Biomedical subjects

J Trinder

Publications and source records attributed to J Trinder.

At least 37 records · Page 2Linked to original sources

PubMed1998

Load compensation as a function of state during sleep onset.

Ventilation decreases and airway resistance increases with the loss of electroencephalogram alpha activity at sleep onset. The aim of this study was to determine whether reflexive load compensation is lost immediately on the loss of alpha activity. Six healthy male subjects were studied under two conditions (load and control-no load), in three states (continuous alpha, continuous theta, and immediately after a transition from alpha to theta), and in two phases (early and late sleep onset). Ventilation and respiratory timing were measured. A comparison of loaded with control conditions indicated that loading had no effect on inspiratory minute ventilation during continuous alpha (differential effect of 0.00 l/min) and only a small, nonsignificant effect in theta immediately after phase 2 transitions (0.31 l/min), indicating a preservation of load compensation at these times. However, there were significant decreases in inspiratory minute ventilation on loaded trials during continuous theta in phase 2 (0.77 l/min) and phase 3 (1.15 l/min) and during theta immediately after a transition in phase 3 (0.87 l/min), indicating a lack of reflexive load compensation. The results indicate that, because reflex load compensation is state dependent, state-related changes in airway resistance contribute to state-related changes in ventilation during sleep onset. However, this effect was slightly delayed with transitions into theta early in sleep.

Adult↗

PubMed1998

Activity of respiratory pump and upper airway muscles during sleep onset.

Ventilation decreases at sleep onset. This change is initiated abruptly at alpha-theta electroencephalographic transitions. The aim of this study was to determine the contributions of reduced activity in respiratory pump muscles and upper airway dilator muscles to this change. Surface electromyograms over the diaphragm (Di) and intercostal muscles and fine-wire intramuscular electrodes in genioglossus (GG) and tensor palatini (TP) muscles were recorded in nine healthy young men. It was shown that phasic Di and both phasic and tonic TP activities were lower during theta than during alpha activity. Breath-by-breath analysis of the changes at alpha-theta transitions during the sleep-onset period showed a number of changes. At alpha-theta transitions, phasic activity of Di, intercostal, and GG muscles fell and rose again, and phasic and tonic activities of TP fell and remained at low levels during theta. With a state transition from theta to alpha, the phasic and tonic activities of the Di, GG, and TP increased dramatically. It is now clear that the fall in ventilation that occurs with sleep is related to a fall in activities of both upper airway dilator muscles and respiratory pump muscles.

Adolescent↗

PubMed1997

Sleep and circadian influences on cardiac autonomic nervous system activity.

To assess the separate contributions of the sleep and circadian systems to changes in cardiac autonomic nervous system (ANS) activity, 12 supine subjects participated in two 26-h constant routines, which were counterbalanced and separated by 1 wk. One routine did not permit sleep, whereas the second allowed the subjects to sleep during their normal sleep phase. Parasympathetic nervous system activity was assessed with respiratory sinus arrhythmia as measured from the spectral analysis of cardiac beat-to-beat intervals. Sympathetic nervous system activity was primarily assessed with the preejection period as estimated from impedance cardiography, although the 0.1-Hz peak from the spectral analysis of cardiac beat-to-beat intervals, the amplitude of the T wave in the electrocardiogram, and heart rate were also measured. Respiratory sinus arrhythymia showed a 24-h rhythm independent of sleep, whereas preejection period only showed a 24-h rhythm if sleep occurred. Thus the findings indicate that parasympathetic nervous system activity is mostly influenced by the circadian system, whereas sympathetic nervous system activity is mostly influenced by the sleep system.

Adult↗

PubMed1997

Gender differences in airway resistance during sleep.

