Blood pressure, plasma NPY and catecholamines during physical exercise in relation to menstrual cycle, ovariectomy, and estrogen replacement

Lewandowski, Jacek; Pruszczyk, Piotr; Elaffi, M; Chodakowska, J; Wocial, B; Switalska, Hanna I.; Januszewicz, W; Zukowska‐Grojec, Zofia

doi:10.1016/s0167-0115(98)00074-3

Cited by 25 publications

(24 citation statements)

References 23 publications

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“…132,133 Exercise has been shown to induce acute increases in blood NPY concentrations in men and women, 134 likely by stimulating release of NPY from sympathetic neurons and the adrenal medulla (although it is yet to be determined whether this consistently occurs in women). 135 Pernow et al 134 first demonstrated that NPY is released only in response to high-intensity exercise (B80% of VO 2 max). In our laboratory, NPY was released at the anaerobic threshold, which varied considerably among individuals, but occurred on average at 76% of VO 2 max.…”

Section: Therapeutic Strategiesmentioning

confidence: 99%

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Scioli-Salter¹,

Forman

Otis

et al. 2015

The Clinical Journal of Pain

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Chronic pain and posttraumatic stress disorder (PTSD) are disabling conditions that affect biological, psychological, and social domains of functioning. Clinical research demonstrates that patients who are affected by chronic pain and PTSD in combination experience greater pain, affective distress, and disability than patients with either condition alone. Additional research is needed to delineate the interrelated pathophysiology of chronic pain and PTSD, with the goal of facilitating more effective therapies to treat both conditions more effectively; current treatment strategies for chronic pain associated with PTSD have limited efficacy and place a heavy burden on patients, who must visit various specialists to manage these conditions separately. This article focuses on neurobiological factors that may contribute to the coprevalence and synergistic interactions of chronic pain and PTSD. First, we outline how circuits that mediate emotional distress and physiological threat, including pain, converge. Secondly, we discuss specific neurobiological mediators and modulators of these circuits that may contribute to chronic pain and PTSD symptoms. For example, neuropeptide Y, and the neuroactive steroids allopregnanolone and pregnanolone (together termed ALLO) have antistress and antinociceptive properties. Reduced levels of neuropeptide Y and ALLO have been implicated in the pathophysiology of both chronic pain and PTSD. The potential contribution of opioid and cannabinoid system factors also will be discussed. Finally, we address potential novel methods to restore the normal function of these systems. Such novel perspectives regarding disease and disease management are vital to the pursuit of relief for the many individuals who struggle with these disabling conditions.

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Section: Therapeutic Strategiesmentioning

confidence: 99%

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Scioli-Salter¹,

Forman

Otis

et al. 2015

The Clinical Journal of Pain

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Section: Sympathetic Nervous System Activitymentioning

confidence: 99%

“…In premenopausal women in follicular phase (elevated estrogen levels) compared with luteal phase (low estrogen levels) of the menstrual cycle, the sympathetic nervous system's control of heart rate is blunted [29] and plasma estrogen concentration is inversely related to blood pressure and to catecholamine responses to exercise stress [30]. Further, studies using head-up tilt [31], treadmill [30], and cold stress [32] all report greater sympathetic activation in postmenopausal compared with premenopausal women. Behavioral stressors also appear to increase sympathetic responses more in postmenopausal compared with premenopausal women [31], and in perimenopausal women, estrogen supplementation reduces sympathetic nervous system reactions and enhances parasympathetic responses to mental stressors, including arithmetic and speech tasks [24,33].…”

Section: Sympathetic Nervous System Activitymentioning

confidence: 99%

Effects of hormone replacement therapy on the sympathetic nervous system and blood pressure

Wyss

Carlson²

2003

Current Science Inc

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Hypertension is a major health problem that significantly contributes to heart disease and stroke. While most studies of hypertension have focused on men, women also experience significant hypertension-related morbidity and mortality. However, the incidence of hypertension and cardiovascular disease is significantly lower in premenopausal women compared with men until the onset of menopause, at which time cardiovascular disease incidence increases dramatically in women and eventually approaches that in men. These observations indicate that the loss of estrogen contributes to menopause-related increases in blood pressure and cardiovascular disease, and suggest that the use of estrogen hormone replacement therapy could decrease the incidence of cardiovascular disease in postmenopausal women. However, new findings from the Women's Health Initiative study suggest that estrogen therapy has few positive benefits and some significant negative effects on the health of postmenopausal women, and these data have caused many to abandon long-term estrogen replacement therapy. Conversely, numerous clinical and basic research studies indicate that estrogen replacement therapy beneficially reduces blood pressure, thereby decreasing the incidence of hypertension and cardiovascular disease. Further, several of these studies suggest that one means by which estrogen lowers blood pressure is by decreasing sympathetic nervous system activity. This review examines the evidence supporting estrogen's ability to modulate sympathetic nervous system tone and thereby decrease arterial pressure.

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“…However, differences in methodology may have had intervening effects on the results. They include selection of time points for exercise testing where estrogen concentrations were not different [12] or where menstrual cycle effects on resting blood pressure were not seen [13,14]. Based on the totality of these observations, we tested the hypotheses that, when resting blood pressure is greater in the early versus the late follicular phase of the menstrual cycle: 1) blood pressure during dynamic exercise is also greater and 2) this greater blood pressure is associated with augmented vasoconstriction.…”

Section: Introductionmentioning

confidence: 99%

Effects of Ovarian Cycle on Hemodynamic Responses during Dynamic Exercise in Sedentary Women

Choi

Stebbins

Nho

et al. 2013

Korean J Physiol Pharmacol

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This study tested the hypothesis that effects of the menstrual cycle on resting blood pressure carry over to dynamic exercise. Eleven healthy females were studied during the early (EP; low estrogen, low progesterone) and late follicular (LP; high estrogen, low progesterone) menstrual phases. Stroke volume (SV), heart rate (HR), cardiac output (CO), systolic blood pressure (SBP), diastolic blood pressure (DBP), and total vascular conductance (TVC) were assessed at rest and in response to mild and moderate cycling exercise during EP and LP. During EP, compared to LP, baseline SBP (111±1 vs. 103±2 mmHg), DBP (71±2 vs. 65±2 mmHg) and mean arterial pressure (MAP) (84±2 vs. 78±1 mmHg) were higher and TVC (47.0±1.5 vs. 54.9±4.2 ml/min/mmHg) was lower (p<0.05). During exercise, absolute values of SBP (Mild: 142±4 vs. 127±5 mmHg; Moderate: 157±4 vs. 144±5 mmHg) and MAP (Mild: 100±3 vs. 91±3 mmHg; Moderate: 110±3 vs. 101±3 mmHg) were also higher, while TVC was lower (Mild: 90.9±5.1 vs. 105.4±5.2 ml/min/mmHg; Moderate: 105.4±5.3 vs. 123.9±8.1 ml/min/mmHg) during EP (p<0.05). However, exercise-induced increases in SBP, MAP and TVC at both work intensities were similar between the two menstrual phases, even though norepinephrine concentrations were higher during LP. Results indicate that blood pressure during dynamic exercise fluctuates during the menstrual cycle. It is higher during EP than LP and appears to be due to additive effects of simultaneous increases in baseline blood pressure and reductions in baseline TVC.

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Blood pressure, plasma NPY and catecholamines during physical exercise in relation to menstrual cycle, ovariectomy, and estrogen replacement

Cited by 25 publications

References 23 publications

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Effects of hormone replacement therapy on the sympathetic nervous system and blood pressure

Effects of Ovarian Cycle on Hemodynamic Responses during Dynamic Exercise in Sedentary Women

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