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The objective of this study was to compare acute effects of prolonged sitting, prolonged standing and sitting interrupted with regular activity breaks on vascular function and postprandial glucose metabolism. In a randomized cross-over trial, 18 adults completed: 1. Prolonged Sitting; 2. Prolonged Standing and 3. Sitting with 2-min walking (5 km/h, 10% incline) every 30 min (Regular Activity Breaks). Flow mediated dilation (FMD) was measured in the popliteal artery at baseline and 6 h. Popliteal artery hemodynamics, and postprandial plasma glucose and insulin were measured over 6 h. Neither raw nor allometrically-scaled FMD showed an intervention effect (p = 0.285 and 0.159 respectively). Compared to Prolonged Sitting, Regular Activity Breaks increased blood flow (overall effect of intervention p<0.001; difference = 80%; 95% CI 34 to 125%; p = 0.001) and net shear rate (overall effect of intervention p<0.001; difference = 72%; 95% CI 30 to 114%; p = 0.001) at 60 min. These differences were then maintained for the entire 6 h. Prolonged Standing increased blood flow at 60 min only (overall effect of intervention p<0.001; difference = 62%; 95% CI 28 to 97%; p = 0.001). Regular Activity Breaks decreased insulin incremental area under the curve (iAUC) when compared to both Prolonged Sitting (overall effect of intervention P = 0.001; difference = 28%; 95% CI 14 to 38%; p<0.01) and Prolonged Standing (difference = 19%; 95% CI 4 to 32%, p = 0.015). There was no intervention effect on glucose iAUC or total AUC (p = 0.254 and 0.450, respectively). In normal-weight participants, Regular Activity Breaks induce increases in blood flow, shear stress and improvements in postprandial metabolism that are associated with beneficial adaptations. Physical activity and sedentary behaviour messages should perhaps focus more on the importance of frequent movement rather than simply replacing sitting with standing., Competing Interests: The authors have declared that no competing interests exist.

New Findings: What is the central question of this study? How does resistance exercise affect peripheral haemodynamics in the active and inactive limb? What is the main finding and its importance? Preliminary data indicate that resistance exercise increases flow and shear rate in the active limb transiently. The same exercise has minimal, short-lasting influence on peripheral haemodynamics in the inactive limb, but further research is required to elaborate on resistance exercise-mediated changes in vascular function in active and inactive limbs., Abstract: Current evidence indicates that to achieve maximum health benefits, regular resistance exercise should be a key component of structured physical activity. Several studies have revealed that regular resistance exercise may be associated with impaired vascular function, although this finding is inconsistent. Proposed explanations for impairment include substantial increases in blood pressure and increased retrograde blood flow in active limbs promoted by resistance exercise. However, few studies have examined the acute haemodynamics of resistance exercise in active - and even fewer in inactive - limbs. The purpose of this study was to characterise the haemodynamic responses in peripheral arteries in active and inactive limbs in response to resistance exercise using upper and lower limbs. Ten participants (five male, five female) familiar with resistance training performed three sets of 10 isotonic repetitions of right-sided bicep curls or knee extensions on separate days. Blood flow, shear rate and muscle oxygenation in the active and inactive limb, and blood pressure were measured before and for 3 min after each set. Blood flow increased in response to resistance exercise in the active limb (∼8-fold and ∼6-fold for the upper and lower limb respectively), with concurrent significant increases in mean and antegrade shear rate. In the inactive limb, blood flow more than doubled for both upper and lower limb exercise, transiently, with no significant change in retrograde shear rate. These acute blood flow profiles following resistance exercise are not indicative of long-term vessel impairment based on current understanding of blood flow and shear stress patterns., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Following exercise, hypotension is often reported and syncope is more likely. It is unresolved whether the postexercise hypotension associated with different exercise intensities contributes to the rate at which syncope develops. What is the main finding and its importance? The physiological events that induce presyncope are the same both before and after exercise; however, more intense exercise accelerated the development of hypocapnia, hypotension and, ultimately, syncope. These data indicate that higher intensity exercise induces a postexercise hypotension that reduces cardiovascular reserve, an earlier development of hypocapnia and, ultimately, cerebral hypoperfusion. After exercise, a reduction in mean arterial pressure is often experienced and is referred to as postexercise hypotension. Whilst syncope is more likely following exercise, it is unknown whether orthostatic tolerance is impacted by any exercise intensity-mediated effect on postexercise