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Early onset neurocirculatory response to static handgrip is associated with greater blood pressure variability in women with posttraumatic stress disorder.

Yoo JK, Badrov MB, Parker RS, Anderson EH, Wiblin JL, North CS, Suris A, Fu Q. Early onset neurocirculatory response to static handgrip is associated with greater blood pressure variability in women with posttraumatic stress disorder. American journal of physiology. Heart and circulatory physiology. 2020 Jan 1; 318(1):H49-H58.

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Abstract:

Posttraumatic stress disorder (PTSD) is a psychiatric illness that is more prevalent in women, and accumulating evidence suggests a link between PTSD and future development of cardiovascular disease. The underlying mechanisms are unclear, but augmented sympathetic reactivity to daily stressors may be involved. We measured muscle sympathetic nerve activity (MSNA), blood pressure (BP), and heart rate responses in 14 women with PTSD and 14 healthy women (controls) during static handgrip (SHG) exercise to fatigue at 40% of maximal voluntary contraction (MVC). Two minutes of postexercise circulatory arrest (PECA) was followed immediately after SHG to fatigue. MVC and the time to fatigue during SHG did not differ between groups (both > 0.05). At the first 30 s of SHG, women with PTSD showed augmented sympathetic neural [mean?± SD, ?MSNA burst frequency (BF): 5?±?4 vs. 2?±?3 bursts/30 s, = 0.02 and ?MSNA total activity (TA): 82?±?58 vs. 25?±?38 arbitrary units/30 s, = 0.004] and pressor (?systolic BP: 10?±?5 vs. 4?±?3 mmHg, = 0.003) responses compared with controls. However, MSNA and BP responses at fatigue and during PECA were not different between groups. More interestingly, the augmented initial neural and pressor responses to SHG were associated with greater awake systolic BP variability during ambulation in women with PTSD (MSNA BF: ? = 0.55, MSNA TA: ? = 0.62, and SBP: ? = 0.69, all < 0.05). These results suggest that early onset exercise pressor response in women with PTSD may be attributed to enhanced mechano- rather than metaboreflexes, which might contribute to the mechanisms underlying the link between PTSD and cardiovascular risk. The novel findings of the current study are that women with posttraumatic stress disorder (PTSD) exhibited augmented sympathetic neural and pressor responses at the first 30 s of submaximal isometric muscle contraction. More interestingly, exaggerated neurocirculatory responses at the onset of muscle contraction were associated with greater ambulatory awake systolic blood pressure fluctuations in women with PTSD. Our findings expand the knowledge on the physiological mechanisms that perhaps contribute to increased risk of cardiovascular disease in such a population.





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