Physical Activity and Stress Reactivity
Summary and Keywords
Cardiovascular disease has been estimated to be responsible for over 30% of deaths worldwide. The traditional cardiovascular risk factors of smoking, obesity, diabetes, physical inactivity, and family history predict about 50% of the variance of new cardiovascular disease cases; therefore, a number of other risk factors must contribute to cardiovascular disease development. One such factor is psychological stress, which has been identified as playing a role in the development of cardiovascular disease. The major research strategy for assessing the impact of psychological stress on cardiovascular disease development is to measure cardiovascular reactivity to laboratory mental stressors. Exaggerated mental stress-induced cardiovascular reactivity and slow stressor recovery have been associated with the development of cardiovascular disease.
In contrast to exposure to psychological stress, there is strong evidence that participation in aerobic exercise leads to a reduction in cardiovascular disease. Participation in regular aerobic exercise generally reduces the cardiovascular response to acute exercise; therefore, researchers have hypothesized that the ability of aerobic exercise to enhance cardiovascular health works partly by modifying the cardiovascular reactivity response to mental stressors. There is mixed evidence to suggest that chronic aerobic exercise decreases or increases cardiovascular reactivity to mental challenge in normotensive, healthy individuals. A decrease in reactivity, however, has been found in those studies that have examined individuals at risk of disease or diseased adults. The optimal volume and intensity of aerobic exercise that brings about maximum decreases in cardiovascular reactivity has yet to be determined. The impact of other forms of exercise on reactivity such as resistance exercise and interval sprinting exercise is starting to be assessed. The challenge for researchers in this area is to identify the mode of exercise that takes the least amount of time but brings about the greatest reduction of levels of stress-induced cardiovascular disease.
Cardiovascular disease has been estimated to be responsible for approximately 31% of deaths worldwide (World Health Organization, 2016). The traditional cardiovascular risk factors of smoking, obesity, diabetes, physical inactivity, and family history predict about 50% of the variance of new cardiovascular disease cases; therefore, a number of other risk factors must contribute to cardiovascular disease development. One such factor is psychological stress, which has been identified as playing a role in the development of cardiovascular disease (Cohen, Janicki-Deverts, & Miller, 2007). The major research strategy for assessing the impact of psychological stress on cardiovascular disease development is to measure cardiovascular reactivity to laboratory mental stressors. Exaggerated mental stress-induced cardiovascular reactivity and slow stressor recovery are hypothesized to lead to the development of cardiovascular disease (Chida & Steptoe, 2010).
Cardiovascular reactivity is typically defined as an increase in cardiovascular response to mental challenge (Treiber et al., 2003). Cardiovascular reactivity responses mainly evoke the sympathetic-adreneomedullary and hypothalamic-pituitary axes that react to stimuli that disrupt the body’s homeostasis. Reactivity has typically been assessed by measuring heart rate (HR) and blood pressure (BP) response to cognitively challenging tasks such as mental arithmetic, the Stroop task, and speech making (Boutcher & Hamer, 2006). Factors such as genetic characteristics (Wu, Snieder, & de Geus, 2010), age, gender, body composition, personality characteristics, and disease states influence patterns of cardiovascular reactivity (Boutcher & Hamer, 2006).
Other factors can amplify the cardiovascular reactivity response. For example, salt sensitivity, caffeine ingestion, and nicotine have been shown to elevate cardiovascular reactivity (Boutcher & Hamer, 2006). Also the nature of the task produces varying patterns of reactivity. Some tasks invoke exaggerated cardiovascular responses, whereas others have a negligible effect. Other tasks elicit central responses such as increases in HR and cardiac output, whereas others bring about peripheral responses such as increases in BP and arterial stiffness. Certain reactivity patterns appear to be more deleterious for cardiovascular health than other patterns (Boutcher & Hamer, 2006). Exaggerated cardiovascular reactivity is related to cardiac disease and hypertension development in humans; however, the underlying pathophysiological mechanisms have not been identified. Blunted cardiovascular reactivity has also been found in obese, depressed, and diabetic individuals, but mechanisms that may mediate the relationship between blunted cardiovascular reactivity and disease are also undetermined. Acute (one bout of exercise) and chronic (regular bouts of exercise over months) aerobic exercise has been shown to both reduce and increase certain aspects of cardiovascular reactivity. Whether exercise-induced lowering or increasing of cardiovascular reactivity leads to reduced cardiovascular disease has not been established.
The purpose of this chapter is to examine the effects of acute and chronic aerobic exercise on cardiovascular reactivity. Specific goals are (1) to describe the reactivity and exercise cardiovascular response, (2) to examine the relationship between reactivity and cardiovascular disease, and (3) to summarize results of research examining the effects of acute and chronic exercise on cardiovascular reactivity.
Cardiovascular Reactivity Response
Cardiovascular reactivity response to mental challenge tasks has been shown to be a relatively stable individual characteristic that tends to be consistent across time and tasks (Hamer, Gibson, Vuoonvirta, Williams, & Steptoe, 2006). The cardiovascular response to an active coping stressor (e.g., Stroop task, mental arithmetic) includes an immediate increase in autonomic activity that results in elevations in HR, BP, cardiac output, total peripheral resistance, skeletal muscle blood flow, and arterial stiffness. An accompanying increase in activity of the adreneomedullary, hypothalamic, and pituitary axes results in a release of a number of stress hormones (e.g., catecholamines, cortisol), and inflammatory cytokines (e.g., interleukin-6, C-reactive protein) that contribute to the reactivity response and elevate the risk of cardiovascular disease (Huang, Webb, Zourdos, & Acevedo, 2013). Other responses activated during exposure to stressors are starting to be examined. For example, the effect of an acute stressor on endothelial function has been investigated by measuring flow-mediated vasodilatation (FMD). Ghiadoni and colleagues (2000) exposed males to mental challenge and showed that FMD was reduced by 50% for 90 minutes following the task. These effects are long lasting as FMD only returned to baseline values after 4 hours. Also hemostatic reactivity that include platelet activation (platelet factor 4 and β-thromboglobulin), hematocrit, and total plasma protein have been found to change in response to laboratory stressors (de Boer, Ring, & Carroll, 2006). Platelet activation has been proposed to be a link between mental stress reactivity and psychiatric and somatic disorders (Koudouovoh-Tripp & Sperner-Unterweger, 2012).
