Acute oral antioxidant consumption does not alter brachial artery flow mediated dilation in young adults independent of exercise training status.

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.

Oral inflammatory load predicts vascular function in a young adult population: a pilot study.

Background: The periodontium is a highly vascularized area of the mouth, and periodontitis initiates negative functional and structural changes in the vasculature. However, mild oral inflammation, including levels experienced by many apparently healthy individuals, has an unclear impact on cardiovascular function. The purpose of this pilot study is to investigate the effects of objectively measured whole mouth oral inflammatory load (OIL) on vascular function in apparently healthy individuals. Methods: In this cross-sectional and correlational analysis, we recruited 28 young (18-30 years) and systemically healthy participants (16 male, 12 female). Using oral neutrophil counts, a validated measure for OIL, we collected participant's mouth rinse samples and quantified OIL. Blood pressure, arterial stiffness (pulse-wave velocity) and endothelial function (brachial artery flow-mediated dilation) were also measured. Results: Only oral neutrophil count significantly predicted flow-mediated dilation % (p = 0.04; R2 = 0.16, ß = - 1.05) and those with OIL levels associated with >2.5 × 105 neutrophil counts (n = 8) had a lower flow-mediated dilation % (6.0 ± 2.3%) than those with counts associated with gingival health with less than 2.5 × 105 neutrophil counts (10.0 ± 5.2%, p = 0.05). There were no significant predictors for arterial stiffness. Conclusion: We found that OIL was a predictor of reduced flow-mediated dilation. An impairment in flow-mediated dilation is an indicator of future possible risk of cardiovascular disease-one of the leading causes of death in North America. Therefore, this study provides evidence for the importance of oral health and that OIL may impact endothelial function.

No acute hyperglycemia induced impairment in brachial artery flow-mediated dilation before or after aerobic exercise training in young recreationally active males.

There is some evidence that transient endothelial dysfunction induced by acute hyperglycemia may be attenuated by a single bout of aerobic exercise. However, the impact of aerobic exercise training on acute hyperglycemia-induced endothelial dysfunction has not been explored. The purpose of this study was to determine the impact of aerobic exercise training on the endothelial function response to acute hyperglycemia. Brachial artery flow-mediated dilation (FMD) was assessed in 24 healthy males (21 ± 1 years) pre-, 60 and 90 min post ingestion of 75 g of glucose. Participants completed a four-week control (CON; n = 13) or exercise training (EX; n = 11) intervention. The EX group completed four weeks of cycling exercise (30 min, 4×/week at 65% work rate peak). Cardiorespiratory fitness ([Formula: see text]O2peak) increased and resting HR decreased in EX, but not CON post-intervention (p < 0.001). Glucose and insulin increased (p < 0.001) following glucose ingestion, with no significant difference pre- and post-intervention. In contrast to previous research, FMD was unaffected by glucose-ingestion, pre- and post-intervention in both groups. In conclusion, acute hyperglycemia did not impair endothelial function, before or after exercise training. Relatively high baseline fitness ([Formula: see text]O2peak ~ 46 mL/kg/min) and young age may have contributed to the lack of impairment observed. Further research is needed to examine the impact of exercise training on hyperglycemia-induced impairments in endothelial function in sedentary males and females.

Cardiac Remodeling in Elite Aquatic Sport Athletes.

