Impaired ventricular filling limits cardiac reserve during submaximal exercise in people with type 2 diabetes

Abstract

BackgroundAttenuated increases in ventricular stroke volume during exercise are common in type 2 diabetes and contribute to reduced aerobic capacity. The purpose of this study was to determine whether impaired ventricular filling or reduced systolic ejection were responsible for the attenuated stroke volume reserve in people with uncomplicated type 2 diabetes.MethodsPeak aerobic capacity and total blood volume were measured in 17 people with diabetes and 16 non-diabetic controls with no evidence of cardiovascular disease. Left ventricular volumes and other systolic and diastolic functional parameters were measured with echocardiography at rest and during semi-recumbent cycle ergometry at 40 and 60% of maximal aerobic power and compared between groups.ResultsPeople with diabetes had reduced peak aerobic capacity and heart rate reserve, and worked at lower workloads than non-diabetic controls. Cardiac output, stroke volume and ejection fraction were not different at rest, but increased less in people with diabetes during exercise. Left ventricular end systolic volume was not different between groups in any condition but end diastolic volume, although not different at rest, was smaller in people with diabetes during exercise. Total blood volume was not different between the groups, and was only moderately associated with left ventricular volumes.ConclusionsPeople with type 2 diabetes exhibit an attenuated increase in stroke volume during exercise attributed to an inability to maintain/increase left ventricular filling volumes at higher heart rates. This study is the first to determine the role of filling in the blunted cardiac reserve in adults with type 2 diabetes.Electronic supplementary materialThe online version of this article (10.1186/s12933-017-0644-1) contains supplementary material, which is available to authorized users.

Exercise capacity in diabetes mellitus is predicted by activity status and cardiac size rather than cardiac function: a case control study

“…3 , the LVEDVI change mirrored that of controls (interaction of exercise and group, P = 0.96) suggesting that there was no impairment in diastolic filling. This is consistent with a recent study by Wilson et al [ 35 ] who also found no difference between changes in LVEDV during exercise in T2DM as compared with controls. Furthermore, the pattern of change in cardiac volumes during exercise in our study are the same as those described for normal physiology using exercise echocardiography [ 45 ] and exercise cardiac magnetic resonance imaging [ 9 , 46 ].…”

“…Wilson et al [ 35 , 36 ] recently reported an almost identical reduction in HR reserve in T2DM subjects as compared with control subjects. They investigated whether this may be attributable to reduced β-adrenoreceptor sensitivity.…”

Clinical outcomes after cardiac rehabilitation in elderly patients with and without diabetes mellitus: The EU-CaRE multicenter cohort study

“…The chronotropic incompetence may, at least in part, also explain the reduced heart rate recovery in our as well as in previous populations with DM [33]. Other factors that potentially contribute to lower VO 2 peak in patients with DM may be reduced diastolic function [34] and lower oxygen extraction by skeletal muscles [35], with the latter being supported by the higher VE/VCO 2 slope [36]. A larger improvement of just over 1 MET, corresponding to 28% was found in a similarly large population of diabetic cardiovascular patients after a 6-week CR [14].…”

Influence of type 2 diabetes on muscle deoxygenation during ramp incremental cycle exercise

“…In addition tempered vasodilator responses of the vascular smooth muscle elicited subsequent to exogenous, direct-acting nitric oxide (NO) donors in the form of glyceryl trinitrate (McVeigh et al, 1992) and sodium nitroprusside (Kingwell et al, 2003;Williams et al, 1996) have also been reported in the respective T2D cohorts. It is pertinent to acknowledge, however, that in the absence of cardiac output (CO) data, we cannot exclude the possibility that impairments in cardiac function (Joshi et al, 2010;Regensteiner et al, 2009;Wilson et al, 2017a;Wilson et al, 2017b) could induce subsequent regional O2 delivery impediments; although peak CO is not significantly reduced in uncomplicated T2D (Baldi et al, 2003;Regensteiner et al, 2009).…”