Search

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]

The purpose of the present study was to clarify the impact of age on the sympathoinhibitory response to cardiopulmonary baroreceptor loading in females. Nine older females (mean ± SD, 70 ± 6 yr) and 11 younger females (20 ± 1 yr) completed the study. A passive leg raising (PLR) test was performed wherein the participants were positioned supine (baseline, 0°), and their lower limbs were passively lifted at 10°, 20°, 30°, and 40° (3 min at each angle). Muscle sympathetic nerve activity (MSNA) was recorded via microneurography of the left radial nerve. The central venous pressure was estimated based on peripheral venous pressure (eCVP), which was monitored using a cannula in the right large antecubital vein. Baseline MSNA was higher in older females than in younger females. MSNA burst frequency (BF) decreased during the PLR test in both older and younger females, but the magnitude of the decrease in MSNA BF was smaller in older females than in younger females (older, −3.5 ± 1.5 vs. younger, −6.3 ± 1.5 bursts/min at 40° from baseline, P = 0.014). The eCVP increased during the PLR in both groups, and there was no difference in the changes in eCVP between the two groups (older, +1.07 ± 0.37 vs. younger, +1.12 ± 0.33 mmHg at 40° from baseline, P = 0.941). These results suggest that inhibition of sympathetic vasomotor outflow during cardiopulmonary baroreceptor loading could be blunted with advancing age in females. NEW & NOTEWORTHY: There were no available data concerning the effect of age on the sympathoinhibitory response to cardiopulmonary baroreceptor loading in females. The magnitude of the decrease in muscle sympathetic nerve activity during passive leg raising (10°–40°) was smaller in older females than in young females. In females, inhibition of sympathetic vasomotor outflow during cardiopulmonary baroreceptor loading could be blunted with advancing age. [ABSTRACT FROM AUTHOR]

Blood flow to the active muscles and arterial blood pressure (ABP) increase during dynamic exercise, whereas blood flow to inactive organs (e.g., splanchnic organs and inactive limbs) declines. Aging leads to exaggerated ABP responses to exercise in females, but whether this is related to greater splanchnic vasoconstriction is unknown. This study sought to clarify the effect of aging in females on celiac artery blood flow during dynamic light-intensity exercise. Twelve healthy young females (YF: 20 ± 2 yr, mean ± SD) and 12 healthy older females (OF: 71 ± 4 yr) performed dynamic knee-extension and knee-flexion exercises at 30% of heart rate reserve for 4 min. The absolute changes from baseline (Δ) for mean arterial blood pressure (MAP), celiac artery mean blood flow (celMBF), and celiac vascular conductance (celVC) during exercise were calculated. ABP was measured using an automated sphygmomanometer, and celMBF was recorded by Doppler ultrasonography. The increase in MAP during exercise was greater in OF than in YF (YF: +14 ± 7 mmHg, OF: +24 ± 13 mmHg, P = 0.028). The celMBF decreased during exercise in both groups, but there was no significant difference in the response between YF and OF (YF: −93.0 ± 66.1 mL/min, OF: −89.6 ± 64.0 mL/min, P = 0.951). The celVC also decreased during exercise and remained lower than baseline during exercise. However, the response was not different between YF and OF (YF: −1.8 ± 1.0 mL/min/mmHg, OF: −1.5 ± 0.6 mL/min/mmHg, P = 0.517). These results demonstrate that aging in females has minimal influence on splanchnic artery hemodynamic responses during dynamic light-intensity exercise, suggesting that exaggerated ABP responses during exercise in OF are not due to greater splanchnic vasoconstriction. NEW & NOTEWORTHY: During exercise, the splanchnic arteries vasoconstrict, contributing to blood flow redistribution and the blood pressure response. Blood pressure responses to exercise are exaggerated with aging in females; however, the physiological mechanism responsible has not been clarified. We show that celiac artery blood flow changes during light-intensity dynamic exercise do not differ with age in females. This indicates the exaggerated blood pressure to exercise with aging is likely not due to a difference in splanchnic vasoconstriction. [ABSTRACT FROM AUTHOR]

Hypertension is recognised as a leading attributable risk factor for cardiovascular disease and premature mortality. Global initiatives towards the prevention and treatment of arterial hypertension are centred around non-pharmacological lifestyle modification. Exercise recommendations differ between professional and scientific organisations, but are generally unanimous on the primary role of traditional aerobic and dynamic resistance exercise. In recent years, isometric exercise training (IET) has emerged as an effective novel exercise intervention with consistent evidence of reductions in blood pressure (BP) superior to that reported from traditional guideline-recommended exercise modes. Despite a wealth of emerging new data and endorsement by select governing bodies, IET remains underutilised and is not widely prescribed in clinical practice. This expert-informed review critically examines the role of IET as a potential adjuvant tool in the future clinical management of BP. We explore the efficacy, prescription protocols, evidence quality and certainty, acute cardiovascular stimulus, and physiological mechanisms underpinning its anti-hypertensive effects. We end the review with take-home suggestions regarding the direction of future IET research. [ABSTRACT FROM AUTHOR]