OBJECTIVE: To characterize and compare the sport-specific cardiac structure of elite swimmers (SW), water polo players (WP), and artistic swimmers (AS). DESIGN: A cross-sectional assessment of elite aquatic athletes' hearts. SETTING: The athletes' village at the 2019 FINA World Championships. PARTICIPANTS: Ninety athletes from swimming (SW) (20 M/17 F), water polo (WP) (21 M/9 F), and artistic swimming (AS) (23 F). ASSESSMENT AND MAIN OUTCOME MEASURES: An echocardiographic assessment of cardiac structure was performed on noncompetition days. RESULTS: Male SW displayed primarily eccentric volume-driven remodeling, whereas male WP had a greater incidence of pressure-driven concentric geometry (SW = 5%, WP = 25%) with elevated relative wall-thickness (RWT) (SW = 0.35 ± 0.04, WP = 0.44 ± 0.08, P < 0.001). Female SW and WP hearts were similar with primarily eccentric-remodeling, but SW and WP had greater concentricity index than artistic swimmers (SW = 6.74 ± 1.45 g/(mL)2/3, WP = 6.80 ± 1.24 g/(mL)2/3, AS = 5.52 ± 1.08 g/(mL)2/3, P = 0.007). AS had normal geometry, but with increased posterior-wall specific RWT (SW = 0.32 ± 0.05, AS = 0.42 ± 0.11, P = 0.004) and greater left atrial area than SW (SW = 9.7 ± 0.9 cm2/m2, AS = 11.0 ± 1.1 cm2/m2, P = 0.003). All females had greater incidence of left ventricular (LV) posterior/septal wall-thickness ≥11 mm than typically reported (SW = 24%, WP = 11%, AS = 17%). CONCLUSIONS: Male athletes presented classic sport-specific differentiation, with SW demonstrating primarily volume-driven eccentric remodelling, and WP with greater concentric geometry indicative of pressure-driven remodeling. Female SW and WP did not display this divergence, likely because of sex-differences in adaptation. AS had unique LV-specific adaptations suggesting elevated pressure under low-volume conditions. The overall incidence of elevated wall-thickness in female athletes may point to an aquatic specific pressure-stress.

Differences in Left Ventricular Function at Rest and during Isometric Handgrip Exercise in Elite Aquatic Sport Athletes.

PURPOSE: Elite swimmers (Sw) have lower diastolic function compared with elite runners, possibly as an adaptation to the aquatic training environment. Water polo players (WP) and artistic swimmers (AS) are exposed to the same hydrostatic pressures as Sw, but they are subject to different training intensities, postures, and hemodynamic stressors. Our purpose was to compare resting and exercising cardiac function in elite Sw, WP, and AS, to characterize the influence of training for aquatic sport on left ventricular (LV) adaptation. METHODS: Ninety athletes (Sw, 20M/17F; WP, 21M/9F; AS, 23F) at the 2019 Fédération Internationale de Natation World Championships volunteered for resting and stress (3 min 30% maximal isometric handgrip) echocardiographic assessment of LV global function and mechanics. RESULTS: Male Sw displayed greater resting systolic and diastolic function compared with WP; however, both groups maintained stroke volume under high-pressure handgrip stress (Sw, ∆-4% ± 12%; WP, ∆-1% ± 13%, P = 0.11). There were no differences between female Sw and WP resting LV function, but Sw demonstrated greater function over AS. During isometric handgrip, all female sport athletes maintained stroke volume (Sw, ∆3% ± 16%; WP, ∆-10% ± 11%; AS, ∆-2% ± 14%, P = 0.46), but WP had improved apical rotation (∆1.7° ± 4.5°), which was reduced in AS (∆-3.1° ± 4.5°) and maintained in Sw (∆-0.5° ± 3.8°, P = 0.04). Unlike Sw and WP, AS displayed a unique maintenance of early filling velocity during handgrip exercise (Sw, ∆-3.5 ± 14.7 cm·s-1; WP, ∆-15.1 ± 10.8 cm·s-1; AS, ∆1.5 ± 15.3 cm·s-1, P = 0.02). CONCLUSIONS: Among male athletes, Sw display primarily volume-based functional adaptations distinct from the mixed volume-pressure adaptations of WP; however, both groups can maintain stroke volume with increased afterload. Female Sw and WP do not demonstrate sport-specific differences like males, perhaps owing to sex differences in adaptation, but have greater volume-based adaptations than AS. Lastly, AS display unique functional adaptations that may be driven by elevated pressures under low-volume conditions.

The impact of repeated, local heating-induced increases in blood flow on lower limb endothelial function in young, healthy females.

