Acute partial sleep restriction does not impact arterial function in young and healthy humans.

Habitual short sleep durations are associated with several cardiovascular diseases. Experimental research generally supports these findings as metrics of arterial function are impaired after complete deprivation of sleep and after longer periods of partial sleep restriction. The acute influence of a single instance of partial sleep restriction (PSR), however, has not been defined. We evaluated arterial structure and function among 32 university-aged participants on two occasions: once after normal habitual sleep (NS), and again the morning after an acute partial sleep restriction (PSR) intervention involving only 3 h of sleep for a single night. Endothelial function was measured using ultrasonography at the brachial artery via flow-mediated dilatation (FMD), and a ramp peak oxygen uptake test was used to evaluate cardiorespiratory fitness. Blood samples were collected from a subset of participants to investigate the influence of circulatory factors on cellular mechanisms implicated in endothelial function. Sleep duration was lower after a night of PSR compared to NS (P < 0.001); however, there were no appreciable differences in any haemodynamic outcome between conditions. FMD was not different between NS and PSR (NS: 6.5 ± 2.9%; PSR: 6.3 ± 2.9%; P = 0.668), and cardiorespiratory fitness did not moderate the haemodynamic response to PSR (all P > 0.05). Ex vivo cell culture results aligned with in vivo data, showing that acute PSR does not alter intracellular processes involved in endothelial function. No differences in arterial structure or function were observed between NS and acute PSR in healthy and young participants, and cardiorespiratory fitness does not modulate the arterial response to acute sleep restriction.

The effects of water temperature on cerebral blood flow during aquatic exercise.

PURPOSE: Recent studies suggest that episodic increases in cerebral blood flow (CBF) may contribute to the improvement in brain health associated with exercise training. Optimising CBF during exercise may enhance this benefit. Water immersion in ~ 30-32 °C augments CBF at rest and during exercise; however, the impact of water temperature on the CBF response has not been investigated. We hypothesised that cycle ergometry in water would increase CBF compared to land-based exercise, and that warm water would attenuate the CBF benefits. METHODS: Eleven young heathy participants (nine males; 23.8 ± 3.1 yrs) completed 30 min of resistance-matched cycle exercise in three separate conditions; non-immersion (Land), 32 °C and 38 °C water immersion up to the level of the waist. Middle cerebral artery velocity (MCAv), blood pressure, and respiratory measures were assessed throughout the exercise bouts. RESULTS: Core temperature was significantly higher in the 38 °C immersion than 32 °C (+ 0.84 ± 0.24 vs + 0.04 ± 0.16, P < 0.001), whilst mean arterial pressure was lower during 38 °C exercise compared to Land (84 ± 8 vs 100 ± 14 mmHg, P < 0.001) and 32 °C (92 ± 9, P = 0.03). MCAv was higher in 32 °C immersion compared to the Land and 38 °C conditions throughout the exercise bout (68 ± 10 vs 64 ± 11 vs 62 ± 12 cm/s, P = 0.03 and P = 0.02, respectively). CONCLUSION: Our findings suggest that cycle exercise in warm water attenuates the beneficial impact of water immersion on CBF velocity due to redistribution of blood flow to subserve thermoregulatory demand. Our findings suggest that, whilst water-based exercise can have beneficial effects on cerebrovascular function, water temperature is a key determinant of this benefit.

Effects of exercise during water immersion on arterial function in humans.

Flow-mediated dilation (FMD) provides a valid bioassay of vascular function in humans. Although water immersion induces hemodynamic effects that modify brachial artery shear stress, it is unclear whether water-based exercise modifies FMD. We hypothesized that exercise in 32°C water would decrease brachial artery shear and FMD relative to land-based exercise, whereas exercise in 38°C would increase brachial shear and FMD. Ten healthy participants (8 males; 23.9 ± 3.3 yr) completed 30 min of resistance-matched cycle exercise in three separate conditions: on land and in 32°C and 38°C water. Brachial artery shear rate area under the curve (SRAUC) was measured throughout each condition, with FMD measured pre- and postexercise. Brachial SRAUC increased during exercise in all conditions and was highest across the 38°C condition compared with Land and 32°C conditions (38°C: 27,507 ± 8,350 vs. Land: 9,908 ± 4,738 vs. 32°C: 13,840 ± 5,861 1/s, P < 0.001). Retrograde diastolic shear was greater during 32°C than both Land and 38°C conditions (32°C:-3,869 ± 2,198 vs. Land:-1,602 ± 1,334 vs. 32°C:-1,036 ± 1,754, P < 0.01). FMD increased as a result of 38°C (6.2 ± 1.9 vs. 8.5 ± 2.7%, P = 0.03), with no change in the Land exercise (6.3 ± 2.4 vs. 7.7 ± 2.4%, P = 0.10) or 32°C condition (6.4 ± 3.2 vs. 6.7 ± 3.2%, P = 0.99). Our findings indicate that cycle exercise in hot water attenuates retrograde shear, increases antegrade shear, and FMD. Exercise in 32°C water induces central hemodynamic changes relative to land-based exercise, but these do not translate to increases in FMD in either condition, likely due to the impact of increased retrograde shear. Our findings indicate that modification of shear has direct acute impacts on endothelial function in humans.

