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OBJECTIVE -Sleep restriction results in decreased insulin sensitivity and glucose tolerance in healthy subjects. We hypothesized that sleep duration is also a determinant of insulin sensitivity in patients with type 1 diabetes.RESEARCH DESIGN AND METHODS -We studied seven patients (three men, four women) with type 1 diabetes: mean age 44 Ϯ 7 years, BMI 23.5 Ϯ 0.9 kg/m 2 , and A1C 7.6 Ϯ 0.3%. They were studied once after a night of normal sleep duration and once after a night of only 4 h of sleep. Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with an infusion of [6,6-2 H 2 ]glucose.RESULTS -Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (469 Ϯ 8.5 vs. 222 Ϯ 7.1 min, P ϭ 0.02). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids (NEFAs), or endogenous glucose production. Endogenous glucose production during the hyperinsulinemic clamp was not altered during the night of sleep restriction compared with the night of unrestricted sleep (6.2 Ϯ 0.8 vs. 6.9 Ϯ 0.6 mol ⅐ kg lean body mass Ϫ1 ⅐ min Ϫ1 , NS). In contrast, sleep restriction decreased the glucose disposal rate during the clamp (25.5 Ϯ 2.6 vs. 22.0 Ϯ 2.1 mol ⅐ kg lean body mass Ϫ1 ⅐ min Ϫ1 , P ϭ 0.04), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by ϳ21% (P ϭ 0.04). Sleep restriction did not alter plasma NEFA levels during the clamp (143 Ϯ 29 vs. 133 Ϯ 29 mol/l, NS).CONCLUSIONS -Partial sleep deprivation during a single night induces peripheral insulin resistance in these seven patients with type 1 diabetes. Therefore, sleep duration is a determinant of insulin sensitivity in patients with type 1 diabetes.

Rationale: Assessing the relative contributions of cardioinhibition and vasodepression to the blood pressure (BP) decrease in tilt-induced vasovagal syncope (T-VVS) requires methods that reflect BP physiology accurately. Objective: To assess the relative contributions of cardioinhibition and vasodepression to T-VVS using novel methods. Methods and Results: We studied the parameters determining BP, i.e. stroke volume (SV), heart rate (HR) and total peripheral resistance (TPR), in 163 patients with T-VVS documented by continuous ECG and video EEG monitoring. We defined the beginning of cardioinhibition as the start of a heart rate decrease (HR) before syncope, and used logarithms of SV-, HR- and TPR-ratios to quantify the multiplicative relation BP=SV·HR·TPR. We defined three stages before syncope and two after it based on direction changes of these parameters. The earliest BP decrease occurred nine minutes before syncope. Cardioinhibition was observed in 91% of patients at a median time of 58 s. before syncope. At that time SV had a strong negative effect on BP, TPR a lesser negative effect, while HR had increased (all p<0.001). At the onset of cardioinhibition, median HR was at 98 bpm higher than baseline. Cardioinhibition thus initially only represented a reduction of the corrective HR increase, but was nonetheless accompanied by an immediate acceleration of the ongoing BP decrease. At syncope, SV and HR contributed similarly to the BP decrease (p<0.001), while TPR did not affect BP. Conclusions: The novel methods allowed the relative effects of SV, HR and TPR on BP to be assessed separately, even though all act together. The two major factors lowering BP in T-VVS were reduced SV and cardioinhibition. We suggest that the term 'vasodepression' in reflex syncope should not be limited to reduced arterial vasoconstriction, reflected in TPR, but should also encompass venous pooling, reflected in SV.

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A patient with reflex epilepsy is described, in whom seizures were induced by bathing in hot water. The literature is reviewed.