Energetics of running in top level marathon runners from Kenya.

On ten top-level Kenyan marathon runners (KA) plus nine European controls (EC, equivalent to KA), we measured maximal oxygen consumption ( _V O2max) and the energy cost of running (Cr) on track during training camps at moderate altitude, to better understand the KA dominance in the marathon. At each incremental running speed, steady-state oxygen consumption ( _V O2) was measured by telemetric metabolic cart, and lactate by electroenzymatic method. The speed requiring _V O2 ¼ _V O2max provided the maximal aerobic velocity (vmax). The energy cost of running was calculated by dividing net _V O2 by the corresponding speed. The speed at lactate threshold (vHAN)was computed from individual Laˆb versus speed curves. The sustainable _V O2max fraction (Fd) at vHAN (FHAN) was computed dividing vHAN by vmax. The Fd for the marathon (Fmar) was determined as Fmar = 0.92 FHAN. Overall, _VO2max (64.9 ± 5.8 vs. 63.9 ± 3.7 ml kg-1 min-1), vmax (5.55 ± 0.30 vs. 5.41 ± 0.29 m s-1) and Cr (3.64 ± 0.28 vs. 3.63 ± 0.31 J kg-1 m-1) resulted the same in KA as in EC. In both groups, Cr increased linearly with the square of speed. FHAN was 0.896 ± 0.054 in KA and 0.909 ± 0.068 in EC; Fmar was 0.825 ± 0.050 in KA and .836 ± 0.062 in EC (NS). Accounting for altitude, running speed predictions from present data are close to actual running performances, if FHAN instead of Fmar is taken as index of Fd. In conclusion, both KA and EC did not have a very high _V O2max, but had extremely high Fd, and low Cr, equal between them. The dominance of KA over EC cannot be explained on energetic grounds

Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men.

We tested whether the kinetics of systemic O2 delivery (Q'aO2) at exercise start was faster than that of lung O2 uptake (V' O2), being dictated by that of cardiac output (Q'), and whether changes in Q' would explain the postulated rapid phase of the V'O2 increase. Simultaneous determinations of beat-by-beat (BBB) Q' and Q' aO2, and breath-by-breath V'O2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/-3.2 years, maximal aerobic power 333 +/- 61 W). V'O2 was determined using Grønlund’s algorithm. Q' was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate (fH, electrocardiograpy) and calibrated against a steadystate method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q'aO2. The Q', Q'aO2 and V'O2 kinetics were analyzed with single and double exponential models. fH, Qst, Q', and V'O2 increased upon exercise onset to reach a new steady state. The kinetics of Q'aO2 had the same time constants as that of Q'. The latter was twofold faster than that of V'O2. The V'O2 kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q' changes fully explained the phase I of V'O2 increase. We suggest that in unsteady states, lung V' O2 is dissociated from muscle O2 consumption. The two components of Q' and Q'aO2 kinetics may reflect vagal withdrawal and sympathetic activation

The role of hole transport between dyes in solid-state dye-sensitized solar cells

In dye-sensitized solar cells (DSSCs) photogenerated positive charges are normally considered to be carried away from the dyes by a separate phase of hole-transporting material (HTM). We show that there can also be significant transport within the dye monolayer itself before the hole reaches the HTM. We quantify the fraction of dye regeneration in solid-state DSSCs that can be attributed to this process. By using cyclic voltammetry and transient anisotropy spectroscopy, we demonstrate that the rate of interdye hole transport is prevented both on micrometer and nanometer length scales by reducing the dye loading on the TiO₂ surface. The dye regeneration yield is quantified for films with high and low dye loadings (with and without hole percolation in the dye monolayer) infiltrated with varying levels of HTM. Interdye hole transport can account for >50% of the overall dye regeneration with low HTM pore filling. This is reduced to about 5% when the infiltration of the HTM in the pores is optimized in 2 μm thick films. Finally, we use hole transport in the dye monolayer to characterize the spatial distribution of the HTM phase in the pores of the dyed mesoporous TiO₂

Cardiac output by model flow method from intra-arterial and finger tip pulse pressure profiles

Modelflow®, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q’ litre· min-1). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q’. We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q’ withModelflow®, so we compared Modelflow® beat-by-beat Q’ values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0 + - 2.9 years; weight, 81.2 + - 12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent Q’ computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly (P < 0.05) lower from the finger than the intra-arterial catheter. The corresponding mean steady-state Q’ obtained from the finger (Q’porta) was significantly (P < 0.05) higher than that computed from the intra-arterial recordings (Q’pia). The line relating beat-by-beat Q’porta and Q’pia was y = 1.55x - 3.02 (r2 = 0.640). The bias was 1.44 litre · min-1 and the precision was 2.84 litre · min-1.The slope of this line was significantly higher than 1, implying a systematic overestimate of Q’ by Q’porta with respect to Q’pia. Consistent with the tested hypothesis, these results demonstrate that pulse pressure profiles from the finger provide inaccurate absolute Q’ values with respect to the radial artery, and therefore cannot be used without correction with a calibration factor calculated previously by measuring Q’ with an independent method

