Scn1a dysfunction alters behavior but not the effect of stress on seizure response.

Mutations in the voltage-gated sodium channel gene SCN1A are responsible for a number of epilepsy disorders, including genetic epilepsy with febrile seizures plus (GEFS+) and Dravet syndrome. In addition, dysfunction in SCN1A is increasingly being linked to neuropsychiatric abnormalities, social deficits and cognitive disabilities. We have previously reported that mice heterozygous for the SCN1A R1648H mutation identified in a GEFS+ family have infrequent spontaneous seizures, increased susceptibility to chemically and hyperthermia-induced generalized seizures and sleep abnormalities. In this study, we characterized the behavior of heterozygous mice expressing the SCN1A R1648H mutation (Scn1a(RH/+)) and the effect of stress on spontaneous and induced seizures. We also examined the effect of the R1648H mutation on the hypothalamic-pituitary-adrenal (HPA) axis response. We confirmed our previous finding that Scn1a(RH/+) mutants are hyperactive, and also identified deficits in social behavior, spatial memory, cued fear conditioning, pre-pulse inhibition and risk assessment. Furthermore, while exposure to a stressor did increase seizure susceptibility, the effect seen in the Scn1a(RH/+) mutants was similar to that seen in wild-type littermates. In addition, Scn1a dysfunction does not appear to alter HPA axis function in adult animals. Our results suggest that the behavioral abnormalities associated with Scn1a dysfunction encompass a wider range of phenotypes than previously reported and factors such as stress exposure may alter disease severity in patients with SCN1A mutations.

Alternating stimulation of synergistic muscles during functional electrical stimulation cycling improves endurance in persons with spinal cord injury.

Therapeutic effects of functional electrical stimulation (FES) cycling for persons with spinal cord injury (SCI) are limited by high rates of muscular fatigue. FES-cycling performance limits and surface mechanomyography (MMG) of 12 persons with SCI were compared under two different stimulation protocols of the quadriceps muscles. One strategy used the standard "co-activation" protocol from the manufacturer of the FES cycle which involved intermittent simultaneous activation of the entire quadriceps muscle group for 400 ms. The other strategy was an "alternation" stimulation protocol which involved alternately stimulating the rectus femoris (RF) muscle for 100 ms and the vastus medialis (VM) and vastus lateralis (VL) muscles for 100 ms, with two sets with a 400 ms burst. Thus, during the alternation protocol, each of the muscle groups rested for two 100 ms "off" periods in each 400 ms burst. There was no difference in average cycling cadence (28 RPM) between the two protocols. The alternation stimulation protocol produced longer ride times and longer virtual distances traveled and used lower stimulation intensity levels with no differences in average MMG amplitudes compared to the co-activation protocol. These results demonstrate that FES-cycling performance can be enhanced by a synergistic muscle alternation stimulation strategy.

Functional electrical stimulation cycling improves body composition, metabolic and neural factors in persons with spinal cord injury.

Persons with spinal cord injury (SCI) are at a heightened risk of developing type II diabetes and cardiovascular disease. The purpose of this investigation was to conduct an analysis of metabolic, body composition, and neurological factors before and after 10 weeks of functional electrical stimulation (FES) cycling in persons with SCI. Eighteen individuals with SCI received FES cycling 2-3 times per week for 10 weeks. Body composition was analyzed by dual X-ray absorptiometry. The American Spinal Injury Association (ASIA) neurological classification of SCI test battery was used to assess motor and sensory function. An oral glucose tolerance (OGTT) and insulin-response test was performed to assess blood glucose control. Additional metabolic variables including plasma cholesterol (total-C, HDL-C, LDL-C), triglyceride, and inflammatory markers (IL-6, TNF-alpha, and CRP) were also measured. Total FES cycling power and work done increased with training. Lean muscle mass also increased, whereas, bone and adipose mass did not change. The ASIA motor and sensory scores for the lower extremity significantly increased with training. Blood glucose and insulin levels were lower following the OGTT after 10 weeks of training. Triglyceride levels did not change following training. However, levels of IL-6, TNF-alpha, and CRP were all significantly reduced.

Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling.

