Periods Of Mental Stress Research Articles

Snacking on Whole Almonds for Six Weeks Increases Heart Rate Variability during Mental Stress in Healthy Adults: A Randomized Controlled Trial.

Cardiac autonomic regulation can be indirectly measured by heart rate variability (HRV). Low HRV, which can be induced by mental stress, is a predictor of risk of sudden cardiac death. Few studies have investigated cause-and-effect relationships between diet and HRV. Nut consumption is associated with CVD risk reduction, but the impact on HRV, particularly in response to stress, is unclear. Men and women (30–70 y) with above average risk of developing CVD were randomly assigned in a 6-week randomized, controlled, parallel arm trial to consume either whole almond or isocaloric control snacks (20% of daily estimated energy requirement). Control snacks contained the average nutrient profile of UK snacks. Five-minute periods of supine heart rate (HR) and HRV were measured at resting and during mental stress (Stroop color-word test) at baseline and six weeks. High frequency (HF) power, which reflects parasympathetic regulation of HR, was increased following almonds during the mental stress task relative to control (mean difference between groups 124 ms2; 95% CI 11, 237; p = 0.031, n = 105), but other indices were unaffected. Snacking on whole almonds instead of typical snacks may reduce risk of CVD partly by ameliorating the suppression of HRV during periods of mental stress.

Cardiovascular and Cerebrovascular Effects in Response to Red Bull Consumption Combined With Mental Stress

The sale of energy drinks is often accompanied by a comprehensive and intense marketing with claims of benefits during periods of mental stress. As it has been shown that Red Bull negatively impacts human hemodynamics at rest, we investigated the cardiovascular and cerebrovascular consequences when Red Bull is combined with mental stress. In a randomized cross-over study, 20 young healthy humans ingested either 355 ml of a can Red Bull or water and underwent 80 minutes after the respective drink a mental arithmetic test for 5 minutes. Continuous cardiovascular and cerebrovascular recordings were performed for 20 minutes before and up to 90 minutes after drink ingestion. Measurements included beat-to-beat blood pressure (BP), heart rate, stroke volume, and cerebral blood flow velocity. Red Bull increased systolic BP (+7 mm Hg), diastolic BP (+4 mm Hg), and heart rate (+7 beats/min), whereas water drinking had no significant effects. Cerebral blood flow velocity decreased more in response to Red Bull than to water (-9 vs -3 cm/s, p <0.005). Additional mental stress further increased both systolic BP and diastolic BP (+3 mm Hg, p <0.05) and heart rate (+13 beats/min, p <0.005) in response to Red Bull; similar increases were also observed after water ingestion. In combination, Red Bull and mental stress increased systolic BP by about 10 mm Hg, diastolic BP by 7 mm Hg, and heart rate by 20 beats/min and decreased cerebral blood flow velocity by -7 cm/s. In conclusion, the combination of Red Bull and mental stress impose a cumulative cardiovascular load and reduces cerebral blood flow even under a mental challenge.

Aerobic exercise acutely prevents the endothelial dysfunction induced by mental stress among subjects with metabolic syndrome: the role of shear rate

Mental stress induces transient endothelial dysfunction, which is an important finding for subjects at cardiometabolic risk. Thus, we tested whether aerobic exercise prevents this dysfunction among subjects with metabolic syndrome (MetS) and whether an increase in shear rate during exercise plays a role in this phenomenon. Subjects with MetS participated in two protocols. In protocol 1 (n = 16), endothelial function was assessed using brachial artery flow-mediated dilation (FMD). Subjects then underwent a mental stress test followed by either 40 min of leg cycling or rest across two randomized sessions. FMD was assessed again at 30 and 60 min after exercise or rest, with a second mental stress test in between. Mental stress reduced FMD at 30 and 60 min after the rest session (baseline: 7.7 ± 0.4%, 30 min: 5.4 ± 0.5%, and 60 min: 3.9 ± 0.5%, P < 0.05 vs. baseline), whereas exercise prevented this reduction (baseline: 7.5 ± 0.4%, 30 min: 7.2 ± 0.7%, and 60 min: 8.7 ± 0.8%, P > 0.05 vs. baseline). Protocol 2 (n = 5) was similar to protocol 1 except that the first period of mental stress was followed by either exercise in which the brachial artery shear rate was attenuated via forearm cuff inflation or exercise without a cuff. Noncuffed exercise prevented the reduction in FMD (baseline: 7.5 ± 0.7%, 30 min: 7.0 ± 0.7%, and 60 min: 8.7 ± 0.8%, P > 0.05 vs. baseline), whereas cuffed exercise failed to prevent this reduction (baseline: 7.5 ± 0.6%, 30 min: 5.4 ± 0.8%, and 60 min: 4.1 ± 0.9%, P < 0.05 vs. baseline). In conclusion, exercise prevented mental stress-induced endothelial dysfunction among subjects with MetS, and an increase in shear rate during exercise mediated this effect.

