Cardiovascular control during exercise in type 2 diabetes mellitus

Abstract

Controlled studies of male and female subjects with type 2 diabetes mellitus (DM) of short duration (~3-5 years) show that DM reduces peak VO2 (L·min(-1) and mL·kg(-1)·min(-1)) by an average of 12-15% and induces a greater slowing of the dynamic response of pulmonary VO2 during submaximal exercise. These effects occur in individuals less than 60 years of age but are reduced or absent in older males and are consistently associated with significant increases in the exercise pressor response despite normal resting blood pressure. This exaggerated pressor response, evidence of exertional hypertension in DM, is manifest during moderate submaximal exercise and coincides with a more constrained vasodilation in contracting muscles. Maximum vasodilation during contractions involving single muscle groups is reduced by DM, and the dynamic response of vasodilation during submaximal contractions is slowed. Such vascular constraint most likely contributes to exertional hypertension, impairs dynamic and peak VO2 responses, and reduces exercise tolerance. There is a need to establish the effect of DM on dynamic aspects of vascular control in skeletal muscle during whole-body exercise and to clarify contributions of altered cardiovascular control and increased arterial stiffness to exertional hypertension.

Figures

Figure 1

A simple conceptual model of cardiovascular control during exercise with links to oxygen uptake, fatigue, and exercise tolerance. Definitions of terms and description of most interrelationships between variables are described in the main text. The length of bidirectional arrows indicates the relative ranges of variables: the regulated variable, mean arterial pressure, varies through a smaller range than controlled variables such as cardiac output and systemic arterial resistance. Dashed bidirectional arrows indicate interactions between two variables. Arterial stiffness is not considered to be a part of a system of cardiovascular regulation and control, but it is influenced by this system (systemic arterial resistance) and also exerts an independent influence on mean arterial pressure.

Figure 2

(a) Effect of type 2 diabetes mellitus (DM) on the dynamic response of pulmonary oxygen uptake during submaximal exercise below the ventilatory threshold. DM blunts the cardiodynamic phase (“1”) and slows the rise (increases the time constant) of the primary phase (“2”). Note that a third phase (“slow component”) is observed at higher intensities and can also be observed in a minority of subjects below the ventilatory threshold, but the effect of DM on this phase is not clear. (b) Effect of DM on the dynamic response of limb blood flow and vascular conductance during submaximal contractions (calf muscle). DM blunts the fast growth phase (“1”), has minimal effect on the rapid decay phase (“2”), and slows the rise (increases the time constant) of the slow growth phase (“3”). Note that a fourth phase, a slow decay, is observed in some subjects but it is not shown in this figure and the effect of DM on it is not clear.