Perinatal ischemic-anoxic and prolonged anoxic insults lead to impaired dopaminergic signaling and are hypothesized to contribute, at least in part, to the pathogenesis of disorders of minimal brain dysfunction such as attention-deficit hyperactivity disorder. We hypothesized that subtle intermittent hypoxic insults, occurring during a period of critical brain development, are also pathogenic to dopaminergic signaling, thereby contributing to behavioral and executive dysfunction. Between postnatal days 7 and 11, rat pups were exposed to either 20-s bursts of isocapnic hypoxic gas, compressed air, or were left undisturbed with the dam. On postnatal days 23 pups were instrumented with electroencephalographic/electromyographic electrodes and sleep-wake architecture was characterized. Locomotor activity was assessed between postnatal days 35 and 38, learning, and working memory evaluated between postnatal days 53 and 64. Rats were killed on postnatal day 80 and tyrosine hydroxylase, vesicular monoamine transporter, dopamine transporter, and dopamine D1 receptors were quantified in the prefrontal cortex, primary sensorimotor cortex, and precommissural striatum by Western blot analyses. Post-hypoxic pups spent less time awake and more time in rapid-eye-movement sleep during the lights-on phase of the circadian cycle, were hyperlocomotive, and expressed impaired working memory. Striatal expression of vesicular monoamine transporter and D1 receptor proteins were increased in post-hypoxic rats, consistent with depressed dopaminergic signaling. These observations lead to the intriguing hypothesis that intermittent hypoxia occurring during a period of critical brain development evokes behavioral and neurochemical alterations that are long lasting, and consistent with disorders of minimal brain dysfunction.

Effects of walking poles on lower extremity gait mechanics.

PURPOSE: The purpose of this study was to determine whether walking with poles reduces loading to the lower extremity during level over ground walking. METHODS: Three-dimensional gait analysis was conducted on 13 healthy adults who completed 10 walking trials using three different poling conditions (selected poles, poles back, and poles front) and without the use of poles (no poles). The inverse dynamics approach was used to calculate kinetic data via anthropometric, kinematic, and kinetic data. RESULTS: All walking with poles conditions increased walking speed (P = 0.0001-0.0004), stride length (P < 0.0001), and stance time (P < 0.0001) compared with the no poles condition. There also was a decrease in anterior-posterior GRF braking impulse (P = 0.0001), a decrease in average vertical GRF walking with poles (P < 0.0001-0.0023), and a decrease in vertical (compressive) knee joint reaction force (P < 0.0001-0.0041) compared with the no poles condition. At the knee, extensor impulse decreased a 7.3% between the no poles and selected poles conditions (P = 0.0083-0.0287) and 10.4% between the no poles and poles back conditions (P < 0.0001). The support moment was reduced between the no poles and poles back (P = 0.0197) and poles front (P = 0.0002) conditions. Ankle plantarflexor work (A2) was reduced in the poles-front condition (P = 0.0334), but no differences were detected in all other ankle, knee or hip power and work variables (P > 0.05). CONCLUSION: There were differences in kinetic variables between walking with and without poles. The use of walking poles enabled subjects to walk at a faster speed with reduced vertical ground reaction forces, vertical knee joint reaction forces, and reduction in the knee extensor angular impulse and support moment, depending on the poling condition used.

A common cause of altered mental status occurring at an uncommon age.

Wernicke's encephalopathy is a neurologic disorder due to a nutritional deficiency of thiamine, characterized by ocular palsies, ataxia, and altered mental activity. While Wernicke's encephalopathy is commonly attributed to alcoholism in the adult population, it has been described in children receiving prolonged parenteral nutrition and those with malignancies and AIDS. The disease, however, is rarely diagnosed in the pediatric population during life. We report a case of Wernicke's encephalopathy in a child with prolonged starvation and aim to improve awareness of a potentially fatal but treatable disease.

Intra-articular knee joint effusion induces quadriceps avoidance gait patterns.

OBJECTIVES: (1) To identify adaptations caused by intra-articular knee joint effusion during walking and (2) to determine if knee joint effusion may be a causative factor in promoting quadriceps avoidance gait patterns. DESIGN: Gait testing of 14 healthy individuals who underwent incremental saline injections of the knee joint capsule.Background. Gait adaptations have been reported in the literature for knee injured and rehabilitating individuals. Knee joint capsular afferent activity can influence knee joint function. METHODS: Gait analysis was employed in a pre- and post-test, repeated measures design to determine lower extremity joint kinematics, kinetics, energetics and thigh EMG adaptations due to intra-articular knee joint effusion. RESULTS: Knee effusion caused an increase in hip and knee flexion through the stance phase. Knee extensor torque, impulse and negative and positive work were diminished with increased effusion levels. Quadriceps activity decreased and hamstring activity increased due to intra-articular knee joint effusion. DISCUSSION: These adaptations cannot be attributed to an injury, surgery or rehabilitation. Thus, the results of this experiment suggest knee joint capsular distention, via knee joint effusion, may be responsible for many gait adaptations reported for knee injured individuals in previous investigations. CONCLUSIONS: Knee joint effusion and the subsequent capsular distention can cause major alterations in the normal gait cycle and can be considered a causative factor promoting the acquisition of quadriceps avoidance gait patterns. RELEVANCE: This study provides reference data on the effects of intra-articular knee joint effusion on gait parameters by which future studies of injured or rehabilitating individuals can be compared.

