Objectives: 
To examine the association between physical fitness, cardiac parasympathetic control, and inflammatory cytokine responses to mental stress. Exercise and physical fitness may act as a buffer to the detrimental effects of psychosocial stress exposure.
Methods: 
Participants were 207 men and women (52 ± 3 years) drawn from the Whitehall II epidemiological cohort. Participants completed two mental stressors consisting of a 5-minute Stroop task and a 5-minute mirror tracing task. Blood samples were obtained during baseline and 45 minutes post stress. Heart rate variability (HRV) was measured during baseline, stress, and recovery. Physical fitness was assessed from a submaximal exercise test.
Results: 
Interleukin (IL)-6 and IL-1 receptor antagonist were increased significantly at 45 minutes post stress. Multiple linear regression analysis, adjusted for age, body mass index, gender, smoking, alcohol, grade of employment, and basal levels of inflammatory markers demonstrated that exercise heart rate (a fitness indicator) was related to IL-6 (β = 0.24; p = .005) and tumor necrosis factor (TNF)-α responses to stress (β = 0.27; p = .002). Exercise heart rate was also related to the HRV response to stress (β = −0.23; p = .02). A higher systolic blood pressure response to exercise was a predictor of TNF-α responses to stress (β = 0.18; p = .03).
Conclusions: 
Physical fitness (as indexed by lower exercise heart rate) is associated with smaller inflammatory cytokine responses to acute mental stress, an effect that may be partly mediated through parasympathetic pathways. This may be one of the mechanisms by which physical fitness confers protection against cardiovascular risk.
IL = interleukin;
TNF = tumor necrosis factor;
HRV = heart rate variability;
CHD = coronary heart disease;
BMI = body mass index.

Exaggerated blood pressure (BP) response to exercise is a strong predictor of cardiovascular disease, although the mechanisms remain unknown. The purpose was to examine the association between systemic markers of vascular inflammation and exercise blood pressure (BP) responses. Participants were 191 healthy men and women (aged 45–59 years). Blood pressure was measured at baseline and during 8 min of steady state cycling ergometry exercise (at 50 W). Markers of vascular inflammation (fibrinogen, von Willebrand factor antigen, tumour necrosis factor-α, interleukin-6 [IL-6], C-reactive protein [CRP]) were measured at baseline together with other traditional risk factors including central adiposity, smoking, alcohol, and habitual physical activity. CRP (β = 0.30, p < 0.001), IL-6 (β = 0.25, p = 0.001), and fibrinogen (β = 0.14, p = 0.04) were associated with exercise systolic BP. The association with CRP remained significant after adjustment for age, sex, resting BP, and other risk factors. Other independent predictors of exercise BP included resting BP, female gender, waist–hip ratio, lower employment grade, and low physical activity level. In summary, central adiposity and vascular inflammatory processes may underlie exaggerated BP responses to acute exercise.