Psychological stress has been proposed as a major contributor to the progression of cardiovascular disease (CVD). Acute mental stress can activate the sympathetic-adrenal-medullary (SAM) axis, eliciting the release of catecholamines (NE and EPI) resulting in the elevation of heart rate (HR) and blood pressure (BP). Combined stress (psychological and physical) can exacerbate these cardiovascular responses, which may partially contribute to the elevated risk of CVD and increased proportionate mortality risks experienced by some occupations (e.g., firefighting and law enforcement). Studies have supported the benefits of physical activity on physiological and psychological health, including the cardiovascular response to acute stress. Aerobically trained individuals exhibit lower sympathetic nervous system (e.g., HR) reactivity and enhanced cardiovascular efficiency (e.g., lower vascular reactivity and decreased recovery time) in response to physical and/or psychological stress. In addition, resistance training has been demonstrated to attenuate cardiovascular responses and improve mental health. This review will examine stress-induced cardiovascular reactivity and plausible explanations for how exercise training and physical fitness (aerobic and resistance exercise) can attenuate cardiovascular responses to stress. This enhanced functionality may facilitate a reduction in the incidence of stroke and myocardial infarction. Finally, this review will also address the interaction of obesity and physical activity on cardiovascular reactivity and CVD.

Exercise elicits intensity-dependent increases in epinephrine (Epi), norepinephrine (NE), cortisol (CORT), and lactate (Lac), whereas at rest the hormonal responses to mental stress include increases in Epi, NE, and CORT, but not Lac. Additionally, elevations in CORT at rest are associated with negative affect. Finally, as exercise intensity increases, perceptions of effort (RPE) increase and affect becomes more negative. The purpose of this study was to examine the responses of Epi, NE, CORT, Lac, RPE, and affect during incremental increases in exercise to maximum. Seven highly-trained male runners completed a discontinuous treadmill protocol that included 10 minutes at 60%, 10 minutes at 75%, 5 minutes at 90%, and 2 minutes at 100% of JOURNAL/jscr/04.02/00124278-200702000-00050/ENTITY_OV0312/v/2017-07-20T235329Z/r/image-pngO2max. Blood samples were collected through an intravenous catheter before, during, and following exercise during the experimental condition, and during a time-matched control condition. RPE and affect were assessed just prior to each blood draw. The Epi, NE, CORT, and Lac displayed the expected incremental increases, however affect became more negative at higher exercise intensities, and RPE increased as exercise intensity increased. Data suggest that CORT follows the same pattern of response to graded exercise as affect. Since perceptual and affective responses to exercise are associated with motivation, these documented negative affective shifts during exercise should be considered in order to develop strategies that lead to enhanced exercise adherence and performance.

Background: Painful diabetic neuropathy (pDN) is the most common cause of neuropathic pain (NP) in the United States. Prolonged continuous theta burst stimulation (pcTBS), a form of repetitive transcranial magnetic stimulation (rTMS), is quick (1–4 minutes) and tolerable for most individuals, compared to high frequency rTMS and can modulate pain thresholds in healthy participants. However, its effects on patients with chronic pain are still unclear. The primary purpose of this preliminary study is to investigate the effects of single session pcTBS targeted at the primary motor cortex (M1) and dorsolateral prefrontal cortex (DLPFC) on a set of self-report measures of pain (SRMP) that assess the (a) sensory-discriminative; (b) affective-motivational; and (c) cognitive-evaluative aspects of pain experience. Methods: For this prospective, single-blind study, forty-two participants with pDN were randomized to receive either pcTBS targeting the M1 or the DLPFC brain regions. SRMP were completed at baseline, post pcTBS and 24h-post pcTBS. A two-way mixed model repeated measures analysis of variance (2 brain regions by 3 time points) was conducted to evaluate the effects of pcTBS stimulation at M1 and DLPFC for each subscale of each SRMP. Results: After a single session of pcTBS targeted at M1 or DLPFC in patients with pDN, statistically significant improvements from baseline to post pcTBS and baseline to 24 h-post pcTBS were observed for different SRMP subscales examining the (a) sensory-discriminative, (b) affective-motivational and (c) cognitive-evaluative components of the pain experience. At 24 h-post pcTBS, none of the participants reported any serious adverse events to the pcTBS treatment, thus demonstrating its feasibility. Conclusions: In pDN patients with NP, our study results demonstrated significant improvement in scores on self-report measures of pain (SRMP) after a single session of pcTBS targeting the M1 and DLPFC brain regions. Future studies should consider utilizing multiple sessions of pcTBS to evaluate its long-term effects on pain perception, safety and tolerability in patients with chronic pain. Clinical Trial Registration: This study was registered on the ClinicalTrials.gov website (NCT04988321).