Exercise may reverse insufficient sleep-associated cardiovascular risk

Regular aerobic exercise may help counteract the adverse effects of insufficient sleep on endothelial function, specifically endothelium-dependent vasodilation and increased endothelin (ET)-1-mediated vasoconstriction, as reported in a study.

The analysis included 36 healthy adults, among whom 16 had normal sleep duration (mean age 57 years, mean sleep duration 7.4 hours/night) and 20 had short sleep duration (mean age 56 years, mean sleep duration 6.2 hours/night). All short sleepers completed a 3-month aerobic exercise training intervention.

Researchers used plethysmography to determine forearm blood flow in response to intra-arterial acetylcholine (ACh), BQ-123 (ETA receptor antagonist), ACh + BQ-123, and sodium nitroprusside.

Results revealed that compared with normal sleepers, short sleepers had lower forearm blood flow responses to Ach (from 4.2 to 12.7 mL/100 mL tissue/min vs from 4.2 to 10.5 mL/100 mL tissue/min; ∼20 percent; p<0.05).

In response to BQ-123, resting forearm blood flow showed a significantly greater increase in the short-sleep group than in the normal-sleep group (∼25 percent vs ∼8 percent). Meanwhile, for ACh + BQ-123, only the short-sleep group exhibited a marked increase in the ACh-mediated vasodilation (∼25 percent).

Among short sleepers, exercise training led to a significantly high ACh-mediated vasodilation (∼20 percent), a low ET-1-mediated vasoconstriction (∼80 percent). Additionally, the vasodilator response to ACh showed no increase with ETA receptor blockade. All these were achieved despite the unchanged nightly sleep duration (mean 6.4 hours/night).