Acute partial sleep deprivation attenuates cardiac output during moderate-intensity cycling in young adults.

Acute partial sleep deprivation (PSD) can attenuate systolic blood pressure (BP) during cycling exercise; however, the mechanisms responsible are unknown. This study aimed to test if acute PSD attenuates cardiac output (Q̇) during cycling. Twenty-five adults (22±3 yrs; 13 females; V̇O2peak: 40.1±7.7 ml.kg-1.min-1) completed a randomized, crossover trial where they slept normally or underwent acute PSD (early awakening; 40% normal sleep duration). BP, Q̇ (impedance cardiography), and middle and posterior cerebral artery blood velocity (transcranial Doppler ultrasound) were assessed at rest, throughout 60 min of moderate-intensity cycling (81±35W), and recovery. Systolic and diastolic BP did not differ at rest or exercise (P≥0.19). Q̇ did not differ at rest (control: 5.0±0.9 L/min vs. PSD: 4.9±0.7 L/min, P>0.99) or 30 min of cycling (control: 11.5±2.7 L/min vs. PSD: 11.0±2.5 L/min, P=0.16), but was attenuated at 60 min of cycling (control: 12.3±3.1 L/min vs. PSD: 11.5±2.6 L/min, P=0.003) and recovery following PSD (control: 7.7±1.9 L/min vs. PSD: 7.2±1.4 L/min, P=0.04). Heart rate and estimated end-diastolic volume did not differ (both, P≥0.82); however, stroke volume tended to be lower (P=0.054), estimated ejection fraction was lower (P=0.02) and total peripheral resistance was augmented (P=0.04) following PSD. Plasma norepinephrine and epinephrine were unchanged at rest but exhibited attenuated increases at 60 min of cycling following PSD (both, P≤0.045). Middle cerebral artery mean velocity tended to decrease during cycling following PSD (P=0.051). Acute PSD can attenuate exercise Q̇ after 30 min of moderate-intensity cycling secondary to a blunted stroke volume, without compensation by increased heart rate.