High‐intensity interval exercise (HIIE) improves cerebral executive function (EF), but the improvement in EF is attenuated after reρeated HIIE, perhaρs because of lower lactate availability for the ...brain. This investigation examined whether imρroved EF after exercise relates to brain lactate uρtake. Fourteen healthy, male subjects performed 2 HIIE protocols separated by 60 min of rest. Blood samples were obtained from the right internal jugular venous bulb and from the brachial artery to determine arterial‐venous differences across the brain for lactate (a‐v difflactate), glucose (a‐v diffglucose), oxygen (a‐v diffoxygen), and brain‐derived neurotrophic factor (BDNF; a‐v diffBDNF). EF was evaluated by the color‐word Stroop task. The first HIIE improved EF for 40 min, whereas the second HIIE improved EF only immediately after exercise. The a‐v diffglucose was unchanged, whereas the a‐v diffBDNF increased similarly after both HIIEs, and the a‐v difflactate increased, but the increase was attenuated after the second HIIE, compared with the first HIIE (P <0.05). The EF after HIIE correlated with the a‐v difflactate(r2 = 0.62; P < 0.01). We propose that attenuated improvement in EF after repeated HIIE relates to reduced cerebral lactate metabolism and is, thereby, linked to systemic metabolism as an example of the lactate shuttle mechanism.— Hashimoto, T., Tsukamoto, H., Takenaka, S., Olesen, N. D., Petersen, L. G., Sørensen, H., Nielsen, H. B., Secher, N. H., Ogoh, S. Maintained exercise‐enhanced brain executive function related to cerebral lactate metabolism in men. FASEB J. 32, 1417‐1427 (2018). www.fasebj.org
Perioperative optimization of spatially resolved near-infrared spectroscopy determined cerebral frontal lobe oxygenation (scO2) may reduce postoperative morbidity. Norepinephrine is routinely ...administered to maintain cerebral perfusion pressure and, thereby, cerebral blood flow, but norepinephrine reduces the scO2. We hypothesized that norepinephrine-induced reduction in scO2 is influenced by cutaneous vasoconstriction.
Fifteen healthy male subjects (25 ± 5 yr, mean ± SD) were studied during: hyperventilation (1.5 kPa end-tidal PcO2 reduction), whole-body heating, administration of norepinephrine (0.15 μg · kg · min; with and without end-tidal carbon dioxide correction), and hypoxia (FiO2: 0.12%). Arterial (saO2), skin, and internal jugular venous oxygen saturations (sjO2) were recorded, and the average cerebral capillary oxygen saturation (scapO2) was calculated.
This study indicates that scO2 is influenced by skin oxygen saturation because whole-body heating increased scO2 by 3.6% (2.1-5.1%; 95% CI) and skin oxygen saturation by 3.1% (1.3-4.9%), whereas scapO2 remained unaffected. Conversely, hyperventilation decreased scO2 by 2.1% (0.4-3.7%) and scapO2 by 5.3% (3.8-6.9%), whereas skin oxygen saturation increased 1.8% (0.5-3.1%). In response to hypoxia, scO2 (10.2%; 6.6-13.7%), scapO2 (7.9%; 6.4-9.4%), and skin oxygen saturation (8.9%; 6.3-11.6%) all decreased. With administration of norepinephrine there was a 2.2% (1.0-4.3%) decrease in skin oxygen saturation and scO2 decreased 6.2% (4.2-8.0%), with scapO2 remaining unaffected.
The results confirm that spatially resolved near-infrared spectroscopy detects cerebral deoxygenation with systemic hypoxic exposure and hyperventilation. However, a commonly used vasopressor norepinephrine disturbs skin oxygen saturation to an extent that influences scO2.