At the onset of non-rapid-eye-movement (NREM) sleep there is a fall in ventilation and an increase in upper airway resistance (UAR). In healthy men there is a progressive increase in UAR as NREM sleep deepens. This study compared the pattern of change in UAR and ventilation in 14 men and 14 women (aged 18-25 yr) both during sleep onset and over the NREM phase of a sleep cycle (from wakefulness to slow-wave sleep). During sleep onset, fluctuations between electroencephalographic alpha and theta activity were associated with mean alterations in inspiratory minute ventilation and UAR of between 1 and 4.5 l/min and between 0.70 and 5.0 cmH2O . l-1 . s, respectively, with no significant effect of gender on either change (P > 0.05). During NREM sleep, however, the increment in UAR was larger in men than in women (P < 0.01), such that the mean levels of UAR at peak flow reached during slow-wave sleep were approximately 25 and 10 cmH2O . l-1 . s in men and women, respectively. We speculate that the greater increase in UAR in healthy young men may represent a gender-related susceptibility to sleep-disordered breathing that, in conjunction with other predisposing factors, may contribute to the development of obstructive sleep apnea.

Adolescent↗

PubMed1997

Correlation between ventilation and EEG-defined arousal during sleep onset in young subjects.

In studies of elderly individuals, ventilation and EEG-defined arousal have been shown to vary periodically and synchronously. Such results have been interpreted as indicating the primacy of sleep/wake state in causing ventilatory instability during sleep onset. However, because the elderly individuals studied were periodic breathers, the results do not unequivocally support this conclusion. In this study the relationship between ventilation and EEG-defined arousal was assessed in a group of 21 young, healthy men in whom ventilatory instability during sleep onset was not periodic. Ventilation and EEG (O1-A2) recordings were collected, and the longest uncontaminated periods from early and late in sleep onset were selected for subsequent analysis. The 84 time series (21 subjects, 2 variables, and 2 occasions in sleep onset) were subjected to spectral analysis to identify periodicity, and the relationship between the two variables was determined by cross-correlational methods. The results indicated that the time series were nonperiodic, yet significant correlations were observed between the two variables. The data support the view that during sleep onset ventilatory instability is driven primarily by variations in sleep/wake arousal level.

Adolescent↗

PubMed1996

Sociotropy, autonomy, and dysphoric emotional responses to specific classes of stress: a psychophysiological evaluation.

The aim of this study was to assess the ability of trait measures of sociotropy and autonomy to predict immediate emotional responses to imagery conditions depicting social rejection and achievement failure. Emotional responses were assessed by self-report techniques and by 2 putative psychophysiological measures of dysphoric mood: heart rate and facial muscle activity. Undergraduate volunteers (N = 100) were assessed for sociotropic and autonomous traits, general levels of depression, and sensory imagery ability, before performing a series of imagery trials depicting neutral and stressful (social rejection and achievement failure) scenes. Results provided support for the role of sociotropy as a vulnerability factor to dysphoric response to social rejection and to a lesser degree for achievement failure, but there was no support for autonomy as a vulnerability factor for either type of stressful script.

Achievement↗

PubMed1996

Inhibition of melatonin secretion onset by low levels of illumination.

Melatonin is a hormone released during darkness under the control of the hypothalamic circadian pacemaker. It has been shown that melatonin is suppressed by light as a function of intensity, with low levels of illumination producing small effects and more intense light greater, but not complete inhibition. The studies which lead to these conclusions administered light subsequent to the secretion pattern being well established. Light as low as 250 lux administered during the normal onset of secretion can reduce melatonin to below detectable levels. The onset of melatonin secretion was delayed for at least an hour during 250 lux exposure and did not rise until termination of light exposure (two hours after control melatonin onset) with higher illumination (500, 1000 and 2500 lux). This tentatively indicates that duration of the inhibition is intensity dependent. It is suggested that the experimental paradigm used in the present study may be a more realistic representation of the effect of normal light exposure (both natural and artificial) on the circadian system, and that findings may be pertinent to the aetiology of certain sleep onset insomnias, which would include delayed sleep phase syndrome (DSPS) and adaptation to shift work.

Adolescent↗

PubMed1996

Cardiac parasympathetic nervous system activity does not increase in anticipation of sleep.