Effects of Perceptually Regulated Exercise Training on Cardiorespiratory Fitness and Peak Power Output in Adults With Spinal Cord Injury: A Systematic Review and Meta-analysis.

OBJECTIVE: To analyze and summarize the effect of regulating exercise training interventions with subjective measures of intensity on cardiorespiratory fitness, measured by peak oxygen uptake (V̇O2peak) and peak power output (POpeak) in adults with spinal cord injury (SCI). DATA SOURCES: Four databases (MEDLINE, Embase, PsycINFO, SPORTDiscus) were searched from inception up until September 1, 2020, and updated November 18, 2021. STUDY SELECTION: Searches combined keywords relating to the topics: SCI, subjective measures of exercise intensity, and exercise. DATA EXTRACTION: Two reviewers independently conducted eligibility screening, data extraction, and assessed the risk of bias. Nine studies were included in the systematic review and meta-analysis, resulting in the inclusion of data from 95 adults with SCI representing both sexes and a diverse range of age, time since injury, lesion level, and lesion completeness classifications. DATA SYNTHESIS: Data were extracted and added to summary tables with 3 outcomes: V̇O2peak, POpeak, and Other. Mean and SD values for V̇O2peak and POpeak were extracted from pre- and post-perceptually regulated exercise training. CONCLUSIONS: All studies used ratings of perceived exertion scale to prescribe exercise intensity. Seven of 8 studies concluded an improvement in V̇O2peak, and 5 studies of 7 concluded an improvement in POpeak. In the outcome Other, 5 studies concluded an improvement, and 3 studies concluded no change. There was evidence for an improvement in cardiorespiratory fitness, measured by V̇O2peak and POpeak after perceptually regulated exercise training in adults with SCI (Grading of Recommendations, Assessment, Development, and Evaluation ratings: Low) (mean difference [MD], 2.92mL/kg/min; 95% confidence interval [CI], 1.30-4.54; P=.0004 and MD, 9.8W; 95% CI, 5.5-14.3; P<.0001, respectively). This review provides critically appraised, cumulative evidence on the use of perceptually regulated exercise training in individuals with SCI.

Influence of hormonal contraceptives on peripheral vascular function and structure in premenopausal females: a review.

Hormonal contraceptives are one of the most widely used prescriptions for premenopausal women worldwide. Although the risk of venous and arterial cardiovascular events (e.g., deep vein thrombosis, arterial clotting) with hormonal contraceptives, specifically oral contraceptive pills, has been established, the literature on early risk indicators, such as peripheral vascular structure and function has yet to be consolidated. The purpose of this review is to summarize literature examining the impact of different hormonal contraceptives on vascular function and structure, including consideration of phasic differences within a contraceptive cycle, and to propose future directions for research. It is evident that hormonal contraceptive use appears to impact both macrovascular and microvascular endothelial function, with phasic differences in some contraceptive types dependent on progestin type, the ratio of ethinyl estradiol-to-progestin, and route of administration. However, hormonal contraceptives do not appear to impact smooth muscle function in the macrovasculature or microvasculature, arterial stiffness, or vascular structure. Underlying mechanisms for observed impacts and areas of future research are discussed. This review provides timely consolidation of research examining hormonal contraceptives and peripheral vascular function and structure and provides guidance on considerations for hormonal contraceptive use in study design.

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives.

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health.Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/.

The impact of the 24-h movement spectrum on vascular remodeling in older men and women: a review.