Microneurographic recordings of muscle sympathetic nerve activity (MSNA) and the succeeding changes in beat-to-beat blood pressure (i.e., sympathetic transduction) provide important insights into the neural control of the circulation in humans. Despite its widespread use, the reliability of this technique remains unknown. Herein, we assessed the intra- and interday test-retest reliability of signal-averaging sympathetic transduction to blood pressure. Data were analyzed from 15 (9 M/6 F) young, healthy participants who completed two baseline recordings of fibular nerve MSNA separated by 60 min (intraday). The interday reliability was obtained in a subset of participants (n = 13, 9 M/4 F) who completed a follow-up MSNA study. Signal-averaging sympathetic transduction was quantified as peak change in diastolic (DBP) and mean arterial pressure (MAP) following a burst of MSNA. Analyses were also computed considering different MSNA burst sizes (quartiles of normalized MSNA) and burst patterns (singlets, couplets, triplets, and quadruplets+), as well as nonburst responses. Intraclass-correlation coefficients (ICCs) were used as the main reliability measure. Peak changes in MAP [intraday: ICC = 0.76 (0.30–0.92), P = 0.006; interday: ICC = 0.91 (0.63–0.97), P < 0.001] demonstrated very good to excellent reliability. Sympathetic transduction of MSNA burst size displayed moderate to very good reliability, though the reliability of MSNA burst pattern was poor to very good. Nonburst responses revealed poor intraday [ICC = 0.37 (−1.05 to 0.80), P = 0.21], but very good interday [ICC = 0.76 (0.18–0.93), P = 0.01] reliability. Intraday reliability measures were consistently lower than interday reliability. Similar results were obtained using DBP. Collectively, these findings provide evidence that the burst-triggering signal-averaging technique is a reliable measure of sympathetic transduction to blood pressure in young, healthy adults. NEW & NOTEWORTHY: We found that signal-averaging sympathetic transduction to blood pressure displayed very good to excellent intra- and interday test-retest reliability in healthy, young adults. Reliability analyses according to muscle sympathetic burst size, burst pattern, and nonburst response were less consistent. Results were similar when using diastolic or mean arterial pressure in the transduction calculation. These findings suggest that the signal-averaging technique can be used with confidence to investigate sympathetic transduction to blood pressure in humans across time. [ABSTRACT FROM AUTHOR]

The purpose of this study was to clarify sex differences in the inhibition of sympathetic vasomotor outflow which is caused by the loading of cardiopulmonary baroreceptors. Ten young males and ten age-matched females participated. The participants underwent a passive leg raising (PLR) test wherein they were positioned supine (baseline, 0º), and their lower limbs were lifted passively at 10º, 20º, 30º, and 40º. Each angle lasted for 3 min. Muscle sympathetic nerve activity (MSNA) was recorded via microneurography of the left radial nerve. Baseline MSNA was lower in females compared to males. MSNA burst frequency was decreased during the PLR in both males (− 6.2 ± 0.4 bursts/min at 40º) and females (− 6.5 ± 0.4 bursts/min at 40º), but no significant difference was detected between the two groups (P = 0.61). These results suggest that sex has minimal influence on the inhibition of sympathetic vasomotor outflow during the loading of cardiopulmonary baroreceptors in young individuals. [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]

This document, published in the journal Clinical Autonomic Research, explores the effects of inhaling cannabis on cardiac autonomic function in humans. The study specifically focuses on the impact of Δ-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), two primary cannabinoids found in cannabis. The researchers found that inhalation of THC-containing cannabis decreased cardiac baroreflex gain and heart rate variability, while CBD did not have the same effect. Additionally, THC increased ventricular repolarization, as indicated by changes in the QT interval. These findings suggest that the physiological effects of cannabis may be influenced by the relative proportions of THC and CBD. [Extracted from the article]

A single high-fat Western meal transiently reduces endothelium-dependent vasodilation at rest, but the interaction with sympathetic vasoconstrictor activity during exercise remains unknown. Herein, we tested the hypothesis that a single high-fat Western meal would impair the ability of contracting skeletal muscle to offset vascular responsiveness to sympathetic activation during exercise, termed functional sympatholysis. In 18 (10 females/8 males) healthy young adults, forearm blood flow (Doppler ultrasound) and beat-to-beat arterial pressure (photoplethysmography) were measured during lower-body negative pressure (LBNP; -20 mmHg) applied at rest and simultaneously during low (15% maximum contraction) and moderate (30% maximum contraction)-intensity rhythmic handgrip exercise. The magnitude of sympatholysis was calculated as the difference of LBNP-induced changes in forearm vascular conductance (FVC) between handgrip and rest. Experiments were performed preprandial and 1 h, 2 h, and 3 h after a high- or low-fat meal. In the preprandial state, LBNP decreased resting FVC (Δ-54 ± 10%), and these responses were attenuated during low (Δ-17 ± 7%)- and moderate (Δ-8 ± 6%)-intensity handgrip exercise. Following a high-fat meal, LBNP induced attenuated decreases in resting FVC (3 h postprandial, Δ-47 ± 10%, P = 0.002 vs. preprandial) and blunted attenuation of FVC during low (3 h postprandial, Δ-23 ± 8%, P = 0.001 vs. preprandial)- and moderate (3 h postprandial, Δ-16 ± 6%, P < 0.001 vs. preprandial)-intensity handgrip exercise. The high-fat meal attenuated the magnitude of sympatholysis during low (preprandial, 38 ± 7 vs. 3 h postprandial, 23 ± 8%, P < 0.001)- and moderate (preprandial, 46 ± 11 vs. 3 h postprandial, 31 ± 10%, P < 0.001)-intensity handgrip exercise. The low-fat meal had no impact on these responses. In conclusion, a single high-fat Western meal modulates sympathetic vasoconstriction at rest and during low- and moderate-intensity handgrip exercise in young healthy adults. [ABSTRACT FROM AUTHOR]

These data suggest that augmented transduction may contribute to greater blood pressure fluctuations that could, over time, lead to a pathological cardiovascular phenotype and blood pressure dysregulation. Larger vasoconstrictor responses to MSNA bursts lead to higher pressor responses, which could contribute to greater blood pressure fluctuations (i.e., larger blood pressure variability). Keywords: Sex differences; Muscle sympathetic nerve activity; Pressor responses; Average-real-variability; Blood pressure regulation EN Sex differences Muscle sympathetic nerve activity Pressor responses Average-real-variability Blood pressure regulation 529 532 4 08/22/23 20230801 NES 230801 Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/s10286-023-00949-7. [Extracted from the article]

