The present study confirms altered sleep duration and quality in OB. Exercise training improves sleep duration, sleep quality and physical activity.

A systematic review of English and French articles using Pubmed/Medline and Embase included studies assessing objective physical activity levels of obstructive sleep apnea (OSA) patients and exploring the effects of exercise training on OSA severity, body mass index (BMI), sleepiness, and cardiorespiratory fitness [peak oxygen consumption (VO2peak)]. Two independent reviewers analyzed the studies, extracted the data, and assessed the quality of evidence. For objective physical activity levels, eight studies were included. The mean number of steps per day across studies was 5,388 (95% CI: 3,831–6,945; p < 0.001), which was by far lower than the recommended threshold of 10,000 steps per day. For exercise training, six randomized trials were included. There was a significant decrease in apnea–hypopnea-index following exercise training (mean decrease of 8.9 events/h; 95% CI: −13.4 to −4.3; p < 0.01), which was accompanied by a reduction in subjective sleepiness, an increase in VO2peak and no change in BMI. OSA patients present low levels of physical activity and exercise training is associated with improved outcomes. Future interventions (including exercise training) focusing on increasing physical activity levels may have important clinical impacts on both OSA severity and the burden of associated co-morbidities. Objective measurement of physical activity in routine OSA management and well-designed clinical trials are recommended.Registration # CRD42017057319 (Prospero).

Study Objectives: Obstructive sleep apnea (OSA) has been associated with hypertension, which is one of the intermediary mechanisms leading to increased cardiovascular morbidity. This study aimed at evaluating the effects of a combination of continuous positive airway pressure (CPAP) and telemedicine support on blood pressure (BP) reduction in high cardiovascular risk OSA patients. Design: A multi-center randomized controlled trial that compared standard CPAP care and CPAP care and a telemedicine intervention. Setting: Sleep clinics in France. Patients or Participants: 107 adult (18-65 years old) OSA patients (AHI > 15 events/h) with a high cardiovascular risk (cardiovascular SCORE > 5% or secondary prevention). Interventions: Patients were randomized to either standard care CPAP (n = 53) or CPAP and telemedicine (n = 54). Patients assigned to telemedicine were equipped with a smartphone for uploading BP measurements, CPAP adherence, sleepiness, and quality of life data; in return, they received pictograms containing health-related messages. Measurements: The main outcome was home self-measured BP and secondary outcomes were cardiovascular risk evolution, objective physical activity, CPAP adherence, sleepiness and quality of life. Results: Self-measured BP did not improve in either group (telemedicine or standard care). Patients in primary prevention showed greater BP reduction with CPAP treatment than those in secondary prevention. Conclusions: CPAP treatment supported by telemedicine alone did not improve blood pressure and cardiovascular risk in high cardiovascular risk OSA patients. This study emphasizes the need for diet and physical activity training programs in addition to CPAP when aiming at decreasing cardiometabolic risk factors in these patients. Clinical Trials Registration: ClinicalTrials.gov identifier: NCT01226641.

This study examines the response of the exhaled nitric oxide (NO) concentration (CNO) and the exhaled NO output (VNO) during incremental exercise and during recovery in six sedentary women, seven sedentary men, and eight trained men. The protocol consisted of increasing the exercise intensity by 30 W every 3 min until exhaustion, followed by 5 min of recovery. Minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production, heart rate, CNO, and VNO were measured continuously. The CNO in exhaled air decreased significantly provided that the exercise intensity exceeded 65% of the peak VO2. It reached similar values, at exhaustion, in all three groups. The VNO increased proportionally with exercise intensity up to exhaustion and decreased rapidly during recovery. At exhaustion, the mean values were significantly higher for trained men than for sedentary men and sedentary women. During exercise, VNO correlates well with VO2, carbon dioxide production, VE, and heart rate. For the same submaximal intensity, and thus a given VO2 and probably a similar cardiac output, VNO appeared to be similar in all three groups, even if the VE was different. These results suggest that, during exercise, VNO is mainly related to the magnitude of aerobic metabolism and that this relationship is not affected by gender differences or by noticeable differences in the level of physical training.