Mental stress elicits sustained and reproducible increases in skin sympathetic nerve activity

Mental stress (MS) is a known trigger of myocardial infarction and sudden death. By activating the sympathetic nervous system, MS may have deleterious effect on the cardiovascular system but this process is not completely understood. The primary aim of this study was to quantify the effect of MS on skin sympathetic nerve activity (SSNA). The secondary aim was to determine the reproducibility of SSNA to MS within a given day and ∼1 week later. Ten subjects (26 ± 1 year) performed two bouts of mental arithmetic lasting 3 min. The bouts were separated by 45 min. One week later the subjects returned to repeat MS. All experiments were conducted in the supine posture during the morning hours. To maintain neutral skin temperature, each subject wore a custom suit (34–35°C). Skin blood flow and sweat rate were measured on the dorsal foot. MS elicited a marked increase in SSNA within the first 10 sec (184 ± 42%; P < 0.01) in all subjects, which was less during the remaining period of MS, but remained elevated (87 ± 20; P < 0.01). The pattern of responses to MS was unchanged during the second bout (10 sec, 247 ± 55%; 3 min average, 133 ± 29%) and during the retest 1 week later (10 sec, 196 ± 55%; 3 min average, 117 ± 36%). MS did not significantly affect cutaneous vascular conductance or sweat rate during any trial. In summary, MS elicits robust and reproducible increases in SSNA in humans, which may be followed over time to observe alterations in the regulation of the autonomic nervous system.

Effect of mental stress on skin sympathetic nerve activity: Are responses reproducible?

The primary aim of this study was to quantify the effect of mental stress (MS) on skin sympathetic nerve activity (SSNA). There is limited quantitative data showing SSNA response to MS. Previous studies report divergent MSNA responses to MS. The second aim was to determine the reproducibility of SSNA to MS within a given day and 1 week later. Ten subjects (26±1 yr.) performed two bouts of mental arithmetic lasting 3 min. The bouts were separated by 45 min. One week later the subjects returned to repeat MS. All experiments were conducted in the supine posture during the morning hours. To maintain neutral skin temperature, each subject wore a custom suit (34–35°C). Skin blood flow and sweat rate were measured on the dorsal foot. MS elicited a marked increase in SSNA within the first 10 s (184±42%; P&lt;0.01) in all subjects, which was less during the remaining period of MS but remained elevated (87±20; P&lt;0.01). The pattern of responses to MS was unchanged during the second bout (10 s, 247±55%; 3 min avg., 133±29%) and during the retest 1 week later (10 s, 196±55%; 3 min avg., 117±36%). MS did not significantly affect cutaneous vascular conductance and sweat rate during any trial. In summary, MS elicits robust and reproducible increases in SSNA in humans. Thus unlike MS effect on MSNA, the pattern of SSNA is consistent during repeated trials on the same day and when performed 1 week later.Supported by NIH (HL109952)

The antithrombotic profile of aspirin. Aspirin resistance, or simply failure?

The antithrombotic profile of aspirin. Aspirin resistance, or simply failure?

Possible mechanisms of aspirin resistance.