This case characterizes the clinical motor, perceived fatigue, gait and balance, cardiovascular, neuromuscular, and cardiopulmonary responses after cycling 7850 km over 85 days in a physically active 57‐year‐old male with idiopathic Parkinson's disease (PD). The participant cycled 73/85 days (86%); averaging 107.5 ± 48.9 km/day over 255.4 ± 108.8 min. Average cycling heart rate was 117 ± 11 bpm. The Unified Parkinson Disease Rating Scale (UPDRS) Part III motor score decreased from 46 to 26 (−44%), while the mean Parkinson Fatigue Scale (PFS‐16) score decreased from 3.4 to 2.3 (−32%). Peak power output on a maximal aerobic exercise test increased from 326 to 357 W (+10%), while peak isotonic power of single‐leg knee extension increased from 312 to 350 W (+12%). Maximal oxygen uptake following the trip was 53.1 mL/min/kg or 151% of predicted. Resting heart rate increased from 48 to 71 bpm (+48%). The systolic and diastolic blood pressure responses to a 2‐min submaximal static handgrip exercise were near absent at baseline (∆2/∆2 mm Hg) but appeared normal post‐trip (∆17/∆9 mm Hg). Gait and static balance measures were unchanged. This case report demonstrates the capacity for physiological and clinical adaptations to a high‐volume, high‐intensity cycling regiment in a physically active middle‐aged male with PD. [ABSTRACT FROM AUTHOR]

Post‐hypoxia sympathoexcitation does not elicit corresponding changes in vascular tone, suggesting diminished sympathetic signalling. Blunted sympathetic transduction following acute hypoxia, however, has not been confirmed and the effects of hypoxia on the sympathetic transduction of mean arterial pressure (MAP) as a function of action potential (AP) activity is unknown. We hypothesized that MAP changes would be blunted during acute hypoxia but restored in recovery and asynchronous APs would elicit smaller MAP changes than synchronous APs. Seven healthy males (age: 24 (3) years; BMI: 25 (3) kg/m2) underwent 20 min isocapnic hypoxia (PETO2: 47 (2) mmHg) and 30 min recovery. Multi‐unit microneurography (muscle sympathetic nerve activity; MSNA) and continuous wavelet transform with matched mother wavelet was used to detect sympathetic APs during baseline, hypoxia, early (first 7 min) and late (last 7 min) recovery. AP groups were classified as synchronous APs, asynchronous APs (occurring outside an MSNA burst) and no AP activity. Sympathetic transduction of MAP was quantified using signal‐averaging, with ΔMAP tracked following AP group cardiac cycles. Following synchronous APs, ΔMAP was reduced in hypoxia (+1.8 (0.9) mmHg) and early recovery (+1.5 (0.7) mmHg) compared with baseline (+3.1 (2.2) mmHg). AP group‐by‐condition interactions show that at rest asynchronous APs attenuate MAP reductions compared with no AP activity (−0.4 (1.1) vs. −2.2 (1.2) mmHg, respectively), with no difference between AP groups in hypoxia, early or late recovery. Sympathetic transduction of MAP is blunted in hypoxia and early recovery. At rest, asynchronous sympathetic APs contribute to neural regulation of MAP by attenuating nadir pressure responses. Key points: Acute isocapnic hypoxia elicits lasting sympathoexcitation that does not correspond to parallel changes in vascular tone, suggesting blunted sympathetic transduction.Signal‐averaging techniques track the magnitude and temporal cardiovascular responses following integrated muscle sympathetic nerve activity (MSNA) burst and non‐burst cardiac cycles. However, this does not fully characterize the effects of sympathetic action potential (AP) activity on blood pressure control.We show that hypoxia blunts the sympathetic transduction of mean arterial pressure (MAP) following synchronous APs that form integrated MSNA bursts and that sympathetic transduction of MAP remains attenuated into early recovery.At rest, asynchronous APs attenuate the reduction in MAP compared with cardiac cycles following no AP activity, thus asynchronous sympathetic APs appear to contribute to the neural regulation of blood pressure.The results advance our understanding of sympathetic transduction of arterial pressure during and following exposure to acute isocapnic hypoxia in humans. [ABSTRACT FROM AUTHOR]

Aims: Patients with sympathetic excess are those most likely to benefit from novel interventions targeting the autonomic nervous system. To inform such personalized therapy, we identified determinants of augmented muscle sympathetic nerve activity (MSNA) in heart failure, versus healthy controls. Methods and results: We compared data acquired in 177 conventionally‐treated, stable non‐diabetic patients in sinus rhythm, aged 18–79 years (149 males; 28 females; left ventricular ejection fraction [LVEF] 25 ± 11% [mean ± standard deviation]; range 5–60%), and, concurrently, under similar conditions, in 658 healthy, normotensive volunteers (398 males; aged 18–81 years). In heart failure, MSNA ranged between 7 and 90 bursts·min−1, proportionate to heart rate (p < 0.0001) and body mass index (BMI) (p = 0.03), but was unrelated to age, blood pressure, or drug therapy. Mean MSNA, adjusted for age, sex, BMI, and heart rate, was greater in heart failure (+14.2 bursts·min−1; 95% confidence interval [CI] 12.1–16.3; p < 0.0001), but lower in women (−5.0 bursts·min−1; 95% CI 3.4–6.6; p < 0.0001). With spline modeling, LVEF accounted for 9.8% of MSNA variance; MSNA related inversely to LVEF below an inflection point of ∼21% (p < 0.006), but not above. Burst incidence was greater in ischaemic than dilated cardiomyopathy (p = 0.01), and patients with sleep apnoea (p = 0.03). Burst frequency correlated inversely with stroke volume (p < 0.001), cardiac output (p < 0.001), and peak oxygen consumption (p = 0.002), and directly with norepinephrine (p < 0.0001) and peripheral resistance (p < 0.001). Conclusion: Burst frequency and incidence exceeded normative values in only ∼53% and ∼33% of patients. Such diversity encourages selective deployment of sympatho‐modulatory therapies. Clinical characteristics can highlight individuals who may benefit from future personalized interventions targeting pathological sympathetic activation. [ABSTRACT FROM AUTHOR]

