Why the study?
Less was known regarding the role of exercise on the vasculature independent of BP under high salt conditions.
Does voluntary wheel running prevent dietary salt-induced arterial stiffness independent of blood pressure in rats?
Does voluntary wheel running prevent dietary salt-induced arterial stiffness independent of blood pressure in rats?
Voluntary wheel running attenuates high salt-induced arterial stiffness in rats independent of blood pressure changes, likely through improved nitric oxide bioavailability and reduced collagen accumulation.
BACKGROUND: Excess dietary salt can lead to the development of arterial stiffness and high blood pressure (BP). Regular physical activity can protect against arterial stiffening and lower BP. Less is known regarding the role of exercise on the vasculature independent of BP under high salt (HS) conditions. The aim of the study was to determine whether wheel running protects against the development of dietary salt-induced arterial stiffness independent of BP. METHODS: Rats were maintained on either normal salt (NS; 0.49% NaCl) or HS (4.0% NaCl) diet for 6 weeks and further divided into a voluntary wheel running (NS-VWR, HS-VWR) or cage control group (NS, HS). Carotid-femoral pulse wave velocity (PWV) was measured using applanation tonometry at baseline (BSL) and 6 weeks. RESULTS: BP was measured weekly and remained unchanged among groups throughout the 6 weeks (P > 0.05). PWV was elevated at 6 weeks in HS compared to baseline (HS-BSL, 3.27 ± 0.17 vs. HS-6 week, 4.13 ± 0.26 m/s; P < 0.05) and was lower at 6 weeks in both VWR groups (NS-VWR, 2.98 ± 0.29, HS-VWR, 3.11 ± 0.23 m/s) when compared to HS at 6 weeks (P < 0.05). This was supported by a significant increase in aortic collagen I in the HS group alone and transforming growth factor beta (TGF-β) was greater in the HS group compared to both NS groups (P < 0.05). Wheel running resulted in a greater aortic phosphorylated eNOS and SOD-2 in HS-WVR (P < 0.05) compared to HS. CONCLUSIONS: These data suggest that VWR may protect against collagen accumulation through a TGF-β-mediated pathway by improving nitric oxide bioavailability and redox balance in rats.
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Guers et al. (2019) studied this question.
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