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Biomedical subjects

M Follenius

Publications and source records attributed to M Follenius.

At least 73 records · Page 4Linked to original sources
PubMed1985

Mental task-induced strain and its after-effect assessed through variations in plasma cortisol levels.

Plasma cortisol levels were measured in 20 healthy men while they carried out mental tasks in intermittent noise. Half the subjects performed a serial short-term memory task and, later on, a multiple-choice task, whereas the other half performed only the multiple-choice task. The aim of the experiment was to determine whether enhanced cortisol release, due to a centrally mediated arousal reaction, depressed the cortisol level when the subjects had to cope with a new task situation. In a previous study, such a regulatory after-effect was revealed in the midday meal-related cortisol peak, but not in a subsequent exercise-induced cortisol peak, although cortisol release in both cases could be related to metabolic changes. The results showed that the second mental task still induced a pronounced rise in cortisol levels. No changes in task performances were found. It is concluded that different regulatory mechanisms are involved in adrenocortical secretion, depending on the origin of the stimulation, and that cortisol responses are closely related to individual coping abilities and strategies.

Adult↗
PubMed1985

ACTH-provoked cortisol peaks during sleep and their effect on the endogenous secretory activity.

The effects of low physiological doses of ACTH on nocturnal plasma cortisol patterns were investigated in six male subjects. Concomitant sleep EEG recordings were analysed in relation to the cortisol level. 250 ng ACTH1-24 (Synacthène), injected through an indwelling catheter at a period of low adreno-cortical activity (2400 h), induced a cortisol peak followed by a four to five-hour period without any cortisol secretion. The same dose of ACTH injected at 0430 h, when cortisol secretory activity was high, did not entirely abolish endogenous secretion, which was diminished for a shorter time (2.5 hr). The ACTH-provoked cortisol peaks of comparable size to endogenous secretory peaks, can suppress cortisol secretion for several hours. This suppressive capacity depends on timing in relation to high or low secretory activity periods. However, spontaneous cortisol peaks have no appreciable effect on further secretory episodes. This difference in suppressive capacities suggests that the 24 hr cortisol rhythm is regulated independently of such feedback mechanisms.

Adrenocorticotropic Hormone↗
PubMed1985

Ultradian oscillations in plasma renin activity: their relationships to meals and sleep stages.

The 24-h pattern of PRA was studied in 6 supine normal subjects, and the relationship between sleep stages and PRA oscillations was analyzed using 18 nighttime profiles and the concomitant polygraphic recordings of sleep. Blood was collected at 10-min intervals. The slow trends obtained by adjusting a third degree polynomial to the 24-h data were not reproducible among individuals, and no circadian pattern was detected. Sustained oscillations in PRA occurred throughout the day. Spectral analysis revealed that PRA oscillated at a regular periodicity of about 100 min during the night. This periodicity was modified during the daytime by meal intake, which induced PRA peaks with large interindividual variations in size. A close relationship was found between the nocturnal PRA oscillations and the alternance of rapid eye movement (REM) sleep and non-REM sleep. Non-REM sleep invariably coincided with increasing or peaking PRA levels. REM sleep occurred as PRA was declining or at nadirs. More precisely, increases in PRA marked the transition from REM sleep to stage II, whereas stages III and IV usually occurred when PRA was highest. This relationship between the periodic nocturnal oscillations in PRA and the alternance of the REM-non-REM cycles may translate a similar oscillatory process in the central nervous system or may be linked to hemodynamic changes during sleep that might be partly controlled by the renin-angiotensin system.

Adult↗
PubMed1984

Endocrine concomitants of sweating and sweat depression.

The effect of humid heat (Ta = 43 degrees C, Pa = 32 Torr) on sweat rate, plasma renin activity and plasma levels of aldosterone and antidiuretic hormone (ADH) was studied in four male subjects before and after repeated heat exposures. Over-sweating and sweat drippage followed by hidromeiosis were observed in three subjects during initial heat exposure. With repeated humid heat exposures increased sweat rates were accompanied by a more intense sweat depression (hidromeiosis) in all four subjects. In our conditions, no changes in plasma levels of aldosterone and ADH or plasma renin activity were observed with hidromeiosis. Plasma renin activity was slightly depressed by repeated exposures, whereas plasma volumes were enhanced, with no significant changes in plasma Na or K. The results suggest that neither ADH nor the components of the renin-angiotensin aldosterone system are involved in the hidromeiotic phenomenon.

Adult↗
PubMed1984

Influence of triazolam on thermal heat balance in poor sleepers.