We examined the influence of sex and age on the relationship between aerobic fitness and muscle sympathetic nerve activity (MSNA) in healthy adults. Data were assessed from 224 volunteers (88 females), aged 18–76 yr, in whom resting MSNA (microneurography) and peak oxygen uptake (V̇o2peak; incremental exercise test) were evaluated. When separated into younger (<50 yr) and older (≥50 yr) subgroups, there were inverse relationships between relative V̇o2peak (mL·kg−1·min−1) and MSNA burst frequency in younger males (R² = 0.21, P < 0.0001) and older females (R2 = 0.36, P < 0.01), but not older males (R² = 0.05, P = 0.08) or younger females (R² = 0.03, P = 0.14). Similar patterns were observed with absolute V̇o2peak (L·min−1) and percent-predicted (based on age, sex, weight, height, and modality), and with burst incidence. Sex and age influence the relationship between aerobic fitness and resting MSNA, and, thus, must be considered as key variables when studying these potential associations; inverse relationships are strongest in younger males and older females. NEW & NOTEWORTHY Our data reveal for the first time that associations between aerobic fitness and resting muscle sympathetic nerve activity are sex and age specific; inverse relationships are evident in younger males (<50 yr) and older females (≥50 yr), but absent in younger females (<50 yr) and older males (≥50 yr). [ABSTRACT FROM AUTHOR]

Glucose ingestion and absorption into the bloodstream can challenge glycemic regulation and vascular endothelial function. Muscular contractions in exercise promote a return to homeostasis by increasing glucose uptake and blood flow. Similarly, muscle hypoxia supports glycemic regulation by increasing glucose oxidation. Blood flow restriction (BFR) induces muscle hypoxia during occlusion and reactive hyperemia upon release. Thus, in the absence of exercise, electric muscle stimulation (EMS) and BFR may offer circulatory and glucoregulatory improvements. In 13 healthy, active participants (27 ± 3 yr, 7 females), we tracked post-glucose (oral 100 g) glycemic, cardiometabolic, and vascular function measures over 120 min following four interventions: 1) BFR, 2) EMS, 3) BFR þ EMS, or 4) control. BFR was applied at 2-min intervals for 30 min (70% occlusion), and EMS was continuous for 30 min (maximum-tolerable intensity). Glycemic and insulinemic responses did not differ between interventions (partial g2 = 0.11–0.15, P = 0.2), however, only BFR þ EMS demonstrated cyclic effects on oxygen consumption, carbohydrate oxidation, muscle oxygenation, heart rate, and blood pressure (all P < 0.01). Endothelial function was reduced 60 min post-glucose ingestion across interventions and recovered by 120 min (5.9 ± 2.6% vs 8.4 ± 2.7%; P < 0.001). Estimated microvascular function was not meaningfully different. Leg blood flow increased during EMS and BFR þ EMS ( þ 656 ± 519 mL·min-1, þ 433 ± 510 mL·min-1 ; P < 0.001); however, only remained elevated following BFR intervention 90 min post-glucose ( þ 94 ± 94 mL·min-1 ; P = 0.02). Superimposition of EMS onto cyclic BFR did not preferentially improve post-glucose metabolic or vascular function among young, active participants. Cyclic BFR increased blood flow delivery 60 min beyond intervention, and BFR þ EMS selectively increased carbohydrate usage and reduced muscle oxygenation warranting future clinical assessments [ABSTRACT FROM AUTHOR]

Baroreflex resetting permits sympathetic long‐term facilitation (sLTF) following hypoxia; however, baroreflex control of action potential (AP) clusters and AP recruitment patterns facilitating sLTF is unknown. We hypothesized that baroreflex resetting of arterial pressure operating points (OPs) of AP clusters and recruitment of large‐amplitude APs would mediate sLTF following hypoxia. Eight men (age: 24 (3) years; body mass index: 24 (3) kg/m2) underwent 20 min isocapnic hypoxia (PETO2${P_{{\rm{ET}}{{\rm{O}}_{\rm{2}}}}}$: 47 (2) mmHg) and 30 min recovery. Multi‐unit microneurography (muscle sympathetic nerve activity; MSNA) and a continuous wavelet transform with matched mother wavelet was used to detect sympathetic APs during baseline, hypoxia, early (first 5 min), and late recovery (last 5 min). AP amplitude (normalized to largest baseline AP amplitude), percentage APs occurring outside a MSNA burst (percentage asynchronous APs), and proportion of APs firing in small (1–3), medium (4–6) and large (7–10) normalized cluster sizes was calculated. Normalized clusters were used to assess baroreflex OPs and sensitivity. Hypoxia increased total MSNA activity, which remained elevated during recovery (P < 0.0001). Baroreflex OPs were shifted rightward for all clusters in recovery, with no effect on slope. Compared to baseline, AP amplitude was elevated by 3 (2)% and 4 (2)% while asynchronous APs were reduced by 9 (5)% and 7 (6)% in early and late recovery, respectively. In early recovery, the proportion of APs firing in large clusters was increased compared to baseline. Hypoxia‐induced sLTF is mediated by baroreflex resetting of AP clusters to higher OPs, reduced asynchronous AP firing, and increased contribution from large‐amplitude APs. Key points: Acute isocapnic hypoxia resets the arterial baroreflex and permits long‐lasting sympathoexcitation, termed sympathetic long‐term facilitation.Our understanding of sympathetic long‐term facilitation following hypoxia in humans is based on multiunit muscle sympathetic nerve activity and does not fully characterize the underlying baroreflex control of sympathetic neuronal subpopulations or their discharge/recruitment strategies.We show that sympathetic long‐term facilitation is mediated by baroreflex resetting of sympathetic action potential clusters to higher arterial pressure operating points, a reduction in the percentage of action potentials firing asynchronously, and a shift toward larger amplitude action potential activity.The results advance our fundamental understanding of how the sympathetic nervous system mediates sympathetic long‐term facilitation following exposure to acute isocapnic hypoxia in humans. [ABSTRACT FROM AUTHOR]

