Effects of psychosocial and physical stress on lactate and anxiety levels.

Both intense physical activity and potent psychosocial stressors increase blood lactate. Raising lactate levels by infusing the chemical can have an anxiogenic effect. Here, we compare the relationship between changes in lactate and anxiety levels resulting from two standardized stressors. We investigated the effects of the Multiple Wingate All-Out Performance Test (WG), a strong physical stressor, and the Trier Social Stress Test (TSST), a well-documented psychosocial stressor, in 32 healthy young men using a crossover design. Before and after each stressor, venous blood was analyzed for lactate levels and the State-Trait-Anxiety Inventory (STAI) was given. Both stressors raised both lactate and anxiety significantly above their baseline levels. While the rise in lactate was much higher for the WG than for the TSST, the rises in anxiety were nearly equal. Individual fitness did not influence the results for lactate or anxiety. No significant relation between lactate and anxiety changes were found. Thus, our results as well as the literature suggest that lactate is an important variable for understanding the impact of sport participation.

Assessing sleep quality using self-report and actigraphy in PTSD.

Sleep disturbance is commonly reported by participants with post-traumatic stress disorder, but objective evidence of poor sleep is often absent. Here we compared self-report and actigraphic evaluations of sleep between veterans with post-traumatic stress disorder and controls. Participants reported their sleep retrospectively for the month before the recording night and on the recording night. On the recording night, they wore an Actiwatch-64 and were instructed to press the marker button upon getting into bed, each time they awoke, and at their final awakening. The post-traumatic stress disorder group reported much worse sleep than controls on the Pittsburgh Sleep Quality Index for the previous month and somewhat poorer sleep on the recording night. However, on the recording night, neither diary nor actigraphic measures of number of awakenings, total time in bed, nor time lying awake after sleep onset differed between participants with and without post-traumatic stress disorder. Diary-reported number of awakenings was fewer than actigraphically captured awakenings. These results suggest a memory bias towards remembering worse sleep on the nights before the recording night.

Psychiatry on trial: the Norway 2011 massacre.

On July 22, 2011, Anders Breivik, a Norwegian citizen, detonated a fertilizer bomb near government buildings in Oslo, killing eight people, and then proceeded to a nearby island where the Labor Party was holding a youth camp. There, he killed 69 people before being arrested. Just before these events, he posted a "compendium" on the Web explaining his actions and encouraging others to do likewise. Much of the ensuing media coverage and trial focused on whether he was sane and whether he had a psychiatric diagnosis. One team of court-appointed psychiatrists found him to be psychotic with a diagnosis of paranoid schizophrenia and legally insane. A second team found him neither psychotic nor schizophrenic and, thus, legally sane. Their contrary opinions were not reconciled by observing his behavior in court. We discuss why experienced psychiatrists reached such fundamentally opposing diagnostic conclusions about a "home-grown" terrorist holding extreme political views.

Autonomic arousal during actigraphically estimated waking and sleep in male veterans with PTSD.

Physiological hyperarousal is manifested acutely by increased heart rate, decreased respiratory sinus arrhythmia, and increased skin conductance level and variability. Yet it is uncertain to what extent such activation occurs with the symptomatic hyperarousal of posttraumatic stress disorder (PTSD). We compared 56 male veterans with current PTSD to 54 males who never had PTSD. Subjects wore ambulatory devices that recorded electrocardiograms, finger skin conductance, and wrist movement while in their normal environments. Wrist movement was monitored to estimate sleep and waking periods. Heart rate, but not the other variables, was elevated in subjects with PTSD equally during waking and during actigraphic sleep (effect sizes, Cohen's d, ranged from 0.63 to 0.89). The length of the sleep periods and estimated sleep fragmentation did not differ between groups. Group heart rate differences could not be explained by differences in body activity, PTSD hyperarousal symptom scores, depression, physical fitness, or antidepressant use.

Separation anxiety disorder in children: disorder-specific responses to experimental separation from the mother.

