway conductance in each subject. In 9 of the 13 subjects tested, inhaled histamine significantly increased P100. This increase was not due to changes in functional residual capacity, which was not affected by aerosolized histamine. Inhalation of isoproterenol abolished the effects of histamine on specific airway conductance and P100. Anesthesia of the airways by lidocaine eliminated the effect of histamine on P100 but did not alter the magnitude of the change in specific airway conductance produced by histamine. We conclude that the increase in occlusion pressure seen after the inhalation of histamine in humans depends on both contraction of bronchial smooth muscle and stimulation of airway receptors.

Effects of expiratory loading on respiration in humans.

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.

Effect of hypoxia on the pressure developed by inspiratory muscles during airway occlusion

The effect of progressive isocapnic hypoxia on the pressure generated by the inspiratory muscle during airway occlusion was studied in 10 awake subjects during normal and obstructed breathing. Isocapnic hypoxia was produced by rebreathing a gas mixture of 6% CO2 in air while the expired gas was passed through a CO2 scrubber so as to maintain PACO2 constant (42.6 mmHg +/- 2.2 SE). Occlusion of the airway was performed randomly for a single breath at FRC. In all 10 subjects maximal pressure (Ppeak) and the pressures measured 100, 200, 300, and 400 ms after the onset of inspiration increased during hypoxia. Furthermore, good correlation was noted between the occlusion pressure response to hypoxia (delta P/DELTA[1/PO2-32]) and simultaneous changes in ventilatory response to hypoxia (delta VI/DELTA[1/PO2-32]). The occlusion pressure response to hypoxia therefore seems to be a reliable measure of respiratory center output. When rebreathing was repeated during inspiratory resistive loading, the occlusion pressure at any given PO2 and delta P/DELTA(1PO2-32) measured in the first 400 ms of inspiration increased in 9 of 10 subjects. Since PACO2 and PAO2 during both control and loaded experiments were the same, the increase in occlusion pressure in the presence of flow-resistive loading appeared to represent a neurally mediated increase in inspiratory motoneuron activity.