Resting beat-to-beat blood pressure variability is a powerful predictor of cardiovascular events and end-organ damage. However, its underlying mechanisms remain unknown. Herein, we tested the hypothesis that a potentiation of GABAergic synaptic transmission by diazepam would acutely increase resting beat-to-beat blood pressure variability. In 40 (17 females) young, normotensive subjects, resting beat-to-beat blood pressure (finger photoplethysmography) was continuously measured for 5-10 min, 60 min after the oral administration of either diazepam (10 mg) or placebo. The experiments were conducted in a randomized, double-blinded, and placebo-controlled design. Stroke volume was estimated from the blood pressure waveform (ModelFlow) permitting the calculation of cardiac output and total peripheral resistance. Direct recordings of muscle sympathetic nerve activity (MSNA, microneurography) were obtained in a subset of subjects (n = 13), and spontaneous cardiac and sympathetic baroreflex sensitivity were calculated. Compared with placebo, diazepam significantly increased the standard deviation of systolic blood pressure (4.7 ± 1.4 vs. 5.7 ± 1.5 mmHg, P = 0.001), diastolic blood pressure (3.8 ± 1.2 vs. 4.5 ± 1.2 mmHg, P = 0.007), and mean blood pressure (3.8 ± 1.1 vs. 4.5 ± 1.1 mmHg, P = 0.002), as well as cardiac output (469 ± 149 vs. 626 ± 259 mL/min, P < 0.001) and total peripheral resistance (1.0 ± 0.3 vs. 1.4 ± 0.6 mmHg/L/min, P < 0.001). Similar results were found using different indices of variability. Furthermore, diazepam reduced MSNA (placebo: 22 ± 6 vs. diazepam: 18 ± 8 bursts/min, P = 0.025) without affecting the arterial baroreflex control of heart rate (placebo: 18.6 ± 6.7 vs. diazepam: 18.8 ± 7.0 ms/mmHg, P = 0.87) and MSNA (placebo: -3.6 ± 1.2 vs. diazepam: -3.4 ± 1.5 bursts/100 Hb/mmHg, P = 0.55). Importantly, these findings were not impacted by biological sex. We conclude that GABAA receptors modulate resting beat-to-beat blood pressure variability in young adults. [ABSTRACT FROM AUTHOR]

In HF patients who quit smoking within the last 15 years, both the time since quitting and pack-years correlated with MSNA burst occurrence, aligning with the time required to ameliorate the increased risk of smoking in HF [[4]]. Elevated MSNA independently predicts mortality in patients with HFrEF [[2]], and understanding the latent risks in those who have recently ceased smoking may have important implications in patient care. We quantified MSNA burst frequency (bursts/min), incidence (bursts/100 heartbeats), and normalized height (% largest burst). Heart failure (HF) increases resting muscle sympathetic nerve activity (MSNA) in those with preserved and, to a greater extent, in those with reduced left ventricular function (heart failure with reduced ejection fraction [HFrEF]) [[1]] and predicts mortality in patients with HFrEF [[2]]. [Extracted from the article]

Signal-averaged sympathetic transduction of blood pressure (BP) is inversely related to resting muscle sympathetic nerve activity (MSNA) burst frequency in healthy cohorts. Whether this represents a physiological compensatory adaptation or a methodological limitation, remains unclear. The current analysis aimed to determine the contribution of methodological limitations by evaluating the dependency of MSNA transduction at different levels of absolute BP. Thirty-six healthy participants (27 ± 7 yr, 9 females) underwent resting measures of beat-to-beat heart rate, BP, and muscle sympathetic nerve activity (MSNA). Tertiles of mean arterial pressure (MAP) were computed for each participant to identify cardiac cycles occurring below, around, and above the MAP operating pressure (OP). Changes in hemodynamic variables were computed across 15 cardiac cycles within each MAP tertile to quantify sympathetic transduction. MAP increased irrespective of sympathetic activity when initiated below the OP, but with MSNA bursts provoking larger rises (3.0 ± 0.9 vs. 2.1 ± 0.7 mmHg; P < 0.01). MAP decreased irrespective of sympathetic activity when initiated above the OP, but with MSNA bursts attenuating the drop (-1.3 ± 1.1 vs. -3.1 ± 1.2 mmHg; P < 0.01). In participants with low versus high resting MSNA (12 ± 4 vs. 32 ± 10 bursts/min), sympathetic transduction of MAP was not different when initiated by bursts below (3.2 ± 1.0 vs. 2.8 ± 0.9 mmHg; P = 0.26) and above the OP (-1.0 ± 1.3 vs. -1.6 ± 0.8 mmHg; P = 0.08); however, low resting MSNA was associated with a smaller proportion of MSNA bursts firing above the OP (15 ± 5 vs. 22 ± 5%; P < 0.01). The present analyses demonstrate that the signal-averaging technique for calculating sympathetic transduction of BP is influenced by the timing of an MSNA burst relative to cyclic oscillations in BP. NEW & NOTEWORTHY The current signal-averaging technique for calculating sympathetic transduction of blood pressure does not consider the arterial pressure at which each muscle sympathetic burst occurs. A burst firing when mean arterial pressure is above the operating pressure was associated with a decrease in blood pressure. Thus, individuals with higher muscle sympathetic nerve activity demonstrate a reduced sympathetic transduction owing to the weighted contribution of more sympathetic bursts at higher levels of arterial pressure. [ABSTRACT FROM AUTHOR]