Serratus anterior muscle activity during selected rehabilitation exercises.

The purpose of this study was to document the electromyographic activity and applied resistance associated with eight scapulohumeral exercises performed below shoulder height. We used this information to design a continuum of serratus anterior muscle exercises for progressive rehabilitation or training. Five muscles in 20 healthy subjects were studied with surface electrodes for the following exercises: shoulder extension, forward punch, serratus anterior punch, dynamic hug, scaption (with external rotation), press-up, push-up plus, and knee push-up plus. Electromyographic data were collected from the middle serratus anterior, upper and middle trapezius, and anterior and posterior deltoid muscles. Each exercise was partitioned into phases of increasing and decreasing force and analyzed for average and peak electromyographic amplitude. Resistance was provided by body weight, an elastic cord, or dumbbells. The serratus anterior punch, scaption, dynamic hug, knee push-up plus, and push-up plus exercises consistently elicited serratus anterior muscle activity greater than 20% maximal voluntary contraction. The exercises that maintained an upwardly rotated scapula while accentuating scapular protraction, such as the push-up plus and the newly designed dynamic hug, elicited the greatest electromyographic activity from the serratus anterior muscle.

Percent of oxygen saturation of arterial hemoglobin among Bolivian Aymara at 3,900-4,000 m.

A range of variation in percent of oxygen saturation of arterial hemoglobin (SaO2) among healthy individuals at a given high altitude indicates differences in physiological hypoxemia despite uniform ambient hypoxic stress. In populations native to the Tibetan plateau, a significant portion of the variance is attributable to additive genetic factors, and there is a major gene influencing SaO2. To determine whether there is genetic variance in other high-altitude populations, we designed a study to test the hypothesis that additive genetic factors contribute to phenotypic variation in SaO2 among Aymara natives of the Andean plateau, a population geographically distant from the Tibetan plateau and with a long, separate history of high-altitude residence. The average SaO2 of 381 Aymara at 3,900-4,000 m was 92+/-0.15% (SEM) with a range of 84-99%. The average was 2.6% higher than the average SaO2 of a sample of Tibetans at 3,800-4,065 m measured with the same techniques. Quantitative genetic analyses of the Aymara sample detected no significant variance attributable to genetic factors. The presence of genetic variance in SaO2 in the Tibetan sample and its absence in the Aymara sample indicate there is potential for natural selection on this trait in the Tibetan but not the Aymara population.

Hemoglobin concentration of high-altitude Tibetans and Bolivian Aymara.

Elevated hemoglobin concentrations have been reported for high-altitude sojourners and Andean high-altitude natives since early in the 20th century. Thus, reports that have appeared since the 1970s describing relatively low hemoglobin concentration among Tibetan high-altitude natives were unexpected. These suggested a hypothesis of population differences in hematological response to high-altitude hypoxia. A case of quantitatively different responses to one environmental stress would offer an opportunity to study the broad evolutionary question of the origin of adaptations. However, many factors may confound population comparisons. The present study was designed to test the null hypothesis of no difference in mean hemoglobin concentration of Tibetan and Aymara native residents at 3,800-4,065 meters by using healthy samples that were screened for iron deficiency, abnormal hemoglobins, and thalassemias, recruited and assessed using the same techniques. The hypothesis was rejected, because Tibetan males had a significantly lower mean hemoglobin concentration of 15.6 gm/dl compared with 19.2 gm/dl for Aymara males, and Tibetan females had a mean hemoglobin concentration of 14.2 gm/dl compared with 17.8 gm/dl for Aymara females. The Tibetan hemoglobin distribution closely resembled that from a comparable, sea-level sample from the United States, whereas the Aymara distribution was shifted toward 3-4 gm/dl higher values. Genetic factors accounted for a very high proportion of the phenotypic variance in hemoglobin concentration in both samples (0.86 in the Tibetan sample and 0.87 in the Aymara sample). The presence of significant genetic variance means that there is the potential for natural selection and genetic adaptation of hemoglobin concentration in Tibetan and Aymara high-altitude populations.