Data regarding possible mechanisms of aspirin (ASA) resistance in patients with recurrent myocardial infarction (MI) or vascular ischemia are limited. Five major possible mechanisms of ASA resistance are documented in the primary literature and are discussed in this paper. These mechanisms include: (1) inadequate blockade of erythrocyte-induced platelet activation; (2) biosynthesis of F2-isoprostane 8-iso-prostaglandin (PGF2alpha), a bioactive product of arachidonic acid peroxidation; (3) stimulation of platelet aggregation by cigarette smoking; (4) ASA resistant platelet aggregability by increased levels of norepinephrine, as seen during excessive exercise or periods of mental stress; and (5) increased platelet sensitivity to collagen. Recognizing mechanisms of platelet activation and identifying reversible risk factors such as smoking and mental stress may help decrease the occurrence of ASA resistance and possibly improve patient outcomes. Until more definitive data become available, when prescribing and dosing ASA for the prevention of MI or vascular ischemia, clinicians should identify possible risk factors for ASA resistance. Whether or not patients at risk for ASA resistance are candidates for additive antiplatelet therapy remains to be determined.

Mental stress enhances the sympathetic fraction of QT variability in an RR-independent way.

In 10 healthy male volunteers aged 19-20, spectral power of the beat-by-beat QT interval was measured at the Traube-Herring-Mayer (THM) band (0.05 to 0.15 Hz) when the subject was at rest and during atrial pacing. After resting in dorsal decubitus for 10 minutes, right atrial pacing was performed at a slight elevation above sinus rhythm as well as at 100 or at 110 beats per minute for 7 minutes each. In addition, during pacing at 100 or 110 bpm, the subject was required to perform a Kraepelin Arithmetic test. There was a statistically significant increase in QT spectral power at the THM band, while heart rate was maintained unchanged during the periods of mental stress versus rest. This experiment confirms the potential independence of the QT interval from heart rate and suggests that THM fraction of QT spectral power has a double subordination: during relaxed rest it follows mostly RR-fluctuation; during stress an RR-independent contribution is added, which presumably reflects the supra-normal sympathetic drive on the ventricles.

Resolution of Sleep Paralysis by Weak Electromagnetic Fields in a Patient with Multiple Sclerosis

Sleep paralysis refers to episodes of inability to move during the onset of sleep or more commonly upon awakening. Patients often describe the sensation of struggling to move and may experience simultaneous frightening vivid hallucinations and dreams. Sleep paralysis and other manifestations of dissociated states of wakefulness and sleep, which reflect deficient monoaminergic regulation of neural modulators of REM sleep, have been reported in patients with multiple sclerosis (MS). A 40 year old woman with remitting-progressive multiple sclerosis (MS) experienced episodes of sleep paralysis since the age of 16, four years prior to the onset of her neurological symptoms. Episodes of sleep paralysis, which manifested at a frequency of about once a week, occurred only upon awakening in the morning and were considered by the patient as a most terrifying experience. Periods of mental stress, sleep deprivation, physical fatigue and exacerbation of MS symptoms appeared to enhance the occurrence of sleep paralysis. In July of 1992 the patient began experimental treatment with AC pulsed applications of picotesla intensity electromagnetic fields (EMFs) of 5Hz frequency which were applied extracerebrally 1–2 times per week. During the course of treatment with EMFs the patient made a dramatic recovery of symptoms with improvement in vision, mobility, balance, bladder control, fatigue and short term memory. In addition, her baseline pattern reversal visual evoked potential studies, which showed abnormally prolonged latencies in both eyes, normalized 3 weeks after the initiation of magnetic therapy and remained normal more than 2.5 years later. Since the introduction of magnetic therapy episodes of sleep paralysis gradually diminished and abated completely over the past 3 years. This report suggests that MS may be associated with deficient REM sleep inhibitory neural mechanisms leading to sleep paralysis secondary to the intrusion of REM sleep atonia and dream imagery into the waking state. Pineal melatonin and monoaminergic neurons have been implicated in the induction and maintenance of REM sleep and the pathogenesis of sleep paralysis and it is suggested that resolution of sleep paralysis in this patient by AC pulsed applications of EMFs was related to enhancement of melatonin circadian rhythms and cerebral serotoninergic neurotransmission.