Calculating the blood pressure (BP) response to a burst of muscle sympathetic nerve activity (MSNA), termed sympathetic transduction, may be influenced by an individual’s resting burst frequency. We examined the relationships between sympathetic transduction and MSNA in 107 healthy males and females and developed a normalized sympathetic transduction metric to incorporate resting MSNA. Burst-triggered signal averaging was used to calculate the peak diastolic BP response following each MSNA burst (sympathetic transduction of BP) and following incorporation of MSNA burst cluster patterns and amplitudes (sympathetic transduction slope). MSNA burst frequency was negatively correlated with sympathetic transduction of BP (r = −0.42; P < 0.01) and the sympathetic transduction slope (r = −0.66; P < 0.01), independent of sex. MSNA burst amplitude was unrelated to sympathetic transduction of BP in males (r = 0.04; P = 0.78), but positively correlated in females (r = 0.44; P < 0.01) and with the sympathetic transduction slope in all participants (r = 0.42; P < 0.01). To control for MSNA, the linear regression slope of the log-log relationship between sympathetic transduction and MSNA burst frequency was used as a correction exponent. In subanalysis of males (38 ± 10 vs. 14 ± 4 bursts/min) and females (28 ± 5 vs. 12 ± 4 bursts/min) with high versus low MSNA, sympathetic transduction of BP and sympathetic transduction slope were lower in participants with high MSNA (all P < 0.05). In contrast, normalized sympathetic transduction of BP and normalized sympathetic transduction slope were similar in males and females with high versus low MSNA (all P > 0.22). We propose that incorporating MSNA burst frequency into the calculation of sympathetic transduction will allow comparisons between participants with varying levels of resting MSNA. [ABSTRACT FROM AUTHOR]

Exercise is a well-known sympathoexcitatory stimulus. However, muscle sympathetic nerve activity (MSNA) can decrease during the onset of muscle contraction. Yet, the underlying mechanisms and neurotransmitters involved in the sympathetic responses at the onset of exercise remain unknown. Herein, we tested the hypothesis that GABAA receptors may contribute to the MSNA responses at the onset of static handgrip in humans. Thirteen young, healthy individuals (4 females) performed 30 s of ischemic static handgrip at 30% of maximum volitional contraction before and following oral administration of either placebo or diazepam (10 mg), a benzodiazepine that enhances GABAA activity. MSNA (microneurography), beat-to-beat blood pressure (finger photopletysmography), heart rate (electrocardiogram), and stroke volume (ModelFlow) were continuously measured. Cardiac output (CO = stroke volume x heart rate) and total vascular conductance (TVC = CO/mean blood pressure) were subsequently calculated. At rest, MSNA was reduced while hemodynamic variables were unchanged after diazepam administration. Before diazepam, static handgrip elicited a significant decrease in MSNA burst frequency (Δ7 ± 2 bursts/min, P < 0.01 vs. baseline) and MSNA burst incidence (Δ16 ± 2 bursts/100 heart beats, P < 0.01 vs. baseline); however, these responses were attenuated following diazepam administration (D-1 ± 2 bursts/min and Δ7 ± 2 bursts/100 heart beats, respectively; P < 0.01 vs. before diazepam). Diazepam did not affect the increases in heart rate, blood pressure, CO, and TVC at the exercise onset. Importantly, the placebo had no effect on any variable at rest or exercise onset. These findings suggest that GABAA receptor activation modulates the MSNA responses at the onset of static exercise in young, healthy humans. [ABSTRACT FROM AUTHOR]

Purpose: Following a shortening or lengthening muscle contraction, torque produced in the isometric steady state is lower (residual torque depression; rTD) or higher (residual torque enhancement; rTE), respectively, compared to a purely isometric contraction at the same final muscle length and level of activation. This is referred to as the history dependence of force. When matching a given torque level, there is greater muscle activation (electromyography; EMG) following shortening and less activation following lengthening. Owing to these differences in neuromuscular activation, it is unclear whether perception of effort is altered by the history dependence of force during plantar-flexion. Methods: Experiment 1 tested whether perception of effort differed between the rTD and rTE state when torque was matched. Experiment 2 tested whether perception of effort differed between the rTD and rTE state when EMG was matched. Finally, experiment 3 tested whether EMG differed between the rTD and rTE state when perception of effort was matched. Results: When torque was matched, both EMG and perception of effort were higher in the rTD compared to rTE state. When EMG was matched, torque was lower in the rTD compared to rTE state while perception of effort did not differ between the two states. When perception of effort was matched, torque was lower in the rTD compared to rTE state and EMG did not differ between the two states. Conclusion: The combined results from these experiments indicate that the history dependence of force alters one's perception of effort, dependent on the level of motor command. [ABSTRACT FROM AUTHOR]

The article presents the Heart failure-specific inverse relationship between the muscle sympathetic response to dynamic leg exercise and VO2peak. Topics discussed include Exercise intolerance, a symptom afflicting the majority of patients with heart failure with reduced ejection fraction (HFrEF), has been attributed classically to a range of disturbances; and the purpose of the present work was to test the hypothesis that the percent predicted VO2peak of patients with HFrEF relates.