hypotension. We examined the effect of exercise intensity on time to presyncope, induced via combined head-up tilt and lower body negative pressure following 1 h of cycling at 30 and 70% of heart rate range. Healthy participants (n = 8; mean ± SD, 28 ± 5 years old) completed orthostatic testing to presyncope before and after exercise. Beat-to-beat middle cerebral artery blood flow velocity (MCAv), mean arterial pressure and cerebral oxygenation (measured by near-infrared spectroscopy) were recorded continuously throughout orthostatic testing. During exercise, heart rates were 95 ± 6 and 147 ± 5 beats min(-1) for 30 and 70% heart rate range, respectively, with average power outputs of 103 ± 22 and 221 ± 45 W, respectively. Time to presyncope occurred 32% sooner after the 70% heart rate range trial (952 ± 484 versus 1418 ± 435 s; P = 0.004). Both before and after exercise, presyncope occurred at the same reduction in MCAv (grouped mean, -30 ± 11 cm s(-1) ), mean arterial pressure (-18 ± 13 mmHg), total oxygenation index (-6 ± 2%) and partial pressure of end-tidal CO2 (-16 ± 8 mmHg; all P > 0.1). At presyncope following exercise, the MCAv response was related more to the change in partial pressure of end-tidal CO2 from the baseline preceding orthostatic testing (r(2)  = 0.50, P = 0.01) than to the hypotension (r(2)  = 0.12, P = 0.17). Presyncope both before and after exercise occurred as a result of the same physiological perturbations, albeit greatly accelerated following more intense exercise., (© 2015 The Authors. Experimental Physiology © 2015 The Physiological Society.)

Regular exercise improves the age-related decline in cerebral blood flow (CBF) and is associated with improved cognitive function; however, less is known about the direct relationship between CBF and cognitive function. We examined the influence of healthy aging on the capability of acute exercise to improve cognition, and whether exercise-induced improvements in cognition are related to CBF and cortical hemodynamics. Middle cerebral artery blood flow velocity (MCAv; Doppler) and cortical hemodynamics (NIRS) were measured in 13 young (24±5 y) and 9 older (62±3 y) participants at rest and during cycling at 30% and 70% of heart rate range (HRR). Cognitive performance was assessed using a computer-adapted Stroop task (i.e., test of executive function cognition) at rest and during exercise. Average response times on the Stroop task were slower for the older compared to younger group for both simple and difficult tasks (P<0.01). Independent of age, difficult-task response times improved during exercise (P<0.01), with the improvement greater at 70% HRR exercise (P=0.04 vs. 30% HRR). Higher MCAv was correlated with faster response times for simple and difficult tasks at rest (R(2)=0.47 and R(2)=0.47, respectively), but this relation uncoupled progressively during exercise. Exercise-induced increases in MCAv were similar and unaltered during cognitive tasks for both age groups. In contrast, prefrontal cortical hemodynamic NIRS measures [oxyhemoglobin (O(2)Hb) and total hemoglobin (tHb)] were differentially affected by exercise intensity, age and cognitive task; e.g., there were smaller increases in [O(2)Hb] and [tHb] in the older group between exercise intensities (P<0.05). These data indicate that: 1) Regardless of age, cognitive (executive) function is improved while exercising; 2) while MCAv is strongly related to cognition at rest, this relation becomes uncoupled during exercise, and 3) there is dissociation between global CBF and regional cortical oxygenation and NIRS blood volume markers during exercise and engagement of prefrontal cognition., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Syncope is widely reported following prolonged exercise. It is often assumed that the magnitude of exercise-induced hypotension (post-exercise hypotension; PEH), and the hypotensive response to postural change (initial orthostatic hypotension; IOH) are predictors of syncope post-exercise. The aim of this study was to determine the relationship between PEH, IOH, the residual IOH and syncope following prolonged exercise. Blood pressure (BP; Finometer) was measured continuously in 19 athletes (47 ± 20 years; BMI: 23.2 ± 2.2 kg m(2); VO(2) max: 51.3 ± 10.8 mL kg(-1) min(-1)) whilst supine and during head-up tilt (HUT) to 60° for 15 min (or to syncope), prior to and following 4 h of running at 70-80% maximal heart rate. Syncope developed in 15 of 19 athletes post-exercise [HUT-time completed, Pre: 14:39 (min:s) ± 0:55; Post: 5:59 ± 4:53; P < 0.01]. PEH was apparent (-7 ± 7 mmHg; -8 ± 8%), but was unrelated to HUT-time completed (r (2) = 0.09; P > 0.05). Although the magnitude of IOH was similar to post-exercise [-28 ± 12 vs. -20 ± 14% (pre-exercise); P > 0.05], the BP recovery following IOH was incomplete [-9 ± 9 vs. -1 ± 11 (pre-exercise); P < 0.05]; however, neither showed a relation to HUT-time completed (r(2) = 0.18, r (2) = 0.01; P > 0.05, respectively). Although an inability to maintain BP is a common feature of syncope post-exercise, the magnitude of PEH, IOH and residual IOH do not predict time to syncope. Practically, endurance athletes who present with greater hypotension are not necessarily at a greater risk of syncope than those who present with lesser reductions in BP.