Quantitative genetic analysis of arterial oxygen saturation in Tibetan highlanders.

This study was designed to test the hypothesis that genetic differences inferred from biological kinship relationships among individuals contribute to individual variation in percentage of oxygen saturation of arterial hemoglobin (SaO2) in a high-altitude native population. SaO2 data were obtained by pulse oximetry from 354 nonpregnant, healthy Tibetan residents of Pen-Dri, two rural agropastoral villages at 3800-4065 m altitude in Lhasa Municipal District, Tibet Autonomous Region, China. Statistical analyses of these data from 46 pedigrees tested the hypothesis of a significant genetic contribution to SaO2 variation. The average SaO2 was 89.4 +/- 0.2%, with a range of 76-97%. Additive genetic effects account for 44% of the interindividual phenotypic variation in SaO2 in the sample. Complex segregation analysis and variance decomposition analysis determined that 21% of the total phenotypic variation could be explained by a major gene influencing SaO2. Homozygotes for the low-SaO2 allele have a mean SaO2 of 83.6%, whereas heterozygotes and homozygotes for the high-SaO2 allele have means of 87.6% and 88.3%, respectively. This confirms findings in another Tibetan sample and extends the known geographic distribution of the major gene. These results suggest the hypothesis that individuals with the dominant allele for higher SaO2 have a selective advantage in their high-altitude hypoxic environment.

[Sleep and respiration at an altitude of 6,400 m (Aconcagua, Argentina]. / Schlaf und Atmung in 6400 m Höhe (Aconcagua, Argentinien).

UNLABELLED: Persons at extreme altitudes are known to experience disturbances in the regulation of ventilation and sleep structure. However, except for simulated studies using the decompression chamber, only single events of sleep or ventilation were measured so far in field studies up to an altitude of 5800 m. Modifying a portable sleep lab (Vitalog HMS 5000), we were able to conduct 7 channel polygraphy on our ascent to the Aconcagua up to an altitude of 6400 m. METHODS: In 6 climbers (age 38-62 y, 1 f, 6 m), ECG, EOG, SaO2, chest and abdominal movements, breathing and snoring sounds, body position, nasal and oral airflow were measured 4 weeks prior to the expedition at an altitude of 500 m, at base camp (4200 m) and in 3 climbers at 6400 m (2nd base camp) at the Aconcagua mountain. All participants had a repeat study at 500 m altitude 4 weeks after the expedition. RESULTS: The total number of obstructive apnoeas and hypopnoeas (OA/H) at night increased at an altitude of 4200 m in the mean of all 6 climbers from 36 to 67.7 compared to 500 m altitude, Central Apneas and Cheyne stokes (CA/CS) increased from 6.7 to 45.2. At 6400 m altitude the OA/H fell to 3 and 4 respectively in 2 climbers and CA to 1 and 2 respectively. In one climber, suffering from recurrent snoring with oxygen desaturation at 500 m altitude level, the number of OA/H and CA/CS increased further to 201 and 322, respectively, at 6400 m. Total sleep time including the REM position increased in all 6 climbers by 10% at base camp in comparison to an altitude of 500 m. Whereas the total sleep time remained constant in the 3 climbers at 6400 m altitude, the REM position declined by 10% in comparison to base camp (4200 m). However, significant fluctuations between individuals were noticed. CONCLUSION: Although significant alterations in sleep and breathing are noticeable at altitudes above 300 m, the respiratory drive in healthy subjects provides for a regular ventilation at high frequency at the extreme altitude above 6000 m. Sleep-related breathing disturbances at low altitude appear to be amplified at high altitudes.

Blood pressure variation among Ethiopians on the Simien Plateau.

This report presents information on determinants of blood pressure variation in a rural sample of 263 Ethiopian highlanders 14-86 years of age, resident at 3530 m on the Simien Plateau. Mean systolic and diastolic blood pressures for males and females were 109/ 75 and 106/73, respectively, and there were no age differences. These findings confirmed that men and women can have low normal blood pressure throughout adulthood. Blood pressures increased with increasing body mass index (BMI) among adult males, although the mean BMI of 19.1 kg/m2 was low compared with US values. This illustrates that BMI variation may be associated with blood pressure variation in men even at low mean values of both. Blood pressure did not vary with adult haemoglobin concentration.

Ventilation and hypoxic ventilatory response of Tibetan and Aymara high altitude natives.

