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Cardiac Output Is Not Related to the Slowed O2 Uptake Kinetics in Type 2 Diabetes


Medicine & Science in Sports & Exercise: June 2011 - Volume 43 - Issue 6 - p 935-942
doi: 10.1249/MSS.0b013e3182061cdb
Clinical Sciences

Purpose: This study aimed to investigate whether cardiac output (CO) responses were related to V˙O2 kinetics during cycling in type 2 diabetes.

Methods: A total of 9 middle-aged women with uncomplicated type 2 diabetes, 9 nondiabetic overweight women, and 11 nondiabetic lean women were recruited. Initially, the ventilatory threshold (VT) and peak V˙O2 were determined during a maximal graded test. Then, on two separate days, subjects completed three 7-min bouts of constant-load cycling at each of three intensities: 50% VT, 80% VT, and midpoint between VT and peak V˙O2 (50% Δ). CO (inert gas rebreathing) was recorded at 30 and 240 s of an additional bout at each intensity. V˙O2 kinetic parameters were determined by fitting a biexponential (50% VT and 80% VT) or triexponential (50% Δ) function to the V˙O2 data.

Results: Peak V˙O2 was significantly lower in type 2 diabetes compared with the two nondiabetic groups (P < 0.05). The time constant of phase 2 was significantly greater (P < 0.05) in type 2 diabetes compared with the nondiabetic heavy and lean groups at 50% VT (34.2 ± 15.7 vs 15.4 ± 7.3 and 20.2 ± 9.7 s) and 80% VT (39.1 ± 9.0 vs 24.8 ± 8.8 and 36.8 ± 7.9 s), but none of the V˙O2 kinetic parameters were different at 50% Δ. CO responses during exercise were not different among the three groups, and at 80% VT, the change in CO from 30 to 240 s was significantly larger in type 2 diabetes compared with the two nondiabetic groups.

Conclusions: The results confirm that type 2 diabetes slows the dynamic response of V˙O2 during light and moderate relative intensity exercise in females but that this occurs in the absence of any slowing of the CO response during the initial period of exercise.

1Department of Physiology, Trinity College Dublin, Dublin, IRELAND; 2Centre for Physical Activity and Nutrition Research, School of Exercise and Nutrition Sciences, Deakin University, Victoria, AUSTRALIA; 3Endocrinology, St. Columcilles and St. Vincent's Hospitals Co., Dublin, IRELAND; and 4Department of Physiology, University of Otago, Dunedin, NEW ZEALAND

Address for correspondence: Mikel Egaña, M.D., Department of Physiology, Trinity College Dublin, Dublin, Ireland; E-mail:

Submitted for publication August 2010.

Accepted for publication November 2010.

©2011The American College of Sports Medicine