Heart rate variability (an index of parasympathetic influence on the heart) and arterial baroreflex sensitivity are both decreased during mental challenge (Boutcher, Nugent, McLaren, & Weltman, 1998). In addition, mental challenge also elevates skeletal muscle vasodilation. This vasodilation in the vascular beds of muscle in response to mental challenge has been suggested to be mainly due to stimulation of β-2 receptors on vascular smooth muscle and endothelial cells by circulating catecholamines in combination with locally mediated nitric oxide release, plus activation of the cardiopulmonary baroreceptors (Hamer, Boutcher, & Boutcher, 2003).
The specific areas in the brain in humans that drive autonomic response to different stressors are poorly identified but include the mesocortical/mesolimbic system and amygdala-hippocampus complex (Sothman, 2006). A related area, the anterior cingulate cortex, is maximally activated during Stroop performance, which suggests that the cingulate responds to conflict occurring between incompatible streams of information processing (Carter et al., 2000). Thus, the significant autonomic response brought about by the Stroop is likely elicited through the activity of the anterior cingulate. The Stroop task has been used extensively as a stressor in reactivity research and typically results in increased cardiac, renal, and splanchnic nerve activity with simultaneous skeletal muscle vasodilation (Boutcher & Boutcher, 2006). The Stroop is attractive for use as a laboratory stressor because of the absence of a significant learning effect and its consistent influence on autonomic reactivity. For example, after 10 minutes of Stroop performance HR, BP, and skeletal muscle vasodilation were all still significantly elevated compared to baseline (Hamer, Boutcher, & Boutcher, 2002).
Given the diversity of the cardiovascular response to mental challenge and further understanding of the reactivity-disease-exercise relationship will be dependent on the ability to assess complex cardiovascular reactivity patterns. Greater use of multiple measures is required so that reactivity patterns and their effect on cardiovascular disease and hypertension development can be established. Ideally, it would be desirable to assess cardiovascular reactivity by measuring cardiac output, total peripheral resistance, cardiac contractility, HR and its determinants, BP, blood flow in different vascular beds, heart and coronary artery status, baroreceptor sensitivity, arterial stiffness, endothelium status, hormonal response, blood platelet response, and genetic influences. It is extremely difficult to simultaneously assess all these measures so a compromise must be made. More information regarding these measures can be obtained from Boutcher and Hamer (2006).
Description of Aerobic, Resistance, and Anaerobic Exercise
Exercise can be broadly divided into aerobic, resistance, and anaerobic (Boutcher & Boutcher, 2016). Combinations of these exercise types include interval sprinting exercise that involves both aerobic and anaerobic modalities and circuit training that utilizes resistance and aerobic exercise. Aerobic exercise includes walking, jogging, cycling, swimming, and rowing. This form of exercise typically involves large muscle groups with a greater employment of slow twitch muscle fibers. Exercise sessions typically last between 30 and 60 minutes of continuous, moderately hard, aerobic exercise. Resistance exercise is a static form of anaerobic exercise that includes free weights, variable machines, and accommodating resistance machines. In contrast to aerobic exercise, resistance exercise mainly involves fast twitch muscle fibers. This exercise is usually more intense than aerobic exercise and involves frequent rest periods. Thus, in a 60-minute free weight workout, actual exercise may account for only 10–15 minutes of the total session. Intermittent anaerobic exercise such as interval sprinting recruits fast and slow twitch fibers and usually involves some type of sprinting over short distances (running or swimming) or short bursts of sprinting on a cycle ergometer (Boutcher, 2011). All three forms of exercise have documented health benefits. For example, regular aerobic exercise has been shown to reduce incidence of coronary disease, decrease insulin resistance, and decrease resting BP (Sharman, La Gerche, & Coombes, 2015). Continuous involvement in aerobic exercise also affects autonomic activity such as changes in arterial and cardiopulmonary baroreceptor sensitivity. Resistance exercise, in the form of weight lifting, has been shown to decrease insulin resistance, whereas interval sprinting exercise has been shown to decrease body fat, visceral fat, and insulin resistance (Dunn, Siu, Freund, & Boutcher, 2014; Heydari, Freund, & Boutcher, 2012; Trapp, Chisholm, Freund, & Boutcher, 2008). As the great majority of studies in the reactivity area have employed aerobic exercise, the acute and long-term responses and adaptations to this form of exercise will be described in greater detail. The ability of interval sprinting exercise (Boutcher, 2011) and resistance exercise (Huang et al., 2013) to influence reactivity and health appears to be a fruitful area for future research.
Acute Cardiovascular Response to Aerobic Exercise
Acute exercise typically involves one bout of continuous exercise performed on a bike or treadmill for between 30 and 50 minutes. The acute cardiovascular response to aerobic exercise and mental challenge is described in Table 1. As can be seen, there are some similarities but there are also distinct differences between the two. For example, the increase in HR that occurs with the start of aerobic exercise is typically a result of parasympathetic withdrawal. In contrast, the increase in HR seen with mental challenge is a result of sympathetic activity plus parasympathetic withdrawal and increased adrenomedullary activity. Systolic BP increases during both mental challenge and aerobic exercise; however, diastolic BP goes up during stress but typically stays the same or goes down during aerobic exercise. Blood levels of catecholamines only rise when aerobic exercise is performed at a moderately hard level, whereas active coping mental challenge such as the Stroop task results in a significant increase in norepinephrine and epinephrine (Boutcher & Boutcher, 2006).