PURPOSE: The purpose of the present study was to examine the effect of repeated, single leg heating on lower limb endothelial function. METHODS: Macrovascular function was assessed with superficial femoral artery (SFA) reactive hyperemia flow-mediated dilation (RH-FMD) and sustained stimulus FMD (SS-FMD). Calf microvascular function was assessed as the peak and area under the curve of SFA reactive hyperemia (RH). Participants (n = 13 females, 23 ± 2 yrs) had one leg randomized to the single leg heating intervention (EXP; other leg: control (CON)). The EXP leg underwent 8 weeks of single leg heating via immersion in 42.5 â„ƒ water for five 35-min sessions/week. At weeks 0, 2, 4, 6, and 8, SFA RH-FMD, SS-FMD (shear stress increased via plantar flexion exercise), and SFA RH flow were measured. RESULTS: None of the variables changed with repeated, single leg heating (interaction week*limb RH-FMD: p = 0.076; SS-FMD: p = 0.958; RH flow p = 0.955). Covariation for the shear stress stimulus did not alter the FMD results. CONCLUSION: Eight weeks of single leg heating did not change SFA endothelial or calf microvascular function. These results are in contrast with previous findings that limb heating improves upper limb endothelial function.

Examining the relationship between arterial stiffness and swim-training volume in elite aquatic athletes.

PURPOSE: Factors such as prone body position, hydrostatic pressure, and intermittent breath-holding subject aquatic athletes to unique physical and environmental stressors during swimming exercise. The relationship between exposure to aquatic exercise and both arterial stiffness and wave reflection properties is not well-understood. This study assessed central artery stiffness and wave reflection properties in elite pool-swimmers (SW), long-distance open-water swimmers (OW), and water polo players (WP) to examine the relationship between these variables and aquatic exercise. METHODS: Athletes competing in SW, OW and WP events at the FINA World Championships were recruited. Carotid-femoral pulse wave velocity, and pulse wave analysis were used to quantify arterial stiffness, and central wave reflection properties. RESULTS: Athletes undertook differing amounts of weekly swimming distance in training according to their discipline (SW: 40.2 ± 21.1 km, OW: 59.7 ± 28.4 km, WP: 11.4 ± 6.3 km; all p < 0.05). Pulse wave velocity (Males [SW: 6.0 ± 0.6 m/s, OW: 6.5 ± 0.8 m/s, WP: 6.7 ± 0.9 m/s], Females [SW: 5.4 ± 0.6 m/s, OW: 5.3 ± 0.5 m/s, WP: 5.2 ± 0.8 m/s; p = 0.4]) was similar across disciplines for females but was greater in male WP compared to male SW (p = 0.005). Augmentation index (Males [SW: - 3.4 ± 11%, OW: - 9.6 ± 6.4%, WP: 1.7 ± 10.9%], Females [SW: 3.5 ± 13.5%, OW: - 13.2 ± 10.7%, WP: - 2.8 ± 10.7%]) was lower in male OW compared to WP (p = 0.03), and higher in female SW compared to OW (p = 0.002). Augmentation index normalized to a heart rate of 75 bpm was inversely related to weekly swim distance in training (r = - 0.27, p = 0.004). CONCLUSIONS: This study provides evidence that the central vasculature of elite aquatic athletes differs by discipline, and this is associated with training load.

Blood flow restriction in the presence or absence of muscle contractions does not preserve vasculature structure and function following 14-days of limb immobilization.

PURPOSE: Limb immobilization causes local vasculature to experience detrimental adaptations. Simple strategies to increase blood flow (heating, fidgeting) successfully prevent acute (≤ 1 day) impairments; however, none have leveraged the hyperemic response over prolonged periods (weeks) mirroring injury rehabilitation. Throughout a 14-day unilateral limb immobilization, we sought to preserve vascular structure and responsiveness by repeatedly activating a reactive hyperemic response via blood flow restriction (BFR) and amplifying this stimulus by combining BFR with electric muscle stimulation (EMS). METHODS: Young healthy adults (M:F = 14:17, age = 22.4 ± 3.7 years) were randomly assigned to control, BFR, or BFR + EMS groups. BFR and BFR + EMS groups were treated for 30 min twice daily (3 × 10 min ischemia-reperfusion cycles; 15% maximal voluntary contraction EMS), 5 days/week (20 total sessions). Before and after immobilization, artery diameter, flow-mediated dilation (FMD) and blood flow measures were collected in the superficial femoral artery (SFA). RESULTS: Following immobilization, there was less retrograde blood velocity (+ 1.8 ± 3.6 cm s-1, P = 0.01), but not retrograde shear (P = 0.097). All groups displayed reduced baseline and peak SFA diameter following immobilization (- 0.46 ± 0.41 mm and - 0.43 ± 0.39 mm, P < 0.01); however, there were no differences by group or across time for FMD (% diameter change, shear-corrected, or allometrically scaled) nor microvascular function assessed by peak flow capacity. CONCLUSION: Following immobilization, our results reveal (1) neither BFR nor BFR + EMS mitigate artery structure impairments, (2) intervention-induced shear stress did not affect vascular function assessed by FMD, and (3) retrograde blood velocity is reduced at rest offering potential insight to mechanisms of flow regulation. In conclusion, BFR appears insufficient as a treatment strategy for preventing macrovascular dysfunction during limb immobilization.