The purpose of this study was to examine the combined cardiorespiratory and cerebrovascular responses to head-up tilt (HUT) in young and older trained and untrained humans following moderate-duration exercise. Middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound), blood pressure (BP; Finometer), and stroke volume (SV) were measured continuously whilst supine and during 60° HUT for 15 min or to pre-syncope in 41 participants [nine young trained; eleven young untrained; twelve older trained; nine older untrained] prior to and following 30 min of treadmill exercise at 70-80% maximal HR. Orthostatic tolerance was not reduced following exercise [Mean (all groups) 14:45 ± 1:19, vs. 14:47 ± 0:43 min:s (before exercise); P = 0.73], and did not differ with age or fitness. Mean MCAv was elevated [~5 ± 11%] whilst supine after exercise in the older participants but reduced [~-4 ± 12%] in the young [P = 0.03]. The postural reductions in MCAv [~-22% vs. -17%; P = 0.02], MAP [~-8% vs. -3%; P = 0.04] and SV [~-28% vs. -23%; P = 0.03] were increased after exercise (vs. pre-exercise). Orthostatic tolerance was not reduced following 30 min of exercise, and did not differ with age or fitness, despite more pronounced post-exercise reductions in MCAv, MAP and SV with postural change., (Copyright © 2010 Elsevier Inc. All rights reserved.)

The purpose of this study was to examine the combined cardiorespiratory and cerebrovascular responses to head-up tilt (HUT) in young (27 ± 4 years) and older (65 ± 5 years) trained and untrained humans. Middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), blood pressure (BP; Finometer) and cardiac output (Q) were measured continuously whilst supine and during 60° HUT for 15 min or to pre-syncope in 41 participants [nine young trained; eleven young untrained; twelve older trained; nine older untrained]. Thirty seven of forty one participants completed 15 min HUT, and orthostatic tolerance did not differ with age or fitness (P = 0.66). Supine MCAv was 30% lower in the older participants but the HUT-induced drop in MCAv was not altered by age [-18% (young) vs. -17% (older)], or fitness. Mean arterial BP was maintained during HUT and not altered by age or fitness. In the untrained, peripheral resistance was elevated [11% vs. -2% (trained); P = 0.01], and Q was reduced [-10% vs. -5% (trained); P = 0.04] with HUT. Despite these age- and fitness-associated differences in some cardiovascular responses to HUT, orthostatic tolerance was similar across groups. Thus, at least in this healthy population, neither age nor fitness impacts on the ability to adapt to postural change., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Background and Objective: Exercise-induced wheeze (EIW) is common. Several treatment options exist. Patients with low fraction of exhaled nitric oxide (F(E)NO) are unlikely to be steroid-responsive and might benefit from non-steroidal therapies. We assessed: the efficacy of cromoglycate, formoterol and montelukast in patients with EIW and low F(E)NO (<35 ppb) in a randomized cross-over trial, and the efficacy of inhaled corticosteroid in a high F(E)NO (>35 ppb) group., Methods: Patients had EIW and airway hyperresponsiveness (AHR) to mannitol and/or exercise. Those with low F(E)NO (n = 19) received cromoglycate (20 mg inh. bd + before challenge tests), formoterol (12 microg inh. bd + before challenge tests) and montelukast (10 mg p.o. od), each for 2 weeks. Those with high F(E)NO (n = 20) took inhaled fluticasone (500 microg) daily for 4 weeks. Primary end-points were: 50% reduction in maximum FEV(1) %fall (clinical protection) and decrease in AHR to mannitol., Results: In patients with low F(E)NO, cromoglycate, formoterol and montelukast significantly decreased AHR to mannitol in 63%, 61% and 47% of patients, respectively. In this group, the magnitude of exercise-induced bronchoconstriction (EIB) was significantly reduced with montelukast and formoterol; between-treatment differences were not significant. Of 6/19 with low F(E)NO and EIB, protection occurred in 67% (cromoglycate), 83% (formoterol) and 50% (montelukast), respectively. In the high F(E)NO group, AHR to mannitol and EIB decreased significantly with fluticasone (P < 0.001, P = 0.005, respectively), and protection occurred in 7/8 (88%) with EIB., Conclusions: In patients with EIW and low F(E)NO, the number of 'responders' to cromoglycate, formoterol and montelukast was similar. In a high F(E)NO population the response to inhaled corticosteroid was highly significant and comparable to previous studies.

