Julian C. Bommarito

The effects of a single night of partial sleep deprivation (PSD) on blood pressure (BP) regulation during cycling exercise remain unclear. We found no differences in BP but attenuated cardiac output during moderate-intensity cycling exercise and recovery following acute PSD in young adults. The blunted cardiac output response following acute PSD occurred after 30 min of cycling and was mediated by an attenuated stroke volume, in concert with an attenuated rise in exercise catecholamines.

Ramadan is a sacred religious practice observed by Muslims that involves abstaining from food and water from sunrise to sunset for 1 month. Prior work has reported that peak oxygen uptake () can decline during Ramadan in parallel with reduced physical activity. We investigated whether dietary nitrate supplementation could attenuate the decrease in during 10 days of Ramadan fasting. In a randomized design, 21 healthy participants (13 females) were assigned to ingest 70 mL of beetroot juice (∼6.45 mmol nitrate; n  = 10), twice a day for 10 days consecutively, or a non‐supplement control ( n  = 11). The was assessed by indirect calorimetry during a maximal cycle ergometer ramp test. After 10 days of Ramadan fasting, the change in body mass was not different between groups [change (∆), −0.91 ± 1.3 vs. −0.27 ± 1.2 kg (control vs. nitrate), P  = 0.25], nor were the changes in resting systolic ( P  = 0.21) or diastolic ( P  = 0.53) blood pressure or urine specific gravity ( P  = 0.17). Subjective sleep quality declined over time in both groups ( P  < 0.01). Participants self‐reported a decline ( n  = 17) or no change ( n  = 4) in regular physical activity, and the number of exercise bouts during the 10 days of Ramadan did not differ between groups (2.5 ± 2.0 vs. 3.3 ± 2.4, P  = 0.44). Absolute decreased in the control group compared with the dietary nitrate supplementation group (∆, −155 ± 168 vs. +67 ± 162 mL min ⁻¹ , P  < 0.01), as did relative to body mass (∆, −2.4 ± 2.5 vs. +0.3 ± 1.9 mL kg ⁻¹ min ⁻¹ , P  = 0.02) and peak power output (∆, −12 ± 16 vs. ∆+2 ± 10 W, P  = 0.04). Dietary nitrate supplementation might represent a practical nutritional strategy to preserve aerobic capacity during Ramadan fasting.

Whether interindividual differences in exercise blood pressure (BP) are mediated by changes in cardiac output or total peripheral resistance remain unclear. We demonstrate in healthy normotensive adults that higher peak exercise systolic BP during cycling is related to a larger cardiac output, whereas the rise in systolic BP per metabolic equivalent is related to a diminished fall in total peripheral resistance. Sex also appears to modulate this relation in those with an exaggerated exercise BP.

Exogenous ketone supplementation can impact cardiovascular regulation, but the effects on muscle sympathetic nerve activity (MSNA) remain unknown. In a randomized, crossover, double‐blind design, 19 participants (23 ± 4 years.; female: n = 9) ingested an oral ketone monoester (KME; 0.4 g/kg) or isocaloric, isovolumetric placebo. Blood pressure, heart rate, brachial artery blood flow, and MSNA (microneurography; n = 14) were assessed at rest before and after ingestion and during two laboratory stressors: 2‐min static handgrip exercise and 2‐min of mental arithmetic. Capillary β‐hydroxybutyrate increased 20 and 40 min post KME ingestion versus placebo (both, p < 0.001). Compared to placebo, KME had no effects on resting mean arterial pressure (Placebo: 78.3 ± 9.3 to 80.2 ± 10.5 mmHg; KME: 76.3 ± 8.3 to 79.5 ± 8.8 mmHg; interaction p = 0.32), heart rate (Placebo: 64.6 ± 12.3 to 69.6 ± 11.0 bpm; KME: 65.3 ± 10.6 to 72.6 ± 11.3 bpm; interaction p = 0.30), or MSNA burst frequency (Placebo: 17.7 ± 7.3 to 17.7 ± 6.7 bursts/minute; KME: 17.5 ± 6.1 to 18.2 ± 7.0 bursts/minute; interaction p = 0.72). Resting brachial artery blood flow and vascular conductance changed over time but did not differ between conditions (interactions, both p > 0.40). Neuro‐cardiovascular responses during exercise (interactions, all p > 0.72) or mental stress (interactions, all p > 0.44) did not differ between conditions. Compared to placebo, acute KME ingestion did not modulate neuro‐cardiovascular measures at rest or during stress in healthy young adults.

Elevated peak blood pressure (BP) during exercise is an independent risk factor for future hypertension, but the mechanisms responsible for inter-individual differences in exercise BP remain poorly studied. Forty-four participants (22±5 years; 18 female) completed a maximal exercise test (modified Bruce protocol) with brachial artery BP measured every 90-seconds (automated auscultation). On a subsequent visit, participants underwent measures of carotid-femoral pulse wave velocity (n=37), superficial femoral artery flow-mediated dilation (n=27), and muscle sympathetic nerve activity (MSNA; microneurography, n=44). Hemodynamic and MSNA data were collected at rest, during handgrip exercise (static and rhythmic), and post-exercise circulatory occlusion. Participants were separated by sex and grouped into tertiles based on peak exercise systolic BP (SBP). Peak exercise SBP differed between tertiles (Tertile 1: 168±16 vs. Tertile 2: 194±14 vs. Tertile 3: 223±17 mmHg, P<0.001), despite no differences in resting SBP ( P=0.12), diastolic BP ( P=0.17), heart rate ( P=0.12), superficial femoral artery flow-mediated dilation ( P=0.85), carotid-femoral pulse wave velocity ( P=0.15), or MSNA (17.8±5.9 vs. 16.8±5.8 vs. 19.0±4.5 bursts/min, P=0.56). MSNA was higher during the final 30-seconds of static handgrip in Tertile 3 compared to both Tertile 1 and 2 (28.8±8.0 vs. 29.3±9.0 vs. 43.7 ± 14.0 bursts/min, both P0.19). Normotensive adults with higher peak SBP during maximal treadmill exercise have augmented MSNA during activation of the muscle metaboreflex.

Following cycling exercise, leg vascular conductance increases, whereas sympathetic nerve traffic is unchanged in young healthy adults. Discordant vascular and sympathetic responses may reflect modulation in vasoconstrictor responsiveness. The current study demonstrated that signal-averaged sympathetic neurovascular transduction was increased by ∼75% following a single bout of cycling exercise. Secondary experiments using local heating suggest that potentiation in sympathetic neurovascular transduction after exercise may occur independent of changes in resting vascular conductance.

Higher peak systolic blood pressure (SBP) during exercise is linked with an increased risk of developing hypertension. It has been suggested that exercise SBP should be normalized to mechanical or metabolic work to account for differences in aerobic fitness. We found that the influence of aerobic fitness on peak SBP or SBP per metabolic equivalent (SBP/MET slope) does not differ between sexes but that the SBP/MET slope is lower in participants with higher aerobic fitness.