Lorenz J.P. van Doornen

The Role of Antioxidant Vitamins and Enzymes in the Prevention of Exercise-Induced Muscle Damage

SummaryA growing amount of evidence indicates that free radicals play an important role as mediators of skeletal muscle damage and inflammation after strenuous exercise. It has been postulated that the generation of oxygen free radicals is increased during exercise as a result of increases in mitochondrial oxygen consumption and electron transport flux, inducing lipid peroxidation. The literature suggests that dietary antioxidants are able to detoxify the peroxides produced during exercise, which could otherwise result in lipid peroxidation, and that they are capable of scavenging peroxyl radicals and therefore may prevent muscle damage.Endogenous antioxidant enzymes also play a protective role in the process of lipid peroxidation. The studies reviewed (rodent and human) show significant increases of malondialdehyde (a product of lipid peroxidation) after exercise to exhaustion, and also favourable changes in plasma antioxidant levels and in antioxidant enzyme activity. In trained individuals and trained rats, the antioxidant enzyme activity increases markedly. In this way, the increased oxidative stress induced by exercise is compromised by increased antioxidant activity, preventing lipid peroxidation.Human studies have shown that dietary supplementation with antioxidant vitamins has favourable effects on lipid peroxidation after exercise. Although several points of discussion still exist, the question whether antioxidant vitamins and antioxidant enzymes play a protective role in exercise-induced muscle damage can be answered affirmatively. The human studies reviewed indicate that antioxidant vitamin supplementation can be recommended to individuals performing regular heavy exercise. Moreover, trained individuals have an advantage compared with untrained individuals, as training results in increased activity of several major antioxidant enzymes and overall antioxidant status. However, future studies are needed in order to be able to give more specific information and recommendations on this topic.

Ambulatory measurement of respiratory sinus arrhythmia and respiration rate

The present study describes a device (AMD43) for ambulatory measurement of respiration rate and respiratory sinus arrhythmia from the combined electrocardiogram (ECG) and thoracic impedance signals. Respiratory time intervals derived from this ambulatory device closely corresponds to those derived from simultaneous recordings with a classical laboratory set-up. Good cross-instrument comparison was also found for respiratory sinus arrhythmia parameters derived with both the peak-to-trough and spectral analyses methods. It is discussed how simultaneous measurement of respiration rate, respiratory sinus arrhythmia may be used to assess cardiac vagal tone in real-life situations.

Overcommitment to work is associated with changes in cardiac sympathetic regulation.

Objective: Work stress is associated with an increased risk for cardiovascular disease (CVD). Exaggerated cardiovascular reactivity to work-related stressors or incomplete recovery after work is a proposed mechanism underlying this increase in risk. This study examined the effects of work stress on 24-hour profiles of the pre-ejection period (PEP), a measure of cardiac sympathetic activity, obtained from ambulatory measurement of the impedance cardiogram. Methods: A total of 67 male white-collar workers (age 47.1 ± 5.2) underwent ambulatory monitoring on 2 workdays and 1 non-workday. Work stress was defined according to Siegrist’s model as 1) a combination of high effort and low reward at work (high imbalance) or 2) an exhaustive work-related coping style (high overcommitment). Results: High overcommitment was associated with shorter absolute PEP levels during all periods on all 3 measurement days, reduced wake-to-sleep PEP differences and reduced PEP variability, as indexed by the SD. Conclusions: Overcommitment to work was associated with an increase in basal sympathetic drive and a reduction in the dynamic range of cardiac sympathetic regulation. Both findings are compatible with the hypothesis that overcommitment induces &bgr;-receptor down-regulation. BP = blood pressure; BMI = body mass index; CVD = cardiovascular disease; ERI = effort-reward imbalance; HR = heart rate; ICG = impedance cardiograms; MANOVA = multivariate analysis of variance; PAI-1 = plasminogen activator inhibitor; PEP = pre-ejection period; SDPEP = SD pre-ejection period; VU-AMS = Vrije Universiteit Ambulatory Monitoring System; WHR = waist to hip ratio.

Bivariate Genetic Analysis of Fasting Insulin and Glucose Levels

The main aim of this study was to estimate the relative influence of genes and environment on fasting insulin levels, which were considered a proxy of insulin resistance. Possible sex differences in genetic and environmental influences, and the origin of the covariance between fasting insulin and glucose were investigated. Subjects were 209 pairs of middle‐aged twins, divided into 5 sex‐by‐zygosity groups. A general bivariate model and a reciprocal causation model including fasting insulin and glucose were used in the analyses. For both quantitative genetic models, a model specifying additive genetic and unique environmental factors, which were the same in males and females, showed the best fit to the data. Heritability estimates were modest and highly similar in both models: 20–25% of the variance in fasting insulin, and around 50% of the variance in fasting glucose levels could be attributed to genetic factors. The two models could not be discriminated on the basis of their fit to the data. A submodel of the general bivariate model suggested that the covariance between glucose and insulin has a unique environmental basis, whereas for the reciprocal causation model both causal paths were needed to explain the phenotypic correlation between insulin and glucose and estimates of the reciprocal paths were of opposite sign, an indication for the expected negative feedback loop. Genet. Epidemiol. 16:426–446, 1999.

Stress, Personality and Serum-Cholesterol Level

It appears that serum-cholesterol level may serve as an important mediator between psychological variables and coronary heart disease (CHD). From a review of the literature it is concluded that (1) psychological stressors significantly elevate serum-cholesterol level and (2) psychological characteristics like the Type A-pattern and depression are positively correlated with serum-cholesterol levels. This suggests that the relationship between CHD and stress and coronary prone behavior may be partially explained by the mediating role of serum-cholesterol. A more careful consideration of psychological variables may be helpful in reducing the substantial amount of unexplained variance in cholesterol levels.

