Syncope is unrelated to supine and postural hypotension following prolonged exercise.

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.

Exercise-induced wheeze: Fraction of exhaled nitric oxide-directed management.

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.

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases.

Cerebral blood flow (CBF) is highly regulated by changes in arterial Pco(2) and arterial Po(2). Evidence from animal studies indicates that various vasoactive factors, including release of norepinephrine, endothelin, adrenomedullin, C-natriuretic peptide (CNP), and nitric oxide (NO), may play a role in arterial blood gas-induced alterations in CBF. For the first time, we directly quantified exchange of these vasoactive factors across the human brain. Using the Fick principle and transcranial Doppler ultrasonography, we measured CBF in 12 healthy humans at rest and during hypercapnia (4 and 8% CO(2)), hypocapnia (voluntary hyperventilation), and hypoxia (12 and 10% O(2)). At each level, blood was sampled simultaneously from the internal jugular vein and radial artery. With the exception of CNP and NO, the simultaneous quantification of norepinephrine, endothelin, or adrenomedullin showed no cerebral uptake or release during changes in arterial blood gases. Hypercapnia, but not hypocapnia, increased CBF and caused a net cerebral release of nitrite (a marker of NO), which was reflected by an increase in the venous-arterial difference for nitrite: 57 +/- 18 and 150 +/- 36 micromol/l at 4% and 8% CO(2), respectively (both P < 0.05). Release of cerebral CNP was also observed during changes in CO(2) (hypercapnia vs. hypocapnia, P < 0.05). During hypoxia, there was a net cerebral uptake of nitrite, which was reflected by a decreased venous-arterial difference for nitrite: -96 +/- 14 micromol/l at 10% O(2) (P < 0.05). These data indicate that there is a differential exchange of NO across the brain during hypercapnia and hypoxia and that CNP may play a complementary role in CO(2)-induced CBF changes.

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: effect of age and 12-week exercise training.

Chronic reductions in cerebral blood flow (CBF) and cerebrovascular reactivity to CO2 are risk factors for cerebrovascular disease. Higher aerobic fitness is associated with higher CBF at any age; however, whether CBF or reactivity can be elevated following an exercise training intervention in healthy individuals is unknown. The aim of this study was to assess the effect of exercise training on CBF and cerebrovascular reactivity at rest and during exercise in young and older individuals. Ten young (23 ± 5 years; body mass index (BMI), 26 ± 3 kg m(-2); [Formula: see text], 35 ± 5 ml kg(-1) min(-1)) and 10 older (63 ± 5 years; BMI, 25 ± 3.0 kg m(-2); [Formula: see text], 26 ± 4 ml kg(-1) min(-1)) previously sedentary individuals breathed 5 % CO2 for 3 min at rest and during steady-state cycling exercise (30 and 70 % heart rate range (HRR)) prior to and following a 12-week aerobic exercise intervention. Effects of training on middle cerebral artery blood velocity (MCAv) at rest were unclear in both age groups. The absolute MCAv response to exercise was greater in the young (9 and 9 cm s(-1) (30 and 70 % HRR, respectively) vs. 5 and 4 cm s(-1) (older), P < 0.05) and was similar following training. Cerebrovascular reactivity was elevated following the 12-week training at rest (2.87 ± 0.76 vs. 2.54 ± 1.12 cm s(-1) mm Hg(-1), P = 0.01) and during exercise, irrespective of age. The finding of a training-induced elevation in cerebrovascular reactivity provides further support for exercise as a preventative tool in cerebrovascular and neurological disease with ageing.

Effect of age on exercise-induced alterations in cognitive executive function: relationship to cerebral perfusion.

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.

Cardiorespiratory and cerebrovascular responses to head-up tilt I: influence of age and training status.

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.

Cardiorespiratory and cerebrovascular responses to head-up tilt II: influence of age, training status and acute exercise.

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.