Blood flow changes in response to exercise have been attributed, among other factors, to the effect of vasodilators factors on the microvasculature, suggesting a close relationship between small blood vessels and conducting arteries. The main purpose of this study was to determine the relationship between the changes in near infrared spectroscopy (NIRS)-derived total haemoglobin ([tHb]) and muscle oxygen saturation (SmO₂) signals and femoral artery blood flow in response to resistance exercise at fast- and slow-velocity muscle contraction. The study randomised crossover design included twelve participants. NIRS and blood flow measurements were continuously monitored before, during, and 5 min after the exercise protocol. There was a significant correlation between [tHb] reperfusion slope ([tHb]_slope) and peak blood flow (BF_peak) after slow- and fast-velocity muscle contraction (r = 0.83, p = 0.0008 and r = 0.72, p = 0.0080, respectively). No significant correlation existed between the SmO₂ reperfusion slope (SmO_{2_slope}) and BF_peak after both slow- and fast-velocity muscle contraction exercise (r = −0.46, p = 0.1253 and r = 0.33, p = 0.2841, respectively). This study demonstrated a strong relationship between the NIRS-derived [tHb] and Doppler ultrasound BF during the recovery period of dynamic resistance exercise at both slow- and fast-velocity contraction.

Adropin is a peptide largely secreted by the liver and known to regulate energy homeostasis; however, it also exerts cardiovascular effects. Herein, we tested the hypothesis that low circulating levels of adropin in obesity and type 2 diabetes (T2D) contribute to arterial stiffening. In support of this hypothesis, we report that obesity and T2D are associated with reduced levels of adropin (in liver and plasma) and increased arterial stiffness in mice and humans. Establishing causation, we show that mesenteric arteries from adropin knockout mice are also stiffer, relative to arteries from wild-type counterparts, thus recapitulating the stiffening phenotype observed in T2D db/db mice. Given the above, we performed a set of follow-up experiments, in which we found that 1) exposure of endothelial cells or isolated mesenteric arteries from db/db mice to adropin reduces filamentous actin (F-actin) stress fibers and stiffness, 2) adropin-induced reduction of F-actin and stiffness in endothelial cells and db/db mesenteric arteries is abrogated by inhibition of nitric oxide (NO) synthase, and 3) stimulation of smooth muscle cells or db/db mesenteric arteries with a NO mimetic reduces stiffness. Lastly, we demonstrated that in vivo treatment of db/db mice with adropin for 4 wk reduces stiffness in mesenteric arteries. Collectively, these findings indicate that adropin can regulate arterial stiffness, likely via endothelium-derived NO, and thus support the notion that “hypoadropinemia” should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D. NEW & NOTEWORTHY Arterial stiffening, a characteristic feature of obesity and type 2 diabetes (T2D), contributes to the development and progression of cardiovascular diseases. Herein we establish that adropin is decreased in obese and T2D models and furthermore provide evidence that reduced adropin may directly contribute to arterial stiffening. Collectively, findings from this work support the notion that “hypoadropinemia” should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D.