Hourly staircase sprinting exercise “snacks” improve femoral artery shear patterns but not flow-mediated dilation or cerebrovascular regulation: A pilot study

2020 ◽  
Author(s):  
Hannah G Caldwell ◽  
Geoff B Coombs ◽  
Hossein Rafiei ◽  
Philip N Ainslie ◽  
Jonathan P. Little
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Femoral Artery ◽  
Vascular Function ◽  
Regional Blood Flow ◽  
Cerebral Metabolism ◽  
Neurovascular Coupling ◽  
Duplex Ultrasound ◽  
Transcranial Doppler Ultrasound ◽  
Flow Mediated Dilation

Healthy males (n=10; 24±4 years; BMI: 24±2 kg/m2) completed two randomized conditions separated by ≥48 hours involving 6-8.5 hours of sitting with (“stair snacks”) and without (sedentary) hourly staircase sprint interval exercise (approx. 14-20 s each). Resting blood flow and shear rates were measured in the femoral artery, internal carotid artery, and vertebral artery (Duplex ultrasound). Flow-mediated dilation (FMD) was quantified as an index of peripheral endothelial function in the femoral artery. Neurovascular coupling (NVC; regional blood flow response to local increases in cerebral metabolism) was assessed in the posterior cerebral artery (transcranial Doppler ultrasound). Femoral artery hemodynamics were higher following the active trial with no change in the sedentary trial, including blood flow (+32±23% vs. -10±28%; P=0.015 and P=0.253, respectively), vascular conductance (+32±27% vs. -15±26%; P=0.012 and P=0.098, respectively), and mean shear rate (+17±8% vs. -8±28%; P=0.004 and P=0.310, respectively). The change in FMD was not different within or between conditions (P=0.184). Global cerebral blood flow (CBF), conductance, shear patterns, and NVC were not different within or between conditions (all P>0.05). Overall, exercise “stair snacks” improve femoral artery blood flow and shear patterns but not peripheral (e.g., FMD) or cerebral (e.g., CBF and NVC) vascular function following prolonged sitting. The study was registered at ClinicalTrials.gov (NCT03374436) Key findings: ● Breaking up 8.5 hours of sitting with hourly staircase sprinting exercise “snacks” improves resting femoral artery shear patterns but not flow-mediated dilation. ● Cerebral blood flow and neurovascular coupling were unaltered following 6 hours of sitting with and without hourly exercise breaks.

Resistive exercise versus resistive vibration exercise to counteract vascular adaptations to bed rest

2010 ◽  
Vol 108 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Noortje T. L. van Duijnhoven ◽  
Dick H. J. Thijssen ◽  
Daniel J. Green ◽  
Dieter Felsenberg ◽  
Daniel L. Belavý ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Vascular Function ◽  
Bed Rest ◽  
Flow Mediated Dilation ◽  
Resistive Exercise ◽  
Vibration Exercise ◽  
Echo Doppler Ultrasound ◽  
The Impact

Bed rest results in marked vascular adaptations, and resistive vibration exercise (RVE) has been shown to be an effective countermeasure. As vibration exercise has practical and logistical limitations, the use of resistive exercise (RES) alone has the preference under specific circumstances. However, it is unknown if RES is sufficient to prevent vascular adaptations to bed rest. Therefore, the purpose of the present study was to examine the impact of RES and RVE on the vascular function and structure of the superficial femoral artery in young men exposed to 60 days of bed rest. Eighteen healthy men (age: 31 ± 8 yr) were assigned to bed rest and randomly allocated to control, RES, or RVE groups. Exercise was applied 3 times/wk for 5–7 min/session. Resting diameter, blood flow, flow-mediated dilation (FMD), and dilator capacity of the superficial femoral artery were measured using echo-Doppler ultrasound. Bed rest decreased superficial femoral artery diameter and dilator capacity ( P < 0.001), which were significantly attenuated in the RVE group ( P < 0.01 and P < 0.05, respectively) but not in the RES group ( P = 0.202 and P = 0.696, respectively). Bed rest significantly increased FMD ( P < 0.001), an effect that was abolished by RVE ( P < 0.005) but not RES ( P = 0.078). Resting and hyperemic blood flow did not change in any of the groups. Thus, RVE abolished the marked increase in FMD and decrease in baseline diameter and dilator capacity normally associated with prolonged bed rest. However, the stimulus provided by RES alone was insufficient to counteract the vascular adaptations to bed rest.

