Nicola J. Paine

Exercise intensity does not influence the efficacy of eccentric exercise as a behavioural adjuvant to vaccination.

Acute exercise prior to vaccination can improve the antibody response to influenza vaccination. However, both the optimal exercise protocol and the mechanisms underpinning this adjuvant effect remain unclear. The aim of the current study was to determine whether exercise intensity influenced the efficacy of the intervention. One hundred and sixty healthy young adults were randomly assigned to a resting control group or one of three intervention groups, who exercised at an intensity of 60%, 85%, or 110% of their pre-determined concentric one repetition maxima. The exercise groups performed 50 repetitions of the eccentric portion of both bicep curl and lateral raise movements. All participants then immediately received a reduced dose (50% recommended dose) influenza vaccine. Antibody titres to the three viral strains contained in the vaccine were measured at baseline and at 28 days post-vaccination. Compared to the control group, exercise enhanced the antibody response to the least immunogenic of the three strains (B/Florida). In addition, the exercise groups showed an augmented response to the A/Uruguay strain compared to control; however, this effect was observed only in men. The intervention had no effect on the antibody responses to the most immunogenic strain, A/Brisbane. Finally, antibody responses were unrelated to the intensity of the exercise bout. In conclusion, our findings provide further evidence of exercise as an adjuvant to enhance vaccination responses. The results further show that responses to the low-immunogenic antigens are particularly responsive to augmentation by acute eccentric exercise.

The time course of the inflammatory response to the Salmonella typhi vaccination

The Salmonella typhi vaccination induces transient increases in inflammatory-responsive cytokines and molecules. For instance, it causes small, mild increases in interleukin-6 (IL-6) within a few hours and C-reactive protein (CRP) within 24h. No study has charted either the time course of the inflammatory response to this vaccine or any associated changes in mood, physical symptoms, and cardiac function. In a blinded crossover experimental design, eight participants received the S. typhi vaccine (vaccination condition) and a saline (control condition) injection on two separate days, at least one week apart. Blood samples and mood ratings were collected at 0, 4, 5, 6, 7, 8 and 24h post-injection, physical symptoms and pain were assessed at 4-8 and 24h post-injection, and cardiovascular function was recorded until 8h post-injection. Repeated measures analyses of variance and polynomial trend analyses compared the timecourse of the response patterns between the two conditions. Whereas there were no temporal changes in the control condition, the vaccination increased granulocytes, IL-6, TNF-α, and CRP (all ps<.05). Specifically, the granulocytes, IL-6 and TNF-α peaked after 6-8h while CRP peaked after 24h. This vaccine-induced mild inflammatory response was not accompanied by any changes in mood or cardiovascular activity. We also found that participants tended to report more pain in the injected limb in the vaccination condition (p<.07). In sum, our study charted the timecourse of key inflammatory-responsive markers following S. typhi vaccination and identified the timing of their modest peaks. It is worth noting that changes in these markers were not accompanied by any notable changes in mood or cardiovascular activity, and thus the S. typhi vaccination is a suitable method to induce increases in inflammatory-responsive markers, without altering mood or cardiovascular parameters.

Goal striving and well-being in sport: the role of contextual and personal motivation.

This investigation sought to clarify mixed results in the literature exploring coach behaviors, basic psychological needs, goal motivation, and well- and ill-being. Regional-level team sport athletes (N = 241) completed questionnaires on the aforementioned variables at the beginning of the season. A subsample (n = 70) provided saliva samples to assess physical ill-being. At the end of the season, athletes (n = 98) reported their goal motivation and attainment. Structural equation modeling demonstrated that coach behaviors were related to needs satisfaction and thwarting, which were related to autonomous and controlled goal motives respectively. Autonomous motives were related to well- and ill-being; controlled motives were only related to ill-being. Over time, only end-of-season autonomous goal motives were related to goal attainment. The findings provide an insight into how coaches can facilitate optimum goal striving and well-being in their athletes.

