Choir singing improves respiratory muscle strength and quality of life in patients with structural heart disease - HeartChoir: a randomised clinical trial.

AIMS OF THE STUDY: Most patients with reduced exercise capacity and acquired or congenital structural heart disease also have a reduced respiratory muscle strength. The aim of this pilot study was to investigate whether choir singing in combination with respiratory muscle training positively influences respiratory muscle strength, exercise capacity and quality of life in this population. METHODS: In this single-centre, randomised and open-label interventional study we compared respiratory muscle strength, exercise capacity and quality of life in patients with acquired or congenital structural heart disease who received either standard of care and a 12-week intervention (weekly choir rehearsal and daily breathing exercises) or standard of care alone. The primary endpoint was the difference in change in maximum inspiratory pressure (∆MIP%predicted). Secondary endpoints included the difference in change in maximum expiratory pressure (∆MEP%predicted), exercise capacity quantified as maximal oxygen uptake during exercise (∆MVO2%predicted) and quality of life quantified by the Minnesota living with heart failure questionnaire (∆MLHFQ score). RESULTS: Overall 24 patients (mean age 65, standard deviation [SD] 19 years, 46% male) were randomised after exclusion. ∆MIP%predicted was significantly higher in the intervention group (∆MIP%predicted +14, SD 21% vs −14, SD 23%; p = 0.008) and quality of life improved significantly (∆MLHFQ score −5, SD 6 vs 3, SD 5; p = 0.006) after 12 weeks. ∆MEP%predicted and ∆MVO2%predicted did not differ between both groups (∆MEP%predicted −3, SD 26% vs −3, SD 16%; p = 1.0 and ∆MVO2%predicted 18, SD 12% vs 10, SD 15%; p = 0.2). CONCLUSIONS: Choir singing in combination with respiratory muscle training improved respiratory muscle strength and quality of life in patients with structural heart disease and may therefore be valuable supplements in cardiac rehabilitation. (Clinical trial registration number: NCT03297918)  .

Cognitive brain responses during circadian wake-promotion: evidence for sleep-pressure-dependent hypothalamic activations.

The two-process model of sleep-wake regulation posits that sleep-wake-dependent homeostatic processes interact with the circadian timing system to affect human behavior. The circadian timing system is fundamental to maintaining stable cognitive performance, as it counteracts growing homeostatic sleep pressure during daytime. Using magnetic resonance imaging, we explored brain responses underlying working memory performance during the time of maximal circadian wake-promotion under varying sleep pressure conditions. Circadian wake-promoting strength was derived from the ability to sleep during an evening nap. Hypothalamic BOLD activity was positively linked to circadian wake-promoting strength under normal, but not under disproportionally high or low sleep pressure levels. Furthermore, higher hypothalamic activity under normal sleep pressure levels predicted better performance under sleep loss. Our results reappraise the two-process model by revealing a homeostatic-dose-dependent association between circadian wake-promotion and cognition-related hypothalamic activity.

Fighting Sleep at Night: Brain Correlates and Vulnerability to Sleep Loss.

OBJECTIVE: Even though wakefulness at night leads to profound performance deterioration and is regularly experienced by shift workers, its cerebral correlates remain virtually unexplored. METHODS: We assessed brain activity in young healthy adults during a vigilant attention task under high and low sleep pressure during night-time, coinciding with strongest circadian sleep drive. We examined sleep-loss-related attentional vulnerability by considering a PERIOD3 polymorphism presumably impacting on sleep homeostasis. RESULTS: Our results link higher sleep-loss-related attentional vulnerability to cortical and subcortical deactivation patterns during slow reaction times (i.e., suboptimal vigilant attention). Concomitantly, thalamic regions were progressively less recruited with time-on-task and functionally less connected to task-related and arousal-promoting brain regions in those volunteers showing higher attentional instability in their behavior. The data further suggest that the latter is linked to shifts into a task-inactive default-mode network in between task-relevant stimulus occurrence. INTERPRETATION: We provide a multifaceted view on cerebral correlates of sleep loss at night and propose that genetic predisposition entails differential cerebral coping mechanisms, potentially compromising adequate performance during night work.