scholarly journals Neurovascular Coupling and Epilepsy: Hemodynamic Markers for Localizing and Predicting Seizure Onset

2007 ◽  
Vol 7 (4) ◽  
pp. 91-94 ◽  
Author(s):  
Theodore H. Schwartz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurovascular Coupling ◽  
Epileptic Activity ◽  
Tissue Hypoxia ◽  
Epileptic Focus ◽  
Seizure Onset

Hemodynamic surrogates of epileptic activity are being used to map epileptic foci with PET, SPECT, and fMRI. However, there are few studies of neurovascular coupling in epilepsy. Recent data indicate that cerebral blood flow, although focally increased at the onset of a seizure, may be temporarily inadequate to meet the metabolic demands of both interictal and ictal epileptic events. Transient focal tissue hypoxia and hyperperfusion may be excellent markers for the epileptic focus and may even precede the onset of the ictal event.

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
AM Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Cerebral Circulation ◽  
Brain Metabolism ◽  
Cerebral Metabolism ◽  
Cerebral Oxygen ◽  
Brain Norepinephrine ◽  
Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

scholarly journals Electro-Metabolic Sensing Through Capillary ATP-Sensitive K+ Channels and Adenosine to Control Cerebral Blood Flow

2021 ◽  
Author(s):  
Maria Sancho ◽  
Nicholas R. Klug ◽  
Amreen Mughal ◽  
Thomas J. Heppner ◽  
David Hill-Eubanks ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Function ◽  
Brain Activity ◽  
List Type ◽  
Capillary Endothelial Cells ◽  
Metabolic Sensing ◽  
Cellular Components

SUMMARYThe dense network of capillaries composed of capillary endothelial cells (cECs) and pericytes lies in close proximity to all neurons, ideally positioning it to sense neuro/glial-derived compounds that regulate regional and global cerebral perfusion. The membrane potential (VM) of vascular cells serves as the essential output in this scenario, linking brain activity to vascular function. The ATP-sensitive K+ channel (KATP) is a key regulator of vascular VM in other beds, but whether brain capillaries possess functional KATP channels remains unknown. Here, we demonstrate that brain capillary ECs and pericytes express KATP channels that robustly control VM. We further show that the endogenous mediator adenosine acts through A2A receptors and the Gs/cAMP/PKA pathway to activate capillary KATP channels. Moreover, KATP channel stimulation in vivo causes vasodilation and increases cerebral blood flow (CBF). These findings establish the presence of KATP channels in cECs and pericytes and suggest their significant influence on CBF.HIGHLIGHTSCapillary network cellular components—endothelial cells and pericytes—possess functional KATP channels.Activation of KATP channels causes profound hyperpolarization of capillary cell membranes.Capillary KATP channels are activated by exogenous adenosine via A2A receptors and cAMP-dependent protein kinase.KATP channel activation by adenosine or synthetic openers increases cerebral blood flow.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

scholarly journals Coronary and cerebral metabolism-blood flow coupling and pulmonary alveolar ventilation-blood flow coupling may be disabled during acute carbon monoxide poisoning

2020 ◽  
Vol 129 (5) ◽  
pp. 1039-1050
Author(s):  
Ronald F. Coburn
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Cerebral Metabolism ◽  
Carbon Monoxide Poisoning ◽  
Alveolar Ventilation ◽  
Physiological Adaptation ◽  
Acute Carbon Monoxide Poisoning ◽  
Flow Coupling ◽  
Adaptation Mechanisms

This article introduces and supports a postulate that the tissue hypoxia component of carbon monoxide poisoning results in part from impairment of physiological adaptation mechanisms whereby tissues can match regional blood flow to O2 uptake, and the lung can match regional blood flow to alveolar ventilation.

Cerebral Blood Flow, Cerebral Metabolism and Cerebrospinal Fluid Biochemistry in Brain-Injured Patients after Exposure to Hyperbaric Oxygen

1976 ◽  
Vol 14 (5) ◽  
pp. 351-364 ◽  
Author(s):  
François Artru ◽  
Bernard Philippon ◽  
Françoise Gau ◽  
Michel Berger ◽  
Raymond Deleuze
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Hyperbaric Oxygen ◽  
Cerebral Metabolism ◽  
Brain Injured ◽  
Injured Patients
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