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Cerebral Blood Flow and PETCO2 on Neuromuscular Function During Environmental Stress

25. januar 2018 opdateret af: Stephen Cheung, Brock University

The Influence of Cerebral Blood Flow and Alkalosis on Neuromuscular Function During Environmental Stress

Environmental stress, such as low oxygen availability (hypoxia), has been associated with impaired neuromuscular performance; however, the mechanisms associated with these performance decrements remain unclear. While the majority of research suggests that the observed fatigue is related to the central nervous system, the influence of changes in cerebral blood flow (CBF) and associated changes in cerebral pH (partial pressure of carbon dioxide; PCO2) remains unexamined. In response to hypoxic stress, humans hyperventilate to maintain oxygen consumption, resulting in a hypocapnia mediated decrease in CBF and cerebral alkalosis (decreased PCO2). Previous research suggests that hyperventilation induces changes in neural excitability and synaptic transmission; however, it remains unclear if these changes are related to hypocapnia mediated decrease in CBF or cerebral alkalosis or both.

The purpose of the proposed research program is to examine the influence of changes in CBF and cerebral alkalosis on neuromuscular function during environmental stress. The research program will consist of 2 separate projects, summarized below in a table outlining the proposed protocols and resultant physiological manipulations. During each manipulation, neuromuscular function will be evaluated and compared to baseline (normoxic) conditions using a repeated measures design.

The research program will consist of 2 separate projects. Project 1 will examine the changes in CBF and alkalosis by using (a) indomethacin (decrease CBF; no change PCO2) and (b) hypocapnia (decrease CBF; decrease PCO2). Using a similar experimental design, Project 2 will examine the change in CBF and alkalosis during hypoxia by using (a) poikilocapnic hypoxia (decrease PO2; decrease CBF; decrease PCO2), (b) isocapnic hypoxia (decrease PO2; no change CBF; no change PCO2) and (c) isocapnic hypoxia + indomethacin (decrease PO2; decrease CBF; no change PCO2). During each manipulation, neuromuscular function will be evaluated and compared to baseline (normoxic) conditions using a repeated measures design.

Therefore, Project 1 will examine the separate and combined effect of changes in CBF and cerebral alkalosis on neuromuscular function independent of environmental manipulations. Subsequently, Project 2 will examine neuromuscular function during hypoxia while controlling CBF and cerebral alkalosis. It is hypothesized that changes in PCO2 and therefore, changes in cerebral alkalosis will contribute to neuromuscular fatigue independent of changes in CBF and oxygen availability.

Studieoversigt

Status

Afsluttet

Betingelser

Intervention / Behandling

Undersøgelsestype

Interventionel

Tilmelding (Faktiske)

8

Fase

  • Fase 4

Kontakter og lokationer

Dette afsnit indeholder kontaktoplysninger for dem, der udfører undersøgelsen, og oplysninger om, hvor denne undersøgelse udføres.

Studiesteder

  • Canada
    • Ontario
      • St Catharines, Ontario, Canada, L2S 3A1
        • Brock University

Deltagelseskriterier

Forskere leder efter personer, der passer til en bestemt beskrivelse, kaldet berettigelseskriterier. Nogle eksempler på disse kriterier er en persons generelle helbredstilstand eller tidligere behandlinger.

Berettigelseskriterier

Aldre berettiget til at studere

18 år til 25 år (Voksen)

Tager imod sunde frivillige

Ja

Køn, der er berettiget til at studere

Han

Beskrivelse

Inclusion Criteria:

  • 18 to 25 yrs old; healthy males

Exclusion Criteria:

  • diagnosed medical condition; NSAID allergy; smoker; high altitude exposure; implants

Studieplan

Dette afsnit indeholder detaljer om studieplanen, herunder hvordan undersøgelsen er designet, og hvad undersøgelsen måler.

Hvordan er undersøgelsen tilrettelagt?