Newcomers acclimatizing to high altitude and adult male Tibetan high altitude natives have increased ventilation relative to sea level natives at sea level. However, Andean and Rocky Mountain high altitude natives have an intermediate level of ventilation lower than that of newcomers and Tibetan high altitude natives although generally higher than that of sea level natives at sea level. Because the reason for the relative hypoventilation of some high altitude native populations was unknown, a study was designed to describe ventilation from adolescence through old age in samples of Tibetan and Andean high altitude natives and to estimate the relative genetic and environmental influences. This paper compares resting ventilation and hypoxic ventilatory response (HVR) of 320 Tibetans 9-82 years of age and 542 Bolivian Aymara 13-94 years of age, native residents at 3,800-4,065 m. Tibetan resting ventilation was roughly 1.5 times higher and Tibetan HVR was roughly double that of Aymara. Greater duration of hypoxia (older age) was not an important source of variation in resting ventilation or HVR in either sample. That is, contrary to previous studies, neither sample acquired hypoventilation in the age ranges under study. Within populations, greater severity of hypoxia (lower percent of oxygen saturation of arterial hemoglobin) was associated with slightly higher resting ventilation among Tibetans and lower resting ventilation and HVR among Aymara women, although the associations accounted for just 2-7% of the variation. Between populations, the Tibetan sample was more hypoxic and had higher resting ventilation and HVR. Other systematic environmental contrasts did not appear to elevate Tibetan or depress Aymara ventilation. There was more intrapopulation genetic variation in these traits in the Tibetan than the Aymara sample. Thirty-five percent of the Tibetan, but none of the Aymara, resting ventilation variance was due to genetic differences among individuals. Thirty-one percent of the Tibetan HVR, but just 21% of the Aymara, HVR variance was due to genetic differences among individuals. Thus there is greater potential for evolutionary change in these traits in the Tibetans. Presently, there are two different ventilation phenotypes among high altitude natives as compared with sea level populations at sea level: lifelong sustained high resting ventilation and a moderate HVR among Tibetans in contrast with a slightly elevated resting ventilation and a low HVR among Aymara.

Role of hypoxemia in sleep apnea-induced sympathoexcitation.

The importance of hypoxemia in determining sympathoexcitation during obstructive sleep apnea was examined by comparing changes in efferent sympathetic nerve activity (SNA) during spontaneous obstructive apneas with hypoxemia alone of similar magnitude and duration induced by 1-4 breaths of 100% nitrogen in six patients with obstructive sleep apnea and with spontaneous apneas while breathing 100% oxygen (apnea without hypoxemia) in three patients. In addition, eight control subjects were studied during induced hypoxemia. The magnitude of sympathoexcitation during spontaneous apneas (103 +/- 15%) was more than twice that observed during induced hypoxemia (47 +/- 14%) during episodes in which the nadir of oxygen desaturation (78 +/- 2 and 75 +/- 2%, respectively) and duration of hypoxemia (27 +/- 3 and 33 +/- 3 s, respectively) were the same (P > 0.20). Similarly, in three patients SNA increased 115% during normoxic spontaneous obstructive apneas, but increased only 43% during hyperoxic spontaneous obstructive apneas in which oxygen saturation did not decrease significantly. Sympathetic neural responses to induced hypoxemia in control subjects (17 +/- 7%) were significantly less than that of the sleep apnea patients. We conclude that hypoxemia contributes importantly, but is not the sole determinant of the sympathoexcitation provoked during episodes of obstructive sleep apnea.

Erythropoietin levels with treatment of obstructive sleep apnea.

The effect of nasal continuous positive pressure (CPAP) treatment on erythropoietin (EPO) was examined by measuring diurnal serum EPO levels before and twice (over the 3rd day and over 1 day on recall after > or = 1 mo of therapy) after initiation of treatment in 12 obstructive sleep apnea syndrome patients with normal hemoglobin, hematocrit, creatinine, blood urea nitrogen, and albumin levels. Over each study day, oxygen saturation was measured by an ambulatory pulse oximetry system. Patients spent 27 +/- 9% (SE) of time below oxygen saturation of 88% vs. 2.1 +/- 0.6% after initiation of nasal CPAP treatment (P < 0.01). The number of desaturation events per hour of sleep before nasal CPAP treatment was 62 +/- 6 vs. 9 +/- 2 with nasal CPAP (P < 0.01). EPO levels measured by radioimmunoassay were drawn every hour before and at 3 days (n = 9) and before and at recall (n = 0) after initiation of CPAP therapy. The mean serum EPO level was higher before treatment (61 +/- 14 mU/ml) than that at 3 days (38 +/- 10 mU/ml, P < 0.01) or at recall (32 +/- 7 mU/ml, P < 0.01). We conclude that nasal CPAP treatment of sleep-disordered breathing will reduce diurnal levels of EPO.