Serum-cholesterol: Sex specific psychological correlates during rest and stress

Abstract In the present study an attempt was made to assess whether male and female students differ in their cholesterol adn catecholamine reaction to examination stress. An answer was also sought to the question of whether cholesterol level and reactivity could be predicted from behavioral traits and mood. In 29 male and female students, cholesterol and urine-catecholamines were measured on an examination day and on a control day. Cholesterol level was found to be higher on the examination day, in both males and females. Although males a larger adrenaline reaction than females, their cholesterol reaction did not differ from that of the females. Specifically with regard to males, 62% of the variance in cholesterol base level and 40% of the variance of the stress induced cholesterol rise, were explained by the psychological variables measured. Achievement motivation and depression contributed to both predictions. No significant predictions could be made in the female group. This demonstrates the necessity of taking sex differences into account in psychophysiological studies. It is suggested to pay greater attention in future research to the mediating role that blood lipids play in the relationship between psychological factors and the risk of coronary heart disease.

The relation of type a behavior and vital exhaustion with physiological reactions to real life stress

Abstract Type A behavior and a Vital Exhaustion/Depression cluster seem to be the most crucial elements of the psychological ‘coronary risk profile’. The question is, what physiological mechanisms intervene between these characteristics and CHD risk. In the present study the relationship was investigated between type A behavior and Vital Exhaustion on the one hand and the reaction of blood pressure, catecholamines and cholesterol to a real life stressor (Ph.D. thesis defence) on the other. Type A was shown to be related to a stronger response of adrenaline and diastolic blood pressure to the stressor. Vital Exhaustion was also positively correlated with the adrenaline reaction, and moreover, with cholesterol base level, stress induced cholesterol change, and noradrenaline and cholesterol stress levels. It was suggested that the relation between Vital Exhaustion and cholesterol parameters may originate in noradrenaline induced lipolysis. Type A and Vital Exhaustion may exert their influence on coronary risk by way of different physiological mechanisms. Type A via exaggerated hemodynamic reactivity, and Vital Exhaustion via lipid metabolism.

Genetic influences on fibrinogen, tissue plasminogen activator-antigen and von Willebrand factor in males and females.

Differences in genetic influence on death from CHD between males and females have been reported. Haemostatic factors have consistently been associated with risk for coronary heart disease (CHD), but sex differences in genetic architecture have not been studied. This study in middle-aged twins investigates whether there are sex differences in means and in genetic and/or environmental variance components of haemostatic risk factors for CHD. A total of 93 monozygotic twin pairs (44 male and 49 female) and 116 dizygotic twin pairs (36 male, 40 female and 40 opposite sex) were available for this study. Structural equation modelling was used to estimate the relative influence of genetic and environmental factors on variation in levels of fibrinogen, tissue plasminogen activator (tPA) antigen and von Willebrand factor (vWF). Mean levels of tPA and vWF increased with age. Oral contraceptive pill (OCP) and menopause had significant influences on levels of fibrinogen and tPA. Genetic influences explained 39, 66 and 72% of the variation in levels of fibrinogen, tPA and vWF, respectively. No quantitative or qualitative differences of genetic influences on haemostatic levels were seen between males and females. Haemostatic factors may account for a significant part of the genetic risk for cardiovascular disease. No difference in genetic architecture for levels of fibrinogen, tPA or vWF was observed between males and females.

Cardiovascular response to mental stress in offspring of hypertensive parents: The Dutch Hypertension and Offspring Study

Objective: To compare blood pressure-regulating mechanisms during mental stress in two groups of offspring with contrasting risk for hypertension. Design: Cardiovascular reactivity to two different types of mental stressors was studied in adolescents and young adults with two hypertensive or two normotensive parents. The two tasks used were intended to evoke either a predominantly adrenergic cardiac response (a memory search task) or a predominantly vascular response (a reaction-time task with visual search and tone avoidance). Methods: Blood pressure and heart rate were recorded at rest and during stress. To study adaptations of the cardiovascular system to mental stress, cardiac output, total peripheral resistance and indices of vagal and sympathetic influences on the heart were measured. Results: The reactivity of systolic blood pressure (SBP) to the memory search task was significantly higher in offspring of hypertensive parents, which resulted in a longer recovery after the task. In contrast, during the reaction-time task, offspring of hypertensive parents had a significantly enhanced reactivity of peripheral resistance, but no differences in heart rate or blood pressure response were observed. No differences between the two groups were found in sympathetic or vagal activity during either task measured by the ratio of pre-ejection time and left ventricular ejection time, and respiratory sinus arrhythmia, respectively. Conclusion: Apart from a higher reactivity of SBP during the memory search task, no other indications supporting the presence of hyperadrenergic activation of the heart in early primary hypertension were found. On the contrary, the results of the present study support the hypothesis that blood pressure responses in prehypertensive subjects are characterized by enhanced vasoconstriction rather than by increased cardiac output.

Developmental Genetic Trends in Blood Pressure Levels and Blood Pressure Reactivity to Stress

This chapter has two main aims. The first is to describe the changes in heritability of blood pressure levels and blood pressure reactivity that occur during the life span. The second is to disentangle the genetic and nongenetic causes of stability and change in these parameters. In order to achieve these goals, both empirical studies and developmental models will be discussed.