Effects of aerobic conditioning on cardiovascular sympathetic response to and recovery from challenge.

Exercise has widely documented cardioprotective effects, but the mechanisms behind these effects are still poorly understood. Here, we test the hypothesis that aerobic training lowers cardiovascular sympathetic responses to and speeds recovery from challenge. We conducted a randomized, controlled trial contrasting aerobic versus strength training on indices of cardiac (pre-ejection period, PEP) and vascular (low-frequency blood pressure variability, LF-BPV) sympathetic responses to and recovery from psychological and orthostatic challenge in 149 young, healthy, sedentary adults. Aerobic and strength training did not alter PEP or LF-BPV reactivity to or recovery from challenge. These findings, from a large randomized, controlled trial using an intent-to-treat design, show that moderate aerobic exercise training has no effect on PEP and LF-BPV reactivity to or recovery from psychological or orthostatic challenge. In healthy young adults, the cardioprotective effects of exercise training are unlikely to be mediated by changes in sympathetic activity.

The association of cardiac vagal control and executive functioning--findings from the MIDUS study.

Cardiac vagal control (CVC), an index of parasympathetic contribution to cardiac regulation, has been linked to enhanced executive functioning (EF). However, findings to date have been based on small or unique samples. Additionally, previous studies assessed the CVC-EF link only during rest or recovery period from a cognitive challenge, but not during both states. In the present study, data on 817 socioeconomically diverse participants were obtained from the Midlife Development in the United States (MIDUS) study. As part of this study, participants completed cognitive tests, including EF, along with laboratory-based measures of CVC during rest and following recovery from a cognitive challenge. Regression analyses adjusting for respiratory rate revealed no effect of CVC at rest or during recovery on a global index of EF. However, exploratory post-hoc analyses of the components of the global EF index revealed a significant association between faster vagal recovery and better attention-switching and response inhibition abilities, as indexed by faster reaction time to the mixed SGST. This association remained significant after controlling for demographic, clinical (BMI, diseases and medications altering cardiac autonomic functioning, etc.), and health behavior covariates (Beta = .148, p = .010). Our findings suggest that future studies may need to investigate the links of CVC to specific EF abilities, rather than global measures of EF. Additionally, our results highlight the importance of assessing CVC during both rest and recovery from a cognitive challenge. The authors discuss the putative neurobiological underpinning of this link, as well as suggestions for future basic and clinical research.

The contributions of disease activity, sleep patterns, and depression to fatigue in systemic lupus erythematosus. A proposed model.

OBJECTIVE: This study describes lupus fatigue multidimensionally and introduces a multivariate model: Sleep problems and depression, through reciprocal effects on each other, act as mediators through which lupus disease activity increases fatigue. METHODS: Self-reported sleep patterns, depression, and fatigue were assessed in 48 women with systemic lupus erythematosus (SLE) and 27 women from the general population. Rheumatologists rated current lupus disease activity. RESULTS: The SLE group reported greater overall fatigue than did the controls. Temporal and affective dimensions of fatigue were more differentiating than sensory or severity dimensions. The SLE group also reported longer sleep latency and total sleep time, but not higher depression. Using 2-stage regression, a form of structural equation modeling, the proposed lupus fatigue model was supported. CONCLUSION: These preliminary results describe fatigue as a multidimensional phenomenon arising out of several contributing factors. They suggest that fatigue treatment strategies should address mediating processes such as sleep and depression, in addition to disease activity.