Aging is associated with increased risk of cardiovascular and cerebrovascular events, which are preceded by early, negative remodeling of the vasculature. Low physical activity is a well-established risk factor associated with the incidence and development of disease. However, recent physical activity literature indicates the importance of considering the 24-h movement spectrum. Therefore, the purpose of this review was to examine the impact of the 24-h movement spectrum, specifically physical activity (aerobic and resistance training), sedentary behavior, and sleep, on cardiovascular and cerebrovascular outcomes in older adults, with a focus on recent evidence (<10 yr) and sex-based considerations. The review identifies that both aerobic training and being physically active (compared with sedentary) are associated with improvements in endothelial function, arterial stiffness, and cerebrovascular function. Additionally, there is evidence of sex-based differences in endothelial function: a blunted improvement in aerobic training in postmenopausal women compared with men. While minimal research has been conducted in older adults, resistance training does not appear to influence arterial stiffness. Poor sleep quantity or quality are associated with both impaired endothelial function and increased arterial stiffness. Finally, the review highlights mechanistic pathways involved in the regulation of vascular and cerebrovascular function, specifically the balance between pro- and antiatherogenic factors, which mediate the relationship between the 24-h movement spectrum and vascular outcomes. Finally, this review proposes future research directions: examining the role of duration and intensity of training, combining aerobic and resistance training, and exploration of sex-based differences in cardiovascular and cerebrovascular outcomes.

Twelve weeks of sprint interval training increases peak cardiac output in previously untrained individuals.

INTRODUCTION: Sprint interval training (SIT), characterized by brief bouts of 'supramaximal' exercise interspersed with recovery periods, increases peak oxygen uptake ([Formula: see text]) despite a low total exercise volume. Per the Fick principle, increased [Formula: see text] is attributable to increased peak cardiac output ([Formula: see text]) and/or peak arterio-venous oxygen difference (a-vO2diff). There are limited and equivocal data regarding the physiological basis for SIT-induced increases in [Formula: see text], with most studies lasting ≤ 6 weeks. PURPOSE: To determine the effect of 12 weeks of SIT on [Formula: see text], measured using inert gas rebreathing, and the relationship between changes in [Formula: see text] and [Formula: see text]. METHODS: 15 healthy untrained adults [6 males, 9 females; 21 ± 2 y (mean ± SD)] performed 28 ± 3 training sessions. Each session involved a 2-min warm-up at 50 W, 3 × 20-s 'all-out' cycling bouts (581 ± 221 W) interspersed with 2-min of recovery, and a 3-min cool-down at 50 W. RESULTS: Measurements performed before and after training showed that 12 weeks of SIT increased [Formula: see text] (17.0 ± 3.7 vs 18.1 ± 4.6 L/min, p = 0.01, partial η2 = 0.28) and [Formula: see text] (2.63 ± 0.78 vs 3.18 ± 1.1 L/min, p < 0.01, partial η2 = 0.58). The changes in these two variables were correlated (r2 = 0.46, p < 0.01). Calculated peak a-vO2diff also increased after training (154 ± 22 vs 174 ± 23 ml O2/L; p < 0.01) and was correlated with the change in [Formula: see text] (r2 = 0.33, p = 0.03). Exploratory analyses revealed an interaction (p < 0.01) such that [Formula: see text] increased in male (+ 10%, p < 0.01) but not female participants (+ 0.6%, p = 0.96), suggesting potential sex-specific differences. CONCLUSION: Twelve weeks of SIT increased [Formula: see text] by 6% in previously untrained participants and the change was correlated with the larger 21% increase in [Formula: see text].

Impact of the menstrual cycle on peripheral vascular function in premenopausal women: systematic review and meta-analysis.