To evaluate the morphology of the “athlete’s heart”, left ventricular (LV) wall thickness (WT) and end-diastolic internal diameter (LVIDd) at rest were addressed in publications on skiers, rowers, ...swimmers, cyclists, runners, weightlifters (
n
= 927), and untrained controls (
n
= 173) and related to the acute and maximal cardiovascular response to their respective disciplines. Dimensions of the heart at rest and functional variables established during the various sport disciplines were scaled to body weight for comparison among athletes independent of body mass. The two measures of LV were related (
r
= 0.8;
P
= 0.04) across athletic disciplines. With allometric scaling to body weight, LVIDd was similar between weightlifters and controls but 7%-15% larger in the other athletic groups, while WT was 9%-24% enlarged in all athletes. The LVIDd was related to stroke volume, oxygen pulse, maximal oxygen uptake, cardiac output, and blood volume (
r
= ~ 0.9,
P
< 0.05), while there was no relationship between WT and these variables (
P
> 0.05). In conclusion, while cardiac enlargement is, in part, essential for the generation of the cardiac output and thus stroke volume needed for competitive endurance exercise, an enlarged WT seems important for the development of the wall tension required for establishing normal arterial pressure in the enlarged LVIDd.
This review focuses on the possibility that autonomic activity influences cerebral blood flow (CBF) and metabolism during exercise in humans. Apart from cerebral autoregulation, the arterial carbon ...dioxide tension, and neuronal activation, it may be that the autonomic nervous system influences CBF as evidenced by pharmacological manipulation of adrenergic and cholinergic receptors. Cholinergic blockade by glycopyrrolate blocks the exercise-induced increase in the transcranial Doppler determined mean flow velocity (MCA Vmean). Conversely, alpha-adrenergic activation increases that expression of cerebral perfusion and reduces the near-infrared determined cerebral oxygenation at rest, but not during exercise associated with an increased cerebral metabolic rate for oxygen (CMRO(2)), suggesting competition between CMRO(2) and sympathetic control of CBF. CMRO(2) does not change during even intense handgrip, but increases during cycling exercise. The increase in CMRO(2) is unaffected by beta-adrenergic blockade even though CBF is reduced suggesting that cerebral oxygenation becomes critical and a limited cerebral mitochondrial oxygen tension may induce fatigue. Also, sympathetic activity may drive cerebral non-oxidative carbohydrate uptake during exercise. Adrenaline appears to accelerate cerebral glycolysis through a beta2-adrenergic receptor mechanism since noradrenaline is without such an effect. In addition, the exercise-induced cerebral non-oxidative carbohydrate uptake is blocked by combined beta 1/2-adrenergic blockade, but not by beta1-adrenergic blockade. Furthermore, endurance training appears to lower the cerebral non-oxidative carbohydrate uptake and preserve cerebral oxygenation during submaximal exercise. This is possibly related to an attenuated catecholamine response. Finally, exercise promotes brain health as evidenced by increased release of brain-derived neurotrophic factor (BDNF) from the brain.
It has been considered whether during whole body exercise the increase in cardiac output is large enough to support skeletal muscle blood flow. This review addresses four lines of evidence for a flow ...limitation to skeletal muscles during whole body exercise. First, even though during exercise the blood flow achieved by the arms is lower than that achieved by the legs (∼160 vs. ∼385 ml·min(-1)·100 g(-1)), the muscle mass that can be perfused with such flow is limited by the capacity to increase cardiac output (42 l/min, highest recorded value). Secondly, activation of the exercise pressor reflex during fatiguing work with one muscle group limits flow to other muscle groups. Another line of evidence comes from evaluation of regional blood flow during exercise where there is a discrepancy between flow to a muscle group when it is working exclusively and when it works together with other muscles. Finally, regulation of peripheral resistance by sympathetic vasoconstriction in active muscles by the arterial baroreflex is critical for blood pressure regulation during exercise. Together, these findings indicate that during whole body exercise muscle blood flow is subordinate to the control of blood pressure.
Purpose
This review presents a perspective on the expansive literature on rowing.
Methods
The PubMed database was searched for the most relevant literature, while some information was obtained from ...books.
