Introduction: Exaggerated blood pressure (BP) responses during exercise are associated with increased risk of clinical cardiovascular outcomes. Partial sleep deprivation (PSD), defined as ≤6 hours of sleep, can increase 24-hour ambulatory BP but the effects on exercise BP have not been studied. We hypothesized that acute PSD would augment the exercise BP response to constant load exercise (below and above estimated lactate threshold) and during a 20-min time trial. Methods: Fourteen, healthy adults (22 ± 3 years; 9 males; VO2peak: 43.2 ± 9.5 ml/kg/min [25.3-60.9]) completed a randomized crossover trial where they slept normally (normal sleep-wake schedule for each participant), or sleep was partially deprived (early awakening, 40% of normal sleep duration). Prior to the testing visits, participants completed two familiarization visits under normal sleep conditions. Each participant completed a 12-minute warm (6-minutes below estimated lactate threshold [moderate intensity; 65 ± 24 W] and 6-minutes above estimated lactate threshold but below respiratory compensation point [heavy intensity; 147 ± 60 W]) followed by a time-trial where they were asked to cycle as far as possible in 20 minutes. BP was assessed at rest (BpTRU, Medical Devices) and on the cycle ergometer every 2 minutes during the warmup and 20-minute time-trial (Tango M2, SunTech Medical). Sleep timing and duration was assessed daily for 1-week prior to each testing visit using self-report and an accelerometer worn on the non-dominate wrist (wGT3X-BT, ActiGraph). Results: Resting systolic ( P=0.08) and diastolic BP ( P=0.06) tended to be higher following PSD (normal sleep: 105 ± 8/62 ± 8 mmHg vs. PSD: 107 ± 6/64 ± 7 mmHg). PSD did not alter VO2 during the moderate- (normal sleep: 1291 ± 394 ml/min vs. PSD: 1258 ± 364 ml/min) and heavy-intensity (normal sleep: 1903 ± 758 ml/min vs. PSD: 1893 ± 724 ml/min) warmup or 20-minute time-trial (normal sleep: 2713 ± 1120 ml/min vs. PSD: 2669 ± 1134 ml/min) or distance covered (normal sleep: 10.16 ± 2.024 km vs. PSD: 10.08 ± 2.145 km) and power output (normal sleep: 175 ± 79 W vs. PSD: 173 ± 79 W) during the 20-min time-trial (all P>0.27). Systolic (normal sleep: 140 ± 17 mmHg vs. PSD: 136 ± 11 mmHg, P=0.14) and diastolic (normal sleep: 67 ± 11 mmHg vs. PSD: 69 ± 8 mmHg, P=0.44) BP did not differ during the moderate-intensity warmup following PSD. However, systolic BP was lower during the heavy-intensity warmup (normal sleep: 165 ± 25 mmHg vs. PSD: 155 ± 22 mmHg, P=0.008) and 20-minute time-trial (normal sleep: 174 ± 20 mmHg vs. PSD: 165 ± 25 mmHg, P=0.05) following PSD. No differences were observed in diastolic BP (all P>0.57). Heart rate during the moderate-intensity warmup (normal sleep: 110 ± 11 bpm vs. PSD: 110 ± 10 bpm), heavy-intensity warmup (normal sleep: 137 ± 14 bpm vs. PSD: 136 ± 14 bpm), and time-trial (normal sleep: 171 ± 16 bpm vs. PSD: 169 ± 19 bpm) did not differ between conditions (all P>0.39). Conclusion: In contrast to our hypothesis, these preliminary findings suggest that a single night of PSD results in lower systolic BP responses during heavy-intensity, but not moderate-intensity, cycling exercise. This research was supported by a Natural Science and Engineering Research Council (NSERC) of Canada Discovery Grant (P.J.M). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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