Tryptophan availability and the susceptibility to stress in multiple sclerosis: a hypothesis.

In his seminal description of the clinical manifestations of multiple sclerosis (MS) in 1868 Charcot suggested that psychological stress is an important factor in the pathogenesis of the disease. MS patients often relate that mental stress exacerbates their symptoms and even provokes attacks of their disease. Moreover, a subgroup of MS patients experiences exacerbation of symptoms following a period of mental stress rather than occurring at times when stress is maximal, i.e., attacks are reported to occur on the rebound from stress. Psychological stress may also contribute to the onset and long term clinical deterioration of the disease. Mental stress is associated with activation of the hypothalamic-pituitary adrenal (HPA) axis resulting in increased release of ACTH and cortisol secretion. Stress-induced activation of the HPA axis is associated with an increased metabolism of cerebral serotonin (5-HT) the synthesis of which is dependent upon the availability of its precursor tryptophan. Thus, increased tryptophan availability may partly underlie the general response to stress. Plasma and CSF tryptophan levels are diminished in chronic MS patients and it is suggested that plasma tryptophan levels are even lower in patients who are stressed. Attenuated increase in the availability of systemic tryptophan in response to stress is thought to underlie the susceptibility of MS patients to stress. This hypothesis is supported by the findings in chronic MS patients of a significantly diminished adrenal cortisol reactivity to insulin-induced hypoglycemia which is considered a stress response mediated through the 5-HT system. Consequently, since patients with MS exhibit an abnormal response to stress it follows that increased tryptophan availability through dietary supplementation would diminish their vulnerability to psychological stress. Additionally, if sustained or repeated stress contributes to progression and clinical deterioration of the disease then chronic tryptophan supplementation also may halt its progression.

Editorial comment: Mental stress, pain perception and risk of silent ischemia

testing has been frequently utilized to evaluate the effects of mental stress induced in the laboratory on hemodynamic variables and the risk of developing myocardial ischemia. The results of these studies had revealed that commonly used psychologic stressors, such as mental arithmetic, color stroop test and the task of public speaking (about unpleasant life experiences), frequently result in development of regional wall motion abnormalities, which are thought to occur secondary to myocardial ischemia in patients with coronary artery disease. It is of interest to note that most patients do not experience chest pain in association with the wall motion abnormalities induced during periods of mental stress. The precise mechanism responsible for lack of symptoms in association with ischemic episodes induced by mental stress in the laboratory, or silent ischemia encountered during daily life, has not been fully elucidated. It has been postulated that alteration in pain threshold might account for the silent nature of ischemic episodes during daily life and during periods of mental stress. However, there has been little evidence to support this hypothesis. The report by Sheps et al. (1) in this issue of the Journal provides valuable information in this area by demonstrating the significance of alterations in pain threshold as well as exploring the role of the opioid system in pain perception in patients with coronary artery disease. The present study. In their study, Sheps et al. (1) have evaluated the effects of psychological stress produced by public speaking on pain threshold and plasma beta-endorphin levels in patients with established diagnosis of coronary artery disease. Pain threshold was measured using a thermal probe technique previously validated by the investigators. Most patients (80%) had a history of stable angina pectoris; 60% had

Differences in pulse rate and heart rate and effects on the calculation of heart rate reactivity during periods of mental stress.

Heart rate and reactivity from pulse and ECG were compared over rest and mental arithmetic periods of 2-min duration each for 32 males and 50 females. Data from the two sources of heart rate were not significantly different during the rest period but did differ significantly during periods of heart rate acceleration and deceleration. Sex effects were also noted, with females having consistently higher heart rates from both sources of measurement. Calculation of heart rate reactivity via five procedures based upon the wider literature revealed significant differences between data from different sources of heart rate. Implications for assessment of heart rate reactivity to laboratory stressors are discussed, with suggestions for future research.