Physiological Determinants of Ultramarathon Trail-Running Performance.

CONTEXT: The physiological determinants of ultramarathon success have rarely been assessed and likely differ in their contributions to performance as race distance increases. PURPOSE: To examine predictors of performance in athletes who completed either a 50-, 80-, or 160-km trail race over a 20-km loop course on the same day. METHODS: Measures of running history, aerobic fitness, running economy, body mass loss, hematocrit alterations, age, and cardiovascular health were examined in relation to race-day performance. Performance was defined as the percentage difference from the winning time at a given race distance, with 0% representing the fastest possible time. RESULTS: In the 50-km race, training volumes, cardiovascular health, aerobic fitness, and a greater loss of body mass during the race were all related to better performance (all P < .05). Using multiple linear regression, peak velocity achieved in the maximal oxygen uptake test (ß = -11.7, P = .002) and baseline blood pressure (ß = 3.1, P = .007) were the best performance predictors for the men's 50-km race (r = .98, r2 = .96, P < .001), while peak velocity achieved in the maximal oxygen uptake test (ß = -13.6, P = .001) and loss of body mass (ß = 12.8, P = .03) were the best predictors for women (r = .94, r2 = .87, P = .001). In the 80-km race, only peak velocity achieved in the maximal oxygen uptake test predicted performance (ß = -20.3, r = .88, r2 = .78, P < .001). In the 160-km race, there were no significant performance determinants. CONCLUSIONS: While classic determinants of running performance, including cardiovascular health and running fitness, predict 50-km trail-running success, performance in longer-distance races appears to be less influenced by such physiological parameters.

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.

Endurance and Sprint Training Improve Glycemia and V˙O2peak but only Frequent Endurance Benefits Blood Pressure and Lipidemia.

PURPOSE: Sprint interval training (SIT) has gained popularity as a time-effective alternative to moderate-intensity endurance training (END). However, whether SIT is equally effective for decreasing cardiometabolic risk factors remains debatable, as many beneficial effects of exercise are thought to be transient, and unlike END, SIT is not recommended daily. Therefore, in line with current exercise recommendations, we examined the ability of SIT and END to improve cardiometabolic health in overweight/obese males. METHODS: Twenty-three participants were randomized to perform 6 wk of constant workload SIT (3 d·wk-1, 4-6 × 30 s ~170% Wpeak, 2 min recovery, n = 12) or END (5 d·wk-1, 30-40 min, ~60% Wpeak, n = 11) on cycle ergometers. Aerobic capacity (V˙O2peak), body composition, blood pressure (BP), arterial stiffness, endothelial function, glucose and lipid tolerance, and free-living glycemic regulation were assessed pre- and posttraining. RESULTS: Both END and SIT increased V˙O2peak (END ~15%, SIT ~5%) and glucose tolerance (~20%). However, only END decreased diastolic BP, abdominal fat, and improved postprandial lipid tolerance, representing improvements in cardiovascular risk factors that did not occur after SIT. Although SIT, but not END, increased endothelial function, arterial stiffness was not altered in either group. Indices of free-living glycemic regulation were improved after END and trended toward an improvement after SIT (P = 0.06-0.09). However, glycemic control was better on exercise compared with rest days, highlighting the importance of exercise frequency. Furthermore, in an exploratory nature, favorable individual responses (V˙O2peak, BP, glucose tolerance, lipidemia, and body fat) were more prevalent after END than low-frequency SIT. CONCLUSION: As only high-frequency END improved BP and lipid tolerance, free-living glycemic regulation was better on days that participants exercised, and favorable individual responses were consistent after END, high-frequency END may favorably improve cardiometabolic health.

Vascular Function Is Differentially Altered by Distance after Prolonged Running.

