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Blood pressure (BP) follows a circadian rhythm, dipping during sleep and surging in the morning. A larger morning BP surge is an independent predictor of cardiovascular events. Acute exercise can produce sustained periods of post-exercise hypotension that last up to 24 h; however, the timing of exercise (morning vs. evening) may influence this response. Whether the timing of exercise influences the morning BP surge remains unknown. The current study investigated the effects of a bout of high-intensity interval exercise (HIIE) performed in the morning versus evening on the magnitude of the morning BP surge in young healthy adults. Twenty-six young, otherwise healthy adults (23 ± 4 years; 15 females) completed a randomized crossover trial where, on different days, they completed a no exercise control visit or performed either morning (0800–1000 h) or evening (1700–1900 h) HIIE. Following each visit, ambulatory BP was assessed in 30 min intervals for 24 hrs. HIIE at either time did not alter the magnitude of the morning BP surge compared to control values (control: 22 ± 5 mmHg; morning exercise: 20 ± 8 mmHg; evening exercise: 22 ± 10 mmHg, P = 0.40) or when grouped separately by sex (visit × sex P = 0.42). A positive correlation existed between Morningness-Eveningness Questionnaire score and the change in nighttime BP following both exercise times (both r = 0.42 and P = 0.04). These findings suggest that HIIE does not attenuate the morning BP surge in young healthy adults and that chronotype can predict nighttime BP responses following HIIE, irrespective of exercise time of day. This study was registered on ClinicalTrials.gov (NCT06702930). [ABSTRACT FROM AUTHOR]

A burst of muscle sympathetic nerve activity (MSNA) induces vasoconstriction that transiently reduces regional vascular conductance and increases systemic blood pressure (BP) over the subsequent 4–8 cardiac cycles. These responses are termed sympathetic neurovascular transduction and sympathetic transduction of BP, respectively. Sympathetic transduction of BP is commonly calculated and interpreted as a proxy measure for regional sympathetic neurovascular transduction despite the systemic nature of BP regulation. The present analysis tested whether the peak change in signal-averaged sympathetic transduction of BP was correlated to the change in regional sympathetic vascular transduction at rest. Fourteen adults (5 females, 23 ± 3 yr) arrived at the laboratory, ate a standardized meal, and rested for 90–120 min. MSNA (fibular nerve microneurography), heart rate (electrocardiography), beat-to-beat BP (finger photoplethysmography), and superficial femoral artery blood flow (Doppler ultrasound) were obtained continuously for 10 min in the supine position. Femoral vascular conductance (FVC) was calculated as blood flow divided by mean arterial BP. The peak change in diastolic BP following a burst of MSNA was correlated to the corresponding nadir change in femoral vascular conductance (r = −0.58 [−0.07 to −0.85], P = 0.03) and superficial femoral artery blood flow (r = −0.54 [−0.17 to −0.83], P = 0.04). The nadir change in diastolic BP in cardiac cycles not following an MSNA burst was correlated to the peak change in femoral vascular conductance (r = −0.42 [−0.83 to 0.00], P = 0.05), but not superficial femoral artery blood flow (r = 0.41 [−0.77 to 0.15], P = 0.14). In conclusion, more commonly assessed sympathetic transduction of BP provides moderate insight into regional sympathetic neurovascular transduction. NEW & NOTEWORTHY: The majority of studies have used signal-averaged sympathetic transduction of blood pressure as a generalized measure of transduction. In this analysis, we show that sympathetic transduction of blood pressure and regional sympathetic vascular transduction were moderately correlated in healthy adults at rest. The moderate strength of this relationship highlights potential differences between regional and systemic assessments of sympathetic transduction and suggests that future work should choose the transduction measure best aligned with the research question. [ABSTRACT FROM AUTHOR]

Low- to moderate-intensity submaximal static contractions are commonly used to study the effects of biological sex on the cardiovascular response to exercise. Under this paradigm, premenopausal females frequently demonstrate smaller blood pressure responses than age-matched males. These differences are preserved during postexercise circulatory occlusion, implicating the muscle metaboreflex as an important driver of sex differences in the blood pressure response to static exercise. The mechanisms responsible for these differences are incompletely understood but often attributed to innate sex differences in skeletal muscle fiber type distribution, muscle metabolism, and/or sympathetic control of the circulation. However, one potential confounding factor is that the majority of studies use relative intensity exercise (e.g., 30% of maximal voluntary contraction), such that on average, females are completing static contractions at a lower absolute intensity. In this review, we summarize human evidence showing that sex differences in blood pressure responses to static exercise are attenuated or abolished when controlling for absolute intensity and muscle strength, either by statistical methods or strength-matched cohorts. We highlight evidence that the effect of higher absolute contraction intensity on exercise blood pressure likely occurs through increased mechanical occlusion of skeletal muscle microvasculature, leading to greater activation of the muscle metaboreflex. These findings highlight an important need to account for absolute intensity when studying and interpreting sex differences in cardiovascular responses to exercise. [ABSTRACT FROM AUTHOR]

