Exercise excess pressure and exercise-induced albuminuria in patients with type 2 diabetes mellitus

• Published in: American journal of physiology. Heart and circulatory physiology 2015-05, Vol.308 (9), p.H1136-H1142
• Main Authors: Climie, Rachel E D, Srikanth, Velandai, Keith, Laura J, Davies, Justin E, Sharman, James E
• Format: Article
• Language: English
• Subjects: Adult; Albuminuria - diagnosis; Albuminuria - etiology; Albuminuria - physiopathology; Albuminuria - urine; Bicycling; Blood Pressure; Diabetes; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - diagnosis; Diabetes Mellitus, Type 2 - physiopathology; Diabetes Mellitus, Type 2 - urine; Diabetic Nephropathies - diagnosis; Diabetic Nephropathies - etiology; Diabetic Nephropathies - physiopathology; Diabetic Nephropathies - urine; Exercise; Female; Humans; Hypertension; Hypertension - diagnosis; Hypertension - etiology; Hypertension - physiopathology; Kidney - physiopathology; Male; Middle Aged; Physiology; Predictive Value of Tests; Proteins; Risk Factors; Time Factors; Vascular Stiffness
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00739.2014

Exercise-induced albuminuria is common in patients with type 2 diabetes mellitus (T2DM) in response to maximal exercise, but the response to light-moderate exercise is unclear. Patients with T2DM have abnormal central hemodynamics and greater propensity for exercise hypertension. This study sought to determine the relationship between light-moderate exercise central hemodynamics (including aortic reservoir and excess pressure) and exercise-induced albuminuria. Thirty-nine T2DM (62 ± 9 yr; 49% male) and 39 nondiabetic controls (53 ± 9 yr; 51% male) were examined at rest and during 20 min of light-moderate cycle exercise (30 W; 50 revolutions/min). Albuminuria was assessed by the albumin-creatinine ratio (ACR) at rest and 30 min postexercise. Hemodynamics recorded included brachial and central blood pressure (BP), aortic stiffness, augmented pressure (AP), aortic reservoir pressure, and excess pressure integral (Pexcess). There was no difference in ACR between groups before exercise (P > 0.05). Exercise induced a significant rise in ACR in T2DM but not controls (1.73 ± 1.43 vs. 0.53 ± 1.0 mg/mol, P = 0.002). All central hemodynamic variables were significantly higher during exercise in T2DM (i.e., Pexcess, systolic BP and AP; P < 0.01 all). In T2DM (but not controls), exercise Pexcess was associated with postexercise ACR (r = 0.51, P = 0.002), and this relationship was independent of age, sex, body mass index, heart rate, aortic stiffness, antihypertensive medication, and ambulatory daytime systolic BP (β = 0.003, P = 0.003). Light-moderate exercise induced a significant rise in ACR in T2DM, and this was independently associated with Pexcess, a potential marker of vascular dysfunction. These novel findings suggest that Pexcess could be important for appropriate renal function in T2DM.