Inflammation and vascular responses to acute mental stress : implications for the triggering of myocardial infarction

There is evidence that mental stress can trigger myocardial infarction. Even though the underlying mechanisms remain to be determined, both inflammation and vascular responses to mental stress have been implicated as contributing factors. This review explores the effects of inflammation on the vascular responses to mental stress. First, the associations between inflammation and resting vascular function are discussed. It is known that increases in inflammation are associated with endothelial dysfunction, with a reduction in nitric oxide a common pathway through which inflammation can influence endothelial function. Second, the effects of mental stress on vascular responses are reviewed. There is ample evidence that in healthy participants, mental stress induces increases in forearm blood flow, which is impaired in those at risk for cardiovascular disease. Even though several mechanisms are discussed, there is evidence that nitric oxide plays an important role in stress-induced vasodilation. Finally, the influences of inflammation on the vascular responses are described. It is hypothesised that inflammation can alter vascular responses to mental stress, most likely due to lower levels of nitric oxide as a result of the inflammation. This poorer vascular response is thought to be an underlying factor through which mental stress can trigger myocardial infarction.

Association of depressive and anxiety symptoms with 24-hour urinary catecholamines in individuals with untreated high blood pressure.

Objective Depression and anxiety are considered risk factors for cardiovascular disease (CVD). The explanatory mechanisms, however, are still to be characterized. One proposed pathophysiological pathway is dysregulation of the autonomic nervous system, including heightened sympathetic nervous system activity. This study examined the relationship between symptoms of depression, anxiety, and sympathetic nervous system activity in individuals with untreated high blood pressure. Methods A total of 140 participants with untreated high blood pressure (55% white, 38.5% female, mean [standard deviation] age = 45.5 [8.55] years) collected urine over a 24-hour period on 3 separate occasions. Urine samples were assayed for mean 24-hour epinephrine (EPI24) and norepinephrine excretion. Depressive symptoms were assessed using the Beck Depression Inventory, with anxiety symptoms assessed using the Spielberger State-Trait Anxiety Inventory. Results Depression and anxiety scores were intercorrelated (r = 0.76, p < .001). EPI24 was positively correlated with anxiety (r = 0.20, p = .02) but not depression (r = 0.02, p = .77), whereas 24-hour urinary norepinephrine excretion was not correlated with anxiety (r = 0.10, p = .21) or with depression (r = 0.07, p = .39). Regression models, accounting for sex, age, body mass index, race, mean systolic ambulatory blood pressure, tobacco use, alcohol use, physical activity, and sleep efficiency confirmed that anxiety was associated with EPI24 excretion (p = .023) and that depressive symptoms were not (p = .54). Conclusions Anxiety was associated with heightened sympathoadrenal activity, suggesting a biological pathway through which anxiety could increase CVD risk. Anxiety and depression may confer increased CVD risk via different mechanisms.

Underlying inflammation has no impact on the oxidative stress response to acute mental stress

INTRODUCTION Mental stress is considered to be a trigger for acute myocardial infarction (MI), with inflammation thought to provide a mechanism. Inflammation is reciprocally linked to oxidative stress, which has also been implicated in MI. The purpose of this study was to assess the effects of experimentally-induced inflammation on the oxidative stress response to mental stress in healthy participants. METHODS Healthy males undertook one of two inflammatory stimuli: typhoid vaccination (Vaccination paradigm, N=17) or eccentric exercise (Eccentric exercise paradigm, N=17). All participants completed a mental arithmetic stress task twice (within-subject design): 6h after the inflammatory stimulus, and during a control non-inflammation condition. Blood samples were taken before, immediately and 30min after the stress task. Plasma was assessed for interleukin-6 (IL-6), protein carbonyls (PC), lipid hydroperoxides (LOOH), total antioxidant capacity (TAC) and nitric oxide metabolites (NOx). RESULTS Vaccination paradigm: IL-6, PC and NOx were significantly higher in the vaccination condition, relative to the control condition (p<.05). PC, TAC, LOOH and NOx were unchanged in response to mental stress in both the vaccination and control conditions. Eccentric Exercise paradigm: IL-6 and TAC were significantly higher in the eccentric exercise condition (p<.05), relative to the control condition. PC, TAC and NOx were unchanged in response to mental stress in both the eccentric exercise and control conditions. CONCLUSIONS Two different inflammatory paradigms were successful in increasing selective plasma markers of inflammation and oxidative stress prior to a mental stress task. However, experimentally induced transient inflammation had no impact on mental stress-induced changes in plasma LOOH, PC, TAC or NOx in young healthy participants.

The effect of acute mental stress on limb vasodilation is unrelated to total peripheral resistance.