The reliability of blood pressure (BP) measured during submaximal and maximal exercise, and confounding effects of biological sex, remain to be fully established but have implications for using exercise BP as a cardiovascular risk factor. We hypothesize that exercise BP test-retest reliability will not differ between sexes but will be higher during submaximal compared to maximal exercise. Eighty-four participants (22 ± 5 yr; 36 females) completed two maximal treadmill tests (modified Bruce protocol) separated by ≥2 days. Exercise BP was measured every 90 s using automated auscultation (Tango M2 monitor). Breath-by-breath oxygen uptake was analyzed. Test-retest reliability was assessed using two-way, mixed-effects, consistency, single-rater intraclass correlation coefficient (ICC) analysis on the total group and separated by sex at submaximal and maximal exercise. Systolic BP during submaximal (ICC = 0.65 [0.49–0.76], P < 0.01) and maximal (ICC = 0.66 [0.52–0.77], P < 0.01) exercise both displayed substantial reliability between visits. In contrast, the SBP/MET slope showed poor submaximal (ICC = 0.12 [−0.09–0.33], P = 0.13) but substantial maximal (ICC = 0.63 [0.48–0.75], P < 0.01) exercise reliability. Females showed substantial reliability in submaximal systolic BP (ICC = 0.73 [0.53–0.85], P < 0.01) and peak systolic BP (ICC = 0.74 [0.54–0.87], P < 0.01) and SBP/MET slope (ICC = 0.78 [0.60–0.88], P < 0.01); the submaximal SBP/MET slope had fair reliability (ICC = 0.28 [−0.06–0.56], P = 0.05). Males showed moderate reliability in submaximal systolic BP (ICC = 0.53 [0.26–0.72], P < 0.01) and peak systolic BP (ICC = 0.41 [0.15–0.62], P < 0.01) and SBP/MET slope (ICC = 0.48 [0.22–0.67], P < 0.01); the submaximal SBP/MET slope had poor reliability (ICC = 0.06 [−0.18–0.31], P = 0.32). Systolic BP showed similar reliability during submaximal and maximal exercise, with females demonstrating higher reliability in exercise systolic BP compared to males. NEW & NOTEWORTHY: Limited work has assessed the reliability of exercise blood pressure (BP) in young healthy males and females. Our results demonstrate that systolic BP test-retest reliability did not differ between submaximal and maximal exercise. Sex-specific analysis found that females had higher reliability in exercise systolic BP than males. Despite the acceptable average reliability, exercise BP measured using automated auscultation possesses wide confidence intervals, which impact sample size requirements in future trials. [ABSTRACT FROM AUTHOR]

Exaggerated blood pressure (BP) responses during exercise are independently associated with future development of hypertension. Partial sleep deprivation (PSD) can increase 24-h ambulatory BP, but the effects on exercise BP are unclear. We hypothesized that acute PSD would augment the BP response to constant load cycling exercise and a 20-min time trial. Twenty-two healthy adults (22 ± 3 yr old; 13 males; V̇ o 2peak, 43.6 ± 8.2 mL·kg−1·min−1) completed a randomized crossover trial in which they either slept normally (normal sleep-wake schedule for each participant) or sleep was partially deprived (early awakening, 40% of normal sleep duration). Each participant completed a 12-min warm-up consisting of two 6-min steps (step 1, 62 ± 25 W; step 2, 137 ± 60 W) followed by a 20-min time trial on a cycle ergometer. PSD did not alter power output during the 20-min time trial [(control vs. PSD) 170 ± 68 vs. 168 ± 68 W, P = 0.65]. Systolic BP did not differ during step 1 of the warm-up (141 ± 15 vs. 137 ± 12 mmHg, P = 0.39) but was lower following PSD during step 2 (165 ± 21 vs. 159 ± 22 mmHg, P = 0.004) and the 20-min time trial (171 ± 20 vs. 164 ± 23 mmHg, P < 0.001). These results were maintained when peak oxygen uptake (V̇ o 2peak) was included as a covariate. Systolic BP responses were modulated by sex (time × visit × sex interaction P = 0.03), with attenuated systolic BP during the warm-up and the 20-min time trial in males but not in females. In contrast to our hypothesis, acute PSD attenuates systolic BP responses during constant load and 20-min time trial cycling exercise; however, these observations appear to be primarily driven by changes in males. NEW & NOTEWORTHY: A single night of partial sleep deprivation (PSD) can increase ambulatory blood pressure (BP) the following day. Despite this phenomenon, the present study found that acute PSD attenuates systolic BP responses to both constant load cycling and a 20-min cycling time trial in young healthy adults. Interestingly, the attenuated systolic BP responses following PSD appeared to be modulated by sex such that attenuations were observed in males but not in females. [ABSTRACT FROM AUTHOR]