Long-Term Cardiovascular Adaptations to Aerobic Exercise
The major long-term cardiovascular adaptations to aerobic exercise are also illustrated in Table 1. These include a number of autonomic, cardiac, and hemostatic changes. For example, low resting HR (bradycardia) typically occurs with regular aerobic exercise such as running. Resting HRs of trained runners are often less than 50 beats per minute (Boutcher, Nugent, & Weltman, 1995). Exercise-induced mechanisms underlying the bradycardia response have not been identified but probably involve changes in parasympathetic receptor sensitivity or flow to the heart and changes to cardiopulmonary baroreceptor sensitivity caused by exercise-induced plasma volume expansion. Also regular aerobic exercise results in decreased arterial, carotid, and cardiopulmonary baroreceptor sensitivity in normotensive individuals although regular exercise can enhance baroreceptor sensitivity in the diseased (Iellamo, Legramante, Massaro, Raimondi, & Galante, 2000). One of the major effects of regular aerobic exercise is the enhancement of mitochondrial biogenesis. Mitochondrial number, volume, and their oxidative enzymes significantly increase with regular aerobic exercise. In contrast, resistance exercise mainly brings about an increase in skeletal muscle protein synthesis. Aerobic exercise typically enhances maximal oxygen uptake (V̇O2max), which is the gold standard measure of aerobic fitness. Other exercise adaptations that influence cardiovascular function are enhanced blood volume and an increased sensitivity to catecholamines and cortisol. As can be seen in Table 1, some responses to mental challenge and aerobic exercise appear to be similar. This relationship has generated the “cross-stressor hypothesis,” which posits that reductions in cardiovascular response to regular bouts of exercise also lead to reduced cardiovascular response to stressors. Sothman (2006) has examined evidence to support this hypothesis and has concluded that animal research shows that exercise training influences stress responsivity; however, the pattern of stress response is variable depending upon the type of challenge. In humans, Sothman (2006) has suggested that the small number of intervention studies in this area have not produced a reliable change in reactivity; therefore, more research needs to be conducted to adequately test the cross-stressor hypothesis. Another related concept is exercise-induced resilience whereby physical fitness increases the ability to withstand and recover from repeated exposure to stressors (Silverman & Deuster, 2014). Proposed biological mechanisms underlying the stress buffering effects of exercise have included a blunted neuroendocrine, reduced inflammation, and increased growth factor expression and neural plasticity response (for an overview, see Silverman & Deuster, 2014).
Table 1. The acute and long-term cardiovascular response to acute and chronic aerobic exercise and mental challenge in healthy, normotensive adults.
Acute mental challenge
Chronic exercise (at rest)
Heart period variability
Skeletal muscle blood flow
Arterial baroreceptor sensitivity
Cardiopulmonary baroreceptor sensitivity
Notes: ⇧ indicates increased;
⇔ no change.
The measurement of maximal aerobic fitness or V̇O2max is best assessed with the use of a metabolic cart that measures gases and ventilation. This involves getting participants to exercise to exhaustion on a treadmill or a stationary bike. Unfortunately, as the carts are expensive and require trained personnel to carry out the testing, researchers have typically not directly assessed fitness levels of participants and instead have used questionnaires or submaximal exercise testing. Both of these methods have problems with participants tending to overestimate their current physical activity levels when assessed by questionnaire. Submaximal testing is also problematic as a maximal HR of 220 minus age is assumed rather being directly measured. A further problem with fitness testing is that there is a genetic contribution to V̇O2max values. Thus, some participants may not be engaged in any form of aerobic exercise but still may appear to be fit when their V̇O2max is assessed. Estimates of the genetic component have varied between 10% and 40% (Bouchard et al., 1999). Another characteristic of fitness testing is that aerobic fitness is highly specific. Thus, a runner may record high aerobic fitness values when running on a treadmill but only moderate values when being tested on a cycle ergometer. Thus, participants may not exhibit reactivity dampening after a bout of cycle exercise if their regular exercise modality is running. The measurement of aerobic fitness is an important aspect of the exercise/reactivity relationship because a significant increase in fitness needs to be shown in order to examine the chronic exercise/reactivity relationship.
Another issue is the contribution to the reactivity response of fitness or exercise adaptation. Aerobic fitness is best measured by a graded exercise test, but values on this test are significantly influenced by genetic factors. Thus, one participant may be genetically endowed and produce a moderately high V̇O2max but may be physically inactive. In contrast, another participant may be a regular jogger (running five times per week at moderate intensity) but also may record a similar moderately high V̇O2max. In the latter case the runner would likely have many of the chronic adaptations described in Table 1, which would be missing in the non-exercising participant. So what is more important for changing the reactivity response? To be physically active and constantly evoke cardiovascular and related systems or to be genetically fit and have the ability to produce moderately high values on the V̇O2max test? The V̇O2max test typically lasts around 10 to 12 minutes and mainly tests participant’s ability to increase their cardiac output.
In summary, aerobic exercise involving walking, jogging, and cycling has been the most studied form of aerobic exercise when examining the exercise/reactivity relationship. There are both similarities and dissimilarities in the cardiovascular response to acute aerobic exercise and mental challenge. Numerous cardiovascular changes occur with participation in regular aerobic exercise and there are many documented health benefits. Issues concern the role of genetic influences on fitness versus regular participation in exercise and the measurement of aerobic fitness.
Cardiovascular Reactivity and Disease Development
Heightened or suppressed reactivity effects on cardiovascular disease are likely to occur through constant exposure to stressors. Heightened cardiovascular reactivity has been linked to unfavorable health outcomes that include the development of preclinical disease markers (Treiber et al., 2003) and the actual development of cardiac disease and essential hypertension (Chida & Steptoe, 2010).
The Effect of Reactivity on the Development of Preclinical Disease Markers
Preclinical disease markers refer to pathogenic changes in cardiovascular structure or function that if continued could progress to cardiovascular disease. The ability of reactivity to accelerate the development of preclinical factors of cardiac disease and hypertension has mainly been examined by assessing the relationship between reactivity and ventricular remodeling, carotid atherosclerosis (Treiber et al., 2003), and vascular smooth muscle hypertrophy (Folkow, 1990). Although relatively few studies have examined the effect of reactivity on these preclinical measures the results appear to be positive. With regard to ventricular modeling, one study has demonstrated a significant association between BP reactivity and change in left ventricular mass. Georgiades, Lemne, de Faire, Lindvall, and Fredrikson (1997) examined reactivity as a predictor of 3-year change in left ventricular mass in middle-aged, borderline hypertensive men. BP and HR reactivity scores were measured in response to mental arithmetic and isometric muscle contraction. Mean arterial pressure reactivity accounted for 15% of the variance in left ventricular mass change over the 3-year period. Similar results have been found with European American and African American youths (Murdison et al., 1998). However, because of the small number of studies in the left ventricular mass/reactivity area, the task characteristics and reactivity measures that best predict left ventricular mass development are undetermined (Treiber et al., 2003).
