Key result
Women with PTSD exhibited augmented pressor responses (∆systolic BP 10 vs 4 mmHg, P=0.003) and sympathetic neural activity during the first 30 seconds of static handgrip compared to controls.
Why the study?
PTSD is linked to future cardiovascular disease, but the underlying mechanisms remain unclear, though augmented sympathetic reactivity to daily stressors may be involved.
Do women with PTSD exhibit augmented neurocirculatory responses to static handgrip exercise compared to healthy controls?
Observational (n=28)
Do women with PTSD exhibit augmented neurocirculatory responses to static handgrip exercise compared to healthy controls?
Absolute Event Rate: 10% vs 4%
p-value: p=0.003
Women with PTSD exhibit exaggerated early sympathetic and pressor responses to isometric exercise, which correlates with greater ambulatory blood pressure variability and may contribute to increased cardiovascular risk.
Augmented sympathetic reactivity during exertion may warrant monitoring in women with PTSD; leaves open causal CVD links and need for prospective trials.
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 P > 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, P = 0.02 and ∆MSNA total activity (TA): 82 ± 58 vs. 25 ± 38 arbitrary units/30 s, P = 0.004] and pressor (∆systolic BP: 10 ± 5 vs. 4 ± 3 mmHg, P = 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: r = 0.55, MSNA TA: r = 0.62, and SBP: r = 0.69, all P < 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. NEW & NOTEWORTHY 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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Yoo et al. (2019) conducted an observational in Posttraumatic stress disorder (PTSD) (n=28). Posttraumatic stress disorder (PTSD) vs. Healthy women was evaluated on ∆systolic BP at the first 30 s of static handgrip (p=0.003). Women with PTSD exhibited augmented pressor responses (∆systolic BP 10 vs 4 mmHg, P=0.003) and sympathetic neural activity during the first 30 seconds of static handgrip compared to controls.
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