The moderating effect of physical activity on cardiovascular reactivity following single fat feedings

Abstract

This experiment examined the effects of consuming a high-fat meal on cardiovascular reactivity and the ability of exercise to act as a moderator between dietary fat consumption and cardiovascular reactivity. Forty healthy, college-age students were randomly assigned to one of four experimental groups: (1) low-fat meal, no exercise; (2) low-fat meal, postprandial exercise; (3) high-fat meal, no exercise; and (4) high-fat meal, postprandial exercise. To induce stress, all participants performed a public speaking task, while heart rate and blood pressure reactivity were measured. Multilevel analyses revealed that consuming a high-fat meal led to heightened mean arterial pressure reactivity. Acute high-intensity exercise resulted in attenuated heart rate and mean arterial pressure reactivity. The results of this study offer insight into how diet and exercise may influence cardiovascular reactivity, which is a key determinant of cardiovascular disease.

Evidence that meal fat content does not impact hemodynamic reactivity to or recovery from repeated mental stress tasks

“…These findings are in agreement with a previous study in which SBP, DBP, and TPR reactivity to a stress task were not influenced by meals that were either low in fat or high in saturated or polyunsaturated fat (Sauder et al 2012) (speech and cold pressor task, ϳ2.5 h postmeal), but are in contrast with other previous findings that blood pressure (Faulk and Bartholomew 2012;Jakulj et al 2007) and TPR (Jakulj et al 2007) reactivity were greater in response to laboratory stressors presented 2 h following consumption of an HFM versus a LFM. The reason for these disparate findings is unclear as all studies used similar subject populations (young, healthy adults), stress tasks (variations of speech tasks, mental arithmetic, and cold-pressor/ ischemia) and quantities of fat (ϳ40-54 g).…”

“…However, endothelial function was not measured during stress, which is the period relevant to hemodynamic reactivity. Unfortunately, endothelial function was not quantified by previous authors (Faulk and Bartholomew 2012;Jakulj et al 2007;Sauder et al 2012), so it is not possible to determine whether this factor played a role in their results.…”

“…The mechanisms of this effect are unclear but have been proposed to involve fat intake-induced endothelial dysfunction (Faulk and Bartholomew 2012;Jakulj et al 2007) and nutrient effects on neural (Barnes et al 2003;Prior et al 2010) and hormonal (Choi et al 1996) stress responses. Since stress reactivity is associated with cardiovascular risk, such interactions with diet are important.…”

“…Dietary fat intake is also an independent risk factor for cardiovascular disease (Stone 1990), and there is some evidence that both a single high-fat meal (HFM) (Faulk and Bartholomew 2012;Jakulj et al 2007) and short-term elevations in dietary fat intake (Straznicky et al 1993) may enhance hemodynamic reactivity to mental stress. The mechanisms of this effect are unclear but have been proposed to involve fat intake-induced endothelial dysfunction (Faulk and Bartholomew 2012;Jakulj et al 2007) and nutrient effects on neural (Barnes et al 2003;Prior et al 2010) and hormonal (Choi et al 1996) stress responses.…”

To email or not to email: The impact of media on psychophysiological responses and emotional content in utilitarian and romantic communication

“…We used multivariate repeated measures GLM using SPSS to analyze the data because it allowed us to examine the psychophysiological and task data with repetition across participants and allows us to assess interaction effects among the independent variables. This type of analysis is typical in psychophysiological studies like this one (Faulk & Bartholomew, 2012;Kordik, Eska, & Schultheiss, 2012;MoyaAlbiol et al, 2013;Ottaviani et al, 2014;Potter & Bolls, 2012;Werner, Kerschreiter, Kindermann, & Duschek, 2013). The means and results of the statistical analysis are presented in Tables 1 and 2. Gender was not found to be a significant factor (F ¼ .193, p ¼ .…”