Report on methods and classification of stress, inattention - sensation
Report on methods and classification of stress, inattention - sensation
Report on methods and classification of stress, inattention - sensation
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D1.1.2<br />
C<strong>on</strong>tract N. IST-507231<br />
ACTH <strong>and</strong> cortisol. The activati<strong>on</strong> <strong>of</strong> HPA <strong>and</strong> SAM leads to increased arousal, which means<br />
that energy is mobilized <strong>and</strong> aids the body in the physical fight or flight. Energy is mobilized<br />
to the brain, heart <strong>and</strong> to the muscles, <strong>and</strong> at the same time the blood flow to the muscles <strong>and</strong><br />
gastrointestinal system is reduced. The energy mobilizati<strong>on</strong>, resulting in an elevated blood<br />
c<strong>on</strong>centrati<strong>on</strong> <strong>of</strong> glucose <strong>and</strong> free fatty lipids, is given priority <strong>and</strong> anabolism is down<br />
regulated (Theorell, 2000). The anabolic processes is central to the body’s defense <strong>of</strong> all<br />
organ systems that need c<strong>on</strong>stant rebuilding <strong>and</strong> restorati<strong>on</strong>. The reduced anabolism<br />
associated with prol<strong>on</strong>ged <strong>stress</strong> is likely to be <strong>of</strong> great importance for <strong>stress</strong> related disease<br />
development.<br />
When the body is exposed to <strong>stress</strong>, a rapid alarm phase starts. However, the alarm phase is an<br />
essential <strong>and</strong> necessary physiological phase, <strong>and</strong> although it may be an unpleasant experience,<br />
it is not associated with illness or disease (Ursin & Eriksen, 2004). If <strong>stress</strong> exposure persists<br />
over time, the sec<strong>on</strong>d stage <strong>of</strong> GAS develops – the resistance phase. During this phase, the<br />
organism achieves a state <strong>of</strong> increased adaptati<strong>on</strong> towards the <strong>stress</strong>or but would be more<br />
susceptible to deleterious effects due to regulatory disturbances (e.g. problems to maintain<br />
homeostasis) <strong>of</strong> the biological <strong>stress</strong> systems (McCarty & Pacak, 2000). If the <strong>stress</strong> exposure<br />
c<strong>on</strong>tinues <strong>and</strong> perhaps increase in intensity, the organism would enter the third phase –<br />
exhausti<strong>on</strong>. This stage is triggered by depleti<strong>on</strong> <strong>of</strong> energy stores, when the <strong>stress</strong> regulatory<br />
systems are worn out.<br />
Selye's proposed n<strong>on</strong>-specific <strong>stress</strong> resp<strong>on</strong>se has been criticized in later research. Recent<br />
animal studies show that <strong>stress</strong>ors have different neuroendocrine pr<strong>of</strong>iles (McCarty & Pacak,<br />
2000). Mas<strong>on</strong> (1968) questi<strong>on</strong>ed the <strong>on</strong>e-dimensi<strong>on</strong>al <strong>stress</strong> c<strong>on</strong>cept <strong>and</strong> emphasized the<br />
physiological balance between energy providing “catabolic” processes <strong>and</strong> regenerative<br />
“anabolic” process (Karasek, Russel, & Theorell, 1982). Thus a large energy mobilizati<strong>on</strong><br />
may be relatively harmless for the body if the subsequent anabolic processes can increase<br />
their compensatory recovery.<br />
The classical markers for acute <strong>stress</strong> are cortisol, epinephrine, heart rate <strong>and</strong> blood pressure,<br />
which will increase rapidly to <strong>stress</strong> exposure. Epinephrine is regarded as maybe the best<br />
indicator <strong>of</strong> the intensity <strong>of</strong> the <strong>stress</strong>or. However, a disadvantage with epinephrine, heart rate<br />
<strong>and</strong> blood pressure is that these measures will not reflect the emoti<strong>on</strong>al value <strong>of</strong> the <strong>stress</strong>or<br />
<strong>and</strong> are rather n<strong>on</strong>-specific. Also activati<strong>on</strong> associated with positive mood <strong>and</strong> pleasant<br />
activities will increase the levels <strong>of</strong> these measures. It has been proposed by some experts<br />
(Lundberg & Frankenhaeuser, 1980), that cortisol is a better marker if the emoti<strong>on</strong>al value is<br />
<strong>of</strong> interest. According to their theory, increased cortisol levels should be associated with<br />
inability to cope, lack <strong>of</strong> c<strong>on</strong>trol <strong>of</strong> the <strong>stress</strong> situati<strong>on</strong>s, <strong>and</strong> depressive mood (Peters et al.,<br />
1998). The empirical evidence for this hypothesis is so far limited.<br />
Ambulatory blood pressure is regarded as <strong>on</strong>e <strong>of</strong> the most feasible markers <strong>of</strong> acute <strong>stress</strong> in<br />
natural c<strong>on</strong>diti<strong>on</strong>s, in particular if <strong>on</strong>e wants to relate physiological resp<strong>on</strong>ses to subjective<br />
percepti<strong>on</strong> <strong>of</strong> <strong>stress</strong> (Pickering, 2000). However, it is important to have c<strong>on</strong>trol over activity<br />
<strong>and</strong> posture, which can have a great impact <strong>on</strong> the results. In a study <strong>of</strong> various activities it<br />
was found that walking increased systolic blood pressure with 12 mm Hg. Being at a meeting<br />
produced an increase <strong>of</strong> 20 mmHg <strong>and</strong> talking in the teleph<strong>on</strong>e increased systolic blood<br />
pressure with 10 mmHg. Sleep decreased systolic blood pressure with 10 mmHg (Pickering,<br />
2000).<br />
An interesting <strong>stress</strong> measure is the fluctuati<strong>on</strong> <strong>of</strong> heart rate over time. Heart rate variability<br />
(HRV) measures frequency fluctuati<strong>on</strong>s across time <strong>and</strong> reflects the aut<strong>on</strong>omic balance, i.e.<br />
whether it is the sympathetic nervous system (SNS) or the parasympathetic nervous system<br />
30/08/2004 9<br />
Karolinska Institutet