Fluctuations in endogenous hormones estrogen and progesterone during the menstrual cycle may offer vasoprotection for endothelial and smooth muscle (VSM) function. While numerous studies have been published, the results are conflicting, leaving our understanding of the impact of the menstrual cycle on vascular function unclear. The purpose of this systematic review and meta-analysis was to consolidate available research exploring the role of the menstrual cycle on peripheral vascular function. A systematic search of MEDLINE, Web of Science, and EMBASE was performed for articles evaluating peripheral endothelial and VSM function across the natural menstrual cycle: early follicular (EF) phase versus late follicular (LF), early luteal, mid luteal, or late luteal. A meta-analysis examined the effect of the menstrual cycle on the standardized mean difference (SMD) of the outcome measures. Analysis from 30 studies (n = 1,363 women) observed a "very low" certainty of evidence that endothelial function increased in the LF phase (SMD: 0.45, P = 0.0001), with differences observed in the macrovasculature but not in the microvasculature (SMD: 0.57, P = 0.0003, I2 = 84%; SMD: 0.21, P = 0.17, I2 = 34%, respectively). However, these results are partially explained by differences in flow-mediated dilation [e.g., discrete (SMD: 0.86, P = 0.001) vs. continuous peak diameter assessment (SMD: 0.25, P = 0.30)] and/or menstrual cycle phase methodologies. There was a "very low" certainty that endothelial function was largely unchanged in the luteal phases, and VSM was unchanged across the cycle. The menstrual cycle appears to have a small effect on macrovascular endothelial function but not on microvascular or VSM function; however, these results can be partially attributed to methodological differences.

Peripheral artery endothelial function responses to altered shear stress patterns in humans.

NEW FINDINGS: What is the central question of this study? What is the effect of altered shear stress pattern, with or without concurrent neurohumoral and metabolic activation, on the acute endothelial function response assessed via brachial artery flow-mediated dilatation? What is the main finding and its importance? Despite generating distinctive shear stress patterns (i.e. increases in anterograde only, anterograde only with neurohumoral and metabolic activation, and both anterograde and retrograde), similar acute improvements were observed in the brachial artery flow-mediated dilatation response in all conditions, indicating that anterograde and/or turbulent shear stress might be the essential element to induce acute increases in endothelial function. ABSTRACT: Endothelial function is influenced by both the direction and the magnitude of shear stress. Acute improvements in endothelial function have mostly been attributed to increased anterograde shear, whereas results from many interventional models in humans suggest that enhancing shear stress in an oscillatory manner (anterograde and retrograde) might be optimal. Here, we determined the acute brachial artery shear stress (SS) and flow-mediated dilatation (FMD) responses to three shear-altering interventions [passive heat stress (HEAT), mechanical forearm compression (CUFF) and handgrip exercise (HGEX)] and examined the relationship between changes in oscillatory shear index (OSI) and changes in FMD. During separate visits, 10 young healthy men (22 ± 3 years old) underwent 10 min of HEAT, CUFF or HGEX in their left forearm. Anterograde and retrograde SS, Reynolds number, OSI and FMD were assessed at rest and during/after each intervention. Anterograde SS increased during all interventions in a stepwise manner (P < 0.05 between interventions), with the change in HGEX (∆37.7 ± 12.2 dyn cm-2 , P < 0.05) > CUFF (∆25.1 ± 11.9 dyn cm-2 , P < 0.05) > HEAT (∆14.5 ± 7.9 dyn cm-2 , P < 0.05). Retrograde SS increased during CUFF (∆-19.6 ± 4.3 dyn cm-2 , P < 0.05). Anterograde blood flow was turbulent (i.e. Reynolds number ≥ |2000|) during all interventions (P < 0.05). The relative FMD improved after all interventions (P = 0.01), and there was no relationship between ∆OSI and ∆FMD. We elicited changes in SS profiles including increased anterograde SS (HEAT and HGEX) and both increased anterograde and retrograde SS (CUFF); regardless of the SS pattern, FMD improved to the same extent. These findings suggest that the presence of anterograde and/or turbulent SS might be the key to optimizing endothelial function in acute assessment protocols.

Associations between arterial stiffness and blood pressure fluctuations after spinal cord injury.