Security devices based on liquid crystals doped with a colour dye

Liquid crystal properties make them useful for the development of security devices in applications of authentication and detection of fakes. Induced orientation of liquid crystal molecules and birefringence are the two main properties used in security devices. Employing liquid crystal and dichroic colorants, we have developed devices that show, with the aid of a polarizer, multiple images on each side of the device. Rubbed polyimide is used as alignment layer on each substrate of the LC cell. By rubbing the polyimide in different directions in each substrate it is possible to create any kind of symbols, drawings or motifs with a greyscale; the more complex the created device is, the more difficult is to fake it. To identify the motifs it is necessary to use polarized light. Depending on whether the polarizer is located in front of the LC cell or behind it, different motifs from one or the other substrate are shown. The effect arises from the dopant colour dye added to the liquid crystal, the induced orientation and the twist structure. In practice, a grazing reflection on a dielectric surface is polarized enough to see the effect. Any LC flat panel display can obviously be used as backlight as well

Lag-Optimized Blood Oxygenation Level Dependent Cerebrovascular Reactivity Estimates Derived From Breathing Task Data Have a Stronger Relationship With Baseline Cerebral Blood Flow

Published: 15 June 2022Cerebrovascular reactivity (CVR), an important indicator of cerebrovascular health, is commonly studied with the Blood Oxygenation Level Dependent functional MRI (BOLD-fMRI) response to a vasoactive stimulus. Theoretical and empirical evidence suggests that baseline cerebral blood flow (CBF) modulates BOLD signal amplitude and may influence BOLD-CVR estimates. We address how acquisition and modeling choices affect the relationship between baseline cerebral blood flow (bCBF) and BOLD-CVR: whether BOLD-CVR is modeled with the inclusion of a breathing task, and whether BOLD-CVR amplitudes are optimized for hemodynamic lag effects. We assessed between-subject correlations of average GM values and within-subject spatial correlations across cortical regions. Our results suggest that a breathing task addition to a resting-state acquisition, alongside lag-optimization within BOLD-CVR modeling, can improve BOLD-CVR correlations with bCBF, both between- and within-subjects, likely because these CVR estimates are more physiologically accurate. We report positive correlations between bCBF and BOLD-CVR, both between- and within-subjects. The physiological explanation of this positive correlation is unclear; research with larger samples and tightly controlled vasoactive stimuli is needed. Insights into what drives variability in BOLD-CVR measurements and related measurements of cerebrovascular function are particularly relevant when interpreting results in populations with altered vascular and/or metabolic baselines or impaired cerebrovascular reserve.This work was supported by the Center for Translational Imaging at Northwestern University. The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health [K12HD073945]. KZ was supported by an NIH-funded training program [T32EB025766]. SM was supported by the European Union’s Horizon 2020 research and innovation program [Marie Skłodowska-Curie grant agreement No. 713673] and a fellowship from La Caixa Foundation [ID 100010434, fellowship code LCF/BQ/IN17/11620063]. CC-G was supported by the Spanish Ministry of Economy and Competitiveness [Ramon y Cajal Fellowship, RYC2017-21845], the Basque Government [BERC 2018-2021 and PIBA_2019_104], and the Spanish Ministry of Science, Innovation and Universities [MICINN; PID2019- 105520GB-100]

Phase I dynamics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men in acute normobaric hypoxia.

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6+/-3.4 yr, 82.1+/-13.7 kg, maximal aerobic power 330+/-67 W), we determined beat-by-beat cardiac output (Q), oxygen delivery (QaO2), and breath-by-breath lung oxygen uptake (VO2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2=0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Qst, by model flow) and heart rate (fH, electrocardiography), and QaO2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q were higher, and Qst and VO2 were unchanged. QaO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for VO2 was unchanged. For fH, Q and QaO2, A1 was lower. Phase I time constant (tau1) for QaO2 and VO2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q and QaO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed

A practical modification to a resting state fMRI protocol for improved characterization of cerebrovascular function

