Shawn D. Youngstedt

Sleep estimation from wrist movement quantified by different actigraphic modalities

Progress in transducer design and empirical characterization of wrist movement has led to diverse wrist activity monitors, each with its unique features and modality of operation. This study compared sleep--wake estimates from nocturnal wrist activity quantified by different motion-quantifying algorithms. Healthy young adults wore an Actillume and a Mini Motionlogger on the same wrist while nocturnal polysomnography data were recorded simultaneously in the laboratory. Activity data were analyzed with ACTION3 using scoring algorithms independently calibrated for each measurement modality. Overall, each modality yielded accurate and reliable sleep estimates relative to polysomnographic estimates (agreement rates: 91.4--96.5%, correlations for sleep duration: 0.79--0.94). Estimates derived from Actillume modalities were comparable to those of Mini Motionloggers, suggesting that the transducers of these two devices performed comparably for monitoring sleep and wakefulness. Wrist movement quantified by the Mini Motionlogger proportional-integrating mode yielded the best accuracy for detection of sleep--wake states.

The Effect of Exercise Training on Obstructive Sleep Apnea and Sleep Quality: A Randomized Controlled Trial

STUDY OBJECTIVES To evaluate the efficacy of a 12-week exercise training program for reducing obstructive sleep apnea (OSA) severity and improving sleep quality, and to explore possible mechanisms by which exercise may reduce OSA severity. DESIGN Randomized controlled trial. SETTING Clinical exercise physiology center, sleep laboratory. PARTICIPANTS Forty-three sedentary and overweight/obese adults aged 18-55 years with at least moderate-severity untreated OSA (screening apnea-hypopnea index [AHI] ≥ 15). INTERVENTIONS Participants randomized to exercise training (n = 27) met 4 times/week for 12 weeks and performed 150 min/week of moderate-intensity aerobic activity, followed by resistance training twice/week. Participants randomized to a stretching control (n = 16) met twice weekly for 12 weeks to perform low-intensity exercises designed to increase whole-body flexibility. MEASUREMENTS AND RESULTS OSA severity was assessed with one night of laboratory polysomnography (PSG) before and following the 12-week intervention. Measures of sleep quality included PSG, actigraphy (7-10 days), and the Pittsburgh Sleep Quality Index. Compared with stretching, exercise resulted in a significant AHI reduction (exercise: 32.2 ± 5.6 to 24.6 ± 4.4, stretching: 24.4 ± 5.6 to 28.9 ± 6.4; P < 0.01) as well as significant changes in oxygen desaturation index (ODI; P = 0.03) and stage N3 sleep (P = 0.03). Reductions in AHI and ODI were achieved without a significant decrease in body weight. Improvements in actigraphic sleep and subjective sleep quality were also noted following exercise compared with stretching. CONCLUSIONS Exercise training had moderate treatment efficacy for the reduction of AHI in sedentary overweight/obese adults, which suggests that exercise may be beneficial for the management of OSA beyond simply facilitating weight loss. TRIAL REGISTRATION Clinicaltrials.gov identification number NCT00956423.

Brain norepinephrine and metabolites after treadmill training and wheel running in rats.

Regional changes in concentrations of brain norepinephrine [NE] and its metabolites after chronic exercise have not been described for exercise protocols not confounded by other stressors. We examined levels of [NE], 3-methoxy-4-hydroxyphenylglycol [MHPG], and 3,4-dihydroxyphenylglycol [DHPG] in the frontal cortex, hippocampus, pons-medulla, and spinal cord after 8 wk of exercise. Male Sprague-Dawley rats (N = 36) were randomly assigned to three conditions: 1) 24-h access to activity wheel running (WR), 2) treadmill running (TR) at 0 degrees incline for 1 h.d-1 at 25-30 m.min-1, or 3) a sedentary control group (C). Levels (nmol.g-1) of [NE], [MHPG], and [DHPG] were assayed by high performance liquid chromatography with electrochemical detection. Planned contrasts (P < 0.05) indicated that exercise training increased succinate dehydrogenase activity (mmol cytochrome C reduced.min-1.g-1 wet weight) in soleus muscle for TR compared with WR or C. [NE] was higher in the pons-medulla and spinal cord for both TR and WR compared with C. [DHPG] was higher in the pons-medulla for TR compared with C, and [MHPG] was higher in the frontal cortex and in the hippocampus for TR compared with C. Our results suggest that treadmill exercise training is accompanied by brain noradrenergic adaptations consistent with increased metabolism of NE in areas containing NE cell bodies and ascending terminals, whereas treadmill running and wheel running are accompanied by increases in levels of NE in the areas of NE cell bodies and the spinal cord, independently of an exercise training effect.

Age-related changes of circadian rhythms and sleep-wake cycles

OBJECTIVES: To compare relationships between the sleep‐wake cycle and endogenous circadian rhythms in young and older adults and to examine correlates between evening naps and circadian rhythms in older adults.

