OBJECTIVE -Alveolar microvascular function is moderately impaired in type 1 diabetes, as manifested by restriction of lung volume and diffusing capacity (DL CO ). We examined whether similar impairment develops in type 2 diabetes and defined the physiologic sources of impairment as well as the relationships to glycemia and systemic microangiopathy. RESEARCH DESIGN AND METHODS-A cross-sectional study was conducted at a university-affiliated diabetes treatment center and outpatient diabetes clinic, involving 69 nonsmoking type 2 diabetic patients without overt cardiopulmonary disease. Lung volume, pulmonary blood flow (Q ), DL CO , membrane diffusing capacity (measured from nitric oxide uptake [DL NO ]), and pulmonary capillary blood volume (V C ) were determined at rest and exercise for comparison with those in 45 healthy nonsmokers as well as with normal reference values.RESULTS -In type 2 diabetic patients, peak levels of oxygen uptake, Q and DL CO , DL NO , and V C at exercise were 10 -25% lower compared with those in control subjects. In nonobese patients (BMI Ͻ30 kg/m 2 ), reductions in DL CO , DL NO , and V C were fully explained by the lower lung volume and peak Q , but these factors did not fully explain the impairment in obese patients (BMI Ͼ30 kg/m 2 ). The slope of the increase in V C with respect to Q was reduced ϳ20% in patients regardless of BMI, consistent with impaired alveolar-capillary recruitment. Functional impairment was directly related to A1C level, retinopathy, neuropathy, and microalbuminuria in a sex-specific manner.CONCLUSIONS -Alveolar microvascular reserves are reduced in type 2 diabetes, reflecting restriction of lung volume, alveolar perfusion, and capillary recruitment. This reduction correlates with glycemic control and extrapulmonary microangiopathy and is aggravated by obesity.

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