Breathing and physical fitness exercises for asthmatic children.
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Previous work has shown that replacing N2 in air with He at the same inspired O2 fraction reduces the exercise-induced alveolar-arterial PO2 difference (AaPO2) in horses but has provided no mechanism explaining this effect. We sought to distinguish among possible causes by using the multiple inert gas elimination technique. Six horses were studied on a high-speed treadmill while they breathed either ambient air or normoxic He-O2. O2 uptake reached 138.0 ml.min-1.kg-1 and was not affected by He-O2. Temperature-corrected arterial PO2 was 76.7 Torr (air) and 86.9 Torr (He-O2) (P < 0.01). Corresponding AaPO2 was 22.3 and 15.9 Torr, respectively (P < 0.01). Mean AaPO2 predicted from ventilation-perfusion inequality did not change with He-O2 (12.7 Torr with air and 11.9 Torr with He-O2). Mean arterial PCO2 was 50.1 Torr with air and 44.1 Torr with He-O2 (P < 0.01); minute ventilation and tidal volume were correspondingly higher by 140 l/min and 1.0 liter, respectively, with He-O2. Pulmonary O2 diffusing capacity, cardiac output, and all ventilation-perfusion dispersion indexes did not change with He-O2. Intrapulmonary shunt was insignificant. Higher ventilation with He-O2 explained only approximately 4 Torr of the 10-Torr rise observed in arterial PO2. The remainder (and the corresponding fall in AaPO2) was due to more complete diffusion equilibration as a consequence of the higher minute ventilation and thus alveolar PO2, which reduced the average slope of the O2 dissociation curve, thereby increasing the ratio of diffusive to perfusive conductance.
It has been suggested that physical training causes a slower, deeper breathing pattern at a given level of ventilation, but there is no convincing evidence to support this. We examined breathing pattern during maximal incremental exercise on a cycle ergometer in 7 males before and after 3-4 weeks of cycle endurance training (TRAINING), and in 6 males before and after a similar period of unaltered physical activity (CONTROL); all subjects were healthy and previously sedentary. After physical training there was a significant increase in peak oxygen uptake, and significant reductions in carbon dioxide output, heart rate (fHR) and minute ventilation (VI) at submaximal workloads; peak VI was significantly increased whereas peak fHR was unchanged. At matched VI levels (moderate, moderately-high, high) the TRAINING subjects' breathing pattern was not significantly altered; there was a power of at least 80% to detect a significant (> 0.30 L) increase in tidal volume (P < 0.05) at moderately high and high ventilation levels. There was no change in the CONTROL subjects' maximal exercise performance, or breathing pattern at matched VI levels, over the same period. Short-term, activity-specific physical training does not significantly affect the breathing pattern adopted by normal humans during progressive exercise.
The oxygen cost of exercise and chemical control of breathing were studied in a subject with Luft's syndrome, a disorder in which skeletal muscle mitochondria have a high "resting" O2 consumption which is imcreased only slightly by stimulation with excess phosphate acceptor, but a normal P/O ratio. The O2 consumption was more than three times normal (1.05 1/min) at rest but could be doubled when stimulated by maximal exercise. The O2 cost of exercise was similar to that of normal subjects. At rest, arterial blood PCO2 and ventilatory response to CO2 were normal, while ventilatory response to hypoxia was four times the predicted value. The data 1) confirm, in vivo, the normal respiratory efficiency of skeletal muscles in this disorder; 2) suggest that in vitro estimates of the extent to which mitochondrial respiration can be stimulated may not correlate with in vivo determinations; and 3) suggests that hypermetabolism per se can cause the ventilatory adjustments which are associated with exercise in normal subjects.
We monitored gas exchange and muscle activity during two commonly used modes of passive leg exercise as a means of assessing the degree of passivity associated with these techniques. Additionally, we measured the rapid changes in ventilation at the start and end of the passive exercise to assess changes that occur in the fast exercise drive to breathe during passive exercise. We monitored seven subjects at rest and during 5 min of passive exercise using (1) cycling movements performed on a tandem bicycle and (2) leg extension movements performed in a chair apparatus. The increase in measured parameters from rest to passive exercise were all higher while using the tandem bicycle compared to the chair apparatus: ventilation [3.09 (0.63) versus 0.35 (0.38) l x min(-1)], leg muscle electromyogram [8.3 (1.6) versus 1.6 (0.6) microV], carbon dioxide production [0.092 (0.018) versus -0.002 (0.001) l x min(-1)] and oxygen consumption [0.158 (0.046) versus -0.008 (0.007) l x min(-1)]. Passive exercise on the tandem bicycle was also associated with a significantly larger fast exercise drive to breathe at both the start and end of motion, compared to the chair apparatus [start: 5.59 (0.74) versus 3.08 (0.79) l x min(-1), end: 3.38 (0.79) versus 1.75 (0.54) l x min(-1)]. The fast exercise drive to breathe at the end of exercise was significantly smaller (60%) than at the start for both modes. We conclude that passive exercise on an upright bicycle contains a significant active component that contributes both neural and metabolic influences toward the physiological adjustments observed. Furthermore, we conclude that adaptation occurs in the fast exercise drive to breathe accompanying passive limb movement.
Fourteen subjects performed cycle exercise at work loads of 0 and 1 kp, each for 3 min, during which the pedal rate was kept constant by various external cues. Six cues were used in order: no cue (N1), a speedometer dial (S), a flashing light (F), a verbal command (V), a metronome sound (M) and no cue, again (N2). An attempt was to study the effect of these cues on breathing pattern in a lower tidel volume (VT) range during exercise, actually VT increasing to 2 times the resting levels. In N1 and N2, exercise was performed at preferred pedal rates, which were 40 +/- 4 (mean +/- S.E.)rpm and 52 +/- 2 rpm, respectively. Pedaling to other four cues was kept at 50 rpm. Ventilatory responses during exercise were similar in all conditions of cue except N1. Increases in respiratory frequency (f) during exercise were similar in S but greater in F at 0-kp load and in V and M at 1-kp load, compared with N2. The greater increases in f in F, V and M were due to greater shortening in inspiratory (T1) and expiratory (TE) durations. In any conditions of cue, T1 and TE decreased with increasing VT in response to exercise. The present study indicates that (1) breathing pattern during rhythmic exercise is affected by external rhythmic stimuli like F, V and M, and (2) there is no such a VT range that TI and TE remain constant in the VT-TI and VT-TE relations during exercise. cycle exercise: rhythmic cue during exercise; breathing pattern.
This study was conducted to determine the impact of maternal exercise on fetal breathing and fetal body movement, which are commonly used for assessing fetal well-being. Twelve healthy patients with a range of gestational ages of 26 to 36 weeks, who actively exercised throughout pregnancy, participated in the study. The patients walked on a motorized treadmill using a modified Bruce protocol until the maternal heart rate reached 75% of the age-predicted maximal heart rate. Fetal activities (fetal breathing and fetal body movement) were continuously monitored with real-time ultrasonography for 20 minutes before and after the standardized exercise test. Our results demonstrate that there is a significant increase in maternal heart rate and blood pressure associated with exercise. In addition, there is a significant decrease in the total duration and frequency of fetal breathing and fetal body movements following acute maternal exercise.
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