Postprandial superior mesenteric artery (SMA) blood flow is associated with the caloric content of a meal. Whether spectral analysis of a peripheral pulse wave or heart rate can model postprandial SMA blood flow is unclear. We hypothesized that altering the caloric content of a meal would evoke dose-response increases in postprandial SMA hyperemia and distinct changes in the pulse wave harmonic spectrum and heart rate. Twenty healthy subjects (10 male, 26 ± 10 yr) completed a randomized cross-over trial, comparing three meals (280, 560, or 840 kcal) on SMA blood flow (Doppler ultrasound), heart rate, and the first to seventh harmonic amplitudes (derived from a finger pulse wave). Supine SMA diameter and blood velocity were collected at baseline and every 15 min throughout 2 h of postprandial recovery. SMA blood flow was smaller across all time points following meal 1 (280 kcal) compared with both meal 2 (560 kcal) and meal 3 (840 kcal) (all P < 0.001), while meal 2 had attenuated responses compared with meal 3 at 60, 90, 105, and 120 min postprandial (all P < 0.01). Distinct changes in heart rate and the amplitude of second to fifth harmonics were observed between meals (all P < 0.05). The changes in harmonic spectrum or heart rate explained 66-69% (adjusted r²) of the variance in postprandial SMA blood flow. These results provide proof-of-concept that easily obtained and noninvasive postprandial harmonic profiles or heart rate may be used to explain changes in SMA blood flow and exploited for the development of wearable technology to noninvasively track caloric intake. [ABSTRACT FROM AUTHOR]

A small proportion of postganglionic muscle sympathetic single units can be inhibited during sympathoexcitatory stressors in humans. However, whether these responses are dependent on the specific stressor or the level of sympathoexcitation remains unclear. We hypothesize that, when matched by sympathoexcitatory magnitude, different stressors can evoke similar proportions of inhibited single units. Multiunit and single-unit muscle sympathetic nerve activity (MSNA) were recorded in seven healthy young males at baseline and during 1) rhythmic handgrip exercise (40% of maximum voluntary contraction) and 2) acute isocapnic hypoxia (partial pressure of end-tidal O2 47 ± 3 mmHg). Single units were classified as activated, nonresponsive, or inhibited if the spike frequency was above, within, or below the baseline variability, respectively. By design, rhythmic handgrip and isocapnic hypoxia similarly increased multiunit total MSNA [Δ273 ± 208 vs. Δ254 ± 193 arbitrary units (AU), P = 0.84] and single-unit spike frequency (Δ8 ± 10 vs. Δ12 ± 13 spikes/min, P = 0.12). Among 19 identified single units, the proportions of activated (47% vs. 68%), nonresponsive (32% vs. 16%), and inhibited (21% vs. 16%) single units were not different between rhythmic handgrip and isocapnic hypoxia (P = 0.42). However, only 9 (47%) single units behaved with concordant response patterns across both stressors (7 activated, 1 nonresponsive, and 1 inhibited during both stressors). During the 1-min epoch with the highest increase in total MSNA during hypoxia (Δ595 ± 282 AU, P < 0.01) only one single unit was inhibited. These findings suggest that the proportions of muscle sympathetic single units inhibited during stress are associated with the level of sympathoexcitation and not the stressor per se in healthy young males. NEW & NOTEWORTHY Subpopulations of muscle sympathetic single units can be inhibited during mild sympathoexcitatory stress. We demonstrate that rhythmic handgrip exercise and isocapnic hypoxia, when matched by multiunit sympathoexcitation, induce similar proportions of single-unit inhibition, highlighting that heterogeneous single-unit response patterns are related to the level of sympathoexcitation independent of the stressor type. Interestingly, only 47% of single units behaved with concordant response patterns between stressors, suggesting the potential for functional specificity within the postganglionic neuronal pool. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In healthy young volunteers, acquisition of blood oxygen level-dependent (BOLD) magnetic resonance (MR) and muscle sympathetic nerve (MSNA) signals during simulation of obstructive or central sleep apnea identified cortical cardiovascular autonomic regions in which the BOLD signal changed synchronously with acute noradrenergic excitation. In the present work, we tested the hypothesis that such Mueller maneuvers (MM) and breath-holds (BH) would elicit greater concomitant changes in mean efferent nerve firing and BOLD signal intensity in patients with moderate to severe obstructive sleep apnea (OSA) relative to age- and sex-matched individuals with no or only mild OSA (Apnea Hypopnea Index, AHI, <15 events/h). Forty-six participants, 24 with OSA [59 ± 8 years; AHI 31 ± 18 events/h (mean ± SD); seven women] and 22 without (58 ± 11 years; AHI 7 ± 4; nine women), performed a series of three MM and three BH, in randomly assigned order, twice: during continuous recording of MSNA from the right fibular nerve and, on a separate day, during T2∗-weighted echo planar functional MR imaging. MSNA at rest was greater in those with OSA (65 ± 19 vs. 48 ± 17 bursts per 100 heart beats; p < 0.01). MM and BH elicited similar heart rate, blood pressure, and MSNA responses in the two cohorts; group mean BOLD data were concordant, detecting no between-group differences in cortical autonomic region signal activities. The present findings do not support the concept that recurring episodes of cyclical apnea during sleep alter cortical or peripheral neural responsiveness to their simulation during wakefulness by volitional Mueller maneuvers or breath-holds. [ABSTRACT FROM AUTHOR]

