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PubMedDate not supplied

The importance of nose-breathing for the systolic blood pressure rise during exercise.

The effect of nose breathing on the systolic blood pressure was examined in ten healthy men. Nose breathing was increased above normal by exercise and tested by maximum bicycle ergometry. When the anterior part of the nose was dilated with Nozovent the nasal airflow increased by on average 29%. In this condition, all ten men could cycle at maximum load without mouth breathing and there was a significantly lower increase (13 mmHg) in the systolic blood pressure than when the nasal dilator was not used. The reason for this lower blood pressure increase is unknown. The hypothesis is put forward, however, that facilitated nose breathing decreases the respiratory work, which in turn lowers the systolic blood pressure during exercise.

Adult↗
PubMed1984

Respiratory frequency and the oxygen cost of exercise.

Although many studies indicate that the spontaneous breathing frequency minimizes breathing work, the consequences of this for exercise energetics have never been investigated. To see if the spontaneous exercise breathing frequency minimizes oxygen uptake, we compared VO2 during treadmill walking (2/3 VO2 max) at several alternative frequencies. The alternative frequencies ranged from the lowest sustainable to a frequency twice the spontaneous value. All eight subjects adjusted tidal volume to comfort. Exercise oxygen uptake was constant, independent of breathing frequency. At the same time, minute ventilation rose to be 65% greater at the highest frequency than at the lowest (P less than 0.01). We then reproduced the various exercise frequencies, tidal volumes, and ventilations during seated isocapnic hyperpnea to measure VO2 with locomotory muscles at rest. Once again, oxygen uptake was constant, independent of breathing frequency. We conclude that the spontaneous exercise breathing frequency fails to minimize VO2 during either exercise or resting reproduction of exercise ventilation.

Adult↗
PubMed2001

Near-infrared spectroscopy determined brain and muscle oxygenation during exercise with normal and resistive breathing.

To elevate effects of carbon dioxide (CO2) retention by way of an increased respiratory load during submaximal exercise (150 W), the concentration changes of oxy- (DeltaHbO2) and deoxy-haemoglobin (DeltaHb) of active muscles and the brain were determined by near-infrared spectroscopy (NIRS) in eight healthy males. During exercise, pulmonary ventilation increased to 33 (28-40) L min-1 (median with range) with no effect of a moderate breathing resistance (reduction of the pneumotach diameter from 30 to 14 and 10 mm). The end-tidal CO2 pressure (PETCO2) increased from 45 (42-48) to 48 (46-58) mmHg with a reduction of only 1% in the arterial haemoglobin O2 saturation (SaO2). During control exercise (normal breathing resistance), muscle and brain DeltaHbO2 were not different from the resting levels, and only the leg muscle DeltaHb increased (4 (-2-10) microM, P < 0.05). Moderate resistive breathing increased DeltaHbO2 of the intercostal and vastus lateralis muscles to 6 +/- (-5-14) and 1 (-7-9) microM(P < 0.05), respectively, while muscle DeltaHb was not affected. Cerebral DeltaHbO2 and DeltaHb became elevated to 6 (1-15) and 1 (-1-6) microM by resistive breathing (P < 0.05). Resistive breathing caused an increased concentration of oxygenated haemoglobin in active muscles and in the brain. The results indicate that CO2 influences blood flow to active skeletal muscle although its effect appears to be smaller than for the brain.

Adult↗
PubMed2003

CO2 does not affect passive exercise ventilatory decline.

Breathing increases abruptly at the start of passive exercise, stimulated by afferent feedback from the moving limbs, and declines toward a steady-state hyperpnea as exercise continues. This decline has been attributed to decreased arterial CO2 levels and adaptation in afferent feedback; however, the relative importance of these two mechanisms is unknown. To address this issue, we compared ventilatory responses to 5 min of passive leg extension exercise performed on 10 awake human subjects (6 men and 4 women) in isocapnic and poikilocapnic conditions. End-tidal Pco2 decreased significantly during poikilocapnic (Delta = -1.5 +/- 0.5 Torr, P < 0.001), but not isocapnic, passive exercise. Despite this difference, the ventilatory responses to passive exercise were not different between the two conditions. Using the fast changes in ventilation at the start (5.46 +/- 0.40 l/min, P < 0.001) and end (3.72 +/- 0.33 l/min, P < 0.001) of passive exercise as measures of the drive to breathe from afferent feedback, we found a decline of 68%. We conclude that the decline in ventilation during passive exercise is due to an adaptation in the afferent feedback from the moving limbs, not a decline in CO2 levels.

Adolescent↗
PubMed2000

Influence of posture, breathing pattern, and type of exercise on minute ventilation estimation by a pacemaker transthoracic impedance sensor.

Previous studies have shown a high correlation between transthoracic impedance minute ventilation (IMV) determined by a pacemaker sensor and actual minute ventilation (VE) measured by standard methods. We hypothesized that several factors (e.g., posture, breathing pattern, and exercise type) could potentially affect the calibration between IMV and VE. In patients with Medtronic Kappa 400 pacemakers, VE (L/min) was monitored using a standard cardiopulmonary metabolic gas analysis system with simultaneous recording of IMV (ohms/min) using DR-180 extended telemetry monitors. Effects of posture and of breathing pattern at rest (19 patients; age 60 +/- 13 years) were evaluated by monitoring each patient under three conditions: (a) slow breathing, supine, (b) slow breathing, sitting, and (c) shallow breathing, supine. Calibration at rest was defined as the ratio of IMV to VE. Effect of type of exercise on calibration compared treadmill versus graded bicycle ergometer exercise (18 patients; age 62 +/- 14 years). Calibration during exercise was defined as: (a) "Begin" (the IMV to VE ratio at VE = 10 L/min, the typical VE value at beginning of exercise), and (b) slope of the IMV/VE regression line. Calibration of IMV/VE was significantly smaller for sitting versus supine position (0.7130.177, P < 0.001) and for shallow versus slow breathing (0.7210.373, P < 0.001), and larger for treadmill versus bicycle exercise (Begin: 1.240.43, P = 0.018; Slope: 1.260.42, P = 0.013). In conclusion, posture, breathing pattern, and type of exercise affect the IMV estimation of the actual VE, possibly by altering the static or dynamic geometry (thus, the impedance) of the intrathoracic viscera.

Arrhythmias, Cardiac↗
PubMed2002

[Effects of pulmonary rehabilitation in patients with pulmonary tuberculosis sequelae].

Pulmonary rehabilitation was evaluated for a mean period of 3.9 weeks in 37 inpatients with pulmonary tuberculosis sequelae. The rehabilitation program consisted of relaxation, breathing retraining, exercise training, respiratory muscle training and instruction. Significant improvement was shown in VC (n = 37) on average from 1.48 l to 1.59 l, in FEV1.0 (n = 37) from 0.93 l to 1.02 l, in PaO2 (n = 35) from 67.1 Torr to 72.4 Torr, in 6-minute walking distance (n = 29) from 303 m to 339 m, in Pimax (n = 17) from 38.5 cmH2O to 47.5 cmH2O, in activity (n = 23) from 19.6 points to 22.5 points, in dyspnea (n = 22) from 18.4 points to 22.5 points and in QOL (n = 25) from 39.0 points to 44.2 points. The effects of pulmonary rehabilitation did not depend on past thoracic surgery for tuberculosis, pattern of ventilatory impairment, findings of chest radiography, or degree of insufficiency. These data suggest that pulmonary rehabilitation is of benefit for improving pulmonary function, exercise tolerance, symptoms and QOL in patients with pulmonary tuberculosis sequelae.

Breathing Exercises↗