Normal Blood Pressure Reactivity to Mental Stress in Patients with Borderline Hypertension

The purpose of the present investigation was to compare the circulatory responses to standardized mental stress in patients with borderline hypertension and in sex-matched control subjects. Seven men and nine women (aged 20–64 yr) with moderately elevated blood pressure and an equal number of normotensive control subjects were exposed to mental stress induced by a modification of the Stroop Color-Word Test. Blood pressure and heart rates were measured every 30 seconds throughout the period of mental stress. The heart rates of persons without and with hypertension, respectively, were as follows (mean ± standard deviation [SD]): at rest, 72 ± 13 vs 79 ± 14 beats/min; peak during mental stress, 94 ± 25 vs 92 ± 17 beats/min; and after stress, 74 ± 12 vs 84 ± 17 beats/min. The blood pressures of persons without and with hypertension, respectively, were as follows: at rest, 120/79 ± 10/8 vs 139/92 ± 13/4 mm Hg; during stress, 144/94 ± 16/8 vs 161/102 ± 16/8 mm Hg; and after stress, 126/81 ± 14/11 vs 143/93 ± 15/5 mm Hg. The results of the present study strongly support the hypothesis that persons with mildly elevated blood pressure do not have a hyperreactive blood pressure regulation system. Although these persons sustain elevated absolute pressure levels, they appear to have pressure responses qualitatively and quantitatively similar to those displayed by normotensive subjects

Spontaneous hypoglycemia in acute gastro-enteritis.

Acute hypoglycemic episodes complicating an acute attack of gastro-enteritis subsided readily with improvement of the underlying disease. In the absence of an organic cause for hypoglycemic attacks, it is suggested that functional hyperinsulism may exist in a subclinical form to become manifest during a period of mental stress and organic inability to take food.

A simple treatment of hypersensitive cervical dentine

A VERY common dental pain is that experienced through hypersensitive cervical dentine, and here will he suggested a very simple and most effective treatment of such areas. A patient usually complains of one or more teeth which are sensitive to sweets, cold, touch, and salts, convinced that he has cavities in which these symptoms are arising. The pain is usually felt on imperfect cemento-enamel junctions which have become denuded of protective gingival tissue by passive or active tooth eruption. The incomplete junction of cementum and. enamel is either of a congenital, abrasive, erosive, traumatic, or carious origin and gives rise to a baring of the dentine which becomes hypersensitive. Hypersensitive dentine is also found in other than the cervical areas of teeth, and these most frequently require operative treatment. If this procedure is neither imperative, possible, nor desired, then the treatment to be offered here often will succeed in palliating the discomfort in these cases too. The pain these cervical areas may register varies in degree. In some instances, there is just enough discomfort to cause the patient to be conscious of an abnormality, and at the other extreme, the pain can be of the greatest severity. It is not unusual to find some sufferers who are rendered uncomfortable in mastication, drinking, toothbrushing, and even in the oral inhalation of cool air. The mere movement of the lip, cheek, or tongue on such an area can give rise to extreme pain. The pain varies in intensity, not only from patient to patient, but also in the same tooth in the same individual, with the degree of reaction depending on various factors, chief among these being the intensity of the stimulus. The pain induced is found to be greater in periods of mental stress, upper respiratory infections, and lowered resistance. Women are found to be more prone to increased dentinal sensitivity during menstruation, pregnancy, and the menopause. More inexplicable but yet certain is the exacerbation of this dental symptom with climatic changes, especially the onset of higher atmospheric humidity. Dentiml Conduction of Pain

Cardiospasm with thoracic stomach and congenital shortening of the esophagus.

An elderly woman, at a period of mental stress, experienced sudden dysphagia. There were intermissions in which swallowing was possible, with a gradual return to normal. Some dyspepsia with flatulence remained. Several years later, again at a time of mental distress, the obstruction recurred. Swallowing of food caused a sense of pressure and fulness behind the sternum. There was no salivation. A roentgenogram after a barium swallow showed moderate dilatation of the esophagus to the level of the seventh thoracic vertebra (fig. 1). The stomach was not well outlined, as there was vomiting of the barium. Esophagoscopic examination demonstrated dilatation of the esophagus without residual food or ulceration and an obstruction at this level. A small Jackson bougie, 12 French, passed through the narrowing when relaxation with the anesthetic occurred. Before this, a filiform bougie would not pass. The transition from tight contraction to partial relaxation of the spasm was