Effect of long-term angiotensin-converting enzyme inhibitor therapy on arterial oxygen saturation in patients with mild to moderate heart failure.

STUDY OBJECTIVE: To evaluate the effects of angiotensin-converting enzyme (ACE) inhibition on continuous pulse oximetry recordings of arterial oxygen saturation (SpO2). DESIGN: Open-label study. SETTING: Cardiology clinics at two large teaching hospitals. PATIENTS: Eight patients with New York Heart Association Functional Class (NYHA FC) II-III heart failure. INTERVENTIONS: Patients were studied after an ACE inhibitor washout (baseline, B), and after 3 months following resumption of therapy (ACE). MEASUREMENTS AND MAIN RESULTS: Monitoring times for B and ACEI were approximately 22 hours. Reduction trends were observed for number (190 +/- 170 vs 125 +/- 67 B vs ACEI), magnitude (8.2 +/- 1.4% vs 7.5 +/- 1.8%), and duration (2.45 +/- 2.8 vs 1.35 +/- 0.8 min) of desaturations/monitoring period, and for nadir SpO2/desaturation (88.1 +/- 1.5% vs 89.9 +/- 3.3%). The B desaturation index [(cumulative desaturation time/monitoring period time) x 100, a measure of hypoxic stress or burden] decreased from 19.4 +/- 8.1% to 11.9 +/- 8.1% at ACEI (p = 0.024). CONCLUSION: Long-term ACE inhibitor therapy improves the profile of SpO2 values over time in patients with NYHA FC II-III heart failure.

Center-based vs patient-based diagnosis and therapy of sleep-related respiratory disorders and the role of the respiratory care practitioner.

Unlike center-based laboratories that follow prescribed technical standards, patient-based studies lack technical standardization. Whereas center-based studies are usually performed by technicians who have met certain professional criteria, patient-based studies can be performed by anyone, even those without clinical training. Although guidelines are currently being developed to direct the use of unattended monitoring in the home, a need exists for specific guidelines that delineate professional qualifications for those who initiate and titrate therapy for patients with sleep-related respiratory disorders. The opportunity exists for respiratory care practitioners to become involved with creating guidelines for patient monitoring and therapeutic intervention, in both center-based and patient-based settings. A need exists for multicenter, peer-reviewed, controlled studies to establish standard recording variables and machine specifications for unattended monitoring devices. Also, the role and cost-benefit ratio of unattended monitoring in healthcare delivery need to be defined. Therefore, with the demand for technology-oriented research, clinical outcome studies, and professional standards, more respiratory care practitioners have the opportunity to expand their practice into the field of sleep medicine.

Arterial oxygen saturation in chronic congestive heart failure.

Continuous, 24-hour, ambulatory pulse oximetry was used in 10 subjects with New York Heart Association functional class II to III heart failure and in 5 age-matched controls to test the prevailing view that arterial oxygen saturation is preserved during wakefulness in chronic mild to moderate heart failure. Subjects with heart failure were stabilized on digitalis and diuretics at the time of the study. All subjects maintained time-activity logs, with an emphasis on self-reported sleep and wakefulness. A desaturation event was defined as a decrease in arterial oxygen saturation > or = 4% from baseline lasting > 5 seconds. Variables assessed included total desaturation events, decrease in arterial oxygen saturation duration/event, nadir of arterial oxygen saturation/event, and desaturation index ([cumulative desaturation time/total monitoring time] x 100). The ratio of self-reported wakefulness:sleep desaturation time was 47:53% for subjects with heart failure versus 64:36% for controls (p = NS). Mean (+/- SEM) time of arterial oxygen saturation < 90% was 123 +/- 67 minutes for subjects with heart failure versus 22 +/- 25 minutes for controls (p < 0.01). Total desaturations were 220 +/- 63 and 76 +/- 35 (p = NS) for the heart failure and control groups, respectively. The heart failure group had a statistically, significantly greater decrease in arterial oxygen saturation, and a longer duration and deeper nadir of the desaturation event than did the age-matched control group. The desaturation index was 21 +/- 3% and 4 +/- 1% for the heart failure and control groups, respectively (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)