Parasympathetic Nervous System (PNS) activity increases while Sympathetic Nervous System (SNS) activity remains relatively stable from wakefulness to NREM sleep. However, it is not clear whether these changes are specifically associated with NREM sleep, or whether they anticipate sleep onset. The latter may occur if ANS activity was influenced by the circadian system. This issue was investigated by conducting spectral analysis of heart beat-to-beat intervals (Periodogram method), collected from 20 healthy male and female subjects at three different times across 24 h; in the morning, just prior to normal sleep onset time, and in slow-wave sleep (SWS). Subjects were supine in all conditions and awake in the first two conditions. The high- and low-frequency peaks, reflecting PNS and SNS activity, respectively, were expressed as proportions of the total power. PNS activity decreased significantly from the morning (0.22) to the presleep period (0.19), before it increased to its maximum during SWS (0.33). In contrast, SNS activity was similar in each of the three conditions (0.07, 0.06, and 0.05 for morning, presleep and SWS, respectively). Thus there do not appear to be changes in PNS activity in anticipation of sleep, as would be predicted on the basis of a circadian influence on the PNS. Instead the increased PNS activity appears to be sleep dependent.

Adolescent↗

PubMed1996

Progressive changes in airway resistance during sleep.

Ventilation (V) decreases during sleep while upper airway resistance (UAR) increases. A number of studies have suggested that in normal healthy individuals the changes in the two variables are reciprocal. Other findings, however, suggest that the relationship between V and UAR may change as non-rapid-eye-movement (NREM) sleep progresses such that most of the change in V occurs early during the sleep period, whereas the most marked changes in UAR occur later during established NREM sleep. However, no study has examined the progressive development of changes in both V and UAR over the NREM sleep period. This study examined V and UAR over one NREM sleep period in two groups of healthy young male subjects: a "slow-wave sleep (SWS) group" (n = 8) in which the subjects obtained the full range of NREM sleep stages from wakefulness to stage 4 NREM sleep and a "no-SWS group" (n = 5) in which the subjects did not attain SWS but spent a prolonged period in stage 2 NREM sleep that was repeatedly interrupted by arousals. Results showed that the most marked changes in V occurred early during the sleep period in association with relatively small increases in UAR. Once NREM sleep became established, further attenuation of V was minimal despite marked and progressive increases in UAR. The progressive increase in UAR occurred in association with increasing delta (0.4- to 3.0-Hz) electroencephalographic activity and did not occur in the no-SWS group. We interpret these findings to indicate that factors in addition to UAR contribute to the reduction in V early in sleep onset, whereas later, during NREM sleep, compensatory mechanisms are activated to allow for maintenance of V in the context of larger increases in UAR.

Adult↗

PubMed1996

Interaction of chemical and state effects on ventilation during sleep onset.

Ventilation varies as a function of state, being higher during wakefulness (as indicated by alpha electroencephalogram activity) than during sleep (theta activity). A recent experiment observed a progressive increase in the magnitude of these state-related fluctuations in ventilation over the sleep-onset period (28). The aim of the present experiment was to test the hypothesis that this effect resulted from chemical (feedback-related) amplification of state effects on ventilation. A hyperoxic condition was used to eliminate peripheral chemoreceptor activity. It was hypothesized that hyperoxia would reduce the amplification of changes in ventilation associated with electroencephalogram state transitions. Ventilation was measured over the sleep-onset period under both hyperoxic and normoxic conditions in 10 young healthy male subjects. Sleep onsets were divided into three phases. Phase 1 corresponded to presleep wakefulness; and phases 2 and 3 corresponded to early and late sleep onset, respectively. The magnitudes of state-related changes in ventilation during phases 2 and 3, and under hyperoxic and normoxic conditions were compared using a phase by condition analysis of variance. Results revealed a significant phase by condition interaction, confirming that hyperoxia reduced the amplification of state-related changes in ventilation by selectively decreasing the magnitude of phase 3 state changes in ventilation. However, some degree of amplification was evident during hyperoxia, thus the results demonstrated that peripheral chemoreceptor activity contributed to the amplification of state-related changes in ventilation but that additional factors may also be involved.

Adolescent↗

PubMed1995

Individual differences in relationship between upper airway resistance and ventilation during sleep onset.