STUDY DESIGN: Cross-sectional. OBJECTIVE: To examine the relationship between arterial stiffness and daily fluctuations in blood pressure (BP) owing to hypotensive events and autonomic dysreflexia (AD) in individuals with a T6 and above spinal cord injury (SCI). SETTING: University-based laboratory in Vancouver, BC, Canada. METHODS: Twenty-six individuals (73% male; 43 (11) years) with a chronic (> 1 year post SCI), traumatic, motor-complete SCI with a neurological level of injury of C4-T6 participated in this study. Arterial stiffness was assessed using carotid-to-femoral pulse wave velocity (cfPWV). BP was measured over a 24-hr period using ambulatory BP monitoring. AD was defined as an increase in systolic BP > 20 mmHg above baseline BP. Hypotensive events were defined as a decrease in systolic BP ≥ 20 mmHg and/or diastolic BP ≥ 10 mmHg below baseline. The severity and frequency of these events were quantified and Pearson and Spearman's correlations between them and cfPWV were performed. RESULTS: AD severity and frequency were not were correlated with cfPWV. For hypotensive events, both the frequency (r = 0.412, P = 0.04) and severity (Δsystolic BP; r = -0.425, P = 0.03) of these events were correlated with cfPWV. The combined total of AD and hypotensive events (9 (5) events/day) was also correlated with cfPWV (r = 0.480, P = 0.01). CONCLUSIONS: Hypotensive events, and the combined frequency of both hypo- and hypertensive events within a 24-hr period are associated with increased arterial stiffness in individuals with T6 and above SCI, suggesting BP instability may play a role in arterial stiffening post SCI.

Comparison between esophageal and intestinal temperature responses to upper-limb exercise in individuals with spinal cord injury.

STUDY DESIGN: Experimental study. OBJECTIVE: Individuals with spinal cord injuries (SCI) may present with impaired sympathetic control over thermoregulatory responses to environmental and exercise stressors, which can impact regional core temperature (Tcore) measurement. The purpose of this study was to investigate whether regional differences in Tcore responses exist during exercise in individuals with SCI. SETTING: Rehabilitation centre in Wakayama, Japan. METHODS: We recruited 12 men with motor-complete SCI (7 tetraplegia, 5 paraplegia) and 5 able-bodied controls to complete a 30-min bout of arm-cycling exercise at 50% V̇O2 peak reserve. Tcore was estimated using telemetric pills (intestinal temperature; Tint) and esophageal probes (Teso). Heat storage was calculated from baseline to 15 and 30 min of exercise. RESULTS: At 15 min of exercise, elevations in Teso (Δ0.39 ± 0.22 °C; P < 0.05), but not Tint (Δ0.04 ± 0.18 °C; P = 0.09), were observed in able-bodied men. At 30 min of exercise, men with paraplegia and able-bodied men both exhibited increases in Teso (paraplegia: Δ0.56 ± 0.30 °C, P < 0.05; able-bodied men: Δ0.60 ± 0.31 °C, P < 0.05) and Tint (paraplegia: Δ0.38 ± 0.33 °C, P < 0.05; able-bodied men: Δ0.30 ± 0.30 °C, P < 0.05). Teso began rising 7.2 min earlier than Tint (pooled, P < 0.01). Heat storage estimated by Teso was greater than heat storage estimated by Tint at 15 min (P = 0.02) and 30 min (P = 0.03) in men with paraplegia. No elevations in Teso, Tint, or heat storage were observed in men with tetraplegia. CONCLUSIONS: While not interchangeable, both Teso and Tint are sensitive to elevations in Tcore during arm-cycling exercise in men with paraplegia, although Teso may have superior sensitivity to capture temperature information earlier during exercise.

Effect of sex, menstrual cycle phase, and monophasic oral contraceptive pill use on local and central arterial stiffness in young adults.

Arterial stiffness is associated with increased cardiovascular disease risk. Previous sex-based investigations of local and central stiffness report inconsistent findings and have not controlled for menstrual cycle phase in women. There is also evidence that sex hormones influence the vasculature, but their impact on arterial stiffness across a natural menstrual (NAT) or oral contraceptive pill (OCP) cycle has been understudied. This study sought to 1) examine potential sex differences in local and central stiffness, 2) compare stiffness profiles between NAT and OCP cycles, and 3) investigate the relationship between duration of OCP use and arterial stiffness. Sex hormone concentrations, ß-stiffness index (local stiffness), and carotid-femoral pulse wave velocity [cfPWV (central stiffness)] were assessed in 53 healthy adults (22 ± 3 yr old, 20 men, 15 NAT women, and 18 OCP women). All participants were tested three times: men on the same day and time 1 wk apart, NAT women in menstrual, midfollicular and luteal phases of the menstrual cycle, and OCP women in placebo, early active and late active pill phases. ß-Stiffness was higher in men than NAT and OCP women ( P < 0.001), whereas cfPWV was similar between groups ( P = 0.09). ß-Stiffness and cfPWV did not differ across or between NAT and OCP cycles ( P > 0.05 for both) and were not associated with duration of OCP use (ß-stiffness: r = 0.003, P = 0.99; cfPWV: r = -0.26, P = 0.30). The apparent sex differences in local, but not central, stiffness highlight the importance of assessing both indexes in comparisons between men and women. Furthermore, fluctuating sex hormone levels do not appear to influence ß-stiffness or cfPWV. Therefore, these stiffness indexes may need to be assessed during only one cycle phase in women in future investigations. NEW & NOTEWORTHY We observed higher local, but not central, arterial stiffness in men than women. We also demonstrated that there are no differences in arterial stiffness between naturally cycling women and women who use monophasic oral contraceptive pills, and that the duration of oral contraceptive pill use does not influence arterial stiffness.

