Faculty Bibliography

First-breath ventilatory responses to graded elastic (delta E) and resistive (delta R) loads from 10 people with spinal muscular atrophy (SMA), 15 people with Duchenne muscular dystrophy (DMD), and 80 able-bodied people were compared. The SMA and DMD groups produced equal tidal volume, respiratory frequency, inspiratory duration (TI), expiratory duration, mean inspiratory airflow, and duty cycle responses to both delta E and delta R. Thus SMA (primarily a motoneuron disorder) and DMD (primarily a muscle disorder) have the same net effect on loaded breathing responses. The SMA and DMD groups failed to duplicate the normal group's short expirations during delta E, long inspirations during delta R, and thus, extended duty cycles during both delta E and delta R. The deficit in load compensation therefore was due to impaired regulation of respiratory timing (reflecting neural mechanisms) but not airflow defense (reflecting mechanical and neural mechanisms). One-fifth of the normal but none of the SMA or DMD subjects actively generated an 'optimal' TI response (defined theoretically as TI greater than 160% control during large delta R and TI less than 75% control during large delta E). This lack of optimal responses, which is the same abnormality exhibited by quadriplegic people, suggests that SMA and DMD also impair human ability to discriminate between large delta R and delta E. These findings support the hypothesis that neuromuscular disorders can lead to disturbances in respiratory perception

Adrenergic mechanisms modulate exercise-induced changes in blood serum K+ concentration ([K+]). Impairment of these same mechanisms may be associated with bronchial hyper-reactivity. If this is accurate, asthmatic subjects should show disturbed K+ regulation during exercise. We measured [K+] and FEV1 in 13 healthy control and in 13 asthmatic subjects pre-exercise, at peak exercise (within 1 min of stopping exercise), and 10 min postexercise. This was done on 2 separate days, one with and one without bronchodilator (BD) pretreatment. Both groups were equally fit, exercising to the same O2 consumption and heart rate. Resting [K+] was normal for both groups (two-day averages were 4.00 +/- 0.07 and 4.09 +/- 0.07 mmol/L, mean +/- SEM, in control and asthmatic subjects, respectively). Without BD pretreatment, at peak exercise, [K+] in control subjects rose by 0.56 +/- 0.08 compared with 0.96 +/- 0.09 in asthmatics (p less than 0.01). After exercise, [K+] returned to baseline (4.12 +/- 0.08) in control subjects but remained elevated in asthmatics (4.60 +/- 0.12, p less than 0.01). Although FEV1 was unchanged in control subjects, in asthmatics it fell after exercise (p less than 0.01). With BD pretreatment: peak exercise [K+] increased by 0.55 +/- 0.09 in control subjects, and by 0.49 +/- 0.01 in asthmatics (p less than 0.01). By 10 min postexercise, it returned to baseline in both groups (4.15 +/- 0.11 for control subjects and 4.32 +/- 0.07 for asthmatics). The asthma group's fall in FEV1 was also abolished. These data indicate that postexercise K+ remains elevated in asthmatics, supporting the suggestion that their adrenergic function is impaired

Pulmonary function after exercise was evaluated in 22 asthmatic subjects before and after a 36-session training sequence of aerobic exercise. Training did not change pulmonary function values, except for a small increase in maximal voluntary ventilation (P less than 0.02), which was attributed to respiratory muscle training. After aerobic training, both external work at a given heart rate and peak O2 consumption increased by 30 and 15%, respectively. At the same minute ventilation (VE), immediate postexercise forced expiratory airflow was higher after training (P less than 0.02), and reduction in forced expiratory airflow during the first 9 min postexercise was less after training (P less than 0.01). The posttraining airflow response to the pretraining work load was, as expected, less than the pretraining response (P less than 0.02). Although the difference in maximal-to-minimal airflow at the same VE was similar before and after training, the airflow increase accounted for 50% of the response after training compared with 16% of the pretraining response. Furthermore the strong negative correlation (P less than 0.01) between maximal and minimal airflow both pre- and posttraining indicates that exercise-induced bronchospasm (EIB) severity is, in part, determined by the degree of exercise-induced bronchodilation. We conclude that aerobic training significantly increases exercise-induced bronchodilation and diminishes EIB

First-breath ventilatory responses to graded elastic and resistive loads were obtained from 15 people with Duchenne muscular dystrophy (DMD), 5 people with facioscapulohumeral MD (FSH), 3 people with Becker MD, and 3 people with limb-girdle MD. For each load tidal volumes from different individuals ranged from relatively small to comparatively large values, indicating a correspondingly wide range of end-inspiratory efforts; strong tidal volume defenders generally employed longer inspirations and higher mean inspiratory airflows than did weak tidal volume defenders; and individual frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the loaded breathing responses of people with MD are qualitatively the same as those of quadriplegic and able-bodied people. Quantitatively, however, the DMD group generated considerably larger tidal volumes than did the FSH group during both elastic and resistive loading. These larger tidal volumes were achieved by both longer inspirations (a neurally mediated phenomenon) and higher mean inspiratory airflows (a mechanically and/or neurally mediated phenomenon). These findings, which could not be attributed to differences in respiratory motor function, suggest that there are differences between the respiratory sensory and/or central functions in the Duchenne and facioscapulohumeral types of MD

The effects of rhythmic input on breath period (TT) under constant metabolic drive were assessed in 10 musically trained and 10 untrained subjects. They tapped to a metronome and then to four musical segments, each for 5 min. Ten of these subjects (5 from each group) also listened to the selections without tapping. TT, beat period (TB), and phase coupling (PC) were assessed during the last 20 breaths of each presentation. TT coefficient of variation decreased significantly (P less than 0.001) in all subjects (base line = 23%; listening = 15%; listening and tapping = 10%). Significant correlation between rhythm and TT, indicating relative entrainment, was found in half of the subjects (r greater than 0.45; P less than 0.01). Significant integer TT/TB ratio and PC, both indicating tight entrainment between rhythm and breathing, were observed in 12 subjects (though not consistently in each one). These data advance the following hypothesis: musical rhythm can be a zeitgeber (i.e., pacemaker), with its ability to entrain respiration dependent on the strength of its signal relative to spurious signals from the higher neural centers that introduce noise into the central pattern generator. Tapping reinforces the zeitgeber, increasing its signal-to-noise ratio and thereby promoting entrainment

This study assessed reduction in expiratory function in 12 asthmatic subjects both after 5 min of cold air provocation (CAP) with dry air conditioned to approximately 0 degrees C and after exercise (to 85% of predicted maximum heart rate) while breathing ambient room air (approximately 21 degrees C and 40% relative humidity). These assessments were done both before and after the following training protocol. Three 5-min periods of isocapnic cold air hyperpnea separated by 5-min rest periods were performed breathing 0 degrees to -10 degrees C air, for 36 sessions over 12 wk. As expected, pretraining expiratory function was significantly reduced (P less than 0.001) after both CAP and exercise. The posttraining reduction in expiratory function after CAP and exercise, however, was significantly less pronounced (largest P less than 0.05). These data support our hypothesis that repeated bouts of cold air challenge result in airway acclimatization to cold air and consequent decrease in exercise-induced bronchospasm. Acclimatization may result directly either by habituation of the airways or by vasodilation leading to increased bronchial blood flow and consequent reduced airway cooling. An unanticipated finding, though, is that repeated cold air challenge may also cause long-term inflammatory changes in the airways. A significant percentage of subjects experienced reduced base-line pulmonary function and overall exacerbation of asthma symptoms during the training period