Sleep-induced hypoventilation is caused partly by inadequate compensation for elevated upper airway resistance (UAR). Some evidence suggests that the effect of UAR on ventilation may vary among individuals. The relationship between minute ventilation (VI) and UAR was examined in 26 healthy young men (average of 10.12 sleep onsets). Variables were analyzed over transitions between wakefulness (defined by alpha electroencephalographic activity) and sleep (theta electroencephalographic activity). Transitions to sleep were associated with increases in UAR in synchrony with reductions in VI, and equally rapid opposite changes occurred with awakenings. The relationship between the magnitudes of the changes in VI and UAR at transitions varied among subjects, accounting for 30% of the variance for alpha-to-theta transitions and 50% of the variance for theta-to-alpha transitions. Results indicated that, although ventilatory changes during sleep onset are partly a consequence of changes in UAR, alterations in UAR do not account fully for alterations in VI. Other factors that may contribute to ventilatory instability during sleep onset include state-related fluctuations in drive to the primary respiratory muscles and variability in compensatory mechanisms.

Adult↗

PubMed1994

Changes in airway resistance during sleep onset.

Ventilation is lower during sleep than wakefulness. An increase in airway resistance has been proposed as the critical factor. As the change in ventilation has been shown to occur abruptly at transitions between alpha and theta electroencephalogram activity, it was of interest to determine whether the increase in airway resistance between wakefulness and sleep also occurs at these transitions. Three young healthy male subjects were run for an average of 15 sleep onsets in each of three conditions. The three conditions were 1) an esophageal balloon was put in place to allow the measurement of airway resistance, 2) in addition to an esophageal balloon the nose was occluded, and 3) there was no esophageal balloon and the nose was not occluded. Ventilation and airway resistance were measured during sleep onset and analyzed as a function of arousal state. In those conditions of the experiment in which airway resistance was affected by state, the changes, like those in ventilation, occurred at transitions between alpha and theta electroencephalogram activity. However, in the three subjects studied, the magnitude of ventilatory changes at alpha-theta transitions and the extent to which changes in ventilation were associated with changes in airway resistance differed between subjects. It was concluded that although inspiratory airway resistance is a major component affecting the state-related changes in ventilation at sleep onset, the degree of its contribution may vary over individuals.

Adult↗

PubMed1992

Respiratory instability during sleep onset.

It has been hypothesized that regulatory control in the respiratory system is state dependent. According to this view respiratory instability during sleep onset is a consequence of repeated fluctuations in arousal state. However, these speculations are based primarily on measurements during stable sleep, not during sleep onset itself. The aim of the present study was to assess changes in ventilation and gas tensions during sleep onset as a function of arousal state. Twenty-one subjects (12 males and 9 females, mean age 20 yr) were assessed over an average of 11.3 sleep onsets. The subject's state was classified as alpha, theta, body movement, or stage 2 sleep, and expiratory tidal volume, minute ventilation, respiratory rate, and end-tidal CO2 and O2 were measured by means of a face mask, valve, and pneumotachograph on a breath-by-breath basis. Respiratory instability during sleep onset was found to be a result of two factors. The first factor was a between-state effect in which transitions from alpha to theta were associated with falls, and from theta to alpha with increases, in ventilation. The magnitude of the change was a positive function of metabolic drive at the time of the state change (as indicated by alveolar PCO2 and PO2 levels). The second was a within-state effect in which ventilation fell during consecutive alpha breaths and increased during consecutive theta breaths. These changes were due to the influence of the relative hyperventilation of the alpha state and the relative hypoventilation of the theta state on metabolic drive.

Adult↗

PubMed1990

Behavioural and EEG responses to auditory stimuli during sleep in newborn infants and in infants aged 3 months.

Two studies were conducted in order to assess EEG and behavioural responsiveness to auditory stimuli as a function of sleep state in infants. The subjects in the first experiment were 11 infants aged 3 months, and in the second study the responsiveness of 8 infants aged 3 months was compared with that of 8 newborn infants. The stimuli ranged in intensity from 36 to 90 dB and were presented using a modification of the method of constant stimuli. The occurrence and intensity of behavioural responses were recorded by a trained observer. Electroencephalogram (EEG) responses were defined as EEG desynchronization and were identified by a Fast Fourier Transform algorithm. The results of the two studies showed that infants were more responsive during active sleep (AS) than during quiet sleep (QS) and gave behavioural responses at lower stimulus intensities than EEG responses. Behavioural responsiveness and EEG responsiveness during AS increased as a function of age, while EEG responsiveness during QS decreased. The marked suppression of EEG responsiveness during QS at 3 months of age is thought to be a consequence of developmental changes in sleep mechanisms--an effect which may have clinical implications.