The influence of a benzodiazepine (triazolam) on the body temperature of poor sleepers during nights disturbed by airplane noises has been examined. Subjects were divided into 3 groups each of 8 men. Following a double-blind design, Group A (controls) received a placebo for 6 consecutive nights, Group B received 0.25 mg triazolam, and Group C received 0.5 mg triazolam on nights N3, N4 and N5. On all other nights Group B and C subjects received placebo. For all 3 groups, nights N3 and N5 were disturbed by 32, semi-randomly distributed airplane noises. Air and wall temperatures (To = 20 degrees C), and air humidity (Tdp = 10 degrees C), were kept constant. Rectal temperature and 4 local skin temperatures were recorded from each subject. Urine samples were collected each morning for measurement of cortisol and catecholamine levels. Noise was found to cause an increase in body heat storage, but only in Group A. Both drug groups showed impairment of body heat balance. The hypothermic action of triazolam could be explained both by a central action of the drug on the thermoregulatory controller and by a peripheral action on blood vessels.

Adult↗
PubMed1982

Cortisol as a sensitive index of heat-intolerance.

The relationship between plasma cortisol levels, core temperatures, heat storage and the appearance of subjective manifestations of heat intolerance were investigated in two groups of 4 and 3 men, respectively. The first group underwent 4 randomized experimental sessions: a control session and three heat-exposure sessions (A: 48 degrees C, 34 Torr, 80 min; B: 55 degrees, 15 Torr, 120 min; C: 48 degrees C, 15 Torr, 180 min). During control periods, the subjects were maintained in a thermoneutral climate (28 degrees C, 10.5 Torr). The second group of subjects was studied before and after five successive daily exposures to hot and humid conditions (D: 43 degrees C, 32 Torr, 165 min). Signs of subjective discomfort in experiments A and B were accompanied by an increase in cortisol values over control day values, and this increase began at a mean rectal temperature of about 38 degrees C. Condition C was well tolerated, the plasma cortisol remained at basal levels and mean rectal temperature averaged 38 degrees C at the end of the exposure. Repeated exposures in condition D improved heat tolerance with a lesser effect on plasma cortisol levels and a lower body temperature at the end of exposure. Circulating cortisol is shown to be a very sensitive index of heat stress heralding the onset of poor tolerance of severe climates. The relation between concomitant levels of cortisol and rectal temperatures, in fit men, is affected by additional factors (hypotension, uncomfortable posture). These reduce tolerance time and are not reflected by body temperatures, but by rapidly increasing cortisol levels.

Adult↗
PubMed1982

Feedback from meal-related peaks determines diurnal changes in cortisol response to exercise.

Diurnal variations in cortisol response to exercise and their relation to the events of the day were assessed by comparing daily cortisol patterns on the control day and on days when exercise was performed at different times. A remarkable midday cortisol peak coincided with the noon meal, but cortisol levels were irregularly affected by an identical meal in the evening. However, the exercise produced equal increases when performed during quiescent periods (i.e. without any secretory peaks at 1000, 1430, 1700, and 2130 h), but peak levels for exercise at 2130 h were significantly lower because of the lower basal levels in the evening. When the same exercise was performed at 1300 h (i.e. coinciding with the postprandial peak), only a brief leveling-off interrupted the decline in cortisol levels. The meal-related evening peak, if any, provoked a similar decrease in response to exercise performed at 2000 h. Similarly, the midday peak itself was reduced by a prior exercise-induced cortisol rise. These results show that the daily cortisol pattern results from the interactions between the meal-related peaks, especially the major midday cortisol peak, and the exercise-induced increases, both of which inhibit the response to subsequent stimulation. The identical responses to exercise at the different quiescent periods tested, despite a general downward trend in basal cortisol levels, establish the primacy of such feedback mechanisms over those responsible for the circadian rhythm.

Adult↗
PubMed1982

Diurnal cortisol peaks and their relationships to meals.

Relationships between diurnal plasma cortisol peaks and meals were evaluated for 30 male subjects divided into 5 groups. At 1300 h, at the time of a slow increase of plasma cortisol in fasting subjects, a reproducible rapidly increasing meal-related peak appeared in all subjects studied. An identical meal at 2000 h led to a lower mean response, with larger interindividual variations. This attenuated evening response does not seem attributable to any daily rhythm in responsiveness nor to changing basal levels, since only slight nonsignificant rises in cortisol appeared after an identical meal at 1000 h. The usual mean cortisol pattern with a midday peak was observed in subjects accustomed to different activity and meal-time schedules, which excludes the role of dietary habits. Satiety did not seen to play a determining role in the response to the 1000 h meal, as was shown by comparing subjects who did or did not have breakfast after overnight fasting. Meal intake was not necessary to provoke peaking in cortisol levels, and it has been established that neural and behavioral factors associated with meal presentation play a predominant role in some subjects. The results given clear evidence of the influence of meal timing on the daily plasma cortisol pattern, but no clue was found as to why eating affects the pituitary-adrenal axis differently according to the time of day. The noon meal may at least have a synchronizing role on normally existing plasma cortisol fluctuations.

Adult↗
PubMed1980

Plasma catecholamines and pituitary adrenal hormones in response to noise exposure.