BACKGROUND: Separation anxiety disorder (SAD) is one of the most common anxiety disorders in childhood and is predictive of adult anxiety disorders, especially panic disorder. However, the disorder has seldom been studied and the attempt to distinguish SAD from other anxiety disorders with regard to psychophysiology has not been made. We expected exaggerated anxiety as well as sympathetic and respiratory reactivity in SAD during separation from the mother. METHOD: Participants were 49 children with a principal diagnosis of SAD, 21 clinical controls (CC) with a principal diagnosis of anxiety disorder other than SAD, and 39 healthy controls (HC) not meeting criteria for any current diagnosis. Analyses of covariance controlling for age were used to assess sympathetic and parasympathetic activation (preejection period and respiratory sinus arrhythmia) as well as cardiovascular (heart rate, mean arterial pressure, total peripheral resistance), respiratory (total breath time, minute ventilation, tidal volume, end-tidal CO(2) , respiratory variability), electrodermal, and self-report (anxiety, cognitions, symptoms) variables during baseline, 4-min separation from, and reunion with the mother. RESULTS: Children with a diagnosis of SAD were characterized by elevated self-reported anxiety responses to separation and increased sympathetic reactivity compared with CC and HC groups. The SAD group also displayed greater vagal withdrawal and higher reactivity in multiple cardiovascular, respiratory, and electrodermal measures compared with the HC group, while corresponding responses were less in the CC group and not significantly different from the other groups. CONCLUSIONS: Separation from the mother elicits greater autonomic, respiratory, and experiential responses in children with SAD. Our findings based on brief experimental separation demonstrate differential subjective and physiological manifestations of specific anxiety diagnoses, thus supporting the validity of the diagnostic category of SAD.

Randomized clinical trial of capnometry-assisted respiratory training in veterans with posttraumatic stress disorder hyperarousal.

OBJECTIVE: To investigate whether capnometry-assisted antihyperventilation respiratory training, successful in treating panic, and sleep hygiene instructions would reduce posttraumatic stress disorder (PTSD) hyperarousal symptoms in U.S. military veterans. METHOD: We conducted a parallel, nonblinded clinical trial and randomized 80 veterans with PTSD hyperarousal into treatment or wait list. Primary treatment outcomes from baseline to 1st follow-up were analyzed using mixed modeling. Baseline physiological measures were compared between the PTSD hyperarousal group and a no-PTSD group (n = 68). RESULTS: Baseline respiration rate but not partial-pressure of end-tidal carbon dioxide (PCO2) was higher in the PTSD hyperarousal group than in the no-PTSD group during 3 min of quiet sitting, indicating no difference in baseline hyperventilation. There was no significant effect of the intervention on PTSD hyperarousal symptoms or hyperventilation compared to wait list, but treatment did lower respiratory rate. CONCLUSION: This intervention did not reduce PTSD hyperarousal symptoms, perhaps due to differences between underlying mechanisms of PTSD hyperarousal and panic disorder or to differences between veteran and civilian populations. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Effects of breathing training on voluntary hypo- and hyperventilation in patients with panic disorder and episodic anxiety.

Anxiety disorders are associated with respiratory abnormalities. Breathing training (BT) aimed at reversing these abnormalities may also alter the anxiogenic effects of biological challenges. Forty-five Panic Disorder (PD) patients, 39 Episodic Anxiety patients, and 20 non-anxious controls underwent voluntary hypoventilation and hyperventilation tests twice while psychophysiological measures were recorded. Patients were randomized to one of two BT therapies (Lowering vs. Raising pCO(2)) or to a waitlist. Before treatment panic patients had higher respiration rates and more tidal volume instability and sighing at rest than did non-anxious controls. After the Lowering therapy, patients had lower pCO(2) during testing. However, neither reactivity nor recovery to either test differed between patients and controls, or were affected by treatment. Although the two treatments had their intended opposite effects on baseline pCO(2), other physiological measures were not affected. We conclude that baseline respiratory abnormalities are somewhat specific to PD, but that previously reported greater reactivity and slower recovery to respiratory challenges may be absent.

Habituation or Normalization? Experiential and Respiratory Recovery From Voluntary Hyperventilation in Treated Versus Untreated Patients With Panic Disorder.

Psychophysiological theories postulate respiratory dysregulation as a mechanism contributing to panic disorder (PD). Additionally, symptomatic and respiratory recovery from voluntary hyperventilation (HVT-recovery) have been shown to lag in PD and it is unclear if HVT-recovery normalizes with treatment. Thirty-seven panic disorder patients were randomized to hypoventilation therapy (TX, n = 20) or waitlist control (WL, n = 17) (Meuret et al., 2008). In a secondary analysis, their HVT-recovery was analyzed at pre- and post-TX/WL, compared to 29 healthy controls (HC). HVT included three phases: 5-min baseline, 3-min hyperventilation, and 8-min recovery. HVT-elicited symptom severity and anxiety were rated following each phase, and end-tidal PCO2 and respiratory rate (RR) were recorded throughout. Treatment, compared to WL, was highly effective in reducing PD pathology (d=2.21, Meuret et al., 2008). At pre-TX/WL, PD demonstrated delayed HVT-recovery PCO2 and higher RR. Treated patients demonstrated normalization of HVT-recovery for PCO2 and RR; however, improvements of HVT-recovery for symptom severity and anxiety did not differ between TX and WL. Results replicate pretreatment HVT respiratory recovery abnormalities in PD and further demonstrate normalization, comparable to HC, following successful treatment. The results provide support for respiratory dysregulation as a feature of PD and demonstrate the utility of HVT respiratory recovery as treatment outcome measure for respiration-based PD therapy.