Results
Following the life span of former rowers paved the way to advocate exercise for health promotion. Rowing involves almost all muscles during the stroke and competition requires a large oxygen uptake, which is challenged by the pulmonary diffusion capacity and restriction in blood flow to the muscles. Unique training adaptations allow for simultaneous engagement of the legs in the relatively slow movement of the rowing stroke that, therefore, involves primarily slow-twitch muscle fibres. Like other sport activities, rowing is associated with adaptation not only of the heart, including both increased internal diameters and myocardial size, but also skeletal muscles with hypertrophy of especially slow-twitch muscle fibres. The high metabolic requirement of intense rowing reduces blood pH and, thereby, arterial oxygen saturation decreases as arterial oxygen tension becomes affected.
Conclusion
Competitive rowing challenges most systems in the body including pulmonary function and circulatory control with implication for cerebral blood flow and neuromuscular activation. Thus, the physiology of rowing is complex, but it obviously favours large individuals with arms and legs that allow the development of a long stroke. Present inquiries include the development of an appropriately large cardiac output despite the Valsalva-like manoeuvre associated with the stroke, and the remarkable ability of the brain to maintain motor control and metabolism despite marked reductions in cerebral blood flow and oxygenation.
Brain-derived neurotrophic factor (BDNF) has an important role in regulating maintenance, growth and survival of neurons.
However, the main source of circulating BDNF in response to exercise is ...unknown. To identify whether the brain is a source
of BDNF during exercise, eight volunteers rowed for 4 h while simultaneous blood samples were obtained from the radial artery
and the internal jugular vein. To further identify putative cerebral region(s) responsible for BDNF release, mouse brains
were dissected and analysed for BDNF mRNA expression following treadmill exercise. In humans, a BDNF release from the brain
was observed at rest ( P < 0.05), and increased two- to threefold during exercise ( P < 0.05). Both at rest and during exercise, the brain contributed 70â80% of circulating BDNF, while that contribution decreased
following 1 h of recovery. In mice, exercise induced a three- to fivefold increase in BDNF mRNA expression in the hippocampus
and cortex, peaking 2 h after the termination of exercise. These results suggest that the brain is a major but not the sole
contributor to circulating BDNF. Moreover, the importance of the cortex and hippocampus as a source for plasma BDNF becomes
even more prominent in response to exercise.
The circulating level of brain-derived neurotrophic factor (BDNF) is reduced in patients with major depression and type-2 diabetes. Because acute exercise increases BDNF production in the hippocampus ...and cerebral cortex, we hypothesized that endurance training would enhance the release of BDNF from the human brain as detected from arterial and internal jugular venous blood samples. In a randomized controlled study, 12 healthy sedentary males carried out 3 mo of endurance training (n = 7) or served as controls (n = 5). Before and after the intervention, blood samples were obtained at rest and during exercise. At baseline, the training group (58 + or - 106 ng x 100 g(-1) x min(-1), means + or - SD) and the control group (12 + or - 17 ng x 100 g(-1) x min(-1)) had a similar release of BDNF from the brain at rest. Three months of endurance training enhanced the resting release of BDNF to 206 + or - 108 ng x 100 g(-1) x min(-1) (P < 0.05), with no significant change in the control subjects, but there was no training-induced increase in the release of BDNF during exercise. Additionally, eight mice completed a 5-wk treadmill running training protocol that increased the BDNF mRNA expression in the hippocampus (4.5 + or - 1.6 vs. 1.4 + or - 1.1 mRNA/ssDNA; P < 0.05), but not in the cerebral cortex (4.0 + or - 1.4 vs. 4.6 + or - 1.4 mRNA/ssDNA) compared with untrained mice. The increased BDNF expression in the hippocampus and the enhanced release of BDNF from the human brain following training suggest that endurance training promotes brain health.
Key points
Sodium nitroprusside lowers blood pressure by vasodilatation but is reported to reduce cerebral blood flow.
In healthy young men sodium nitroprusside reduced blood pressure, total ...peripheral resistance, and arterial CO2 tension and yet cerebral blood flow was maintained, with an increase in internal carotid artery blood flow and cerebrovascular conductance.
Sodium nitroprusside induces both systemic and cerebral vasodilatation affecting internal carotid artery more than vertebral artery flow.