Results from a small number of studies also indicate that exaggerated reactivity may be predictive of the development of carotid atherosclerosis. In two studies, measurement of longitudinal change in disease suggested that preexisting clinical or subclinical disease may moderate the observed relationship between reactivity and carotid atherosclerosis. Barnett, Spence, Manuck, and Jennings (1997) assessed reactivity to the Stroop Color and Word interference task in men and women and then monitored change in carotid plaque progression over a two-year period. Systolic BP reactivity but not HR or diastolic BP reactivity explained 7% of the variance associated with change in carotid plaque area. Matthews and colleagues (1998) examined stress reactivity in healthy middle-aged women and found that pulse pressure (systolic minus diastolic BP) reactivity rather than BP reactivity was significantly associated with future carotid plaque thickness development.
Repeated episodes of skeletal muscle blood flow hyper-reactivity may contribute to the development of hypertension. An over-perfusion of vascular beds has been suggested to be responsible for a remodeling process involving hypertrophy of vascular smooth muscle that eventually cause permanent increases in vascular resistance (Folkow, 1990). The muscle vasodilatation that is brought about during exposure to mental challenge is mediated by both sympathetic withdrawal and β-adrenergic stimulated catecholamine release. Catecholamines possess trophic properties that have been shown to enhance vascular smooth muscle growth. Enhanced vascular smooth muscle growth plays a significant role in the vascular remodeling process that is integral to the development of hypertension (Folkow, 1990). Macnair (2000) has also described a link between a vascular remodeling process and low levels of physical activity. It was suggested that over-perfusion of inactive muscle, with a low requirement for oxygen, would produce a chain of events resulting in the production of angiotensin II, which is one of the strongest vasoconstricting hormones. This could lead to a vascular remodeling process with the vasomotor system becoming hypersensitive to vasoconstrictor stimuli resulting in the resistance changes described by Folkow (1990). Thus, individuals who respond to mental challenge with exaggerated muscle vasodilatation may be at greater risk of developing smooth muscle hypertrophy leading to the development of hypertension. The exaggerated skeletal muscle blood flow reactivity but higher resting peripheral vascular resistance typically found in young offspring of hypertensive parents supports this hypothesis. For example, it has been shown that young normotensives with a family history of hypertension had 25% higher peripheral vascular resistance (inability to maximally vasodilate skeletal muscle vascular beds) than that of young normotensives without a family history of hypertension (Takeshita et al., 1982). Thus, despite demonstrating normal BP, males with a family history of hypertension tend to possess exaggerated skeletal muscle blood flow reactivity but reduced maximal vascular vasodilatory ability. However, genetics may also contribute to the vascular changes of the offspring of hypertensives as it is plausible they could be born with thickened arterial walls and decreased lumen diameter. Thus, those individuals who possess thickened arterial walls and decreased lumen diameter and also respond to stress with an exaggerated skeletal muscle blood flow may be especially vulnerable to the development of hypertension.
Collectively, results of these studies provide preliminary evidence to indicate that BP and pulse pressure reactivity may contribute to the development of left ventricular mass and carotid atherosclerosis. Individuals, such as offspring of hypertensives, who respond to mental challenge with exaggerated muscle vasodilatation may be at greater risk of developing long-term elevated peripheral vascular resistance and hypertension.
The Effect of Reactivity on Cardiovascular Disease
Support for reactivity influence on cardiovascular disease (cardiac disease and hypertension) comes directly and indirectly by animal and human research. The result of animal research has been summarized by Boutcher and Hamer (2006). Overall, animal studies have demonstrated a causal relationship between cardiovascular reactivity and the development of cardiac disease and hypertension. In human research the evidence is not as strong as that of the animal literature; however, there is some support for a relationship between reactivity, cardiac events, and hypertension development (Chida & Steptoe, 2010).
Numerous laboratory studies using stressors such as mental arithmetic and public
speaking have demonstrated that acute mental stress induces myocardial ischemia in coronary artery patients. For example, Jiang et al. (1996) recorded deaths and incidence of cardiovascular incidents over a 5-year period after assessing infarct patient’s reactivity to mental stress and found that cardiac problems were associated with stress-induced ischemia. Jain, Burg, Soufer, and Zaret (1995) also exposed cardiac patients to stress and found similar results.
Individuals with a parental history of hypertension demonstrate exaggerated BP and HR, forearm blood flow, sympathetic nervous activity, and endothelin-1 release (Noll et al., 1996) in response to mental challenge. Heightened cardiovascular reactivity has also been linked to the development of hypertension. Matthews and colleagues (2004) tested the hypothesis that individuals who demonstrate BP reactivity during psychological stress are at risk for developing hypertension. Hypertensive status during 13 years of follow-up in a sample of 4100 normotensive Black and White men and women (aged 18 to 30 years) enrolled in the CARDIA study was assessed. BP responses to cold pressor, star tracing, and video game tasks were measured. After adjustment for a number of covariates it was found that the larger the BP response to the tasks, the earlier hypertension occurred. It was concluded that young adults who show a large BP response to psychological stress may be at risk for hypertension as they approach midlife. Also Jennings and colleagues (1986) examined 756 males from the Kuopio Ischemic study and found that systolic BP reactivity was related to carotid intima-media thickness after 7 years of follow-up independent of established risk factors. Importantly, the association between BP reactivity and later BP elevation has also been established in normotensive children and adolescents.
Recovery to mental stressors has not been examined to the same extent as reactivity to mental stressors; however, delayed BP stressor recovery has been reported to be associated with risk factors for coronary heart disease. For example, Steptoe, Donald, O’Donnell, Marmot, and Deanfield (2006) monitored post-stress systolic BP response from middle-aged men and women and found a link between delayed systolic BP recovery and carotid intima-media thickness (a coronary heart disease marker). This delayed BP recovery after mental stress was a predictor for a future increase in BP (Steptoe & Marmot, 2005). In addition, a delay in post-stress systolic BP was accompanied with hemostatic responses that may contribute to coronary heart disease pathology (Steptoe & Marmot, 2005). Trivedi, Sherwood, Strauman, and Blumenthal (2008) have also shown the importance of post-stress recovery BP. They exposed 182 participants to mental challenge and found that BP recovery to stressors was an independent predictor of real-life BP measured by an ambulatory device. Also de Boer and colleagues (2006) reported an elevated hematocrit during mental stress and recovery, suggesting a possible link between hemoconcentration and acute cardiovascular events. A delay in recovery from both exercise and mental challenge has also been shown to be linked to cardiovascular disease risk (Cole, Blackstone, Pashkow, Snader, & Lauer, 1999).