Brachial artery endothelial function is stable across a menstrual and oral contraceptive pill cycle but lower in premenopausal women than in age-matched men.

Sex hormone concentrations differ between men, premenopausal women with natural menstrual cycles (NAT), and premenopausal women using oral contraceptive pills (OCP), as well as across menstrual or OCP phases. This study sought to investigate how differences in sex hormones, particularly estradiol, between men and women and across cycle phases might influence brachial artery endothelial function. Fifty-three healthy adults (22 ± 3 yr, 20 men, 15 NAT women, and 18 second-, third-, or fourth-generation OCP women) underwent assessments of sex hormones and endothelial [flow-mediated dilation (FMD) test] and smooth muscle [nitroglycerin (NTG) test] function. Men were tested three times at 1-wk intervals, and women were tested three times throughout a single menstrual or OCP cycle (NAT: menstrual, midfollicular, and luteal phases and OCP: placebo/no pill, "early", and "late" active pill phases). Endogenous estradiol concentration was comparable between men and women in their NAT menstrual or OCP placebo phase ( P = 0.36) but increased throughout a NAT cycle ( P < 0.001). Allometrically scaled FMD did not change across a NAT or OCP cycle but was lower in both groups of women than in men ( P = 0.005), whereas scaled NTG was lower only in NAT women ( P = 0.001). Changes in estradiol across a NAT cycle were not associated with changes in relative FMD ( r2 = 0.01, P = 0.62) or NTG ( r2 = 0.09, P = 0.13). Duration of OCP use was negatively associated with the average relative FMD for second-generation OCP users only ( r = -0.65, P = 0.04). Our findings suggest that brachial endothelial function is unaffected by cyclic hormonal changes in premenopausal women but may be negatively impacted by longer-term use of second-generation OCPs. NEW & NOTEWORTHY We demonstrate that brachial artery flow-mediated dilation does not change across a menstrual or oral contraceptive pill cycle in premenopausal women but is lower in women than in men. Although unaffected by within-cycle changes in estradiol, brachial flow-mediated dilation is negatively correlated with duration of oral contraceptive pill use for second-generation pills.

Cardiovascular aging and the microcirculation of skeletal muscle: using contrast-enhanced ultrasound.

Skeletal muscle is the largest and most important site of capillary-tissue exchange, especially during high-energy demand tasks such as exercise; however, information regarding the role of the microcirculation in maintaining skeletal muscle health is limited. Changes in microcirculatory function, as observed with aging, chronic and cardiovascular diseases, and exercise, likely precede any alterations that arise in larger vessels, although further investigation into these changes is required. One of the main barriers to addressing this knowledge gap is the lack of methodologies for quantifying microvascular function in vivo; the utilization of valid and noninvasive quantification methods would allow the dynamic evaluation of microvascular flow during periods of clinical relevance such as during increased demand for flow (exercise) or decreased demand for flow (disuse). Contrast-enhanced ultrasound (CEUS) is a promising noninvasive technique that has been used for diagnostic medicine and more recently as a complementary research modality to investigate the response of the microcirculation in insulin resistance, diabetes, and aging. To improve the reproducibility of these measurements, our laboratory has optimized the quantification protocol associated with a bolus injection of the contrast agent for research purposes. This brief report outlines the assessment of microvascular flow using the raw time-intensity curve incorporated into gamma variate response modeling. CEUS could be used to compliment any macrovascular assessments to capture a more complete picture of the aging vasculature, and the modified methods presented here provide a template for the general analysis of CEUS within a research setting.

Brachial artery endothelial function is unchanged after acute sprint interval exercise in sedentary men and women.

