The effect of flow limitation on the cardiorespiratory response to arousal from sleep under controlled conditions of chemostimulation in healthy older adults.

The influence of flow limitation on the magnitude of the cardiorespiratory response to arousal from sleep is of interest in older people, because they experience considerable flow limitation and frequent arousals from sleep. We studied older flow-limiting subjects, testing the hypothesis that the cardiorespiratory activation response would be larger when arousal occurred during flow limitation, compared to no flow limitation, and chemical stimuli were controlled. In 11 older adults [mean ± standard deviation (SD) age: 68 ± 5 years] ventilation was stabilized using continuous positive airway pressure, and flow limitation was induced by dialling down the pressure. Partial pressure of end-tidal carbon dioxide (PetCO(2)) was maintained by titration of the inspired CO(2) and hyperoxia was maintained using 40% O(2) balanced with nitrogen. Flow limitation at the time of arousal did not augment cardiovascular activation response (heart rate P = 0.7; systolic blood pressure P = 0.6; diastolic blood pressure P = 0.3), whereas ventilation was greater following arousals during flow limitation compared to no flow limitation (P < 0.001). The pre-post-arousal differences in ventilation reflected significant pre-arousal suppression (due to flow limitation) plus post-arousal activation. In summary, the cardiovascular response to arousal from sleep is not influenced by flow limitation at the time of arousal, when chemical stimuli are controlled in older adults. This finding may contribute to the decreased cardiovascular burden associated with sleep-disordered breathing reported in older adults, although our data do not exclude the possibility that flow limitation in the presence of mild hypoxic hypercapnia could increase the cardiovascular response to arousal.

On the nature of cardiovascular activation at an arousal from sleep.

STUDY OBJECTIVES: The intent of the study was to explore the nature and function of the cardiovascular activation response that occurs at an arousal from sleep. DESIGN: Four experiments were conducted. The first compared the pattern of physiologic response to orienting and startle stimuli and arousal from sleep. The second and third measured the amplitude of the cardiovascular arousal response as a function of the trait of fearfulness and the threat value of the arousing stimulus, respectively. The final experiment assessed the effect of arousal duration. SETTING: The experiments were conducted in the sleep laboratory of the Department of Psychology, University of Melbourne. PARTICIPANTS: A total of 42 (24 women and 18 men) healthy individuals between the ages of 18 and 24 participated in the experiments. INTERVENTIONS: The experiments manipulated the stimuli to which participants were exposed (orienting and startle stimuli and arousal from sleep), the threat value of stimuli used to arouse participants from sleep, and individual differences in fearfulness. MEASUREMENTS AND RESULTS: The major dependent variables were heart rate, blood pressure, and a measure of peripheral vasoconstriction (digital pulse volume). In addition, in the first study, the galvanic skin response and orbicularis oculi electromyographic activity were measured. Experiment 1 showed that the pattern of physiologic response at an arousal from sleep differed, with a substantially larger cardiovascular component, from responses to orienting and startle stimuli. Experiments 2a and 2b indicated that the magnitude of the cardiovascular response at an arousal was unrelated to either individual differences in fearfulness or differences in the threat value of arousing stimuli. The final experiment showed that the cardiovascular response at an arousal was not a return to waking levels of activity but, rather, was a transient activation response. CONCLUSIONS: The study supported the view that the cardiovascular activation response at an arousal from sleep is a transient, reflex-like response that is different from the response that occurs during normal wakefulness.

Nature's clocks and human mood: the circadian system modulates reward motivation.

