Chest wall oscillation at 1 Hz reduces spontaneous ventilation in healthy subjects during sleep.

STUDY OBJECTIVE: The objective was to determine whether external chest wall oscillation (ECWO) during sleep (1) reduced spontaneous ventilation while maintaining adequate gas exchange over several hours, (2) influenced the quality and distribution of sleep, and (3) increased the number of respiratory events. DESIGN: Prospective controlled study with counterbalanced order of intervention. SETTING: Pulmonary function sleep laboratory. PARTICIPANTS: Seven healthy volunteers. INTERVENTION: One night of ECWO at 1 Hz (I:E = I:I; oscillation mean [SEM] from - 11.1 [0.7] to 6.0 [0.7] cm H2O) and a night during which the cuirass was applied without ECWO. MEASUREMENTS AND RESULTS: ECWO resulted in a significant decrease in spontaneous minute ventilation (VE) in all stages of sleep. ECWO was associated with a reduction in the total sleep time and a reduction in rapid eye movement (REM) sleep. The number of stage changes and the sleep efficiency did not change significantly. The mean PCO2 was similar between the control and cuirass nights (44 to 46 mm Hg). There was a significant decrease in the mean PCO2 during stage 1 (41 [2] mm Hg) and stage 2 (42 [2] mm Hg) sleep during the ECWO night. The mean arterial oxygen saturation (SaO2) was maintained at 96 to 97% throughout sleep during the control, cuirass, and ECWO nights. The apnea + hypopnea index increased (p < 0.05) during ECWO mostly due to an increase in the number of hypopneas in stage 2 sleep. During ECWO, 18 of 30 respiratory events were associated with an arousal, whereas only 2 events were associated with an arousal during the control night. CONCLUSIONS: ECWO can be tolerated for several hours and will assist ventilation while maintaining normal mean PCO2 and mean SaO2 during sleep. Monitoring of the apnea + hypopnea index and the SaO2 is recommended at the time of application. Clinical trials to define the most appropriate indications for ECWO are now necessary.

Dystrophin, vinculin, and aciculin in skeletal muscle subject to chronic use and disuse.

Dystrophin is a subsarcolemmal protein that interacts with cytoskeletal actin and a glycoprotein complex in the plasma membrane. One potential function of dystrophin is its ability to stabilize the sarcolemmal membrane during muscle contraction. We hypothesized 1) that chronic muscle use and disuse would alter the expression of dystrophin as a compensatory mechanism designed to prevent muscle damage, and 2) that other subsarcolemmal cytoskeletal proteins (vinculin, M-vinculin, aciculin 60/63 kDa) that colocalize with dystrophin in muscle adherens junctions would be changed in parallel. Chronic muscle use induced by voluntary running or 10-Hz chronic stimulation did not alter dystrophin levels in rat muscle. In contrast, muscle disuse induced by 6 d of microgravity, or 7 and 21 d of denervation, increased dystrophin levels by 1.8-, 1.9- and 3.2-fold, respectively. Thus, this increase in dystrophin levels appears to be dependent on the duration of muscle disuse, independent of the presence of the nerve. Denervation also induced 3.3-fold increases in vinculin and aciculin 60 kDa, in parallel with dystrophin. However, in contrast to its effects on dystrophin, chronic stimulation increased the levels of vinculin and aciculin 60 kDa by 3.4- and 6.4-fold, respectively. Thus, both the removal and the augmentation of muscle activity resulted in increases of these two cytoskeletal proteins. The data indicate that the concentrations of these proteins are independently regulated. They further indicate that chronic muscle use is not a stimulus for the induction of dystrophin levels, suggesting that normal levels are sufficient for the protective effect on the sarcolemma that dystrophin may confer. The results reveal an interesting area of muscle plasticity, and the adaptation observed may have profound implications for the structure and function of skeletal muscle responding to changes in contractile activity.

Blood flow, mitochondria, and performance in skeletal muscle after denervation and reinnervation.

Tibialis anterior (TA) muscles of rats underwent bilateral peroneal nerve crush (NC) or denervation (D) and were compared with sham-operated (SO) animals to determine the effect of reinnervation on blood flow, mitochondria, metabolites, and muscle performance. After surgery, animals were left for 2, 7, 21, or 42 days (NC and SO groups) or 2, 7, or 21 days (D group; n = 7-11.day-1.group-1), after which TA muscles were stimulated in situ at 1 Hz. alpha-Motoneuron reinnervation of muscle was complete 21 days after NC. Blood flow increased 10-fold above SO values in nonstimulated TA muscle 7 days after NC and D (P < 0.05). By 21 days, blood flow to nonstimulated TA muscle in NC animals returned to SO values but remained elevated (P < 0.05) in D muscle. Thus restoration of neural control of blood flow to resting muscle likely occurred by 21 days post-NC. Blood flow to stimulated muscle was not affected by NC or D, indicating the probable importance of metabolic factors in regulating blood flow during 1-Hz contractions. Cytochrome-c oxidase activity decreased (P < 0.05) below SO values 7 days after NC and D. By 21 days, cytochrome-c oxidase activity in TA muscles of NC animals returned to SO values, while values in denervated TA muscle continued to decrease. Despite these changes, endurance performance of TA muscle was not affected by D or NC at any time. These results suggest that reinnervation processes controlling blood flow and muscle function occur along similar time courses and that muscle blood flow is more closely related to endurance performance than is muscle oxidative capacity under these contraction conditions.