NEW FINDINGS: What is the central question of this study? What is the acute brachial artery endothelial function response to sprint interval exercise and are there sex-based differences? What is the main finding and its importance? Brachial artery endothelial function did not change in either men or women following an acute session of SIT consisting of 3 × 20 s 'all-out' cycling sprints. Our findings suggest this low-volume protocol may not be sufficient to induce functional changes in the brachial artery of sedentary, but otherwise healthy adults. ABSTRACT: Sprint interval training (SIT) is a potent metabolic stimulus, but studies examining its acute effects on brachial artery endothelial function are limited. The influence of oestradiol on the acute arterial response to this type of exercise is also unknown. We investigated the brachial artery endothelial function response to a single session of SIT in sedentary healthy men (n = 8; 22 ± 4 years) and premenopausal women tested in the mid-follicular phase of the menstrual cycle (n = 8; 21 ± 3 years). Participants performed 3 × 20 s 'all-out' cycling sprints interspersed with 2 min of active recovery. Brachial artery flow-mediated dilatation (FMD) and haemodynamic parameters were measured before and 1 and 24 h post-exercise. Despite attenuations in some haemodynamic parameters at 1 h post-exercise, there were no changes in absolute (P = 0.23), relative (P = 0.23) or allometrically scaled FMD (P = 0.38) following a single session of SIT. Resting and peak dilatory diameters did not change in men or women (P > 0.05 for all) and there were no interactions between time and sex for any measure (P > 0.05). Oestradiol was not correlated with relative FMD at baseline (r = -0.22, P = 0.42) or with the change in relative FMD from baseline to 1 h post-exercise (r = 0.24, P = 0.40). Overall, brachial artery FMD appears to be unchanged in men and women following an acute session of SIT, and the higher oestradiol concentrations in women do not augment the baseline or post-exercise FMD response. The 3 × 20 s model of low-volume sprint interval exercise may not be sufficient to alter brachial artery endothelial function in healthy men and women.

Cardiac and haemodynamic influence on carotid artery longitudinal wall motion.

NEW FINDINGS: What is the central question of this study? Carotid artery longitudinal wall motion (CALM) is a bidirectional forward and backward motion of the arterial wall; however, there is no evidence in humans for what controls CALM despite proposals for pulse pressure, left ventricular motion and shear rate. What is the main finding and its importance? Carotid artery longitudinal wall motion responses were heterogeneous when manipulating sympathetic activation and endothelium-independent vasodilatation, leading to non-significant group responses. However, individual CALM responses were associated with left ventricular rotation and shear rate. These findings are important when interpreting changes in CALM in humans with acute or chronic experimental designs. Carotid artery longitudinal wall motion (CALM) has recently attracted interest as an indicator of arterial health; however, the regulation of CALM is poorly understood. We conducted a series of studies aimed at manipulating pulse pressure (PP), left ventricular (LV) motion and carotid shear rate, which have been previously suggested to regulate various components of CALM pattern and magnitude. To determine the regulatory influences on CALM, 15 healthy men (22 ± 2 years old) were exposed to three acute interventions: the serial subtraction test (SST); the cold pressor test (CPT); and exposure to sublingual nitroglycerine (NTG). The SST elicited increases in PP (P < 0.01), apical LV rotation (P < 0.01) and carotid shear rate (P < 0.01), with no changes in CALM (P > 0.05). Likewise, the CPT elicited increases in PP (P = 0.01), basal LV rotation (P = 0.04) and carotid shear rate (P = 0.01), with no changes in CALM (P > 0.05). Conversely, exposure to NTG elicited no change in PP (P = 0.22), basal (P = 0.65) or apical LV rotation (P = 0.45), but did decrease carotid shear rate (P < 0.01), without altering CALM (P > 0.05). Considerable individual variability in CALM responses prompted further analyses where all three interventions were pooled for change scores. Changes in LV basal rotation were related to changes in systolic retrograde CALM (B = -0.025, P = 0.03), whereas changes in carotid shear rate were related to changes in diastolic CALM displacement (B = 0.0009, P = 0.01). The interventions were underpinned by relationships between CALM and both LV basal rotation and local shear rate at the individual level, indicating that cardiac and haemodynamic factors may influence CALM in humans.

Assessing Ventilatory Threshold in Individuals With Motor-Complete Spinal Cord Injury.