Mental stress can trigger myocardial infarction, with poor vascular responses to stress implicated as a pathway. Vascular stress reactivity can be assessed by different methods, such as total peripheral resistance (TPR) and forearm blood flow (FBF). Little is known about how these vascular assessments are linked. This was examined in two separate studies. Healthy men (Study 1: N = 29, Study 2: N = 23) completed rest and mental arithmetic (Study 1: 8 min, Study 2: 16 min). In both studies, heart rate, mean arterial pressure, and FBF increased in response to stress. In Study 1, no changes in TPR were seen, but Study 2 found stress-induced increases in TPR. FBF was not linked to TPR at any time (all ps > .05). It appears that limb vasculature and TPR responses to stress do not give the same information about impairments of the vasculature. These findings are relevant to the interpretation of prior research findings and the design of future studies on stress and vascular responses.

Eccentric-exercise induced inflammation attenuates the vascular responses to mental stress.

Mental stress has been identified as a trigger of myocardial infarction (MI), with inflammation and vascular responses to mental stress independently implicated as contributing factors. This study examined whether inflammation moderates the vascular responses to mental stress. Eighteen healthy male participants completed a stress task under two counter balanced conditions. In the exercise condition, a morning bout of eccentric exercise (12×5 repetitions of unilateral eccentric knee extension at 120% intensity of concentric one repetition maximum) was used to increase levels of inflammatory-responsive cytokines during an afternoon stress session scheduled 6h later. In the control condition, participants sat and relaxed for 45min, 6h prior to the afternoon stress session. Forearm blood flow, calf blood flow (measured in the leg which completed the exercise task), blood pressure, heart rate and cardiac output were assessed at rest and in response to mental stress. As expected, interleukin-6 was higher (p=.02) 6h post exercise, i.e., at the start of the stress session, as compared to the no-exercise control condition. Mental stress increased forearm blood flow, calf blood flow, blood pressure, heart rate, and cardiac output in both conditions (ps<.001). Stress-induced calf blood flow was attenuated in the exercise condition compared to the control condition (p<.05) which was not the case for forearm blood flow. This study found that the inflammatory response to eccentric exercise attenuated the vascular responses to mental stress locally at the site of eccentric exercise-induced inflammation. The observed impairment in vascular responses to stress associated with increased levels of inflammation suggests a mechanism through which inflammation might increase the risk for MI.

Do Women With Anxiety or Depression Have Higher Rates of Myocardial Ischemia During Exercise Testing Than Men

Background—Women diagnosed with coronary artery disease (CAD) typically experience worse outcomes relative to men, possibly through diagnosis and treatment delays. Reasons for these delays may be influenced by mood and anxiety disorders, which are more prevalent in women and have symptoms (eg, palpitations and fatigue) that may be confounded with CAD. Our study examined sex differences in the association between mood and anxiety disorders and myocardial ischemia in patients with and without a CAD history presenting for exercise stress tests. Methods and Results—A total of 2342 patients (women n=760) completed a single photon emission computed tomographic exercise stress test (standard Bruce Protocol) and underwent a psychiatric interview (The Primary Care Evaluation of Mental Disorders) to assess mood and anxiety disorders. Ischemia was assessed using single photon emission computed tomography, with odds ratio used to calculate the effect of sex and mood/anxiety on the presence of ischemia during stress testing by CAD history in a stratified analyses, adjusted for relevant covariates. There was a sex by anxiety interaction with ischemia in those without a CAD history (P=0.015): women with anxiety were more likely to exhibit ischemia during exercise than women without anxiety (odds ratio, 1.75; 95% confidence interval, 1.05–2.89). No significant effects were observed for men nor mood. Conclusions—Women with anxiety and no CAD history had higher rates of ischemia than women without anxiety. Results suggest that anxiety symptoms, many of which overlap with those of CAD, might mask CAD symptoms among women (but not men) and contribute to referral and diagnostic delays. Further research is needed to confirm this hypothesis.

Induced mild systemic inflammation is associated with impaired ability to improve cognitive task performance by practice

Elevated inflammatory levels are linked to poorer cognition, but experimental confirmation is lacking. This report examined associations between cognitive performance and inflammation induced by exercise and vaccination. Thirty-six (exercise N = 18, vaccination N = 18) healthy males completed a paced auditory serial addition test (PASAT), which is a multifaceted measure of cognitive function. The task was completed in placebo and elevated inflammation states. Improvements in PASAT performance were related to inflammation. In the exercise study, IL-6 during the first PASAT negatively correlated with PASAT improvement (p = .022). In the vaccination study, increases in C-reactive protein between PASATs correlated with reduced PASAT improvement (p < .001). Inflammation was linked to reduced improvements in cognitive performance. Further research should identify the specific cognitive functions affects and the underlying mechanisms.