Exercise training is recommended to improve the quality of life in those living with Parkinson's disease (PD); however, the optimal prescription to improve cardiorespiratory fitness and disease-related motor symptoms remains unknown. Twenty-nine participants with PD were randomly allocated to either 10 wk of high-intensity interval training (HIIT) (n = 15; 6 female) or moderate-intensity continuous training (MICT) (n = 14; 5 female). The primary outcome was the change in maximal oxygen consumption (V̇ o 2peak). Secondary outcomes included changes in the Unified Parkinson's Disease Rating Scale (UPDRS) Part III motor score, Parkinson's Fatigue Scale (PFS)-16, resting and exercise cardiovascular measures, gait, balance, and knee extensor strength and fatigability. Exercise training increased V̇ o 2peak (main effect of time, P < 0.01), with a clinically meaningful difference in the change following HIIT versus MICT (Δ3.7 ± 3.7 vs. 1.7 ± 3.2 mL·kg−1·min−1, P = 0.099). The UPDRS motor score improved over time (P < 0.001) but without any differences between HIIT versus MICT (Δ−9.7 ± 1.3 vs. −8.4 ± 1.4, P = 0.51). Self-reported subjective fatigue (PFS-16) decreased over time (P < 0.01) but was similar between HIIT and MICT groups (P = 0.6). Gait, balance, blood pressure (BP), and heart rate (HR) were unchanged with training (all P > 0.09). Knee extensor strength increased over time (P = 0.03) but did not differ between HIIT versus MICT (Δ8.2 ± 5.9 vs. 11.7 ± 6.2 Nm, P = 0.69). HIIT alone increased the muscular endurance of the knee extensors during an isotonic fatigue task to failure (P = 0.04). In participants with PD, HIIT and MICT both increased V̇ o 2peak and led to improvements in motor symptoms and perceived fatigue; HIIT may offer the potential for larger changes in V̇ o 2peak and reduced knee extensor fatigability. NEW & NOTEWORTHY: The optimal exercise prescription to improve cardiorespiratory fitness and disease-related motor symptoms in adults with Parkinson's disease remains unknown. In a single-center randomized trial consisting of either 10 wk of high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT), we found that both training modes increased V̇ o 2peak, with a larger clinically meaningful difference following HIIT. Both exercise modes improved motor symptoms and subjective fatigue, whereas HIIT increased the muscular endurance of the knee extensors. [ABSTRACT FROM AUTHOR]

Discharge of postganglionic muscle sympathetic nerve activity (MSNA) is related poorly to blood pressure (BP) in adults. Whether neural measurements beyond the prevailing level of MSNA can account for interindividual differences in BP remains unclear. The current study sought to evaluate the relative contributions of sympathetic-BP transduction and sympathetic barore- flex gain on resting BP in young adults. Data were analyzed from 191 (77 females) young adults (18-39 years) who underwent continuous measurement of beat-to-beat BP (finger photoplethysmography), heart rate (electrocardiography), and fibular nerve MSNA (microneurography). Linear regression analyses were computed to determine associations between sympathetic-BP transduction (signal-averaging) or sympathetic baroreflex gain (threshold technique) and resting BP, before and after controlling for age, body mass index, and MSNA burst frequency. K-mean clustering was used to explore sympathetic phenotypes of BP control and consequential influence on resting BP. Sympathetic-BP transduction was unrelated to BP in males or females (both R² < 0.01; P > 0.67). Sympathetic baroreflex gain was positively associated with BP in males (R² = 0.09, P < 0.01), but not in females (R² < 0.01; P = 0.80), before and after controlling for age, body mass index, and MSNA burst frequency. K-means clustering identified a subset of participants with average resting MSNA, yet lower sympathetic-BP transduction and lower sympathetic baroreflex gain. This distinct subgroup presented with elevated BP in males (P < 0.02), but not in females (P = 0.10). Sympathetic-BP transduction is unrelated to resting BP, while the association between sympathetic baroreflex gain and resting BP in males reveals important sex differences in the sympathetic determination of resting BP. [ABSTRACT FROM AUTHOR]

