β-Adrenergic Responsiveness in the Type 2 Diabetic Heart

Wilson, Genevieve A.; Wilson, Luke C.; Lamberts, Regis R.; Majeed, Kamran; Lal, Sunil K.; Wilkins, Gerard T.; Baldi, James C.

doi:10.1249/mss.0000000000001184

Cited by 16 publications

(8 citation statements)

References 37 publications

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“…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.…”

Section: Discussionmentioning

confidence: 97%

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

Roberts

Burns

MacIsaac

et al. 2018

Cardiovasc Diabetol

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BackgroundThe reasons for reduced exercise capacity in diabetes mellitus (DM) remains incompletely understood, although diastolic dysfunction and diabetic cardiomyopathy are often favored explanations. However, there is a paucity of literature detailing cardiac function and reserve during incremental exercise to evaluate its significance and contribution. We sought to determine associations between comprehensive measures of cardiac function during exercise and maximal oxygen consumption (peak), with the hypothesis that the reduction in exercise capacity and cardiac function would be associated with co-morbidities and sedentary behavior rather than diabetes itself.MethodsThis case–control study involved 60 subjects [20 with type 1 DM (T1DM), 20 T2DM, and 10 healthy controls age/sex-matched to each diabetes subtype] performing cardiopulmonary exercise testing and bicycle ergometer echocardiography studies. Measures of biventricular function were assessed during incremental exercise to maximal intensity.ResultsT2DM subjects were middle-aged (52 ± 11 years) with a mean T2DM diagnosis of 12 ± 7 years and modest glycemic control (HbA1c 57 ± 12 mmol/mol). T1DM participants were younger (35 ± 8 years), with a 19 ± 10 year history of T1DM and suboptimal glycemic control (HbA1c 65 ± 16 mmol/mol). Participants with T2DM were heavier than their controls (body mass index 29.3 ± 3.4 kg/m2 vs. 24.7 ± 2.9, P = 0.001), performed less exercise (10 ± 12 vs. 28 ± 30 MET hours/week, P = 0.031) and had lower exercise capacity (peak = 26 ± 6 vs. 38 ± 8 ml/min/kg, P < 0.0001). These differences were not associated with biventricular systolic or left ventricular (LV) diastolic dysfunction at rest or during exercise. There was no difference in weight, exercise participation or peak in T1DM subjects as compared to their controls. After accounting for age, sex and body surface area in a multivariate analysis, significant positive predictors of peak were cardiac size (LV end-diastolic volume, LVEDV) and estimated MET-hours, while T2DM was a negative predictor. These combined factors accounted for 80% of the variance in peak (P < 0.0001).ConclusionsExercise capacity is reduced in T2DM subjects relative to matched controls, whereas exercise capacity is preserved in T1DM. There was no evidence of sub-clinical cardiac dysfunction but, rather, there was an association between impaired exercise capacity, small LV volumes and sedentary behavior.

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Section: Discussionmentioning

confidence: 97%

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

Roberts

Burns

MacIsaac

et al. 2018

Cardiovasc Diabetol

View full text Add to dashboard Cite

show abstract

“…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).…”

Section: Discussionmentioning

confidence: 99%

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

Gildea

Rocha

McDermott

et al. 2019

Respiratory Physiology & Neurobiology

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We tested the hypothesis that type 2 diabetes (T2D) alters the profile of muscle fractional oxygen (O2) extraction (near-infrared spectroscopy) during incremental cycle exercise. Seventeen middle-aged individuals with uncomplicated T2D and 17 controls performed an upright ramp test to exhaustion. The rate of muscle deoxygenation (i.e. deoxygenated haemoglobin and myoglobin concentration, Δ[HHb+Mb]) profiles of the vastus lateralis muscle were normalised to 100% of the response, plotted against % power output (PO) and fitted with a double linear regression model. Peak oxygen uptake was significantly (P<0.05) reduced in individuals with T2D. The %Δ[HHb+Mb]/%PO slope of the first linear segment of the double linear regression function was significantly (P<0.05) steeper in T2D than controls (1.810.61 vs 1.350.43). Both groups displayed a near-plateau in Δ[HHb+Mb] at an exercise intensity (%PO) not different among them. Such findings suggest that a reduced O2 delivery to active muscles is an important underlying cause of exercise intolerance during a maximum graded test in middle-aged individuals with T2D.

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“…Indeed, Peterson et al [ 15 ] found that resting early diastolic filling was inversely proportional to exercising stroke volume in healthy older people, suggesting that resting measurements of diastolic function have an arbitrary relationship with LV filling during exercise. In contrast, LV contractile responses to β-adrenergic stimulation are often [ 29 – 33 ] but not always [ 34 ] reduced in the diabetic heart, providing evidence that impaired systolic responses during exercise could limit cardiac reserve. In addition, a recent paper found that end diastolic volume responses to exercise were blunted, but end systolic volume responses were unchanged in adolescents with type 1 diabetes during supine exercise [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

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

Wilson

Wilkins

Cotter

et al. 2017

Cardiovasc Diabetol

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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.

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β-Adrenergic Responsiveness in the Type 2 Diabetic Heart

Cited by 16 publications

References 37 publications

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

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

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

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

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