Design detaljer

  • Primært formål: Grundvidenskab
  • Tildeling: Randomiseret
  • Interventionel model: Enkelt gruppeopgave
  • Maskning: Enkelt

Våben og indgreb

Deltagergruppe / Arm
Intervention / Behandling
Eksperimentel: Drug
Indomethacin 1.2 mg kg 1 dose
Medicin: Indomethacin
Placebo komparator: Placebo
flour capsule
Medicin: Placebo

Hvad måler undersøgelsen?

Primære resultatmål

Resultatmål
Foranstaltningsbeskrivelse
Tidsramme
Hvilemotorisk tærskel
Tidsramme: Skift fra baseline 90 minutter
Motorisk fremkaldte potentialer registreres fra muskler efter transkraniel magnetisk stimulering af motorisk cortex. Den hvilende motoriske tærskel er defineret som den minimale stimulationsintensitet, der kræves for at fremkalde et motorisk fremkaldt potentiale. Hvilemotortærskel vil blive kvantificeret i millivolt.
Skift fra baseline 90 minutter
Maksimal frivillig kontraktion
Tidsramme: Skift fra baseline 90 minutter
Under testning af maksimal frivillig kontraktion (MVC) vil deltagernes højre arm blive fastgjort i en specialfremstillet enhed, der bruges til at isolere underarmsfleksion og til at måle kraftproduktion af flexor carpi radialis-musklen. Deltagerne vil blive bedt om at producere en 5-sekunders MVC og vil blive verbalt opfordret til at opretholde maksimal kraftproduktion under hele kontraktionens varighed. MVC vil blive kvantificeret som den maksimale kraftproduktion i newtonmeter.
Skift fra baseline 90 minutter
H-Reflex Amplitude
Tidsramme: Change from baseline 90-minutes
The H-Reflex is an indirect measure of motor neuron excitability. Initially, a maximal M-wave (M-max) will be elicited by stimulating (1 ms in duration; 15 s between stimuli) the median nerve incrementally (2 V increments) until the largest waveform is observed. The peak-to-peak amplitude of this waveform is considered M-max. Using similar procedures as above, a sub-maximal M-wave of 5% M-max will be elicited and the amplitude of the resultant H-reflex (a small waveform observed following the submaximal M-wave) will be calculated. The amplitude of the H-reflex will be quantified in milllivolts.
Change from baseline 90-minutes
H-reflex latency
Tidsramme: Change from baseline 90-minutes
The H-Reflex is an indirect measure of motor neuron excitability. Initially, a maximal M-wave (M-max) will be elicited by stimulating (1 ms in duration; 15 s between stimuli) the median nerve incrementally (2 V increments) until the largest waveform is observed. The peak-to-peak amplitude of this waveform is considered M-max. Using similar procedures as above, a sub-maximal M-wave of 5% M-max will be elicited and the amplitude of the resultant H-reflex (a small waveform observed following the submaximal M-wave) will be calculated. The onset latency of the H-reflex will be quantified in milliseconds.
Change from baseline 90-minutes
Voluntary Activation
Tidsramme: Change from baseline 90-minutes
The level of neural drive to muscle during contraction is termed voluntary activation and will be estimated by interpolation of a single supramaximal motor evoked potential during the 5-second MVC contraction. If extra force is evoked by the 'superimposed' stimulus then either the stimulated axons were not all recruited voluntarily or they were discharging at sub-tetanic rates. Therefore, voluntary activation will be quantified as the amplitude of maximal voluntary force production, relative to the amplitude of the supramaximal MEP.
Change from baseline 90-minutes

