Menopause is considered to be a risk factor for sleep-disordered breathing, but this hypothesis has not been adequately tested. The association of premenopause, perimenopause, and postmenopause with sleep-disordered breathing was investigated with a population-based sample of 589 women enrolled in the Wisconsin Sleep Cohort Study. Menopausal status was determined from menstrual history, gynecologic surgery, hormone replacement therapy, follicle-stimulating hormone, and vasomotor symptoms. Sleep-disordered breathing was indicated by the frequency of apnea and hypopnea events per hour of sleep, measured by in-laboratory polysomnography. Multivariable logistic regression was used to estimate odds ratios for having 5 or more and 15 or more apnea and hypopnea events per hour. Odds ratios (95% confidence interval), adjusted for age, body habitus, smoking, and other potential confounding factors, for 5 or more apnea and hypopnea events per hour were 1.2 (0.7, 2.2) with perimenopause and 2.6 (1.4, 4.8) with postmenopause; odds ratios for 15 or more apnea and hypopnea events per hour were 1.1 (0.5, 2.2) with perimenopause and 3.5 (1.4, 8.8) with postmenopause. The menopausal transition is significantly associated with an increased likelihood of having sleep-disordered breathing, independent of known confounding factors. Evaluation for sleep-disordered breathing should be a priority for menopausal women with complaints of snoring, daytime sleepiness, or unsatisfactory sleep.

The pilot, unsupervised walking intervention increased the MPA of overweight and obese women during pregnancy.

Sport-related concussion is an important topic in nearly all sports and at all levels of sport for children and adolescents. Concussion knowledge and approaches to management have progressed since the American Academy of Pediatrics published its first clinical report on the subject in 2010. Concussion's definition, signs, and symptoms must be understood to diagnose it and rule out more severe intracranial injury. Pediatric health care providers should have a good understanding of diagnostic evaluation and initial management strategies. Effective management can aid recovery and potentially reduce the risk of long-term symptoms and complications. Because concussion symptoms often interfere with school, social life, family relationships, and athletics, a concussion may affect the emotional well-being of the injured athlete. Because every concussion has its own unique spectrum and severity of symptoms, individualized management is appropriate. The reduction, not necessarily elimination, of physical and cognitive activity is the mainstay of treatment. A full return to activity and/ or sport is accomplished by using a stepwise program while evaluating for a return of symptoms. An understanding of prolonged symptoms and complications will help the pediatric health care provider know when to refer to a specialist. Additional research is needed in nearly all aspects of concussion in the young athlete. This report provides education on the current state of sport-related concussion knowledge, diagnosis, and management in children and adolescents.

Background: Unrecognized obstructive sleep apnea (OSA) may lead to poor asthma control despite optimal therapy. Our objective was to evaluate the relationship between OSA risk and asthma control in adults. Methods: Patients with asthma seen routinely at tertiary-care clinic visits completed the validated Sleep Apnea Scale of the Sleep Disorders Questionnaire (SA-SDQ) and Asthma Control Questionnaire (ACQ). An ACQ score of Ն 1.5 defi ned not-well-controlled asthma, and an SA-SDQ score of Ն 36 for men and Ն 32 for women defi ned high OSA risk. Logistic regression was used to model associations of high OSA risk with not-well-controlled asthma (ACQ full version and short versions). Results: Among 472 subjects with asthma, the mean 6 SD ACQ (full version) score was 0.87 6 0.90, and 80 (17%) subjects were not well controlled. Mean SA-SDQ score was 27 6 7, and 109 (23%) subjects met the defi nition of high OSA risk. High OSA risk was associated, on average, with 2.87-times higher odds for not-well-controlled asthma (ACQ full version) (95% CI, 1.54-5.32; P 5 .0009) after adjusting for obesity and other factors known to worsen asthma control. Similar independent associations were seen when using the short ACQ versions. Conclusions: High OSA risk is signifi cantly associated with not-well-controlled asthma independent of known asthma aggravators and regardless of the ACQ version used. Patients who have diffi culty achieving adequate asthma control should be screened for OSA.CHEST 2010; 138(3):543-550Abbreviations: ACQ 5 Asthma Control Questionnaire; CPAP 5 continuous positive airway pressure; GERD 5 gastroesophageal refl ux disease; OSA 5 obstructive sleep apnea; PEFR 5 peak expiratory fl ow rate; PSG 5 polysomnography; SA-SDQ 5 Sleep Apnea Scale of the Sleep Disorders Questionnaire

SummaryAstrocytes from familial amyotrophic lateral sclerosis (ALS) patients or transgenic mice are toxic specifically to motor neurons (MNs). It is not known if astrocytes from sporadic ALS (sALS) patients cause MN degeneration in vivo and whether the effect is specific to MNs. By transplanting spinal neural progenitors, derived from sALS and healthy induced pluripotent stem cells (iPSCs), into the cervical spinal cord of adult SCID mice for 9 months, we found that differentiated human astrocytes were present in large areas of the spinal cord, replaced endogenous astrocytes, and contacted neurons to a similar extent. Mice with sALS but not non-ALS cells showed reduced non-MNs numbers followed by MNs in the host spinal cord. The surviving MNs showed reduced inputs from inhibitory neurons and exhibited disorganized neurofilaments and aggregated ubiquitin. Correspondingly, mice with sALS but not non-ALS cells showed declined movement deficits. Thus, sALS iPSC-derived astrocytes cause ALS-like degeneration in both MNs and non-MNs.

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Lactic acid has played an important role in the traditional theory of muscle fatigue and limitation of endurance exercise performance. It has been called a waste product of anaerobic metabolism and has been believed to be responsible for the uncomfortable "burn" of intense exercise and directly responsible for the metabolic acidosis of exercise, leading to decreased muscle contractility and ultimately cessation of exercise. Although this premise has been commonly taught, it is not supported by the scientific literature and has led to a great deal of confusion among the sports medicine and exercise science communities. This review will provide the sports medicine clinician with an understanding of contemporary lactate theories, including lactate's role in energy production, its contributions to metabolic acidosis, and its function as an energy substrate for a variety of tissues. Lactate threshold concepts will also be discussed, including a practical approach to understanding prediction of performance and monitoring of training progress based on these parameters.