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Arterial Spin Labeling: A Magnetic Resonance Imaging Technique for Measuring Cerebral Perfusion
Published in Alexander D. Poularikas, Stergios Stergiopoulos, Advanced Signal Processing, 2017
Keith St. Lawrence, Daron G. Owen, Frank S. Prato
The ingeniousness of Kety was to recognize that the Fick principle, which had been previously used to measure cardiac output in man, could be adapted to measure CBF. His approach was to introduce into the blood a chemically inert tracer that would readily diffuse across the blood–brain barrier (BBB) and accumulate in tissue [13]. Based on the conservation of mass, the Fick principle states that the amount of tracer in brain at time t equals the difference between the amount entering and leaving by blood flow [12]: Cb(t)=F⋅∫0t(Ca(u)−Cv(u))du In this equation, Cb(t), Ca(t) and Cv(t) are the concentrations of tracer in brain, arterial blood and venous blood, respectively, and F is cerebral blood flow, which is typically expressed as ml of blood/g of tissue/min or ml of blood/100 g of tissue/min. The first application of this approach required subjects to inhale nitrous oxide while blood samples were acquired from a peripheral artery and the jugular vein to determine Ca(t) and Cv(t), respectively [13]. If the inhalation period is long enough to allow the cerebral tissue and blood tracer concentrations to equilibrate, denoted as t→ ∞, then Cb(∞) can be defined by: Cb(∞)=λCv(∞) where λ is the partition coefficient and is the ratio between the tissue and blood tracer concentrations at equilibrium [12]. The partition coefficient is generally expressed in units of ml blood/g tissue and the values for water in whole brain, grey matter and white matter are 0.9, 0.98 and 0.82 ml/g, respectively [23]. With the tissue concentration defined by Equation 18.2, CBF can be determined from Equation 18.1.
Effect of a novel 90-second “Gear” exercise programme on markers of inflammation and cardiorespiratory fitness measurements in person at risk of cardiovascular disease
Published in Research in Sports Medicine, 2022
N. Rugbeer, D. Constantinou, G. Torres
The primary finding of the study is that the GEP-DT and GEP-OT increased power output (load), peak oxygen consumption and metabolic equivalent at ventilatory threshold post six weeks of training. The GEP-OT group demonstrated a substantial decrease in interleukin-6 post six weeks of training; however, the probability value was insignificant. There was a significant difference within the GEP-OT group for VT-L, VT-Rf and VO2peak-L. The physiological exercise benefits derived by the GEP-DT and GEP-OT are explained by the Fick principle (VO2max = CO x [CaO2 – CvO2]), were CO is cardiac output and [CaO2 – CvO2] is the arteriovenous difference in oxygen, which is an essential determinant of myocardial ischaemia (Guazzi et al., 2017).
Submaximal heart rate seems inadequate to prescribe and monitor intensified training
Published in European Journal of Sport Science, 2019
Twan ten Haaf, Carl Foster, Romain Meeusen, Bart Roelands, Maria Francesca Piacentini, Selma van Staveren, Leo Koenderman, Jos J. de Koning
In line with previous work (Le Meur et al., 2014), submaximal heart rate in our study decreased both in AF and FOR athletes. Also, the correlation analyses revealed no associations between the change in heart rate and performance. This suggests that the observed change in submaximal heart rate in our study is rather a general effect of intensified training (i.e. the TFL), than that it is associated with underperformance. This can possibly be explained by the finding that, despite a decreased (sub)maximal heart rate after the TFL, ⩒O2 was unchanged at all exercise intensities. The negative association between the pre- versus post-TFL changes in heart rate and O2pulse at low and medium exercise intensity illustrates that ⩒O2 was maintained through compensation by an increased stroke volume and/or arteriovenous oxygen difference. A case study from the 1970s applied the direct Fick principle to reveal that stroke volume decreased and arteriovenous oxygen difference increased after jogging across the United States for 6 days per week, for 2.5 months (Bruce, Kusumi, Culver, & Butler, 1975). Similarly, an experimental study using impedance cardiography showed a decrease in stroke volume, and an increase in arteriovenous oxygen difference in overreached but not in acute fatigued athletes (Le Meur et al., 2014). It is, therefore, speculated that an increased arteriovenous oxygen difference compensated for the decrease in heart rate in our study, but further research in necessary to evaluate this hypothesis.
Cardiopulmonary parameters and organ blood flows for workers expressed in terms of VO2 for use in physiologically based toxicokinetic modeling
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Pierre Brochu, Jessie Ménard, Sami Haddad
The physiological mass balance between whole body VO2 (L/min), Q (L/min) and the arterial (CaO2) and mixed venous (CvO2) blood oxygen contents (ml of O2/ml of blood), is outlined by the eponymous Fick principle as follows (Fick 1870; Guyton and Hall 2006):