OBJECTIVE: To assess the feasibility of measuring ventilatory threshold (VT) in higher-level motor-complete spinal cord injury (SCI) using 4 different analysis methods based on noninvasive gas exchange. DESIGN: Observational. SETTING: Laboratory testing. PARTICIPANTS: Individuals with C4-T6 motor-complete SCI (16 paraplegia, 22 tetraplegia; American Spinal Injury Association Impairment Scale A/B; 42±10 years old). INTERVENTIONS: Not applicable. MAIN OUTCOME: VT from a graded arm cycling test to volitional exhaustion using 4 methods: ventilatory equivalents, excess CO2, V-slope, and combined method. RESULTS: VT could be identified in all individuals with paraplegia, but in only 68% of individuals with tetraplegia. Individuals without observable VT completed the graded exercise test with lower ventilatory rate, peak power output, and peak oxygen consumption (Vo2peak) (all P<.05), compared to those with a detectable VT. Bland-Altman plots indicate minimal bias between methods (range: 0.01-0.03 L/min), with 95% limits of agreement of the difference within 0.25 L/min. Absolute V.o2 at VT with individual methods were all correlated to peak power output (r>0.74; P<.01) and Vo2peak (r>0.91; P<.01), with negligible differences between methods. CONCLUSIONS: The assessment of VT is a feasible alternative to peak exercise testing for aerobic fitness in individuals with higher-level, motor-complete SCI, although care should be taken when interpreting VT in individuals with tetraplegia who have lower cardiorespiratory fitness and lower peak power outputs.

Effect of sex on the acute skeletal muscle response to sprint interval exercise.

NEW FINDINGS: What is the central question of this study? Are there sex-based differences in the acute skeletal muscle response to sprint interval training (SIT)? What is the main finding and its importance? In response to a SIT protocol that involved three 20 s bouts of 'all-out' cycling, the expression of multiple genes associated with mitochondrial biogenesis, metabolic control and structural remodelling was largely similar between men and women matched for fitness. Our findings cannot explain previous reports of sex-based differences in the adaptive response to SIT and suggest that the mechanistic basis for these differences remains to be elucidated. A few studies have reported sex-based differences in response to several weeks of sprint interval training (SIT). These findings may relate to sex-specific responses to an acute session of SIT. We tested the hypothesis that the acute skeletal muscle response to SIT differs between sexes. Sedentary but healthy men (n = 10) and women (n = 9) were matched for age (22 ± 3 versus 22 ± 3 years old) and cardiorespiratory fitness [45 ± 7 versus 43 ± 10 ml O2  (kg fat-free mass)-1  min-1 ], with women tested in the mid-follicular phase of their menstrual cycles. Subjects performed three 20 s 'all-out' cycling efforts against a resistance of 5% of body mass, interspersed with 2 min of recovery. Relative mean power outputs [7.6 ± 0.5 versus 7.5 ± 0.9 W (kg fat-free mass)-1 ] were similar between men and women (P > 0.05). Furthermore, there were no differences in the exercise-induced changes in mRNA expression of PGC-1α, PRC, PPARD, SIRT1, RIP140, HSL, HKII, PDK4, PDP1, FOXO3, MURF-1, Myf5, MyoD and VEGFA at 3 h of recovery versus rest (P < 0.05, main effect of time). The only sex-specific responses to exercise were an increase in the mRNA expression of GLUT4 and LPL in women only and Atrogin-1 in men only (P < 0.05). Women also had higher expression of HKII and lower expression of FOXO3 compared with men (P < 0.05, main effect of sex). We conclude that the acute skeletal muscle response to SIT is largely similar in young men and women. The mechanistic basis for sex-based differences in response to several weeks of SIT that has been previously reported remains to be elucidated.

Cardiovascular profile in postural orthostatic tachycardia syndrome and Ehlers-Danlos syndrome type III.

The cardiovascular profile of postural orthostatic tachycardia syndrome + Ehlers-Danlos syndrome hypermobility type (POTS + EDSIII) has not been described, despite suggestions that it plays a role in orthostatic intolerance. We studied nine individuals diagnosed with POTS + EDSIII and found that the arterial stiffness and cardiac profiles of patients with POTS + EDSIII were comparable to those of age- and sex-matched controls, suggesting an alternate explanation for orthostatic intolerance.