The ability of reactivity to predict clinical cardiovascular disease in humans, however, has not been viewed as strong by some authors. For example, Treiber et al. (2003) concluded that the evidence linking reactivity with clinical events in healthy adults is sparse. However, these authors do point out that most studies examining the association between cardiovascular disease and new clinical events in patients with preexisting hypertension or cardiovascular disease do show a significant relationship between BP reactivity and health risk. Chida and Steptoe (2010), however, carried out a meta-analytic review to evaluate the association between cardiovascular responses to laboratory tasks and later cardiovascular risk status. Results indicated that greater BP reactivity to stress and slow recovery after mental stress predicted poor future cardiovascular status and progression of cardiovascular disease risk. The most consistent finding was a small, positive relationship between BP reactivity and future development of high BP and hypertension. Only cognitive tasks were significantly associated with later cardiovascular risk status, and the association between greater reactivity and future cardiovascular risk was more pronounced in men compared to women. The strongest associations between negative cardiovascular risk outcomes were found for systolic and diastolic BP reactivity, whereas the most consistent cardiovascular outcome was hypertension. Lovallo (2010) has pointed out that although this meta-analysis showed that the strength of association between a BP reactivity score and development of hypertension was small the relationship was clinically meaningful. For example, Chida and Steptoe (2010) suggest that people with high reactivity BP scores would have a 23% increase in risk of developing hypertension. In the Framingham study, after a follow-up of 34 years, an increase of 20 mmHg in resting systolic BP was associated with a 25% increase in carotid stenosis (Lovallo, 2010).
In summary, it seems that BP reactivity is a consistent independent predictor of future hypertension status when long-term follow-ups are conducted in adults and adolescents. Delayed BP recovery to stressors is also predictive of future BP levels. Results also indicate that patients with daily life ischemia demonstrate exaggerated reactivity to mental challenge.
The Effects of Acute Aerobic Exercise on the Reactivity Response
The logic behind examining the effects of acute exercise (one bout of exercise) on reactivity is that repeated bouts of acute exercise, on a regular basis, may reduce stress-induced reactivity. For example, one vigorous bout of aerobic exercise has been shown to significantly reduce resting BP of hypertensive participants for over 10 hours post exercise (Pescatello, Fargo, Leach, & Scherzer, 1991). With regard to cardiovascular reactivity there is stronger evidence to support an acute exercise reactivity lowering effect compared to results of research examining the effects of chronic exercise. The majority of studies in this area have shown a lowering of mental challenge reactivity after an acute bout of aerobic exercise whereas a minority have shown no effect (see Boutcher & Hamer, 2006; Hamer, Taylor, & Steptoe, 2006). Acute exercise reactivity reducing effects have mainly been documented for BP reactivity; however, post-exercise reduction in total peripheral vascular resistance has also been found.
It is likely that lack of significant findings in some studies occurred because the intensity and duration of exercise employed was too light or too short. Studies that have found significant results have typically used higher intensity aerobic exercise (>60% V̇O2max) for at least 20 minutes and have completed reactivity testing within the first hour of exercise recovery. For example, Steptoe, Kearsley, and Walters (1993) showed that a significant reactivity reduction was only induced by high-intensity cycle exercise (50% versus 70% V̇O2max). Also Alderman, Arent, Landers, and Rogers (2007) examined cardiovascular reactivity to a mental stressor as a function of time (5, 30, or 60 minutes) following exercise. Results indicated that low (50–55% V̇O2max) and high-intensity (75–80% V̇O2max) exercise significantly reduced HR and systolic and diastolic BP and increased HR recovery. The greatest HR recovery, however, was observed only after the high-intensity exercise bout.
Hamer and colleagues (2006) performed a review of randomized controlled trials that examined the effect of acute aerobic exercise on BP reactivity. Of 15 randomized control trials 10 demonstrated significant reductions in post-exercise BP reactivity. Studies using a greater exercise dose showed bigger effects with the minimum effective dose being 30 minutes at 50% V̇O2max. Authors concluded that an acute bout of aerobic exercise had a significant impact on BP reactivity to mental challenge.
It is likely that acute exercise will have the greatest effect on the cardiovascular variables that display the greatest reactivity. This was confirmed by Hamer, Jones, and Boutcher (2006) who examined the effects of acute exercise on cardiac and vascular response to mental challenge in males at risk of hypertension. Offspring of hypertensives consistently display an enhanced peripheral vasodilatation response to mental challenge. A moderately stressful task (Stroop) was performed for 10 minutes after 20 minutes of moderate intensity cycle ergometry exercise at 75% of HR reserve and on a separate occasion after an attentional control task. Similar to the results of previous studies the offspring of hypertensives displayed an enhanced peripheral vasodilatation response to the Stroop task. However, this enhanced response was significantly blunted in offspring hypertensive participants following an acute bout of aerobic exercise so that differences in the skeletal muscle vasodilatation response were no longer observed in comparison with men without familial risk of hypertension.
In summary, there is evidence to suggest that vigorous acute aerobic physical exercise decreases certain aspects of reactivity to mental challenge. A decrease in BP reactivity has been consistently found in those studies that have employed a high-intensity bout of aerobic exercise. Preliminary evidence indicates that skeletal muscle blood flow reactivity after exercise is also decreased in individuals displaying exaggerated vascular reactivity or risk of hypertension.
The major effect of acute exercise appears to be a lowering of skeletal muscle blood flow and BP reactivity. Possible underlying mechanisms for the lowering of skeletal blood flow during mental challenge include reduced catecholamine production, decreased β-adrenergic receptor responsiveness, and increased α-adrenergic mediated vasoconstriction response to stressors (Boutcher & Hamer, 2006).
The Effects of Chronic Aerobic Exercise on the Reactivity Response
Researchers examining the effects of chronic exercise (e.g., regular walking, jogging, running for months) on reactivity have utilized both cross-sectional and longitudinal approaches.
