Sleep Loss Impairs Inspiratory Muscle Endurance

Abstract

Sleep loss is common in patients with respiratory disorders. To determine whether sleep loss affects respiratory muscle function, we compared respiratory muscle and pulmonary functions after normal sleep with those measured after a 30-h sleepless period in 30 normal male subjects. The respiratory muscle strength was estimated by the maximal static inspiratory and expiratory pressures. Inspiratory muscle endurance was determined by the product of pressure load and the sustained time, i.e., pressure-time index, while the subject breathed against an inspiratory pressure load on a modified Nickerson-Keens device. We found that inspiratory muscle endurance was decremented from 871 +/- 61 to 638 +/- 69 cm H2O.min after sleep deprivation. Twelve-second maximal voluntary ventilation was also significantly reduced after sleep loss. Nevertheless, the respiratory muscle strength, FEV1, and FVC were unaltered. We therefore conclude that inspiratory muscle endurance may deteriorate after a 30-h sleep loss.

Bed rest and hypoxic exposure affect sleep architecture and breathing stability

“…Sleep architecture is affected in all trials, with the most noticeable shifts occurring in the combined HBR condition. There appears to be a direct relationship between breathing stability and mean night SpO 2 when otherwise healthy adults are confined to bed, echoing published data that have reported ventilatory drive changes in patients (Schiffman et al, 1983;Chen and Tang, 1989), and lower hypoxic chemoresponsiveness in susceptible individuals at high altitude (Nespoulet et al, 2012). The initial increase in ventilation during exposure to hypoxia (i.e., hypoxic ventilatory response; HVR) is highly variable (Hirshman et al, 1975).…”

“…These disruptions are often attributed to noise, interruptions to complete diagnostic tests, or other environmental factors (Freedman et al, 1999). Healthy subjects sleep-deprived 24-30-h can experience 17-24% decreases in ventilatory responsiveness to hypercapnia, and increased respiratory muscle fatigue (Chen and Tang, 1989). Evidence alludes to prolonged time spent in bed altering patients' ventilatory drive; sleep deprivation per se may play a role in ventilatory chemoreceptor mechanisms, although these findings are not universally supported (Spengler and Shea, 2000).…”

Physiologic correlates of dyspnea in patients with morbid obesity

“…Experimental studies in normal subjects showed that sleep loss might alter inspiratory muscle performance. 29 This mechanism could explain in part the impairment of IME. Consistent with this finding, IME was significantly lower in OSAS patients compared to OHS patients, OSAS patients exhibiting an AHI higher than OHS patients (37.2726.0 vs 28.6726.5).…”

Respiratory failure in tuberculosis: a modern perspective

“…The UK has largely been spared the effects of the worldwide increase in tuberculosis over the last [10][11][12][13][14][15][16][17][18][19][20] years. This respite is likely to be only temporary and in the past, as probably in the future, the incidence of tuberculosis in this country has been much greater.…”