To evaluate the immediate effect of exposure to a high level of noise on the sympatho-adrenal and pituitary-adrenal systems, measurements were made of circulating catecholamines, growth hormone, ACTH, and cortisol in seven normal male subjects. They were studied on two random experimental days: a control day and a noise-exposure day with an intermittent noise alternating between 99 dB (A) and 45 dB (A) for 2 h. Analysis did not reveal any variation in the plasma levels of norepinephrine (NE), epinephrine (E) or dopamine (D), measured every 20 min, which might have been related to noise exposure. Similarly, analysis of the 2-h urine samples collected from 8 a.m. to 2 p.m. revealed no significant changes in urinary catecholamine excretion. Plasma levels of GH and ACTH did not differ significantly from those for control days, but cortisol showed a brief, significant levelling-off in its pattern during the exposure period. The data demonstrate that exposure to a high level of noise, although considered as "unpleasant", does not induce any important endocrinological changes in man. These conclusions differ from those for studies on animals where reactions to noise may be related to a more general stressing situation.

Adrenocorticotropic Hormone↗
PubMed1980

Plasma catecholamines and pituitary adrenal hormones related to mental task demand under quiet and noise conditions.

Plasma levels of catecholamines and pituitary adrenal hormones were measured in 20 min samples from eight subjects, in one control session and two experimental sessions, while they performed a short-term memory task under quiet of noise conditions. Performing the task led to significant increase in the plasma levels of cortisol, adrenaline and noradrenaline, whereas no variations in growth hormone and dopamine were observed. Similarly, significant changes occurred in urinary catecholamine excretion. A significant correlation was found between individual plasma cortisol increments and error-rates assessed from an accuracy of recall variable. For adrenaline and noradrenaline, an early response apparently linked with an anticipatory process preceded the task. Exposure to noise did slightly amplify cortisol response to the task, but during the first experimental session, with or without noise, the task elicited greater cortisol increases in all subjects than during the second session. These results provide evidence for a relationship between sympathoadrenocortical activity and attentional demand, whereas cortisol increments seem to be more specifically related to better coping with the task. Frequent hormone level measurements during a prolonged mental task might clarify the complex relationship between time-related bodily hormonal changes, performance and subjective feelings.

Adrenocorticotropic Hormone↗
PubMed1979

Plasma aldosterone, renin activity, and cortisol responses to heat exposure in sodium depleted and repeleted subjects.

The effect of 90-min heat exposure (46 degrees C, 35 mbar) on plasma aldosterone (PA) patterns was studied and the respective roles of plasma renin activity (PRA), adrenocorticotropin (ACTH), Na+ and K+ concentrations in the control of PA response were in investigated in eight subjects on a low sodium diet and in five subjects on a high sodium diet. In all subjects, transitory PA increases of varying importance were observed, which were not related to sweat losses (less than 1% bodyweight) or to rectal temperature rise. In sodium-repleted subjects, basal PA and PRA levels as well as heat-induced rises were low (mean PA peak level = 12.62 +/- 1.15 ng/100 ml). They were enhanced by sodium depletion and PA reached a mean peak level of 34.07 +/- 2.73 ng/100 ml. But, in both conditions, the heat-induced PA peaks were 3-times higher than the initial levels. PA correlated with PRA in all but one of the sodium-repleted subjects and in 6 of the 8 sodium-depleted subjects. ACTH release, as measured by plasma cortisol (PC) levels, occurred in those subjects who noted an increased feeling of annoyance and discomfort. Thus, PA correlated positively with PC in 4 sodium-depleted subjects. A high sodium intake improved heat-tolerance. Plasma K+ and Na+ concentrations were not significantly modified by exposure to heat. PA increases can occur without concomitant changes in PRA, PC, K+ or Na+, which suggests that an additional factor may play a role in aldosterone regulation during acute heat exposure.

Adult↗
PubMed1975

Influence of timing and intensity of musclar exercise on temporal patterns of plasma cortisol levels.

Plasma concentrations of cortisol were measured in 9 subjects form 0800 h to 1800 h at 10-min intervals during resting periods and 5 min intervals during exercise and recovery. This was done to assess to effect of exercise on the patterns of plasma cortisol levels. At 1000 h, 90 min exercise at a moderate work level (55% of Vo2 max) produced a transient rise in plasma cortisol which averaged 11.9 pg/100 ml (SE plus or minus 1.2) and introduced subsequent suppression of meal-related increase, At a lower work load (25% of Vo2 max) a similar transient rise occurred, avering 11.7 pg/100 ml (SE plus or minus 2.2); latency rate of concentration change and magnitude and not significatntly different from those at a moderate work load. A strenous work level was required to produce a more rapid response with an increased secretion rate. When 90 min exercise at a moderate work levels was preformed at 1300 h. (i.e. coinciding with postprandial cortisol concentration peak), the increase in plasma cortisol concentration (1.3 pg/100ml (SE plus or minus 0.3) was significantly lower than that induced by the same exercise performed in the morning. These results demonstrate that high plasma levels of cortisol diminish the subsequent stress response and that exercise-induced and meal-induced increases are not active.

Adult↗