Cross-Sectional Exercise Studies and the Reactivity Response
Cross-sectional studies typically have compared the reactivity responses of aerobically trained or physically fit individuals with that of the untrained or sedentary. Some studies have found different HR and BP reactivity responses (e.g., baseline HR minus HR response to the stressor) between trained and untrained adults, whereas others have found no differences (Boutcher & Hamer, 2006). A consistent finding of cross-sectional studies is that aerobically trained individuals typically demonstrate lower absolute HR response to mental stress (e.g., Boutcher et al., 1995). Resting HRs during rest and to mental challenge in the trained are influenced by cardiac parasympathetic activity. Thus, the parasympathetic and sympathetic response to mental challenge may be changed by aerobic training. Boutcher and colleagues (1998) showed that trained compared to untrained males during the Stroop task showed greater decreases in parasympathetic control of the heart. Thus, trained individuals may possess greater parasympathetic reactivity and reduced sympathetic reactivity to mental challenge. This greater parasympathetic withdrawal to mental challenge of trained participants also exists in older males (Boutcher, Nurhayati, & McLaren, 2001) and pre-pubescent boys (Franks & Boutcher, 2003).
Longitudinal Exercise Studies and the Reactivity Response
The overall effect of chronic aerobic exercise on reactivity in both cross-sectional and longitudinal studies has been assessed by a number of meta-analyses. For example, Crews and Landers (1987) found that chronic aerobic exercise was associated with a HR reactivity reduction. Another meta-analysis, however, failed to replicate these results. Jackson and Dishman (2006) performed a meta-regression analysis of 73 studies that examined whether cardiorespiratory fitness reduced cardiovascular reactivity during and after acute laboratory stress. Results indicated that aerobic fitness was associated with slightly greater HR reactivity but quicker HR recovery to mental challenge. Authors observed that the effects were smallest in the better controlled studies. Fitness was not associated with reduced stress responses, such as HR and BP, which were the variables examined in most of the studies reviewed.
Another meta-analysis was conducted in the same year (Forcier et al., 2006) to evaluate whether physical fitness attenuates cardiovascular reactivity and improves recovery from acute psychological stressors. Thirty-three randomized control trials met selection criteria and 18 were included in the recovery analysis. In contrast, to Jackson and Dishman (2006) fit individuals showed significantly attenuated HR and systolic BP reactivity and a trend toward attenuated diastolic BP reactivity. Fit individuals also showed faster HR recovery but no significant differences in systolic BP or diastolic BP recovery were found. No significant moderators emerged. The disparate findings of these two meta-analyses are difficult to explain. For example, Jackson and Dishman (2006) found that in the better controlled studies (randomized control studies) fitter participants exhibited slightly greater reactivity; in contrast, Forcier and colleagues (2006) examined the results of randomized control studies only and found the opposite results (fitness attenuated HR and systolic BP reactivity). Results may have been influenced by differing study entry criteria and use of different meta-analysis models. A limitation of the randomized control trial is that fitness levels achieved after relatively short training regimens (usually two to six months) are markedly lower than that of regular exercisers who have been participating in exercise for years. Thus, bigger reactivity reductions may be found with individuals who have exercised for years rather than months. Consequently, fitness and adaptation to short-term exercise programs may underestimate the reactivity lowering effects of regular aerobic exercise. More recently, Ramirez and Wipfli (2013) have pointed out that these prior meta-analyses have included methodologically weak studies. Consequently, they conducted a meta-analysis using more stringent study inclusion criteria. The resultant analysis revealed a moderate effect (effect size = −.31) for exercise-induced lowering of cardiovascular reactivity. The major variable influenced by chronic aerobic exercise was a lowering of BP reactivity. A second meta-analysis, in the same article, using the animal literature also showed moderate reductions in hormone and catecholamine reactivity to stressors in rats allowed to engage in aerobic training (Ramirez & Wipfli, 2013).
Results of the Jackson and Dishman (2006) and Forcier et al. (2006) meta-analyses indicated that aerobic fitness was related to quicker HR recovery to mental challenge although this effect was small. As mentioned previously, a delay in recovery from both exercise and mental challenge has also been shown to be linked to cardiovascular disease risk (Cole et al., 1999), thus, a quicker HR and BP recovery to stressors may contribute to reduced cardiovascular disease risk. Studies examining HR and BP recovery patterns and their relationship to cardiovascular risk need to be carried out to further explore the exercise reactivity/recovery phenomenon. Also, as pointed out by Jackson and Dishman (2006), future studies should examine other autonomic, hemodynamic, and vascular responses aside from HR and BP.
Also studies in this area have typically examined exercise/reactivity relationships in low risk, healthy individuals. It is likely, however, that aerobic exercise training, similar to acute exercise, may produce a far greater reduction in reactivity in those participants who display greater reactivity or higher resting cardiovascular levels (e.g., high BP). Research evidence supporting this hypothesis again comes from the hypertension literature. Hypertension development has a genetic influence with up to 50% of hypertension risk being inherited. Offspring of hypertensives, which have a hypertensive parent or grandparent, also consistently display enhanced skeletal muscle blood flow to mental stress. For example, we compared vascular reactivity responses of aerobically trained and untrained offspring hypertensives to a Stroop challenge (Hamer et al., 2002). Skeletal muscle blood flow reactivity to the Stroop, measured by occlusion plethysmography, was significantly lower in the trained offspring hypertensives. Thus, aerobic exercise training is likely to produce a greater reduction in reactivity in those participants who possess greater reactivity.
Similar to the offspring hypertensive cross-sectional results there is preliminary longitudinal evidence with hypertensive individuals supporting the ability of aerobic exercise training to produce a far greater reduction in reactivity in diseased participants. For example, Georgiades and colleagues (2000) investigated the effect of chronic exercise on reactivity in hypertensive participants. Cardiovascular reactivity during public speech, anger interview, mirror trace, and cold pressor was assessed before and after a six-month aerobic exercise training program. Systolic and diastolic BP, total peripheral vascular resistance, and HR reactivity were all significantly reduced in the exercise compared to control group.