Age Factors↗

PubMed1990

Ventilation during sleep onset in young adult females.

Ventilation is known to decrease from wakefulness to non-rapid-eye-movement sleep. In males, the change is associated with the commencement of theta activity in the electroencephalogram (EEG). The magnitude of the decrease is greater than that required by the reduction in metabolic rate at sleep onset and it has been suggested that the nonmetabolic component reflects the loss of a wakefulness drive to respiration. The effect of sleep onset on ventilation in female subjects was of interest because previous studies on changes in respiratory activity during sleep in this population have produced inconsistent results, a phenomenon that may relate to the menstrual cycle and the role of progesterone in respiratory activity. The present experiment sought to investigate ventilation during sleep onset in young adult females as a function of the menstrual cycle, and to compare the results with data collected from male subjects in an earlier experiment. Sleep onset was studied in five subjects in a series of single subject designs. The data were consistent with those of the male subjects and showed decreases in ventilation associated with the onset of theta activity in the EEG. Furthermore, no menstrual phase differences were apparent. The results indicate that in females, as in males, sleep is associated with loss of a wakefulness drive to ventilation.

Adolescent↗

PubMed1990

The effect of afternoon body heating on body temperature and slow wave sleep.

Recent evidence suggests that body temperature at sleep onset affects the subsequent level of slow wave sleep. According to one hypothesis, the actual temperature is the critical factor determining the relationship. An alternative proposal is that it is the rate of fall of body temperature following sleep onset. These hypotheses were tested by measuring rectal temperature and sleep, following late afternoon passive heating in a warm bath and during a control condition. Passive heating increased rectal temperature, which then returned rapidly toward the control level. However, immediately before lights out rectal temperature was still higher in the passive heating condition, a difference that continued throughout the night. Following passive heating the amount of slow wave sleep was higher in the early part of the night. These results support the hypothesis that body temperature at sleep onset and the amount of slow wave sleep are positively related.

Adult↗

PubMed1989

Effect of sleep and circadian cycle on sleep period energy expenditure.

Energy expenditure is lower during sleep than relaxed wakefulness. However, there is disagreement as to the particular metabolic changes that produce the difference. The present study assessed the contribution of sleep, circadian cycle, and the specific dynamic action effect of the evening meal to the sleep period fall in metabolic rate. Five subjects were tested for a total of nine nights under three conditions in a repeated-measures design. Subjects were confined to bed throughout their usual sleep period but were instructed to go to sleep 0, 3, or 6 h after their usual time for lights out. O2 consumption was measured in all conditions for the 0.5 h before and after each of the times for lights out and then throughout the sleep period after lights out. The results demonstrated that changes in energy expenditure during the sleep period are a function of both sleep and circadian cycle. In this study, the contribution of the two components was approximately equal. However, the effect of sleep was rapid asymptoting within 15 min of sleep onset, whereas that of circadian cycle was constant over the assessment period.

Adult↗

PubMed1988

The effect of exercise on sleep: the negative view.

Theories of sleep typically view sleep as having a compensatory relationship to wakefulness. This hypothesis leads to the prediction that physical exercise will cause both sleep duration and the amount of slow wave sleep (SWS) to be higher on the following night. Three previous reviews of the literature, while not agreeing in detail, have generally supported the hypothesis. It is argued that, in two of these reviews in particular, the extent of the positive evidence was overstated. Consistent with this interpretation the subsequent literature is also negative with regard to the hypothesis. Further, physical fitness, which occurs as a result of long periods of physical training, is not consistently associated with either longer sleep durations, or higher levels of SWS. While there is some evidence that exercise may have indirect effects on sleep under a limited range of circumstances, there is no evidence to support the hypothesis that physical exercise directly causes, or is reliably associated with, longer sleep durations or higher levels of SWS.

Exercise↗