PURPOSE: Ultraendurance exercise is steadily growing in popularity; however, the effect of increasingly prolonged durations of exercise on the vascular endothelium is unknown. The aim of this study was to characterize the effect of various ultramarathon running distances on vascular form and function. METHODS: We evaluated vascular endothelial function via flow-mediated dilation (FMD) in the superficial femoral artery, as well as microvascular function, inflammatory factors, and central artery stiffness, before and after participants completed 25-km (7M:2F), 50-km (11M:10F), 80-km (9M:4F), or 160-km (9M:2F) trail races all run on the same day and course. RESULTS: Completion required 149 ± 20, 386 ± 111, 704 ± 130, and 1470 ± 235 min, with corresponding average paces of 6.0 ± 0.8, 7.7 ± 2.2, 8.6 ± 1.3, and 9.6 ± 1.3 min·km-1, respectively. At baseline, there were no differences in participant characteristics across race distance groups. Shear rate stimulus trended toward an increase after the race (P = 0.07), but resting postrace artery diameter (P < 0.001) was elevated to a similar extent in all conditions. There was a reduction in FMD after the 50-km race (Δ -1.9% ± 2.2%, P < 0.01), but not the 25-km (Δ +0.3% ± 2.9%, P = 0.8), the 80-km (Δ -1.5% ± 3.2%, P = 0.1), or the 160-km (Δ +0.5% ± 2.5%, P = 0.5) race. Inflammatory markers increased most after 160 km, but arterial stiffness and microvascular function were not differently affected by race distance. CONCLUSIONS: Although the superficial femoral artery baseline diameter was larger postexercise regardless of race distance, only the 50-km race reduced FMD, whereas a short-duration higher-intensity race (25 km) and longer-duration lower-intensity races (160 km) did not. Therefore, a 50-km ultramarathon may represent the intersection between higher-intensity exercise over a prolonged duration, causing reduced endothelial function not seen in shorter or longer distances.

Alterations in Cardiac Function Following Endurance Exercise Are Not Duration Dependent.

Cardiac function has been shown to transiently decrease following prolonged exercise, with greater durations related to increased impairment. However, the prospective assessment of exercise duration on cardiac performance is rare, and the influence of relative exercise intensity is typically not assessed in relation to these changes. The aim of this study was to determine whether progressively longer running distances over the same course would elicit greater cardiac impairment. The present investigation examined cardiac alterations in 49 athletes, following trail-running races of 25, 50, 80, and 160 km, performed on the same course on the same day. Echocardiography, including conventional and speckle tracking imaging, was performed with legs-raised to 60° to mitigate alterations in preload both pre- and post-race. Race-intensities were monitored via heart rate (HR). Following the races, mean arterial pressure (Δ-11 ± 7 mmHg, P < 0.0001), and HR (Δ19 ± 14 bpm, P < 0.0001) were altered independent of race distance. Both left and right ventricular (LV and RV) diastolic function were reduced (ΔLV E/A -0.54 ± 0.49, P < 0.0001; ΔRV A' + 0.02 ± 0.04 m/s, P = 0.01) and RV systolic function decreased (ΔTAPSE -0.25 ± 0.9 cm, P = 0.01), independent of race distance. Cardiac impairment was not apparent using speckle tracking analysis with cubic spline interpolation. While race duration was unrelated to cardiac alterations, increased racing HR was related to greater RV base dilation (r = -0.37, P = 0.03). Increased time spent at higher exercise intensities was related to reduced LV ejection fraction following 25 km (r = -0.81, P = 0.03), LV systolic strain rate following 50 km (r = 0.59, P = 0.04), and TAPSE (r = -0.81, P = 0.03) following 80 km races. Increased running duration did not affect the extent of exercise-induced cardiac fatigue, however, intensity may be a greater driver of cardiac alterations.

Acute aerobic exercise impairs aspects of cognitive function at high altitude.