Obesity and Depression and the Reactivity Response
With regard to other populations a growing literature has examined the effect of fitness and reactivity in children, older adults, gender, and ethnicity. Briefly, greater reactivity has been documented in fitter children and trained older men and postmenopausal women (see Boutcher & Hamer, 2006) and certain ethnic groups. Also a number of research groups have examined blunted reactivity to mental stressors. Obese individuals demonstrate alterations in their hemodynamic response to mental challenge. Although HR reactivity to mental challenge is similar in both lean and obese, vascular reactivity is dissimilar. For example, the enhanced skeletal muscle blood flow response of lean participants to mental challenge is typically reduced in the obese, whereas cardiac output response is blunted (Sung, Wilson, Izzo, Ramirez, & Dandona, 1997). The inability to vasodilate skeletal muscle during mental challenge results in increased systemic vascular resistance that is accompanied by an increase in BP (Seematter, 2000). It has also been found that obese, depressed adults who possessed poorer self-reported health in the West of Scotland 20-7 study also demonstrated blunted HR, SBP, and DBP reactivity (Phillips, 2011). Importantly, blunted HR and BP reactivity and mortality has also been demonstrated in patients with heart failure. Kupper, Denollet, Widdershoven, and Kopp (2015) exposed 100 heart patients to a public speech task and found that at follow-up 31 patients had died. Blunted diastolic BP reactivity to mental challenge was independently associated with all-cause mortality in heart failure patients.
Obesity and being overweight has also been reported to be associated with disturbances in autonomic control of the cardiovascular system determined by heart rate variability and baroreceptor sensitivity assessment. Also the blunted skeletal muscle blood flow response to mental challenge has been observed to be greater in obese individuals with high levels of insulin resistance (Ribeiro et al., 2005). Endothelial dysfunction and a loss of the vasodilatory effect of insulin to stimulate production of the vasodilator nitric oxide from endothelium have been proposed as mechanisms for blunted skeletal muscle blood flow during mental challenge (Steinberg, Brechtel, Johnson, Fineberg, & Baron, 1994). Thus, hyperinsulinaemia in both normal and overweight individuals may induce blunted skeletal muscle blood flow response to mental challenge. The ability of exercise-increased insulin sensitivity to reverse blunted reduced skeletal muscle blood flow reactivity is an important future research area as a growing body of research suggests that chronic psychosocial stress significantly contributes to the pathogenesis of insulin-related abnormalities and cardiovascular disease by creating dysregulation of the sympathoadrenal system and hypothalamic-pituitary-adrenal axis.
Interval Sprinting and Resistance Exercise and the Reactivity Response
With regard to interval sprinting and resistance exercise few studies have examined their acute or chronic effects on reactivity. Nevertheless, a small number of studies have indicated that these forms of exercise are an important area for future research. For example, interval sprinting exercise, a form of anaerobic exercise (Boutcher, 2011), compared to aerobic exercise, produced a significantly greater acute impact on the autonomic nervous system (ANS) assessed by HR and plasma catecholamine levels (Trapp, Chisholm, & Boutcher, 2007). As acute interval sprinting produces a significant cardiovascular response it is feasible that regular exposure to interval sprinting compared to aerobic exercise will result in greater reactivity change to mental challenge. Support for this notion has been provided by Heydari and colleagues (2013a) who exposed overweight males to 12 weeks of interval sprinting. This form of anaerobic training resulted in reduced HR and arterial stiffness and increased baroreceptor sensitivity (BRS) and muscle blood flow during mental challenge and at rest (Heydari et al., 2013b). One study has examined the effect of acute resistance exercise (e.g., one bout of weight training) on stress reactivity of obese and lean women (Franklin, Ali, Goslawski, Wang, & Phillips, 2014). Brachial-artery flow-mediated dilation was reduced in both groups of women after acute resistance exercise although dilation in the obese was lower compared to the lean. Another study examined the effect of combined acute aerobic and resistance exercise (circuit exercise). Moreira, Lima, Silva, and Simoes (2014) exposed 20 adults to the cold pressor test after performing 3 sets of knee extension, bench press, knee flexion, rowing in the prone position, squats, shoulder press, and 5 minutes of aerobic exercise at 75 to 85% of age-predicted maximum HR. The combined exercise circuit session resulted in significant post-hypotension and an attenuated BP response to the cardiovascular stress test. Although few resistance exercise studies examining reactivity effects appears to have been carried out, Huang and colleagues (2013) reviewed the physiological and biochemical adaptations of regular weight training and have provided a strong case for a potential reactivity lowering effect. Consequently, studies examining the effect of regular weight training on cardiovascular, autonomic, hemodynamic, and biochemical reactivity need to be carried out.
In summary, results of the majority of meta-analyses indicate that chronic aerobic exercise is associated with slightly lower HR and BP reactivity and quicker HR recovery to mental challenge in normotensive, healthy individuals. A greater decrease in HR and BP reactivity, however, has been found in studies that have examined diseased adults (e.g., hypertensives) and a greater decrease in exaggerated skeletal muscle blood flow reactivity in individuals at risk (e.g., offspring of hypertensives). Blunted skeletal muscle blood flow reactivity and increased BP reactivity has been commonly found in the overweight and viscerally obese.
Mechanisms Underlying the Exercise Effects on the Reactivity Response
The possible mechanisms underlying chronic aerobic exercise effects on reactivity are undetermined. The major effect of chronic exercise appears to a lowering of absolute HR during stress and a slightly quicker post-stress HR recovery. Possible mechanisms for absolute HR lowering during mental challenge include increased parasympathetic sensitivity (Boutcher & Hamer, 2006) whereas mechanisms underlying quicker HR recovery are undetermined but probably involve exercise-induced autonomic modulation.
For example, a large number of studies have demonstrated that autonomic modulation on the cardiovascular system is altered after exercise training in healthy young adults, older sedentary individuals, clinical populations, and obese/overweight individuals (Amano, Kanda, Ue, & Moritani, 2000). Some studies have examined obese and overweight individuals and have combined exercise and diet restriction, and collectively have found a favorable modification of autonomic profile (Facchini et al., 2003). How exercise-induced changes in autonomic function impact on stress reactivity and recovery, however, is undetermined.
As illustrated in Figure 1 it is likely that chronic exercise is more effective at reducing reactivity of those individuals who possess enhanced reactivity. Exaggerated reactivity (e.g., enhanced BP or skeletal muscle blood flow response) is displayed by individuals with and without apparent risk factors. Mechanisms underlying hyper-reactivity is undetermined but probably involves abnormal baroreceptor sensitivity. For example, it has been demonstrated that the exaggerated forearm skeletal muscle blood flow response of offspring hypertensives to a Stroop challenge is significantly reduced when cardiopulmonary receptors are inhibited by lower negative body pressure (Hamer et al., 2003). Thus, abnormal skeletal muscle blood flow reactivity of offspring hypertensives is significantly influenced by overly sensitive cardiopulmonary baroreceptors. Importantly, chronic aerobic exercise consistently results in plasma volume expansion and can change cardiopulmonary baroreceptor sensitivity.
