Psychological, cardiovascular, and metabolic correlates of individual differences in cortisol stress recovery in young men
Introduction
Glucocorticoids play a central role in stress responses (Chrousos and Gold, 1992). The development of assays from saliva has greatly extended the possibilities for assessing cortisol responses in human psychobiological research (Kirschbaum and Hellhammer, 2000). The concentration of saliva free cortisol typically increases in response to acute psychological stressors such as problem-solving tasks and socially evaluative speech, with the rise being delayed by some minutes in comparison with electrodermal or cardiovascular responses. There are, however, substantial differences in cortisol reactivity, and a proportion of individuals demonstrate very little acute cortisol stress response. The magnitude of cortisol responses is influenced by situational characteristics such as task difficulty (Pruessner et al., 1999), lack of control (Peter et al., 1998), social support during stress (Kirschbaum et al., 1995a), and harassment during behavioural challenge (Earle et al., 1999). Individual factors also affect cortisol responses, including gender and age (Kirschbaum et al., 1992, Nicolson et al., 1997).
Although the association between cortisol level and clinical depression is well established (Checkley, 1996), the relationship between individual differences in cortisol responses to standardised challenges and psychological factors in healthy populations have been inconsistent. No associations between cortisol reactivity and trait anxiety, depression, perceived stress or personality factors were found by van Eck et al. (1996) or Schommer et al. (1999) and Schommer et al. (1999). In a group of long-term unemployed men and women, Grossi et al. (1998) reported that participants with low basal cortisol and low responses to acute stress were more anxious and depressed. But Kirschbaum et al. (1995b) found that individuals who displayed persistent cortisol responses over 5 days of testing were more depressed and had lower self-esteem than less responsive individuals. In a previous analysis of the present data set, we found no association between cortisol responses and social support or recent aversive life events (Roy et al., 1998).
There is also uncertainty about the relationship between cortisol reactivity and cardiovascular stress responses. Cardiovascular activation and cortisol release are both part of the acute stress response, and there is a substantial functional interrelationship between hypothalamic–pituitary–adrenocortical (HPA) and sympathoadrenal responses (Axelrod and Reisine, 1984). Studies to date have classified individuals on the basis of cardiovascular reactivity, then assessed cortisol responses. No association between cardiac reactivity and cortisol responses were observed by Manuck et al. (1991), while another study showed that heart rate reactivity predicted cortisol responses to an aversive but not an appetitive task, even though norepinephrine responses were comparable to the two situations (Lovallo et al., 1990). Three relatively small scale experiments from one research group have all found evidence for positive associations between cardiovascular and cortisol responses. Sgoutas-Emch et al. (1994) pre-screened male students for heart rate reactivity to a stress test, then found that high cardiac reactors showed greater cortisol responses to a second task. A study of 24 female students showed positive associations between heart rate and blood pressure responses and cortisol reactions (Uchino et al., 1995). The third study found no association between heart rate reactivity and cortisol responses among older women; rather, cortisol responsivity was correlated with stress-induced blood pressure increases (Cacioppo et al., 1995).
There is evidence to suggest that cortisol may act permissively to heightened stress-induced cardiovascular function. Glucocorticoids allow catecholamines to exert their full actions by promoting epinephrine synthesis and inhibiting catecholamine re-uptake (Munck and Naray-Fejes-Toth, 1994). It is therefore logical to assess the impact of cortisol reactivity on cardiovascular function rather than vice versa. In the present analysis, we classified individuals on the basis of cortisol change, and treated cardiovascular measures as dependent variables. In addition, we tested the hypothesis put forward by Sapolsky et al. (2000) that cortisol basal levels rather than stress-induced cortisol responses are likely to be more important as modulators of cardiovascular reactivity.
The purpose of this study was to further understanding of individual differences in acute cortisol responsivity to psychological stress. Instead of classifying responsivity in terms of increases in cortisol from pre-stress levels, we evaluated individual differences in the magnitude of stress recovery. There is growing interest in evaluating the rate of stress recovery in psychobiological research, and failure to adapt after stress termination may lead to dysregulation of protective mechanisms (Linden et al., 1997). McEwen (1998) has argued that failure of stress recovery may be indicative of sustained allostatic load. A pattern of large cortisol stress responses followed by rapid recovery is observed in dominant as opposed to subordinate baboons (Sapolsky, 1995), while delayed HPA recovery may be associated with inadequate responses, leading to the mobilisation of compensatory mechanisms. In the present study, we defined stress recovery by calculating differences between peak cortisol responses to tasks and levels recorded at the end of a 30 min post-stress resting period. We hypothesised that individuals showing large recovery effects would also have higher cortisol levels in response to stressors. The study was limited to men, since there are consistent sex differences in acute cortisol stress responsivity that would have complicated the analysis (Kirschbaum et al., 1992).
A final issue studied in this analysis was the association between cortisol stress responses and lipid levels. Recent evidence has implicated dysregulation of HPA function in cardiovascular disease risk, particularly insulin resistance, and lipid levels may be affected by glucocorticoid concentration in the circulation (Andrews and Walker, 1999). Phillips et al. (1998) showed in a sample of middle aged men that cortisol levels recorded at 9.00 a.m. were positively associated with blood pressure, insulin resistance and plasma triglyceride concentration, and negatively correlated with high density lipoprotein (HDL) cholesterol. Longitudinal cohort studies indicate that plasma cortisol concentration in adult life is negatively associated with birth weight, itself a cardiovascular disease risk factor (Phillips et al., 2000). Elevated cortisol and high total/HDL-cholesterol ratios have also been linked in indices of allostatic load (Seeman et al., 1997). We therefore predicted that high cortisol stress recovery would be associated with unfavourable lipid profiles, including elevated low density lipoprotein (LDL) cholesterol, low HDL-cholesterol, and a high total/HDL cholesterol ratio.
Section snippets
Participants
Ninety-three male probationary firefighters (age range 19–32) from the London Fire & Civil Defence Authority took part in the study soon after completing basic training. Eleven firefighters were not included in the analyses due to incomplete data. Female probationary firefighters were not included in the study as they represented fewer than 1% of the graduates across the recruiting year.
Cortisol
Saliva samples were collected using cotton dental rolls (Salivettes, Sarstedt) held in the mouth until
Cortisol responses during the laboratory session
The average salivary cortisol values recorded during the laboratory session from the high and low stress recovery groups are shown in Fig. 1. Repeated measures analysis of variance over the seven cortisol samples showed a main effect of recovery group (F(1,80)=5.73, P=0.019), and sample (F(6,480)=19.7, P<0.001), together with a significant recovery group by sample interaction (F(6,480)=5.53, P<0.001). It is evident from Fig. 1 that both groups showed a decrease in cortisol between the
Discussion
This study was carried out with a sample of healthy young men newly recruited to the demanding occupation of firefighting. They had all undergone extensive evaluations of their capacity to carry out this work, and had successfully completed training. The results therefore represent findings in comparatively fit young men, and this may be relevant to their interpretation.
Participants were classified into stress recovery groups on the basis of the magnitude of differences between cortisol
Acknowledgements
This research was supported by the Medical Research Council, UK. The authors are grateful to the London Fire and Civil Defence Authority for their co-operation.
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