Diversity of effective treatments of panic attacks: what do they have in common?

By comparing efficacious psychological therapies of different kinds, inferences about common effective treatment mechanisms can be made. We selected six therapies for review on the basis of the diversity of their theoretical rationales and evidence for superior efficacy: psychoanalytic psychotherapy, hypercapnic breathing training, hypocapnic breathing training, reprocessing with and without eye-movement desensitization, muscle relaxation, and cognitive behavior therapy. The likely common element of all these therapies is that they reduce the immediate expectancy of a panic attack, disrupting the vicious circle of fearing fear. Modifying expectation is usually regarded as a placebo mechanism in psychotherapy, but may be a specific treatment mechanism for panic. The fact that this is seldom the rationale communicated to the patient creates a moral dilemma: Is it ethical for therapists to mislead patients to help them? Pragmatic justification of a successful practice is a way out of this dilemma. Therapies should be evaluated that deal with expectations directly by promoting positive thinking or by fostering non-expectancy.

Supplementing sleep actigraphy with button pressing while awake.

OBJECTIVE/BACKGROUND: Wrist-worn sleep actigraphs are limited for evaluating sleep, especially in sleepers who lie awake in bed without moving for extended periods. Sleep logs depend on the accuracy of perceiving and remembering times of being awake. Here we evaluated pressing an event-marker button while lying awake under two conditions: self-initiated pressing every 5 to 10 minutes or pressing when signaled every 5 minutes by a vibration pulse from a wristband. We evaluated the two conditions for acceptability and their concordance with actigraphically scored sleep. PARTICIPANTS AND METHODS: Twenty-nine adults wore actigraphs on six nights. On nights 1 and 4, they pressed the marker to a vibration signal, and on nights 2 and 5, they self-initiated presses without any signal. On nights 3 and 6, they were told not to press the marker. Every morning they filled out a sleep log about how they had slept. RESULTS: The vibration band was unacceptable to 42% of the participants, who judged it too disturbing to their sleep. Self-initiated pressing was acceptable to all, although it reduced log reported sleep depth compared to a no pressing condition. Estimations of sleep onset latency were considerably longer by button pressing than by actigraphy. Agreement of epoch-by-epoch sleep scoring by actigraphy and by button pressing was poor (kappa = 0.23) for self-initiated pressing and moderate (kappa = 0.46) for pressing in response to a vibration. CONCLUSIONS: Self-initiated button pressing to indicate being awake while lying in bed is acceptable to many, interferes little with sleep, and adds substantially to the information given by actigraphy.

Changes in respiration mediate changes in fear of bodily sensations in panic disorder.

The purpose of the study was to examine whether changes in pCO(2) mediate changes in fear of bodily sensation (as indexed by anxiety sensitivity) in a bio-behavioral treatment for panic disorder that targets changes in end-tidal pCO(2). Thirty-five panic patients underwent 4 weeks of capnometry-assisted breathing training targeting respiratory dysregulation. Longitudinal mediation analyses of the changes in fear of bodily symptoms over time demonstrated that pCO(2), but not respiration rate, was a partial mediator of the changes in anxiety sensitivity. Results were supported by cross lag panel analyses, which indicated that earlier pCO(2) levels predicted later levels of anxiety sensitivity, but not vice versa. PCO(2) changes also led to changes in respiration rate, questioning the importance of respiration rate in breathing training. The results provide little support for changes in fear of bodily sensations leading to changes in respiration, but rather suggest that breathing training targeting pCO(2) reduced fear of bodily sensations in panic disorder.

Do blood phobia patients hyperventilate during exposure by breathing faster, deeper, or both?