Activity wheel running reduces escape latency and alters brain monoamine levels after footshock

We examined the effects of chronic activity wheel running on brain monoamines and latency to escape foot shock after prior exposure to uncontrollable, inescapable foot shock. Individually housed young (approximately 50 day) female Sprague-Dawley rats were randomly assigned to standard cages (sedentary) or cages with activity wheels. After 9-12 weeks, animals were matched in pairs on body mass. Activity wheel animals were also matched on running distance. An animal from each matched pair was randomly assigned to controllable or uncontrollable inescapable foot shock followed the next day by a foot shock escape test in a shuttle box. Brain concentrations of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-hydroxytryptamine (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed in the locus coeruleus (LC), dorsal raphe (DR), central amygdala (AC), hippocampus (CA1), arcuate nucleus, paraventricular nucleus (PVN), and midbrain central gray. After prior exposure to uncontrollable foot shock, escape latency was reduced by 34% for wheel runners compared with sedentary controls. The shortened escape latency for wheel runners was associated with 61% higher NE concentrations in LC and 44% higher NE concentrations in DR compared with sedentary controls. Sedentary controls, compared with wheel runners, had 31% higher 5-HIAA concentrations in CA1 and 30% higher 5-HIAA concentrations in AC after uncontrollable foot shock and had 28% higher 5-HT and 33% higher 5-HIAA concentrations in AC averaged across both foot shock conditions. There were no group differences in monoamines in the central gray or in plasma prolactin or ACTH concentrations, despite 52% higher DA concentrations in the arcuate nucleus after uncontrollable foot shock and 50% higher DOPAC/DA and 17% higher 5-HIAA/5-HT concentrations in the PVN averaged across both foot shock conditions for sedentary compared with activity wheel animals. The present results extend understanding of the escape-deficit by indicating an attenuating role for circadian physical activity. The altered monoamine levels suggest brain regions for more direct probes of neural activity after wheel running and foot shock.

Influence of exercise on human sleep.

Several research paradigms have been used to examine the influence of exercise on sleep. Epidemiological studies show that exercise is perceived as helpful in promoting sleep and suggest that regular physical activity may be useful in improving sleep quality and reducing daytime sleepiness. Additional epidemiological inquiry is clearly warranted based on the available evidence. Acute exercise experiments that have measured sleep physiology directly from subjects who either performed, or refrained from, daytime exercise indicate that exercise is associated with a small, but reliable increase in Stage 2 and slow wave sleep. The mechanism(s) that underlie exercise-associated increases in SWS is unknown. However, there is evidence that links elevations in daytime core body temperature to increases in SWS. Acute exercise experiments were found to be associated with a reduction in REM sleep and a delay in REM onset latency that were larger in magnitude than the effects observed for Stage 2 and SWS. These REM sleep observations highlight the need for continued study of the consequences of exercise on both circadian and homeostatic aspects of sleep. The delay in REM onset latency observed in the naturalistic acute exercise studies was consistent with the results of experiments in which environmental factors were more rigorously controlled and showed that physical exercise, or a concomitant, can induce a phase delay in markers of the human circadian pacemaker. It is worth pointing out that the most sophisticated and rigorous experiments from a standpoint of understanding sleep, such as those involving constant routines, bed rest, and temporal isolation, have for the most part used exercise in a crude manner. Because exercise is a stressor with diverse psychophysiological consequences that depends in part upon the interaction of multiple factors (e.g., the setting; degree of environmental heat stress; the activity history and fitness of the subject; the duration, intensity, and timing of the exercise bout; body position, etc.), understanding the influence of exercise on sleep will be stymied until carefully designed sleep studies also use exercise in an equally sophisticated and systematic way. Exercise is widely believed to have large effects on sleep. However, the scientific evidence does not strongly support this common belief. This incongruity may well be explained in part by considering the paradigms that have been used to study exercise and sleep.(ABSTRACT TRUNCATED AT 400 WORDS)

Phase-Shifting Human Circadian Rhythms With Exercise During the Night Shift

Appropriately timed exercise can phase shift the circadian rhythms of rodents. The purpose of this study was to determine whether exercise during the night shift could phase delay the temperature rhythm of humans to align with a daytime sleep schedule. Exercise subjects (N = 8) rode a stationary cycle ergometer for 15 min every h during the first 3 of 8 consecutive night shifts, whereas control subjects (N = 8) remained sedentary. All subjects wore dark welders goggles when outside after the night shift until bedtime, and then slept in dark bedrooms. Sleep was delayed 9 h from baseline. Rectal temperature was continuously measured. There were fewer evening-types and more morning-types in the exercise group than in the control group, which should have made phase delay shifts more difficult for the exercise group. Nevertheless, a majority of the exercise subjects (63%) had large temperature rhythm phase delay shifts ( > 6 h in the last 4 days relative to baseline), whereas only 38% of the control subjects had large shifts. An ANCOVA showed that, when morningness-eveningness was accounted for (as the covariate), the exercise group had a significantly larger temperature rhythm phase shift than the control group. As expected, there was a correlation between the temperature rhythm phase shift and morningness-eveningness in the control group, with greater eveningness resulting in larger phase shifts. However, there was no such relationship in the exercise group; exercise facilitated temperature rhythm phase shifts regardless of circadian type. These results suggest that exercise might be used to promote circadian adaptation to night shift work.