Sekundære resultatmål

Resultatmål
Foranstaltningsbeskrivelse
Tidsramme
Mellemhjernearterie blodgennemstrømningshastighed
Tidsramme: Skift fra baseline 90 minutter
Blodstrømningshastigheden i den midterste cerebrale arterie (MCA) vil blive målt non-invasivt af en 2-MHz transkraniel Doppler (TCD) ultralydssonde, fastgjort bilateralt til et behageligt pandebånd og fastgjort anteriort til den zygomatiske bue, rostralt af pinna. Doppler-prober vil blive pacet over de temporale vinduer (nær øret) og vil forblive på plads under hele forsøgsprotokollens varighed. MCA-hastigheden vil blive kvantificeret i cm/s.
Skift fra baseline 90 minutter
Brachial Artery Blood flow
Tidsramme: Change from baseline 90-minutes
Brachial artery blood flow will be measured non-invasively using a high-resolution ultrasound machine. Participants will lie supine with their forearm extended in a comfortable position. Blood flow measurements will be taken in the top 1/3 of the upper arm over the duration of 10 cardiac cycles (approximately 60 seconds). Blood flow will be quantified in L/min.
Change from baseline 90-minutes
Internal Carotid Artery Blood Flow
Tidsramme: Change from baseline 90-minutes
Internal carotid artery (ICA) blood flow will be measured non-invasively using a high-resolution ultrasound machine. Participants will lie supine with a slight extension of the neck and at 45° of lateral flexion away from the side being scanned. ICA measurements will be taken 1 cm superior to the common carotid bifurcation over the duration of 10 cardiac cycles (approximately 60 seconds). Blood flow will be quantified in L/min.
Change from baseline 90-minutes
Blood pressure
Tidsramme: Change from baseline 90-minutes
Beat by beat blood pressure will be calculated from the blood pressure waveform using finger photoplethysmography (Nexfin, bmeye), with a finger cuff placed directly over the middle finger on the left hand. Blood pressure will be quantified in mmHg.
Change from baseline 90-minutes
Pulse oximetry
Tidsramme: Change from baseline 90-minutes
A pulse oximetry probe will be placed over a finger to provide a continuous, non-invasive measurement of the blood oxygen saturation to confirm that the end-tidal forcing system is controlling oxygen delivery at the desired levels during each experiment. Oxygen saturation will be quantified as a percentage.
Change from baseline 90-minutes
Heart Rate
Tidsramme: Change from baseline 90-minutes
Heart rate will be measured by electrocardiogram. Heart rate will be quantified in beats per minute.
Change from baseline 90-minutes
End-Tidal Gas Concentrations
Tidsramme: Change from baseline 90-minutes
The end-tidal concentrations of oxygen and carbon dioxide will be measured and reported in mmHg.
Change from baseline 90-minutes

Samarbejdspartnere og efterforskere

Det er her, du vil finde personer og organisationer, der er involveret i denne undersøgelse.

Sponsor

Brock University

Efterforskere

  • Ledende efterforsker: Stephen Cheung, PhD, Brock University

Datoer for undersøgelser

Disse datoer sporer fremskridtene for indsendelser af undersøgelsesrekord og resumeresultater til ClinicalTrials.gov. Studieregistreringer og rapporterede resultater gennemgås af National Library of Medicine (NLM) for at sikre, at de opfylder specifikke kvalitetskontrolstandarder, før de offentliggøres på den offentlige hjemmeside.

Studer store datoer

Studiestart

1. april 2013

Primær færdiggørelse (Faktiske)

1. juni 2015

Studieafslutning (Faktiske)

1. december 2016

Datoer for studieregistrering

Først indsendt

20. marts 2013

Først indsendt, der opfyldte QC-kriterier

10. april 2013

Først opslået (Skøn)

12. april 2013

Opdateringer af undersøgelsesjournaler

Sidste opdatering sendt (Faktiske)

29. januar 2018

Sidste opdatering indsendt, der opfyldte kvalitetskontrolkriterier

25. januar 2018

Sidst verificeret

1. januar 2018

Mere information

Begreber relateret til denne undersøgelse

Yderligere relevante MeSH-vilkår

Andre undersøgelses-id-numre

  • 12-167

Disse oplysninger blev hentet direkte fra webstedet clinicaltrials.gov uden ændringer. Hvis du har nogen anmodninger om at ændre, fjerne eller opdatere dine undersøgelsesoplysninger, bedes du kontakte register@clinicaltrials.gov. Så snart en ændring er implementeret på clinicaltrials.gov, vil denne også blive opdateret automatisk på vores hjemmeside .

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Placeringer

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