Exercise training may have greater effects on individuals with certain clinical conditions or middle-aged and older people in which arterial, carotid, and cardiopulmonary baroreceptor sensitivity is decreased or increased. Interestingly, Somers, Conway, Johnston, and Sleight (1991) reported an increase in arterial baroreceptor sensitivity brought about by aerobic exercise training in hypertensive patients and middle-aged and older healthy men. Whether baroreceptor changed sensitivity, brought about by chronic exercise, impacts on reactivity response to mental challenge, however, is undetermined.
The ability of chronic exercise to reduce the catecholamine response to stress is an important finding as Flaa, Eide, Kjeldson, and Rostrup (2008) have shown that sympathoadrenal reactivity predicts obesity. Arterial plasma epinephrine and norepinephrine concentrations were measured in 99 men at rest and during mental challenge and a cold pressor test. BMI, waist circumference, and triceps skin-fold thickness was measured after 18 years of follow-up. The epinephrine response to the mental stress test was negatively related to BMI and waist circumference change. After correcting for level of exercise, BMI, waist circumference, and triceps skin-fold thickness, reactivity was found to be a consistent negative predictor of future BMI and waist circumference and triceps skin-fold thickness. Authors concluded that the epinephrine response to mental stress was a negative predictor of future body composition after 18 years of follow-up. Consequently, it is feasible that regular aerobic exercise may reduce catecholamine reactivity and thus may help reduce the development of obesity.
In summary, there is evidence to suggest that chronic aerobic exercise may decrease certain aspects of reactivity to mental challenge. The decrease in absolute HR has been consistently found in those cross-sectional studies that have examined individuals displaying resting bradycardia and in those longitudinal studies that have resulted in decreases in resting HR. Results of the majority of meta-analyses indicate that chronic aerobic exercise is associated with slightly lower HR and BP reactivity and quicker HR recovery to mental challenge in normotensive, healthy individuals. A greater decrease in HR and BP reactivity, however, has been found in studies that have examined diseased adults (e.g., hypertensives) and a greater decrease in enhanced skeletal muscle blood flow reactivity in individuals at risk (e.g., offspring of hypertensives). Thus, the ability of chronic exercise to reduce reactivity is likely to be far greater in those individuals who display exaggerated reactivity.
Figure 1 illustrates a schematic describing individual reactivity factors, amplifiers, and disease-inducing mechanisms leading to the development of cardiac disease and hypertension. There are numerous possible intervention points for acute and chronic exercise. For example, acute and chronic exercise has been shown to influence autonomic reactivity by reducing catecholamine response to mental challenge. Also, as discussed, disease-inducing mechanisms such as left ventricular modeling, carotid atherosclerosis, vascular hypertrophy, endothelial dysfunction, arterial stiffness, and autonomic degradation could all be positively influenced by exercise. Also acute and chronic exercise has the potential to directly and indirectly influence the impact of individual reactivity factors. Exercise has been shown to reduce subcutaneous and visceral fat, lower hyper-reactivity, and improve cardiovascular health. Regular exercise improves insulin sensitivity, which may counter the pattern of reduced skeletal muscle blood flow and enhanced BP response to mental stressors typically displayed by the overweight and obese. Exercise may also negate the effect of reactivity amplifiers by enhancing the quality of sleep and lowering the reactivity effects of substances such as caffeine and nicotine and nutrients such as fat and sugar. Other individual factors not displayed in Figure 1 and are not amendable to change include age, gender, and genetic influences. Future research is required to validate these proposed effects so the utility of using acute and chronic exercise to reduce the effects of cardiovascular reactivity can be established.
Future Research Recommendations and Conclusions
The major issues for future research in this area include better methods of reactivity assessment, use of more realistic stressors, identification of the exercise damping/enhancing reactivity mechanisms, and determination of exercise/reactivity clinical outcomes (Boutcher & Hamer, 2006). Multiple measures of reactivity using rapid multiple cardiac and vascular assessment are needed to identify patterns of reactivity. More research examining the effects of acute and chronic exercise on those individuals displaying hyper-reactivity is also needed. Blunted reactivity to stressors, such as those found in the obese, should also be examined and the ability of acute and chronic exercise to restore the optimal reactivity response determined. Also other related biological processes thought to underlie the association between stress and heart disease (e.g., neuroendocrine, inflammatory, and haemostatic pathways; Silverman & Deuster, 2014) should be investigated. Also the identification of “reactivity” genes is an important future research area. Wu and colleagues (2010) performed a meta-analysis on all published twin studies that assessed HR or BP reactivity to the cold pressor test or various mental stress tasks to assess the importance of genetic factors on reactivity. For reactivity to mental stress the pooled heritability estimate ranged from 0.26 to 0.43. This review of genetic association studies revealed a number of genes, mostly within the sympathoadrenal pathway, which could partially account for the heritability of cardiovascular stress reactivity.
There is only limited support for the generalizability of laboratory reactivity tasks, thus Zanstra and Johnston (2011) have called for the use of more ecologically valid stressors. Also the identification of mechanisms underlying stress and heart disease and which are affected by exercise would be beneficial. Little is known about the relationship between reactivity, exercise, and clinical health outcomes; therefore, the effects of exercise-induced reactivity reductions and their impact on cardiovascular disease are required.
In conclusion, there is evidence to suggest that vigorous acute aerobic physical exercise decreases BP reactivity in those studies that have employed a high-intensity bout of aerobic exercise. Preliminary evidence indicates that skeletal muscle blood flow reactivity after acute exercise is also decreased in individuals displaying exaggerated muscle blood flow reactivity. With regard to chronic aerobic exercise there is evidence to suggest that it may decrease certain aspects of reactivity to mental challenge. A decrease in absolute HR has been consistently found in those cross-sectional studies that have examined individuals displaying resting bradycardia and in those longitudinal studies that have resulted in decreases in resting HR. Results of the majority of meta-analyses indicate that chronic aerobic exercise is associated with slightly lower HR and BP reactivity and quicker HR recovery to mental challenge in normotensive, healthy individuals. A greater decrease in HR and BP reactivity, however, has been found in studies that have examined diseased individuals.
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