Endothelium-dependent vasodilation can be tested using a variety of shear stress paradigms, some of which may involve the production of reactive oxygen species. The purpose of this study was to compare different methods for assessing endothelial function and their specific involvement of reactive oxygen species and influence of aerobic training status. Twenty-nine (10 F) young and healthy participants (VO2max: 34–74 mL·kg−1·min−1) consumed either an antioxidant cocktail (AOC; vitamin C, vitamin E, α-lipoic acid) or placebo (PLA) on each of two randomized visits. Endothelial function was measured via three different brachial artery flow-mediated dilation (FMD) tests: reactive hyperemia (RH-FMD: 5 min cuff occlusion and release), sustained shear (SS-FMD: 6 min rhythmic handgrip), and progressive sustained shear (P-SS-FMD: three intensities of 3 min of rhythmic handgrip). Baseline artery diameter decreased (all tests: 3.8 ± 0.5 to 3.7 ± 0.6 mm, p = 0.004), and shear rate stimulus increased (during RH-FMD test, p = 0.021; during SS-FMD test, p = 0.36; during P-SS-FMD test, p = 0.046) following antioxidant consumption. However, there was no difference in FMD following AOC consumption (RH-FMD, PLA: 8.1 ± 2.6%, AOC: 8.2 ± 3.5%, p = 0.92; SS-FMD, PLA: 6.9 ± 3.9%, AOC: 7.8 ± 5.2%, p = 0.15) or FMD per shear rate slope (P-SS-FMD: PLA: 0.0039 ± 0.0035 mm·s−1, AOC: 0.0032 ± 0.0017 mm·s−1, p = 0.28) and this was not influenced by training status/fitness (all p > 0.60). Allometric scaling did not alter these outcomes (all p > 0.40). Reactive oxygen species may not be integral to endothelium-dependent vasodilation tested using reactive, sustained, or progressive shear protocols in young males and females, regardless of fitness level. [ABSTRACT FROM AUTHOR]

Blood pressure (BP) follows a circadian rhythm intertwined with the sleep-wake cycle. Acute partial sleep deprivation (PSD; sleep = 6 h) can increase BP, associated with increased cardiovascular risk. Acute exercise can reduce BP for up to 24 h, a phenomenon termed postexercise hypotension. The present study tested whether aerobic exercise could mitigate the augmented 24-h ambulatory BP caused by acute PSD. Twenty-four young otherwise healthy adults (22 ± 3 yr; 14 females; selfreported chronotypes: 6 early/10 intermediate/8 late; Pittsburgh sleep quality index: 17 good/7 poor sleepers) completed a randomized crossover trial in which, on different days, they slept normally (2300-0700), restricted sleep [0330-0700 (PSD)], and cycled for 50 min (70-80% predicted heart rate maximum) before PSD. Ambulatory BP was assessed every 30 min until 2100 the next day. Acute PSD increased 24-h systolic BP (control 117 ± 9 mmHg, PSD 122 ± 9 mmHg; P < 0.001) and prior exercise attenuated (exercise þ PSD 120 ± 9 mmHg; P = 0.04 vs. PSD) but did not fully reverse this response (exercise þ PSD, P = 0.02 vs. control). Subgroup analysis revealed that the 24-h systolic BP reduction following exercise was specific to late types (PSD 119 ± 7 vs. exercise þ PSD 116 ± 6 mmHg; P < 0.05). Overall, habitual sleep quality was negatively correlated with the change in daytime systolic BP following PSD (r = -0.56, P < 0.01). These findings suggest that the ability of aerobic cycling exercise to counteract the hemodynamic effects of acute PSD in young adults may be dependent on chronotype and that habitual sleep quality can predict the daytime BP response to acute PSD. [ABSTRACT FROM AUTHOR]