Effects of moderate aerobic exercise training on chronic primary insomnia

OBJECTIVE To evaluate the effect of long-term moderate aerobic exercise on sleep, quality of life, and mood of individuals with chronic primary insomnia, and to examine whether these effects differed between exercise in the morning and exercise in the late afternoon. METHODS Nineteen sedentary individuals with chronic primary insomnia, mean age 45.0 (standard error [SE] 1.9) years, completed a 6-month exercise training protocol, randomized to morning and late-afternoon exercise groups. RESULTS Combining polysomnographic data across both time points, this study found a significant decrease in sleep onset latency (from 17.1 [SE 2.6] min to 8.7 [SE 1.4] min; P<0.01) and wake time after sleep onset (from 63.2 [SE 12.8] min to 40.1 [SE 6.0] min), and a significant increase in sleep efficiency (from 79.8 [SE 3.0]% to 87.2 [SE 1.6]%) following exercise. Data from sleep diaries revealed significant improvement in sleep onset latency (from 76.2 [SE 21.5] min to 80.3 [SE 7.4] min) sleep quality (from 41.5 [SE 5.2]% to 59.4 [SE 6.6]%) and feeling rested in the morning (from 50.8 [SE 5.3] to 65.1 [SE 5.0]). There were generally no significant differences in response between morning and late-afternoon exercise. Following exercise, some quality-of-life measures improved significantly, and a significant decrease was seen in the following Profile of Mood State measures: tension-anxiety (from 7.2 [SE 1.0] to 3.5 [SE 1.0]), depression (from 5.9 [SE 1.2] to 3.3 [SE 1.1]) and total mood disturbance (from 9.2 [SE 4.8] to -1.7 [SE 4.8]). These effects did not vary between morning and late-afternoon exercise. CONCLUSION Long-term moderate aerobic exercise elicited significant improvements in sleep, quality of life and mood in individuals with chronic primary insomnia.

Increased open field locomotion and decreased striatal GABAA binding after activity wheel running.

Open-field behavior has been used to model reductions in anxiety-related behaviors in the rat after chronic physical activity. Plausible mechanisms for the increased open field locomotion observed after physical activity have not been studied. Open field locomotion is decreased by gamma-aminobutyric acid (GABA) and its agonists, and increased by GABA antagonists, in the ventral striatum. Hence, we tested the hypothesis that increased open field locomotion following chronic physical activity would be accompanied by a decrease in the number of GABAA receptors in the corpus striatum. Young (approximately 55 days) male Sprague-Dawley rats (N = 24) were randomly assigned to three conditions: 24-h access to an activity wheel (AW), running for 1 h without shock 6 days/week on a motorized treadmill (TM), or sedentary control (C). Open field locomotion (total and center squares traversed), defecation, and urination were assessed on each of 3 consecutive days prior to and again after 8 weeks of physical activity. Open field locomotion (total and center squares) increased after activity wheel running, decreased after treadmill training, and did not change for control animals. GABAA receptor density indicated by [3H] bicuculline binding (fmol/mg) was lower for activity wheel animals compared with treadmill animals and controls. GABA concentration (mumol/g) was not different between activity wheel and treadmill groups but was higher for both groups contrasted with controls. Our findings of decreased GABAA density in the corpus striatum concomitant with an increase in open field locomotion are consistent with an anxiolytic effect of chronic activity wheel running.

Actigraphy suggests age-related differences in napping and nocturnal sleep

The aim of this study was to contrast the time distribution of out‐of‐bed napping in young and older adults through recordings of wrist activity, and to evaluate the correlates of napping with nocturnal sleep. Seventy‐three young adults between 18 and 32 years and 60 older adults between 60 and 75 years of age participated in the study. Subjects were selected for good general health and had few sleep complaints. They wore wrist‐activity monitors and kept daily sleep logs for 1 week. Automatic sleep scoring was edited by the authors, supplemented by sleep logs and illumination data as well as activity data. Napping episodes were modestly increased in older adults, but there was no difference in the daily duration of napping. Older adults napped more in the evening (especially within 2 h before bedtime), whereas young adults napped more in the afternoon. The older adults with evening naps (n = 31) showed earlier nocturnal wake‐up times and decreased nocturnal sleep duration compared with the older adults without evening naps (n = 29). There was no difference in nocturnal sleep between young adults with afternoon naps (n = 32) and without afternoon naps (n = 41). In determining the effects of napping on nocturnal sleep, timing of napping and age are important. Maintaining alertness during the evening (e.g. by bright light exposure or moderate exercise) would be a possible approach to delay wake‐up times in older adults.