View clinical trials related to Intermittent Hypoxia.
Filter by:The purpose of the study is to determine the effect of a single exposure of intermittent hypoxia on erythropoietin levels and hemoglobin mass in young adults, older adults and patients with type 2 diabetes.
This study aims to determine the effect of acute mild intermittent hypoxia on ankle plantarflexor muscle output during balance regulation and walking in younger and older adults. Fifteen younger adults and 15 older adults will be recruited to participate in the cross-over design study that requires 2 visits (at least 1-week apart). Participants will be pseudo-randomly assigned to receive either intermittent hypoxia or sham during the first visit, and then switch over to receive sham or intermittent hypoxia during the 2nd visit. Muscle activation patterns and kinetic and kinematics during standing and walking will be recorded before and after the intermittent hypoxia/sham. It is hypothesized that compared to the sham condition, both younger and older participants will show greater increases in ankle plantarflexor muscle activation during gait and balance assessments following intermittent hypoxia.
The objective of the present study is to determine whether intermittent hypoxia protects against ischemia-reperfusion injury in young and older healthy individuals. The investigators hypothesize that intermittent hypoxia will attenuate the reduction in flow-mediated dilation following ischemia-reperfusion injury.
Low oxygen at altitude causes pauses in breathing during sleep, called central sleep apnea. Central sleep apnea causes repeated awakenings and poor sleep. Low oxygen itself and the induced oxidative stress can damage mental function which is likely worsened by poor sleep. Reduced mental function due to low oxygen can pose a serious danger to mountain climbers. However there is also mounting evidence that even in populations of people that live at high altitudes and are considered adapted, low oxygen contributes to reductions in learning and memory. Therefore there is a serious need for treatments which may improve sleep, control of breathing and mental function during low oxygen.Therefore this study aims to determine how melatonin effects control of breathing, sleep and mental performance during exposure to low oxygen.
Intermittent Hypoxia and Caffeine in Infants Born Preterm (ICAF) Our proposal will address the critical question: is persisting intermittent hypoxia (IH) in preterm infants associated with biochemical, structural, or functional injury, and is this injury attenuated with extended caffeine treatment? The investigators will study the effects of caffeine on IH in 220 preterm infants born at ≤30 weeks + 6 days gestation. Infants who are currently being treated with routine caffeine, and who meet eligibility criteria, will be enrolled between 32 weeks + 0 days and 36 weeks + 6 days PMA. At enrollment, infants will be started on continuous pulse oximeter recording of O2 saturation and heart rate. If, based on standard clinical criteria, the last dose of routine caffeine is given on or before the day the infant is 36 weeks + 5 days PMA, then on the day following their last dose of routine caffeine treatment, infants will be randomized (110/group) to extended caffeine treatment or placebo. Randomized infants should begin receiving study drug (i.e. 5 mg/kg/of caffeine base, or equal volume of placebo) on the day of randomization, but no later than the third calendar day following the last dose of routine caffeine. Prior to 36 weeks + 0 days PMA, study drug will be given once daily (i.e. 5mg/kg/day) and beginning at 36 weeks + 0 days PMA, study drug will be given twice daily (i.e. 10 mg/kg/day). The last dose of study drug will be given at 42 weeks + 6 days PMA. Pulse oximeter recordings will continue 1 additional week after discontinuing study drug. Two caffeine levels will be obtained, the 1st at one week after beginning study drug, and the 2nd at a target date of 40 weeks + 0 days PMA, but no later than the last day of study drug, whether in hospital or at home. Inflammatory biomarkers will be measured at study enrollment and again at 38 weeks + 0 days PMA, or within 2 calendar days prior to hospital discharge, whichever comes first. Quantitative MRI/MRS should be obtained between study enrollment and 3 calendar days after starting study drug and again at a target date of 43 weeks + 0 days, but no later than 46 weeks + 6 days PMA.
Rehabilitation approaches introduce a stimulus to a motor system, with the goal to enhance motor function to patients. For example, exposure to brief and intermittent episodes of mild hypoxia has shown to strengthen synaptic pathways to respiratory and skeletal muscle motor neurons. In humans with spinal cord injury, exposure to intermittent hypoxia (IH) alone or in combination with rehabilitative strategies has shown enhanced motor function. Another strategy known as inspiratory threshold loading, which involves breathing against pressure threshold loads, results in improved inspiratory muscle strength. Although there is evidence supporting the use of IH alone or in combination with other rehabilitative strategies in improving motor function in humans, the impact of exposure to IH or IH with inspiratory threshold loading on inspiratory muscle function and ventilation in humans is unknown.
Patients with sleep apnea syndrome have repeated apneic events that induce periodic hypoxia-reoxygenation, drawing away an overproduction of oxidants. This exaggerated generation of oxidants is associated with a dysfunction of the vascular endothelium that evolves, in its turn, towards cardiovascular diseases such as systemic hypertension, stroke, and myocardial infarction. The major aim of our study is to examine the effect of CPAP treatment on biochemical (markers of oxidative stress) and functional (endothelium-dependent vascular relaxation reactivity) abnormalities at 1 and 4 weeks of treatment.