It is known that cerebral blood flow declines with age in sedentary adults, although previous studies have involved small sample sizes, making the exact estimate of decline imprecise and the effects of possible moderator variables unknown. Animal studies indicate that aerobic exercise can elevate cerebral blood flow; however, this possibility has not been examined in humans. We examined how regular aerobic exercise affects the age-related decline in blood flow velocity in the middle cerebral artery (MCAv) in healthy humans. Maximal oxygen consumption, body mass index (BMI), blood pressure and MCAv were measured in healthy sedentary (n = 153) and endurance-trained (n = 154) men aged between 18 and 79 years. The relationships between age, training status, BMI and MCAv were examined using analysis of covariance methods. Mean +/- s.e.m. estimates of regression coefficients and 95% confidence intervals (95% CI) were calculated. The age-related decline in MCAv was -0.76 +/- 0.04 cm s(-1) year(-1) (95% CI = -0.69 to -0.83, r(2) = 0.66, P < 0.0005) and was independent of training status (P = 0.65). Nevertheless, MCAv was consistently elevated by 9.1 +/- 3.3 cm s(-1) (CI = 2.7-15.6, P = 0.006) in endurance-trained men throughout the age range. This approximately 17% difference between trained and sedentary men amounted to an approximate 10 year reduction in MCAv 'age' and was robust to between-group differences in BMI and blood pressure. Regular aerobic-endurance exercise is associated with higher MCAv in men aged 18-79 years. The persistence of this finding in older endurance-trained men may therefore help explain why there is a lower risk of cerebrovascular disease in this population.

Endurance exercise induces cardiovascular adaptations; the athletic phenotypes of the heart and arteries are well characterized, but few studies have investigated the effects of chronic exercise on the venous system. The aim of this study was to describe the anatomy and function of lower-limb deep and superficial veins in athletes compared with controls. Endurance-trained athletes and untrained controls (13 males, 7 females per group) were examined using ultrasound to measure vein diameter and flow, and air plethysmography to assess calf venous volume dynamics and muscle pump function at rest, during a single step, ambulation (10 steps) and after acute treadmill exercise (30 min (80% age-predicted heart rate maximum). Diameters of three of the seven deep veins assessed were larger in athletes (P 0.0167) and more medial calf perforators were detectable (5 vs. 3, P = 0.0039). Calf venous volume was 22% larger in athletes (P = 0.0057), and calf muscle pump ejection volume and ambulatory venous volume after 10 steps were both greater in athletes (20 and 46% respectively, P 0.0482). Following acute exercise, flow recovery profiles in deep and superficial veins draining the leg were not different between groups, despite athletes performing approximately four times more work. After exercise, venous volume and ejection volume were reduced by (20% in athletes with no change in controls (interaction, P 0.0372) and although ambulatory venous volume reduced, this remained greater in athletes. These findings highlight venous adaptations that compensate for the demands of regular endurance exercise, all of which are suited to enhance flow through the lower-limb venous system. NEW & NOTEWORTHY Although much literature exists describing adaptations to the heart and arteries in response to endurance exercise training, less is known about the effects on the venous system. Characteristics of “the athlete’s vein” described here include deep and perforator vein remodeling, improved drainage, and greater calf venous volume at rest and on calf muscle pump activation. Following exercise, athletes demonstrated prompt flow recovery and appropriate volume reductions, and veins beneficially adapt to better tolerate the demands of regular physical activity. [ABSTRACT FROM AUTHOR]