Existing literature on reward motivation pays scant attention to the fact that reward potential of the environment varies dramatically with the light/dark cycle. Evolution, by contrast, treats this fact very seriously: In all species, the circadian system is adapted to optimize the daily rhythm of environmental engagement. We used 3 standard protocols to demonstrate that human reward motivation, as measured in the dynamics of positive affect (PA), is modulated endogenously by the circadian clock. Under naturalistic conditions, 13.0% of PA variance was explained by a 24-hr sinusoid. In a constant routine protocol, 25.0% of PA variance was explained by the unmasked circadian rhythm in core body temperature (CBT). A forced desynchrony study showed PA to align with CBT in exhibiting circadian periodicity independent of a 28-hr sleep/wake cycle. It is concluded that the circadian system modulates reward activation, and implications for models of normal and abnormal mood are discussed.

The cardiorespiratory activation response at an arousal from sleep is independent of the level of CO(2).

Arousal from sleep is associated with transient cardiorespiratory activation. Traditionally, this response has been understood to be a consequence of state-dependent changes in the homeostatic control of ventilation. The hypothesis predicts that the magnitude of ventilatory and cardiac responses at an arousal will be a function of the intensity of concurrent respiratory stimuli (primarily PCO(2)). Alternatively, it has been proposed that increased cardiorespiratory activity is due to reflex activation. This hypothesis predicts that the magnitude of the cardiorespiratory response will be independent of respiratory stimuli. To compare these hypotheses we measured minute ventilation (V(i)), heart rate (HR) and blood pressure (BP) during wakefulness and stage 2 sleep, while manipulating P(et)CO(2). Further, we assessed the magnitude of the response of these variables to an arousal from sleep at the various levels of P(et)CO(2). The subjects were male aged 18-25 years. P(et)CO(2) was manipulated by clamping it at four levels during wakefulness [wake eucapnic, sleep eucapnic (Low), and sleep eucapnic +3 mmHg (Medium) and +6 mmHg (High)] and three levels during sleep (Low, Medium and High). The average number of determinations for each subject at each level was 14 during wakefulness and 25 during sleep. Arousals were required to meet American Sleep Disorders Association criteria and were without body movement. The results indicated that average increases in V(i), HR and BP at arousal from sleep did not significantly differ as a function of the level of P(et)CO(2) present at the time of the arousal (all P > 0.05). Further, the magnitude of the ventilatory response to an arousal was significantly less than the values predicted by the homeostatic hypothesis (P < 0.05). We conclude that, in normal subjects, the cardiorespiratory response to an arousal from sleep is not because of a homeostatic response, but of a reflex activation.

The influence of sleep onset on the diurnal variation in cardiac activity and cardiac control.

Heart rate (HR), blood pressure (BP) and autonomic nervous system (ANS) activity vary diurnally, with a reduction in HR and BP, and a shift to vagal dominance during the dark phase. However, the cause of these changes, particularly the relative influence of sleep and circadian mechanisms, remains uncertain. The present study assessed the effect of sleep onset on HR, BP, high frequency (HF) component of heart rate variability (HRV), low frequency/high frequency (LF/HF) ratio and pre-ejection period (PEP). Sleep onset was dissociated from circadian influences by having subjects go to sleep at two different circadian phases, their normal time of sleep onset (normal sleep onset, NSO), and after a delay of 3 h (delayed sleep onset, DSO). The assumption was that changes caused by sleep onset would occur in association with sleep onset, irrespective of its timing, while circadian effects would have a consistent circadian phase and be independent of when sleep onset occurred. Thirteen and 17 subjects were run in the NSO and DSO conditions, respectively. Following a 1-h adaptation period, data collection began 2 h before subjects' normal time of sleep onset and continued until morning awakening. The lights were turned out after 2 h in the NSO condition and 5 h in the DSO condition. Subjects were required to maintain a supine position throughout the experimental sessions. The night-time decrease in HR was found to be due to both sleep onset and a circadian influence, with the circadian component being more prominent. In contrast, the fall in BP was largely due to a sleep onset effect. Increased vagal activity, as reflected in the HF component and a shift to vagal dominance in the LF/HF ratio, appeared to be primarily a function of the sleep system, while sympathetic activity, as assessed by PEP, reflected a circadian influence.