Hypoxia-mediated cognitive dysfunction can be transiently mitigated by exercise in a laboratory-based setting. Whether this effect holds true in the context of high altitude hypoxia has not been determined. We investigated the effect of acute aerobic exercise on cognitive function (CF) at low (1400m) and high altitude (4240m). Fifteen volunteers (24.1±3.5yrs; 9 females) exercised for 20-min at 40-60% of their heart rate reserve at low and high altitude. CF was assessed before and 10-min after exercise using a tablet-based battery of executive function tests. A sea-level control group (n=13; 24.2±2.4 years; 9 females) performed time-matched CF tests to assess the contribution of a learning effects due to repeated testing. Measures of resting CF were unaffected by ascent to high altitude. Following high altitude exercise, performance significantly worsened on the digit symbol substitution task - a test of processing speed, working memory, and visuospatial attention (z=0.01 vs. -0.59, p=0.02, η2=0.35). No effect was found on other measures of CF following exercise. There was no association between changes in peripheral oxygen saturation and changes in CF following high altitude exercise (r=0.22, p=0.44), but higher hemoglobin concentration at high altitude was associated with a decline in CF following exercise at high altitude (r=-0.65, p=0.02). Acute aerobic exercise performed at high altitude impairs some aspects of CF, whereas other CF tests remain unchanged. The strong ecological validity of this study warrants attention and follow-up investigations are needed to better characterize selective impairment of CF with high altitude exercise.

Evidence of a limb- and shear stress stimulus profile-dependent impact of high-intensity cycling training on flow-mediated dilation.

Lower limb endurance training can improve conduit artery flow-mediated dilation (FMD) in response to transient increases in shear stress (reactive hyperemia; RH-FMD) in both the upper and lower limbs. Sustained increases in shear stress recruit a partially distinct transduction pathway and elicit a physiologically relevant FMD response (SS-FMD) that provides distinct information regarding endothelial function. However, the impact of training on SS-FMD is not well understood. The purpose of this study was to determine the impact of cycling training on handgrip exercise-induced brachial artery (BA) FMD (BA SS-FMD) and calf plantar-flexion-induced superficial femoral artery (SFA) FMD (SFA SS-FMD). RH-FMD was also assessed in both arteries. Twenty-eight young males were randomized to control (n = 12) or training (n = 16) groups. The training group cycled 30 min/day, 3 days/week for 4 weeks at 80% heart rate reserve. FMD was assessed in the BA and SFA before and after the intervention via Duplex ultrasound. Results are means ± SD. Training did not impact SS-FMD in either artery, and SFA RH-FMD was also unchanged (p > 0.05). When controlling for the shear rate stimulus via covariate analysis, BA RH-FMD improved in the training group (p = 0.05) (control - pre-intervention: 5.7% ± 2.4%, post-intervention: 5.3% ± 2.4%; training - pre-intervention: 5.4% ± 2.5%, post-intervention: 7.2% ± 2.4%). Thus, endurance training resulted in nonuniform adaptations to endothelial function, with an isolated impact on the BA's ability to transduce a transient increase in shear stress. Novelty Training did not alter SS-FMD in the arm or leg. RH-FMD was augmented in the arm only. Thus training adaptations were limb- and shear stress profile-specific.

Effects of dynamic arm and leg exercise on muscle sympathetic nerve activity and vascular conductance in the inactive leg.

The influence of muscle sympathetic nerve activity (MSNA) responses on local vascular conductance during exercise are not well established. Variations in exercise mode and active muscle mass can produce divergent MSNA responses. Therefore, we sought to examine the effects of small- versus large-muscle mass dynamic exercise on vascular conductance and MSNA responses in the inactive limb. Thirty-five participants completed two study visits in a randomized order. During visit 1, superficial femoral artery (SFA) blood flow (Doppler ultrasound) was assessed at rest and during steady-state rhythmic handgrip (RHG; 1:1 duty cycle, 40% maximal voluntary contraction), one-leg cycling (17 ± 3% peak power output), and concurrent exercise at the same intensities. During visit 2, MSNA (contralateral fibular nerve microneurography) was acquired successfully in 12/35 participants during the same exercise modes. SFA blood flow increased during RHG (P < 0.0001) and concurrent exercise (P = 0.03) but not cycling (P = 0.91). SFA vascular conductance was unchanged during RHG (P = 0.88) but reduced similarly during concurrent and cycling exercise (both P < 0.003). RHG increased MSNA burst frequency (P = 0.04) without altering burst amplitude (P = 0.69) or total MSNA (P = 0.26). In contrast, cycling and concurrent exercise had no effects on MSNA burst frequency (both P ≥ 0.10) but increased burst amplitude (both P ≤ 0.001) and total MSNA (both P ≤ 0.007). Across all exercise modes, the changes in MSNA burst amplitude and SFA vascular conductance were correlated negatively (r = -0.43, P = 0.02). In summary, the functional vascular consequences of alterations in sympathetic outflow to skeletal muscle are most closely associated with changes in MSNA burst amplitude, but not frequency, during low-intensity dynamic exercise.NEW & NOTEWORTHY Low-intensity small- versus large-muscle mass exercise can elicit divergent effects on muscle sympathetic nerve activity (MSNA). We examined the relationships between changes in MSNA (burst frequency and amplitude) and superficial femoral artery (SFA) vascular conductance during rhythmic handgrip, one-leg cycling, and concurrent exercise in the inactive leg. Only changes in MSNA burst amplitude were inversely associated with SFA vascular conductance responses. This result highlights the functional importance of measuring MSNA burst amplitude during exercise.

