Subjective sleep quality and ethnicity are interactively related to standard and situation-specific measures of pain catastrophizing.

OBJECTIVE: Sleep quality and ethnicity are related to a host of general health outcomes including the experience of pain, yet it remains unclear whether poor sleep quality and ethnicity might interactively affect pain catastrophizing and laboratory-evoked acute pain reports. The current study examined the cross-sectional associations of subjective sleep quality, ethnicity, and their interaction with pain catastrophizing and pain reports. DESIGN: Healthy (N = 149), ethnically diverse (58% Caucasian American, 23% Asian American, 19% African American) young adults were subjected to a cold pressor task (CPT). Prior to CPT, participants completed the Pittsburgh Sleep Quality Index and a standard version of the Pain Catastrophizing Scale (PCS). Following CPT, participants completed a situation-specific version of the PCS. RESULTS: Adjusted analyses revealed a significant sleep quality by ethnicity interaction for standard catastrophizing reports. Particularly, African Americans with poor overall sleep quality reported the greatest level of catastrophizing on the standard PCS relative to their Caucasian American and Asian American counterparts. Furthermore, African Americans with poorer sleep efficiency reported greater catastrophizing on the situation-specific PCS compared with Caucasian American and Asian Americans. Catastrophizing was significantly correlated with pain reports. CONCLUSIONS: These results suggest that African Americans with poorer sleep quality may be at greater risk for catastrophizing, a known contributor to more intense pain and increased pain-related emotional distress. Whether interventions that improve the sleep quality of ethnic minorities affect pain catastrophizing is in need of investigation.

Mechanism of greater oxygen desaturation during walking compared with cycling in patients with COPD.

BACKGROUND: Patients with COPD exhibit greater oxyhemoglobin desaturation during walking than with cycling. The purpose of this investigation was to investigate differences in ventilatory responses and gas exchange as proposed mechanisms for this observation. METHODS: Arterial blood gas and lactate levels were measured in 12 patients with COPD (aged 68 ± 6 years) during incremental treadmill and cycle exercise. The primary outcome to assess the ventilatory response to exercise was Pao2. The primary outcome to assess impairment in exercise gas exchange was the difference between partial pressures of alveolar and arterial oxygen (Pao2 - Pao2). RESULTS: Pao2 in patients was significantly lower at peak exercise for treadmill walking (51.4 ± 6.8 mm Hg) compared with cycling (60.4 ± 10.7 mm Hg) (P = .002). The initial increase in Pao2 with cycling occurred prior to the onset of the anaerobic threshold. At peak exercise, Pao2 was significantly higher with cycling compared with walking (P = .004). The anaerobic threshold occurred at a lower oxygen consumption during cycling than walking (P = .001), and peak lactate levels were higher with cycling (P = .019). With progressive exercise, Pao2 - Pao2 increased similarly during treadmill and cycle exercise. CONCLUSIONS: The higher Pao2 during cycling minimized the magnitude of oxyhemoglobin desaturation compared with walking. The enhanced respiratory stimulation during cycling appears due to an initial neurogenic process, possibly originating in receptors of exercising muscles, and a subsequent earlier onset of anaerobic metabolism with higher lactate levels during cycling.