Exercise-Induced Changes in Plasma Atrial Natriuretic Peptide and Brain Natriuretic Peptide Concentrations in Healthy Subjects With Chronic Sleep Deprivation

Tanabe, Kazuhiko; Yamamoto, Akiko; Suzuki, Noriyuki; Akashi, Yoshihiro J.; Seki, Atsushi; Samejima, Hisanori; Oya, Misa; Murabayashi, Taizo; Nakayama, Masaru; Yokoyama, Yasuhiro; Osada, Naohiko; Omiya, Kazuto; Miyake, Fumihiko; Murayama, Masahiro

doi:10.1253/jcj.63.447

Cited by 13 publications

(13 citation statements)

References 16 publications

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“…However, the response of BNP to exercise remains controversial with another study showing no pathologically elevated BNP concentrations in highly trained road cyclists [22], following a road-cycling race. Graded sub-maximal or maximal ergometric tests in healthy subjects however, showed only minor changes post-exercise [4,17,32,43,45,47]. NT-proBNP concentration was not correlated with any of the other laboratory markers or training parameters that were recorded in this study.…”

Section: Neurohormone Nt-probnpcontrasting

confidence: 62%

Responses of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Cardiac Troponin I (cTnI) to Competitive Endurance Exercise in Recreational Athletes

et al. 2005

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The present study was designed to investigate whether the stress of a half-marathon race can induce myocardial cell injury or left ventricular dysfunction in moderately trained runners of both gender, as assessed by post-race plasma concentrations of biochemical cardiac-specific markers and by quantitative echocardiographic measurements. We examined 12 male (mean+/-SD); age: 42.8+/-7.3 yr; height: 177.6+/-7.4 cm; body mass: 75.6+/-9.4 kg; BMI: 24.1+/-1.8 and 13 female (mean+/-SD); age: 39.0+/-6.5 yr; height: 164.6+/-6.2 cm; body mass: 58.4+/-9.8 kg; BMI: 21.5+/-3.4 recreational runners, who completed a half-marathon race. Blood samples were collected from each subject before the half-marathon race as well as 20 min and 2 h post-race and cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured. Quantitative echocardiographic analyses of wall dimensions and ejection fraction were also obtained from 14 of 25 subjects within 1 wk after the race. Both blood markers showed significant changes (p<0.05-0.001) over the time course of the three blood draws. A significant percentage of laboratory analytes analyzed in this study were outside the reference ranges and fulfilled conventional criteria for cardiac muscle damage. However, echocardiography within one week following the competition did not show any evidence that running a half-marathon competition damages the myocardium. Strenuous endurance exercise in middle-aged recreational runners induces a significant elevation of biochemical cardiac-specific markers, which may reflect transient subclinical myocardial damage, but can also reflect a physiological reparative or adaptive process.

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Section: Neurohormone Nt-probnpcontrasting

confidence: 62%

Responses of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Cardiac Troponin I (cTnI) to Competitive Endurance Exercise in Recreational Athletes

et al. 2005

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“…Preclinical studies show that central · 2 -adrenergic and opioid receptors are involved in the release of plasma ANP [30][31][32]. Whether the increased CSF norepinephrine or ß-endorphin concentrations observed in PTSD patients [33,34] reflect central neuroendocrine adaptations responsible for the plasma ANP alterations needs further study meticu-Kellner/Yassouridis/Hübner/Baker/ Wiedemann lously controlled for factors that influence ANP secretion, such as sleep pattern and sports activity [35]. Furthermore, whether the low plasma ANP concentrations found in our study are a consequence of PTSD symptoms, of traumatization, or indicate an increased vulnerability to develop PTSD needs to be clarified.…”

Section: Discussionmentioning

confidence: 99%

Endocrine and Cardiovascular Responses to Corticotropin-Releasing Hormone in Patients with Posttraumatic Stress Disorder: A Role for Atrial Natriuretic Peptide?