BACKGROUND: Recently we found that patients with blood-injection-injury (BII) phobia tend to hyperventilate when exposed to feared stimuli. Hyperventilation results from increases in minute ventilation above levels required by metabolic demand and can result from increases in either frequency or depth of breathing, or a combination of both. METHOD: In order to determine which of these factors contributed most to hyperventilation in BII phobia we analyzed breathing patterns of BII phobia patients (N=12) and non-anxious controls (N=14), recorded with respiratory inductance plethysmography. Participants viewed ten film clips of either an emotionally positive, negative, or neutral quality, as well as surgery and asthma-relevant clips. During five film clips (one from each category) they also tensed their leg muscles. RESULTS: Minute ventilation was markedly increased in blood phobia patients compared to other groups during surgery films. Also, tidal volume and irregularity of tidal volume showed strong increases, while respiration rate was not affected. Leg muscle tension increased ventilation in general but far below the extent brought about by hyperventilation in BII phobia. Patients who were breathing deeper during exposure reported stronger symptoms of dizziness, light-headedness and faintness. In general, patients showed a higher rate of spontaneous sighs throughout all film presentations, but not at baseline. CONCLUSION: Thus, hyperventilation in blood phobia is produced by excessively deep and irregular breathing and may contribute to fainting responses. Behavioral interventions for BII phobia could benefit from attention to this aspect of dysfunctional breathing.

Changes in pCO2, symptoms, and lung function of asthma patients during capnometry-assisted breathing training.

In a recent pilot study with asthma patients we demonstrated beneficial outcomes of a breathing training using capnometry biofeedback and paced breathing assistance to increase pCO(2) levels and reduce hyperventilation. Here we explored the time course changes in pCO(2), respiration rate, symptoms and lung function across treatment weeks, in order to determine how long training needs to continue. We analyzed in eight asthma patients whether gains in pCO(2) and reductions in respiration rate achieved in home exercises with paced breathing tapes followed a linear trend across the 4-week treatment period. We also explored the extent to which gains at home were manifest in weekly training sessions in the clinic, in terms of improvement in symptoms and spirometric lung function. The increases in pCO(2) and respiration rate were linear across treatment weeks for home exercises. Similar increases were seen for in-session measurements, together with gradual decreases in symptoms from week to week. Basal lung function remained stable throughout treatment. With our current protocol of paced breathing and capnometry-assisted biofeedback at least 4 weeks are needed to achieve a normalization of pCO(2) levels and reduction in symptoms in asthma patients.

Circadian affective, cardiopulmonary, and cortisol variability in depressed and nondepressed individuals at risk for cardiovascular disease.

Depression is a risk factor for cardiovascular disease (CVD) perhaps mediated by hypothalamic-pituitary-adrenal (HPA) axis or vagal dysregulation. We investigated circadian mood variation and HPA-axis and autonomic function in older (55 years) depressed and nondepressed volunteers at risk for CVD by assessing diurnal positive and negative affect (PA, NA), cortisol, and cardiopulmonary variables in 46 moderately depressed and 19 nondepressed volunteers with elevated CVD risk. Participants sat quietly for 5-min periods (10:00, 12:00, 14:00, 17:00, 19:00, and 21:00), and then completed an electronic diary assessing PA and NA. Traditional and respiration-controlled heart rate variability (HRV) variables were computed for these periods as an index of vagal activity. Salivary cortisols were collected at waking, waking+30min, 12:00, 17:00, and 21:00h. Cortisol peaked in the early morning after waking, and gradually declined over the day, but did not differ between groups. PA was lower and NA was higher in the depressed group throughout the day. HRV did not differ between groups. Negative emotions were inversely related to respiratory sinus arrhythmia in nondepressed participants. We conclude that moderately depressed patients do not show abnormal HPA-axis function. Diurnal PA and NA distinguish depressed from nondepressed individuals at risk for CVD, while measures of vagal regulation, even when controlled for physical activity and respiratory confounds, do not. Diurnal mood variations of older individuals at risk for CVD differ from those reported for other groups and daily fluctuations in NA are not related to cardiac autonomic control in depressed individuals.

Feedback of end-tidal pCO2 as a therapeutic approach for panic disorder.

BACKGROUND: Given growing evidence that respiratory dysregulation is a central feature of panic disorder (PD) interventions for panic that specifically target respiratory functions could prove clinically useful and scientifically informative. We tested the effectiveness of a new, brief, capnometry-assisted breathing therapy (BRT) on clinical and respiratory measures in PD. METHODS: Thirty-seven participants with PD with or without agoraphobia were randomly assigned to BRT or to a delayed-treatment control group. Clinical status, respiration rate, and end-tidal pCO(2) were assessed at baseline, post-treatment, 2-month and 12-month follow-up. Respiratory measures were also assessed during homework exercises using a portable capnometer as a feedback device. RESULTS: Significant improvements (in PD severity, agoraphobic avoidance, anxiety sensitivity, disability, and respiratory measures) were seen in treated, but not untreated patients, with moderate to large effect sizes. Improvements were maintained at follow-up. Treatment compliance was high for session attendance and homework exercises; dropouts were few. CONCLUSIONS: The data provide preliminary evidence that raising end-tidal pCO(2) by means of capnometry feedback is therapeutically beneficial for panic patients. Replication and extension will be needed to verify this new treatment's efficacy and determine its mechanisms.

