Does exercise improve self-reported sleep quality in non-remitted major depressive disorder?

BACKGROUND: Sleep disturbances are persistent residual symptoms following remission of major depressive disorder (MDD) and are associated with an increased risk of MDD recurrence. The purpose of the current study was to examine the effect of exercise augmentation on self-reported sleep quality in participants with non-remitted MDD. Method Participants were randomized to receive selective serotonin reuptake inhibitor (SSRI) augmentation with one of two doses of exercise: 16 kilocalories per kilogram of body weight per week (KKW) or 4 KKW for 12 weeks. Depressive symptoms were assessed using the clinician-rated Inventory of Depressive Symptomatology (IDS-C). The four sleep-related items on the IDS-C (Sleep Onset Insomnia, Mid-Nocturnal Insomnia, Early Morning Insomnia, and Hypersomnia) were used to assess self-reported sleep quality. RESULTS: Significant decreases in total insomnia (p < 0.0001) were observed, along with decreases in sleep onset, mid-nocturnal and early-morning insomnia (p's <0.002). Hypersomnia did not change significantly (p = 0.38). Changes in total, mid-nocturnal and early-morning insomnia were independent of changes in depressive symptoms. Higher baseline hypersomnia predicted a greater decrease in depression severity following exercise treatment (p = 0.0057). No significant moderating effect of any baseline sleep on change in depression severity was observed. There were no significant differences between exercise treatment groups on total insomnia or any individual sleep item. CONCLUSIONS: Exercise augmentation resulted in improvements in self-reported sleep quality in patients with non-remitted MDD. Given the prevalence of insomnia as a residual symptom following MDD treatment and the associated risk of MDD recurrence, exercise augmentation may have an important role in the treatment of MDD.

Regression of left ventricular hypertrophy in hypertension. Effects of prazosin therapy.

Left ventricular hypertrophy is a common consequence of chronic hypertension. Although the hypertrophic response can be considered an adaptive mechanism in the initial stages, its progression is associated with increased cardiovascular morbidity and mortality rates. Therefore, reversal of left ventricular hypertrophy may provide considerable clinical benefits to hypertensive patients. Although treatment of hypertension per se is important, blood pressure alone may not explain the course of the hypertrophic process. Not all antihypertensive drugs cause a reversal of hypertrophy, though they may produce equal effects on blood pressure. Factors other than the severity of blood pressure may play a role in the genesis of left ventricular hypertrophy. Adrenergic inhibitors cause its regression, whereas direct vasodilators may promote progression. In this study, therapy with the alpha-adrenergic inhibitor prazosin resulted in significant regression of left ventricular hypertrophy in a group of patients with moderate-to-severe hypertension. This study utilized a new technique--[123I]phenylpentadecanoic acid myocardioscintigraphy--to measure the left ventricular mass. In this study, it was shown that monotherapy with prazosin produced significant relative reductions in systolic and diastolic blood pressure, along with significant reductions in left ventricular mass.

The early morning rise in blood pressure is related mainly to ambulation.

The marked increase in cardiovascular events that occur in the early morning hours could be related to a significant rise in blood pressure at this time but there is uncertainty as to whether this rise in pressure occurs before, at, or after awakening. Automatic blood pressure and pulse measurements were taken twice on 15 normotensive subjects and three times on 11 untreated hypertensive subjects starting before the onset of sleep and at 10 min intervals for 1 h before and 60 to 90 min after awakening. In random order, all subjects either remained supine or immediately arose and ambulated on the first two occasions. The hypertensives had a third study involving ingestion of 10 mg nifedipine after awakening and remaining supine for the next 60 min. The blood pressure and pulse changed little before and after awakening if the subjects remained supine. They rose rapidly and significantly immediately upon arising. The rise in pressure upon arising was blunted by the prior ingestion of nifedipine. The early morning rise in blood pressure and pulse is mainly related to arising from bed. Possible ways to reduce the abrupt rise in blood pressure and the increase in cardiovascular events that occur after arising are suggested.