Cerebral autoregulation maintains cerebral blood flow (CBF) despite marked changes in mean arterial pressure (MAP). Sodium nitroprusside (SNP) reduces blood pressure by vasodilatation but is reported to lower CBF, probably by a reduction in its perfusion pressure. We evaluated the influence of SNP on CBF and aimed for a 20% and then 40% reduction in MAP, while keeping MAP ≥ 50 mmHg, to challenge cerebral autoregulation. In 19 healthy men (age 24 ± 4 years; mean ± SD) duplex ultrasound determined right internal carotid (ICA) and vertebral artery (VA) blood flow. The SNP reduced MAP (from 83 ± 8 to 69 ± 8 and 58 ± 4 mmHg; both P < 0.0001), total peripheral resistance, and arterial CO2 tension (P aC O2; 41 ± 3 vs. 39 ± 3 and 37 ± 4 mmHg; both P < 0.01). Yet ICA flow increased with the moderate reduction in MAP but returned to the baseline value with the large reduction in MAP (336 ± 66 vs. 365 ± 69; P = 0.013 and 349 ± 82 ml min–1; n.s.), while VA flow (114 ± 34 vs. 112 ± 38 and 110 ± 42 ml min–1; both n.s.) and CBF ((ICA + VA flow) × 2; 899 ± 135 vs. 962 ± 127 and 918 ± 197 ml min–1; both n.s.) were maintained with increased cerebrovascular conductance. In conclusion, CBF is maintained during SNP‐induced reduction in MAP despite reduced P aC O2 and the results indicate that SNP dilates cerebral vessels and increases ICA flow.
Key points
Sodium nitroprusside lowers blood pressure by vasodilatation but is reported to reduce cerebral blood flow.
In healthy young men sodium nitroprusside reduced blood pressure, total peripheral resistance, and arterial CO2 tension and yet cerebral blood flow was maintained, with an increase in internal carotid artery blood flow and cerebrovascular conductance.
Sodium nitroprusside induces both systemic and cerebral vasodilatation affecting internal carotid artery more than vertebral artery flow.
New Findings
What is the central question of this study?
High‐intensity interval exercise (HIIE) is recommended for its favourable haemodynamic stimulation, but excessive haemodynamic fluctuations ...may stress the brain: is the cerebral vasculature protected against exaggerated systemic blood flow fluctuation during HIIE?
What is the main finding and its importance?
Time‐ and frequency‐domain indices of aortic–cerebral pulsatile transition were lowered during HIIE. The findings suggest that the arterial system to the cerebral vasculature may attenuate pulsatile transition during HIIE as a defence mechanism against pulsatile fluctuation for the cerebral vasculature.
High‐intensity interval exercise (HIIE) is recommended because it provides favourable haemodynamic stimulation, but excessive haemodynamic fluctuations may be an adverse impact on the brain. We tested whether the cerebral vasculature is protected against systemic blood flow fluctuation during HIIE. Fourteen healthy men (age 24 ± 2 years) underwent four 4‐min exercises at 80–90% of maximal workload (Wmax) interspaced by 3‐min active rest at 50–60% Wmax. Transcranial Doppler measured middle cerebral artery blood velocity (CBV). Systemic haemodynamics (Modelflow) and aortic pressure (AoP, general transfer function) were estimated from an invasively recorded brachial arterial pressure waveform. Using transfer function analysis, gain and phase between AoP and CBV (0.39–10.0 Hz) were calculated. Stroke volume, aortic pulse pressure and pulsatile CBV increased during exercise (time effect: P < 0.0001 for all), but a time‐domain index of aortic–cerebral pulsatile transition (pulsatile CBV/pulsatile AoP) decreased throughout the exercise bouts (time effect: P < 0.0001). Furthermore, transfer function gain reduced, and phase increased throughout the exercise bouts (time effect: P < 0.0001 for both), suggesting the attenuation and delay of pulsatile transition. The cerebral vascular conductance index (mean CBV/mean arterial pressure; time effect: P = 0.296), an inverse index of cerebral vascular tone, did not change even though systemic vascular conductance increased during exercise (time effect: P < 0.0001). The arterial system to the cerebral vasculature may attenuate pulsatile transition during HIIE as a defence mechanism against pulsatile fluctuation for the cerebral vasculature.
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