et al. 2003

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Hypothalamic-pituitary-adrenocortical (HPA) axis data, such as low plasma cortisol concentrations in spite of increased corticotropin-releasing hormone (CRH) levels in patients with posttraumatic stress disorder (PTSD), are difficult to interpret. Atrial natriuretic peptide (ANP) may be an explanatory link in the neuroendocrine pathophysiology of the disorder, since it is a neuromodulator with antianxiety effects that inhibits HPA activity at multiple levels. Seventeen patients with chronic PTSD and 17 healthy control subjects were given 100 µg of human CRH at 3 p.m. ANP, adrenocorticotropic hormone (ACTH), and cortisol levels in plasma as well as blood pressure and heart rate were measured during basal conditions and after CRH stimulation. Basal ANP levels were significantly lower in PTSD patients in comparison with normal controls, but the response to CRH was undistinguishable. In contrast to our expectation, no significant differences in basal or CRH-stimulated ACTH or cortisol parameters could be observed. Systolic and diastolic blood pressures at baseline and after CRH were significantly elevated in PTSD patients. All group differences remained significant after controlling for basal blood pressure and/or body mass index. Our data do not support a role of ANP in abnormal HPA axis regulation in PTSD. However, the persistently low ANP plasma levels in PTSD patients despite elevated blood pressure may serve to facilitate anxiety behavior and have adverse long-term cardiovascular consequences. Further studies to assess ANP secretion in PTSD patients and to clarify its pathophysiological impact are needed.

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“…CO measurement by an invasive method, the direct Fick method, or thermodilution, seemed to be difficult to perform during an exercise test in an outpatient department. Although the reliability of thoracic bioimpedance has been reported in two of our previous · · · · studies, 15,22) CO measurement using an invasive method is recommended in order to arrive at more definite conclusions.…”

Section: )mentioning

confidence: 95%

“…The measurement of CO with the thoracic bioimpedance method has been described elsewhere. 14,15) Briefly, thoracic bioimpedance was used to measure the pulsatile change in resistance to injected microcurrents for the calculation of stroke volume. Cardiac index (CI) was calculated as CO/body surface area, calculated on a beat-by-beat basis and represented as the average of 16 accepted beats.…”

Section: Subjectsmentioning

confidence: 99%

Relationship Between Impaired Chronotropic Response, Cardiac Output During Exercise, and Exercise Tolerance in Patients with Chronic Heart Failure

et al. 2003

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SUMMARYThe present study was undertaken to investigate the relationship between the extent of impaired chronotropic response and cardiac output during exercise, and exercise tolerance in patients with chronic heart failure. The subjects consisted of 24 patients (mean 60.1 ± 14.0 years) who had mild chronotropic incompetence. Cardiopulmonary exercise testing was performed in all patients, and heart rate (HR), anaerobic threshold (AT), maximum oxygen uptake (peak VO 2 ), slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO 2 slope), and exercise time were measured. Cardiac output (CO) was measured by a thoracic bioimpedance method and cardiac index (CI) was calculated. Plasma norepinephrine (NE) was measured at rest and immediately after the exercise test. The changes in HR, NE, and CI from the resting state to immediately after exercise were calculated as ∆HR, ∆NE, and ∆CI, respectively. The ∆NE was converted to a logarithmic scale and ∆HR/log∆NE was used as a parameter of HR response to sympathetic nerve stimulation. The results were as follows: HR and NE in the resting state had no correlation with AT and with peak VO 2 . ∆HR/log∆NE correlated positively with both AT and peak VO 2 , and negatively with the VE/VCO 2 slope. ∆HR/ log∆NE correlated positively with peak CI, %∆CI, and ∆CI/exercise time. The data suggest that one of the mechanisms of low exercise tolerance in chronic heart failure patients was due to an inadequate increase in CO response against exercise caused by an impaired HR response to increased NE. (Jpn Heart J 2003; 44: 515-525)

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Exercise-Induced Changes in Plasma Atrial Natriuretic Peptide and Brain Natriuretic Peptide Concentrations in Healthy Subjects With Chronic Sleep Deprivation

Cited by 13 publications

References 16 publications

Responses of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Cardiac Troponin I (cTnI) to Competitive Endurance Exercise in Recreational Athletes

Responses of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Cardiac Troponin I (cTnI) to Competitive Endurance Exercise in Recreational Athletes

Endocrine and Cardiovascular Responses to Corticotropin-Releasing Hormone in Patients with Posttraumatic Stress Disorder: A Role for Atrial Natriuretic Peptide?

Relationship Between Impaired Chronotropic Response, Cardiac Output During Exercise, and Exercise Tolerance in Patients with Chronic Heart Failure

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