Abstract
Emerging evidence suggests that type 2 diabetes (T2D) may impair the ability to properly adjust the circulation during exercise with augmented blood pressure (BP) and an attenuated contracting skeletal muscle blood flow (BF) response being reported. This review provides a brief overview of the current understanding of these altered exercise responses in T2D and the potential underlying mechanisms, with an emphasis on the sympathetic nervous system and its regulation during exercise. The research presented support augmented sympathetic activation, heightened BP, reduced skeletal muscle BF, and impairment in the ability to attenuate sympathetically mediated vasoconstriction (i.e., functional sympatholysis) as potential drivers of neurovascular dysregulation during exercise in T2D. Furthermore, emerging evidence supporting a contribution of the exercise pressor reflex and central command is discussed along with proposed future directions for studies in this important area of research.
Highlights
Type 2 diabetes (T2D) negatively impacts cardiovascular health, contributing to a high risk of premature mortality (Raghavan et al, 2019)
A recent study by Holwerda et al (2016a) linked the augmented blood pressure (BP) responses to exercise in type 2 diabetes (T2D) with elevated sympathetic nerve activity (SNA) demonstrating, for the first time, that T2D patients, independent of coexisting hypertension, had exaggerated muscle SNA (MSNA) responses to isometric handgrip exercise compared to nondiabetic controls (Figure 1)
In terms of vasoconstrictors, blocking endothelin-1 receptors during rhythmic handgrip exercise has been shown to enhance muscle blood flow (BF) responses in T2D patients but not in healthy controls, indicating augmented endothelin 1-mediated vasoconstriction during exercise in T2D (Schreuder et al, 2014). These findings suggest that attenuated vasodilation via reduced nitric oxide (NO) and ATP, in combination with enhanced vasoconstrictor influence via endothelin-1, may impair the ability to appropriately regulate contracting skeletal muscle BF in T2D. These changes in nonadrenergic pathways, along with the heightened MSNA and impaired functional sympatholysis, likely contribute to the exaggerated BP response to exercise reported in T2D patients
Summary
Type 2 diabetes (T2D) negatively impacts cardiovascular health, contributing to a high risk of premature mortality (Raghavan et al, 2019). A recent study by Holwerda et al (2016a) linked the augmented BP responses to exercise in T2D with elevated SNA demonstrating, for the first time, that T2D patients, independent of coexisting hypertension, had exaggerated MSNA responses to isometric handgrip exercise compared to nondiabetic controls (Figure 1) Another common feature reported in studies examining exercise responses in T2D has been reductions in contracting skeletal muscle BF (Menon et al, 1992; Kingwell et al, 2003; Lalande et al, 2008; Mac Ananey et al, 2011; Kiely et al, 2014; O’Connor et al, 2015; Groen et al, 2019; Bock et al, 2020). For complementary details on exercise impairments in T2D, the reader is referred to other excellent reviews (Reusch et al, 2013; Green et al, 2015; Poitras et al, 2018; Kim et al, 2020; Nesti et al, 2020)
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