Intermittent fasting and exercise provide neuroprotection from age‐related cognitive decline. A link between these two seemingly distinct stressors is their capability to steer the brain away from exclusively glucose metabolism. This cerebral substrate switch has been implicated in upregulating brain‐derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning and memory, and may underlie some of these neuroprotective effects. We examined the isolated and interactive effects of (1) 20‐h fasting, (2) 90‐min light exercise, and (3) high‐intensity exercise on peripheral venous BDNF in 12 human volunteers. A follow‐up study isolated the influence of cerebrovascular shear stress on circulating BDNF. Fasting for 20 h decreased glucose and increased ketones (P ≤ 0.0157) but had no effect on BDNF (P ≥ 0.4637). Light cycling at 25% of peak oxygen uptake (V̇O2peak${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$) increased serum BDNF by 6 ± 8% (independent of being fed or fasted) and was mediated by a 7 ± 6% increase in platelets (P < 0.0001). Plasma BDNF was increased from 336 pg l−1 [46,626] to 390 pg l−1 [127,653] by 90‐min of light cycling (P = 0.0128). Six 40‐s intervals at 100% of V̇O2peak${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ increased plasma and serum BDNF, as well as the BDNF‐per‐platelet ratio 4‐ to 5‐fold more than light exercise did (P ≤ 0.0044). Plasma BDNF was correlated with circulating lactate during the high‐intensity intervals (r = 0.47, P = 0.0057), but not during light exercise (P = 0.7407). Changes in cerebral shear stress – whether occurring naturally during exercise or induced experimentally with inspired CO2 – did not correspond with changes in BDNF (P ≥ 0.2730). BDNF responses to low‐intensity exercise are mediated by increased circulating platelets, and increasing either exercise duration or particularly intensity is required to liberate free BDNF. Key points: Intermittent fasting and exercise both have potent neuroprotective effects and an acute upregulation of brain‐derived neurotrophic factor (BDNF) appears to be a common mechanistic link.Switching the brain's fuel source from glucose to either ketone bodies or lactate, i.e. a cerebral substrate switch, has been shown to promote BDNF production in the rodent brain.Fasting for 20 h caused a 9‐fold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest.Prolonged (90 min) light cycling exercise increased plasma‐ and serum‐derived BDNF irrespective of being fed or fasted and seemed to be independent of changes in cerebral shear stress.Six minutes of high‐intensity cycling intervals increased every metric of circulating BDNF by 4 to 5 times more than prolonged low‐intensity cycling; the increase in plasma‐derived BDNF was correlated with a 6‐fold increase in circulating lactate irrespective of feeding or fasting.Compared to 1 day of fasting with or without prolonged light exercise, high‐intensity exercise is a much more efficient means to increase BDNF in circulation. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question to the study?Are primary indices of heat adaptation (e.g., expansion of plasma volume and reduction in resting core temperature) differentially affected by the three major modes of short‐term heat acclimation, that is, exercise in the heat, hot water immersion and sauna?What it the main finding and its importance?The three modes elicited typical adaptations expected with short‐term heat acclimation, but these were not significantly different between modes. This comparison has not previously been made and highlights that individuals can expect similar adaptation to heat regardless of the mode used. Heat acclimation (HA) can improve heat tolerance and cardiovascular health. The mode of HA potentially impacts the magnitude and time course of adaptations, but almost no comparative data exist. We therefore investigated adaptive responses to three common modes of HA, particularly with respect to plasma volume. Within a crossover repeated‐measures design, 13 physically active participants (five female) undertook four, 5‐day HA regimes (60 min/day) in randomised order, separated by ≥4 weeks. Rectal temperature (Tre) was clamped at neutrality via 36.6°C (thermoneutral) water immersion (TWI; i.e., control condition), or raised by 1.5°C via heat stress in 40°C water, sauna (55°C, 52% relative humidity), or exercise in humid heat (40°C, 52% relative humidity; ExH). Adaptation magnitude was assessed as the pooled response across days 4–6, while kinetics was assessed via the 6‐day time series. Plasma volume expansion was similar in all heated conditions but only higher than TWI in exercise in the heat (ExH) (by 4%, P = 0.036). Approximately two‐thirds of the expansion was attained within the initial 24 h and was moderately related to that present on day 6, regardless of HA mode (r = 0.560–0.887). Expansion was mediated by conservation of both sodium and albumin content, with little evidence for these having differential roles between modes (P = 0.706 and 0.320, respectively). Resting Tre decreased by 0.1–0.3°C in all heated conditions, and systolic blood pressure decreased by 4 mmHg, but not differentially between conditions (P ≥ 0.137). In conclusion, HA mode did not substantially affect the magnitude or rate of adaptation in key resting markers of short‐term HA. [ABSTRACT FROM AUTHOR]