Short-Term Physical Inactivity Induces Endothelial Dysfunction

Figures

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  FIGURE 1. Physical activity data for individuals at baseline, following step-reduction and resuming activity, including daily average step count (A), TEE (B), daily waking sedentary time (<1.5 METS) (C), daily light activity (1.5–3 METS) (D), daily moderate activity (3–6 METS) (E), and daily vigorous activity (>6 METS) (F). Data are presented as mean ± SD; *P < 0.05 main effect of time.

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  FIGURE 2. Data for individuals at baseline, following step- reduction and resumption of activity. Flow mediated dilation; FMD (A), V.⁢O2 peak (B), lower limb lean mass (C), total body fat (D), liver fat; IHCL (E), and whole-body IS (F). Data are presented as mean ± SD; *P < 0.05 main effect of time.

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  FIGURE 3. Mechanisms of short-term (14 days) physical inactivity and its role in the development of cardio-metabolic complications. Low levels of physical activity are associated with reduced shear stress; brachial artery endothelial function is compromised as a consequence of 14 days inactivity, as such NO mediated endothelium vasodilation is worsened. Low levels of physical activity alter insulin and AMPK signaling pathways in skeletal muscle and reduce GLUT4 translocation and glucose uptake. Skeletal muscle insulin resistance means additional glucose substrate for de novo lipogenesis in adipose tissue and the liver with expansion of adipose tissue and intra-hepatic lipid. Systemic insulin resistance, higher levels of circulating NEFA and TG are observed. Vascular insulin resistance may also contribute to peripheral insulin resistance in part due to reduced blood flow. In contrast, in habitually active individuals shear stress mediates endothelial-mediated vasodilatation (which together with intact skeletal muscle AMPK and insulin signaling) contributes to preserved peripheral insulin resistance. This figure is adapted from Bowden Davies et al. (2019) with full permissions from the…