The impact of acute mental stress on brachial artery flow-mediated dilation in women diagnosed with depression.

Endothelial function, assessed by flow-mediated dilation (FMD), may be transiently attenuated in healthy adults following acute mental stress. However, the impact of acute mental stress on endothelial function in the context of clinical depression is unknown. This study examined the impact of acute mental stress on FMD in women with a diagnosis of a depressive disorder. Forty-three otherwise healthy women (33 ±â€¯14 years) participated. Brachial artery diameter and blood velocity were assessed with ultrasound. FMD was assessed immediately prior to and 15 min following the Trier Social Stress Test (TSST). The FMD protocol included 5 min of forearm cuff occlusion (pressure = 250 mm Hg), followed by release. Shear stress was estimated by calculating shear rate (SR = brachial artery blood velocity/diameter). Stress reactivity was assessed via changes in mean arterial pressure (MAP), heart rate (HR) and salivary cortisol. Results are mean ±â€¯SD. A significant stress response was elicited by the TSST [MAP, HR and salivary cortisol increased (p < 0.05)]. Neither the SR stimulus nor FMD response differed pre-versus post-stress (p = 0.124 and p = 0.641, respectively). There was a modest negative correlation between cortisol reactivity and change in FMD from pre- to post-stress (R = -0.392, p = 0.011). To conclude, acute mental stress did not consistently impair endothelial function in women diagnosed with a depressive disorder; however, higher cortisol reactivity may increase the likelihood of post-stress endothelial dysfunction. Further research is required to better understand the factors influencing the relationship between acute mental stress, cortisol and endothelial function in women with depression.

Systemic vascular dysfunction is associated with emphysema burden in mild COPD.

BACKGROUND: Cardiovascular diseases play a major role in morbidity and mortality in the earlier stages of COPD. We hypothesized that systemic vascular dysfunction would be present even in patients who are currently considered at "low-risk" for negative cardiovascular outcomes, i.e., those with largely preserved FEV1, few exacerbations and only mild burden of respiratory symptoms (GOLD spirometric grade 1, clinical group A). METHODS: 16 patients (FEV1 = 86 ±â€¯13%) and 16 age- and gender-matched controls underwent measurements of: a) central arterial stiffness by pulse wave velocity, b) brachial flow-mediated dilation and c) forearm muscle oxygenation by near-infrared spectroscopy. Computed tomography quantified emphysema (% of low attenuation areas (LAA)) and airway disease. RESULTS: Patients and controls were well matched for key clinical variables including co-morbidities burden. Thirteen patients presented with more than 5% LAA: emphysema extension was negatively related to transfer factor for carbon monoxide (TLCO) (r = -0.63; p = .01). Compared to controls, patients had higher central arterial stiffness, lower normalized (to shear stress) flow-mediated dilation, delayed time to peak flow-mediated dilation and poorer muscle oxygenation (p < .05). TLCO and emphysema, but not airway disease, were significantly related to each of these functional abnormalities (r values ranging from 0.51 to 0.66; p < .05). CONCLUSION: Systemic vascular dysfunction is present in the earlier stages of COPD, particularly in patients with greater emphysema burden and low TLCO. Regardless FEV1, patients showing those structural and functional abnormalities might be at higher risk of negative events thereby deserving closer follow-up for early detection of cardiovascular disease.