Acute elevations in inflammatory cytokines have been demonstrated to increase aortic and left ventricular stiffness and reduce endothelial function in healthy subjects. As vascular and cardiac functions are often transiently reduced following prolonged exercise, it is possible that cytokines released during exercise may contribute to these alterations. The a priori aims of this study were to determine whether vaccine-induced increases in inflammatory cytokines would reduce vascular and left ventricular function, whether vascular alterations would drive cardiac impairments, and whether this would be potentiated by moderate exercise. In a randomized crossover fashion, 16 male participants were tested under control (CON) and inflammatory (INF) conditions, wherein INF testing occurred 8 h following administration of an influenza vaccine. On both days, participants underwent measures of echocardiography performed during light cycling (stress-echocardiography), carotid-femoral pulse wave velocity (cf-PWV), and superficial femoral flow-mediated dilation (FMD) before and after cycling for 90 min at ∼85% of their first ventilatory threshold. IL-6 increased significantly (Δ1.9 ± 1.3 pg/mL, P < 0.001), whereas TNFα was nonsignificantly augmented (Δ0.05 ± 0.11 pg/mL, P = 0.09), 8 h following vaccination. Vascular function was unaltered following cycling or inflammation (all P > 0.05). The use of echocardiography during light cycling revealed cardiac alterations traditionally expected to occur only with greater exercise loads, with reduced systolic (e.g., longitudinal strain CON: Δ3.3 ± 4.4%, INF: Δ1.7 ± 2.7%, P = 0.002) and diastolic function (e.g., E/A ratio CON: Δ-0.32 ± 0.34 a.u., INF:Δ-0.25 ± 0.27 a.u., P = 0.002) following cycling, independent of inflammation. The vaccine reduced stroke volume (SV) (main effect of condition P = 0.009) before-and-after cycling. These findings indicate that reduced cardiac function following exercise occurs largely independent of additional inflammatory load. [ABSTRACT FROM AUTHOR]

Cigarette smoking is among the most detrimental behaviors to cardiovascular health, resulting in arterial stiffening, endothelial dysfunction, and structural/functional alterations to the myocardium. Similar to cigarettes, cannabis is commonly smoked, and next to alcohol, is the most commonly used recreational substance in the world. Despite this, little is known about the long-term cardiovascular effects of smoking cannabis. This study explored the associations of cardiovascular structure and function with cannabis use in ostensibly healthy young participants (n = 35). Using echocardiography, carotid-femoral pulse wave velocity (cfPWV), and brachial flow-mediated dilation (FMD), we performed a cross-sectional assessment of cardiovascular function in cannabis users (n = 18) and controls (n = 17). There were no differences in cardiac morphology or traditional resting measures of systolic or diastolic function between cannabis users and controls (all P > 0.05), whereas cannabis users demonstrated reduced peak apical rotation compared with controls (cannabis users: 5.5 ± 3.8, controls: 9.6 ± 1.5; P = 0.02). Cannabis users had higher cfPWV compared with controls (cannabis users: 5.8 ± 0.6 m/s, controls: 5.3 ± 0.7 m/s; P = 0.05), whereas FMD was similar between cannabis users and controls (cannabis users: 8.3 ± 3.3%, controls: 6.8 ± 3.6%; P = 0.7). Young, healthy, and cannabis users demonstrate altered cardiac mechanics and greater aortic stiffness. Further studies should explore causal links between cannabis smoking and altered cardiovascular function. [ABSTRACT FROM AUTHOR]

Elevated large-artery stiffness is recognized as an independent predictor of cardiovascular and all-cause mortality. The mechanisms responsible for such stiffening are incompletely understood. Several recent cross-sectional and acute experimental studies have examined whether sympathetic outflow, quantified by microneurographic measures of muscle sympathetic nerve activity (MSNA), can modulate large-artery stiffness in humans. A major methodological challenge of this research has been the capacity to evaluate the independent neural contribution without influencing the dynamic blood pressure dependence of arterial stiffness. The focus of this review is to summarize the evidence examining 1) the relationship between resting MSNA and large-artery stiffness, as determined by carotid-femoral pulse wave velocity or pulse wave reflection characteristics (i.e., augmentation index) in men and women; 2) the effects of acute sympathoexcitatory or sympathoinhibitory maneuvers on carotid-femoral pulse wave velocity and augmentation index; and 3) the influence of sustained increases or decreases in sympathetic neurotransmitter release or circulating catecholamines on large-artery stiffness. The present results highlight the growing evidence that the sympathetic nervous system is capable of modulating arterial stiffness independent of prevailing hemodynamics and vasomotor tone. [ABSTRACT FROM AUTHOR]

Fluctuations in diastolic pressure modulate muscle sympathetic nerve activity (MSNA) through the arterial baroreflex. A higher sympathetic baroreflex sensitivity (sBRS) to pressure falls compared with rises has been reported; however, the underlying mechanisms are unclear. We assessed whether beat-to-beat falling and rising diastolic pressures operate on two distinct baroreflex response curves. Twenty-two men (32 ± 8 yr) underwent sequential bolus injections of nitroprusside and phenylephrine (modified Oxford test) with continuous recording of heart rate, blood pressure, and MSNA. The weighted negative linear regression slope between falling or rising diastolic pressure and MSNA burst incidence quantified sBRSfall and sBRSrise, respectively. The diastolic pressure evoking a MSNA burst incidence of 50 (T50) was calculated. sBRSfall was greater than sBRSrise (-6.24 ± 2.80 vs. -4.34 ± 2.16 bursts·100 heartbeats-1·mmHg-1, P = 0.01) and had a narrower operating range (14 ± 8 vs. 20 ± 10 mmHg, P = 0.01) that was shifted rightward (T50, 75 ± 9 and 70 ± 11 mmHg, P < 0.001). At diastolic pressures below baseline, sBRSfall was less than sBRSrise (-1.81 ± 1.31 vs. -3.59 ± 1.70 bursts·100 heartbeats-1·mmHg-1, P = 0.003) as low absolute pressures operated closer to the saturation plateau on the falling, compared with the rising pressure curve. At pressures above baseline, sBRSfall was greater than sBRSrise (-5.23 ± 1.94 and -3.79 ± 1.67 bursts·100 heartbeats-1·mmHg-1, P = 0.03). These findings demonstrate that the sympathetic arterial baroreflex possesses two response curves for processing beat-to-beat diastolic pressure falls and rises. The falling pressure curve is rightward shifted, which reduces sensitivity to falling pressure at low absolute pressures. This demonstrates that the direction of the hysteresis is influenced by the prevailing pressure level relative to each baroreflex response curve. [ABSTRACT FROM AUTHOR]