Introduction Combining exercise training with hypoxic exposure has been recently proposed as a new therapeutic strategy to improve health status of obese individuals. Whether hypoxic exercise training (HET) provides greater benefits regarding body composition and cardiometabolic parameters than normoxic exercise training (NET) remains, however, unclear. We hypothesized that HET would induce greater improvement in exercise capacity and health status than NET in overweight and obese individuals. Methods Twenty-three subjects were randomized into 8-wk HET (11 men and 1 woman; age, 52 ± 12 yr; body mass index, 31.2 ± 2.4 kg·m−2) or NET (eight men and three women; age, 56 ± 11 yr; body mass index, 31.8 ± 3.2 kg·m−2) programs (three sessions per week; constant-load cycling at 75% of maximal heart rate; target arterial oxygen saturation for HET 80%, FiO2 ~0.13, i.e., ~3700 m a.s.l.). Before and after the training programs, the following evaluations were performed: incremental maximal and submaximal cycling tests, measurements of pulse-wave velocity, endothelial function, fasting glucose, insulin and lipid profile, blood NO metabolites and oxidative stress, and determination of body composition by magnetic resonance imaging. Results Peak oxygen consumption and maximal power output increased significantly after HET only (peak oxygen consumption HET + 10% ± 11% vs NET + 1% ± 10% and maximal power output HET + 11% ± 7% vs NET + 3% ± 10%, P < 0.05). Submaximal exercise responses improved similarly after HET and NET. Except diastolic blood pressure which decreased significantly after both HET and NET, no change in vascular function, metabolic status and body composition was observed after training. Hypoxic exercise training only increased nitrite and reduced superoxide dismutase concentrations. Conclusions Combining exercise training and hypoxic exposure may provide some additional benefits to standard NET for obese individual health status.

The aim of this study was to determine whether the power output associated with a maximal lactate steady state (MLSS) (.W(MLSS)) can be assessed using a single incremental cycling test. Eleven recreational sportsmen (age: 22+/-1 years, height: 175+/-6 cm, weight: 71+/-5 kg) volunteered to participate in the study. For each subject the first and second ventilatory thresholds (VT(1) and VT(2), respectively) and the power output corresponding to (respiratory exchange ratio) RER=1.00 were determined during an incremental test to exhaustion. Thereafter, each subject performed several 30-min constant load tests to determine MLSS. The workload used in the first constant test was set to the .W(RER=1.00) determined during the incremental test. .W(VT1) (175+/-24 W) and .W(VT2) (265+/-31 W) were significantly different from .W(MLSS )(220+/-36 W). Whereas, .W(RER=1.00) (224+/-33 W) was similar to .W(MLSS). HR, RER and .VE were significantly different between the 10th and the 30th minutes when exercising at .W(RER=1.00) and at .W(MLSS). In contrast, .VO(2) and .VCO(2) were stable over those 30-min constant tests. Power output at VT(1), RER=1.00 and VT(2) were all correlated to .W(MLSS) but the relationship was stronger between RER=1.00 and MLSS (R (2)=0.95). The present study shows that the power output associated with a RER value equal to 1.00 during an incremental test does not differ from that determined for MLSS. Hence, the MLSS can be estimated with a single exercise test.

Chronic intermittent hypoxia (IH) is described as the major detrimental factor leading to cardiovascular morbimortality in obstructive sleep apnea (OSA) patients. OSA patients exhibit increased infarct size after a myocardial event, and previous animal studies have shown that chronic IH could be the main mechanism. Endoplasmic reticulum (ER) stress plays a major role in the pathophysiology of cardiovascular disease. High-intensity training (HIT) exerts beneficial effects on the cardiovascular system. Thus, we hypothesized that HIT could prevent IH-induced ER stress and the increase in infarct size. Male Wistar rats were exposed to 21 days of IH (21-5% fraction of inspired O2, 60-s cycle, 8 h/day) or normoxia. After 1 wk of IH alone, rats were submitted daily to both IH and HIT (2 ϫ 24 min, 15-30m/min). Rat hearts were either rapidly frozen to evaluate ER stress by Western blot analysis or submitted to an ischemia-reperfusion protocol ex vivo (30 min of global ischemia/ 120 min of reperfusion). IH induced cardiac proapoptotic ER stress, characterized by increased expression of glucose-regulated protein kinase 78, phosphorylated protein kinase-like ER kinase, activating transcription factor 4, and C/EBP homologous protein. IH-induced myocardial apoptosis was confirmed by increased expression of cleaved caspase-3. These IH-associated proapoptotic alterations were associated with a significant increase in infarct size (35.4 Ϯ 3.2% vs. 22.7 Ϯ 1.7% of ventricles in IH ϩ sedenary and normoxia ϩ sedentary groups, respectively, P Ͻ 0.05). HIT prevented both the IH-induced proapoptotic ER stress and increased myocardial infarct size (28.8 Ϯ 3.9% and 21.0 Ϯ 5.1% in IH ϩ HIT and normoxia ϩ HIT groups, respectively, P ϭ 0.28). In conclusion, these findings suggest that HIT could represent a preventive strategy to limit IHinduced myocardial ischemia-reperfusion damages in OSA patients.obstructive sleep apnea; intermittent hypoxia; ischemia-reperfusion; high-intensity aerobic training; endoplasmic reticulum stress NEW & NOTEWORTHYWe demonstrated that intermittent hypoxia induced cardiac proapoptotic ER stress and increased infarct size, which were prevented by high-intensity aerobic training. These results strengthen the need for early identification of patients with sleep apnea at risk for cardiovascular complications and suggest that exercise can be used as a new preventive strategy for these patients.

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