Sympathetic activation in broadly defined generalized anxiety disorder.

The definition of generalized anxiety disorder (GAD) has been narrowed in successive editions of DSM by emphasizing intrusive worry and deemphasizing somatic symptoms of hyperarousal. We tried to determine the clinical characteristics of more broadly defined chronically anxious patients, and whether they would show physiological signs of sympathetic activation. A group whose chief complaint was frequent, unpleasant tension over at least the last six weeks for which they desired treatment, was compared with a group who described themselves as calm. Participants were assessed with structured interviews and questionnaires. Finger skin conductance, motor activity, and ambient temperature were measured for 24h. Results show that during waking and in bed at night, runs of continuous minute-by-minute skin conductance level (SCL) declines were skewed towards being shorter in the tense group than in the calm group. In addition, during waking, distributions of minute SCLs were skewed towards higher levels in the tense group, although overall mean SCL did not differ. Thus, the tense group showed a failure to periodically reduce sympathetic tone, presumably a corollary of failure to relax. We conclude that broader GAD criteria include a substantial number of chronically anxious and hyperaroused patients who do not fall within standard criteria. Such patients deserve attention by clinicians and researchers.

Psychophysiological reactions to two levels of voluntary hyperventilation in panic disorder.

Panic disorder (PD) patients usually react with more self-reported distress to voluntary hyperventilation (HV) than do comparison groups. Less consistently PD patients manifest physiological differences such as more irregular breathing and slower normalization of lowered end-tidal pCO(2) after HV. To test whether physiological differences before, during, or after HV would be more evident after more intense HV, we designed a study in which 16 PD patients and 16 non-anxious controls hyperventilated for 3 min to 25 mmHg, and another 19 PD patients and another 17 controls to 20 mmHg. Patients reacted to HV to 20 mmHg but not to 25 mmHg with more self-reported symptoms than controls. However, at neither HV intensity were previous findings of irregular breathing and slow normalization of pCO(2) replicated. In general, differences between patients and controls in response to HV were in the cognitive-language rather than in the physiological realm.

Hypoventilation Therapy Alleviates Panic by Repeated Induction of Dyspnea.

BACKGROUND: Previous research has shown that hypoventilation therapy reduces panic symptoms in part by increasing basal partial pressure of carbon dioxide (PCO2) levels. We tested an additional pathway by which hypoventilation therapy could exert its therapeutic effects: through repeated interoceptive exposure to sensations of dyspnea. METHODS: A total of 35 patients with panic disorder were trained to perform exercises to raise their end-tidal PCO2 levels using a portable capnometry device. Anxiety, dyspnea, end-tidal PCO2, and respiratory rate were assessed during each exercise across 4 weeks of training. Mixed-model analysis examined whether within-exercise levels of dyspnea were predictive of reduction of panicogenic cognitions. RESULTS: As expected, within-exercise anxiety and respiratory rate decreased over time. Unexpectedly, PCO2 dropped significantly from the beginning to the end of exercise, with these drops becoming progressively smaller across weeks. Dyspnea increased and remained consistently above basal levels across weeks. As hypothesized, greater dyspnea was related to significantly lower panicogenic cognitions over time even after controlling for anxiety and PCO2. Additional exploratory analyses showed that within-exercise increases in dyspnea were related to within-exercise increases in anxiety but were not related to within-exercise increases in PCO2. CONCLUSIONS: In support of the interoceptive exposure model, we found that greater dyspnea during hypoventilation exercises resulted in lower panicogenic cognitions even after the effect of PCO2 was taken into account. The findings offer an additional important target in panic treatment.

Muscle relaxation therapy for anxiety disorders: it works but how?

Muscle relaxation therapy (MRT) has continued to play an important role in the modern treatment of anxiety disorders. Abbreviations of the original progressive MRT protocol [Jacobson, E. (1938). Progressive relaxation (2nd ed.). Chicago: University of Chicago Press] have been found to be effective in panic disorder (PD) and generalized anxiety disorder (GAD). This review describes the most common MRT techniques, summarizes recent evidence of their effectiveness in treating anxiety, and explains their rationale and physiological basis. We conclude that although GAD and PD patients may exhibit elevated muscle tension and abnormal autonomic and respiratory measures during laboratory baseline assessments, the available evidence does not allow us to conclude that physiological activation decreases over the course of MRT in GAD and PD patients, even when patients report becoming less anxious. Better-designed studies will be required to identify the mechanisms of MRT and to advance clinical practice.