Available online 24 June 2021.Cerebrovascular reactivity (CVR), defined here as the Blood Oxygenation Level Dependent (BOLD) response to a CO 2 pressure change, is a useful metric of cerebrovascular function. Both the amplitude and the timing (hemo- dynamic lag) of the CVR response can bring insight into the nature of a cerebrovascular pathology and aid in understanding noise confounds when using functional Magnetic Resonance Imaging (fMRI) to study neural ac- tivity. This research assessed a practical modification to a typical resting-state fMRI protocol, to improve the characterization of cerebrovascular function. In 9 healthy subjects, we modelled CVR and lag in three resting- state data segments, and in data segments which added a 2–3 minute breathing task to the start of a resting-state segment. Two different breathing tasks were used to induce fluctuations in arterial CO 2 pressure: a breath-hold task to induce hypercapnia (CO 2 increase) and a cued deep breathing task to induce hypocapnia (CO 2 decrease). Our analysis produced voxel-wise estimates of the amplitude (CVR) and timing (lag) of the BOLD-fMRI response to CO 2 by systematically shifting the CO 2 regressor in time to optimize the model fit. This optimization inher- ently increases gray matter CVR values and fit statistics. The inclusion of a simple breathing task, compared to a resting-state scan only, increases the number of voxels in the brain that have a significant relationship between CO 2 and BOLD-fMRI signals, and improves our confidence in the plausibility of voxel-wise CVR and hemody- namic lag estimates. We demonstrate the clinical utility and feasibility of this protocol in an incidental finding of Moyamoya disease, and explore the possibilities and challenges of using this protocol in younger populations. This hybrid protocol has direct applications for CVR mapping in both research and clinical settings and wider applications for fMRI denoising and interpretation.This research was supported by the Eunice Kennedy Shriver Na- tional Institute of Child Health and Human Development of the Na- tional Institutes of Health under award number K12HD073945. The pediatric dataset and cerebral palsy dataset were collected with sup- port of National Institutes of Health award R03 HD094615–01A1. The authors would like to acknowledge Marie Wasielewski and Carson Ingo for their support in acquiring these data. K.Z. was supported by an NIH-funded training program (T32EB025766). S.M. was supported by the European Union’s Horizon 2020 research and innovation pro- gram (Marie Sk ł odowska-Curie grant agreement No. 713673), a fel- lowship from La Caixa Foundation (ID 100010434, fellowship code LCF/BQ/IN17/11620063) and C.C.G was supported by the Spanish Ministry of Economy and Competitiveness (Ramon y Cajal Fellowship, RYC-2017- 21845), the Basque Government (BERC 2018–2021 and PIBA_2019_104) and the Spanish Ministry of Science, Innovation and Universities (MICINN; PID2019–105520GB-100)

ICA-based denoising strategies in breath-hold induced cerebrovascular reactivity mapping with multi echo BOLD fMRI

Available online 6 March 2021.Performing a BOLD functional MRI (fMRI) acquisition during breath-hold (BH) tasks is a non-invasive, robust method to estimate cerebrovascular reactivity (CVR). However, movement and breathing-related artefacts caused by the BH can substantially hinder CVR estimates due to their high temporal collinearity with the effect of interest, and attention has to be paid when choosing which analysis model should be applied to the data. In this study, we evaluate the performance of multiple analysis strategies based on lagged general linear models applied on multi- echo BOLD fMRI data, acquired in ten subjects performing a BH task during ten sessions, to obtain subject-specific CVR and haemodynamic lag estimates. The evaluated approaches range from conventional regression models, i.e. including drifts and motion timecourses as nuisance regressors, applied on single-echo or optimally-combined data, to more complex models including regressors obtained from multi-echo independent component analysis with different grades of orthogonalization in order to preserve the effect of interest, i.e. the CVR. We compare these models in terms of their ability to make signal intensity changes independent from motion, as well as the reliability as measured by voxelwise intraclass correlation coefficients of both CVR and lag maps over time. Our results reveal that a conservative independent component analysis model applied on the optimally-combined multi-echo fMRI signal offers the largest reduction of motion-related effects in the signal, while yielding reliable CVR amplitude and lag estimates, although a conventional regression model applied on the optimally-combined data results in similar estimates. This work demonstrates the usefulness of multi-echo based fMRI acquisitions and independent component analysis denoising for precision mapping of CVR in single subjects based on BH paradigms, fostering its potential as a clinically-viable neuroimaging tool for individual patients. It also proves that the way in which data-driven regressors should be incorporated in the analysis model is not straight-forward due to their complex interaction with the BH-induced BOLD response.This research was supported by the European Union’s Horizon 2020 research and innovation program ( Marie Sk ł odowska-Curie grant agreement No. 713673 ), a fellowship from La Caixa Foundation (ID 100010434 , fellowship code LCF/BQ/IN17/11620063 ), the Spanish Ministry of Economy and Competitiveness ( Ramon y Cajal Fellowship, RYC-2017- 21845 ), the Spanish State Research Agency (BCBL “Severo Ochoa ”excellence accreditation, SEV- 2015-490 ), the Basque Govern- ment ( BERC 2018-2021 and PIBA_2019_104 ), the Spanish Ministry of Science, Innovation and Universities (MICINN; PID2019-105520GB-100 and FJCI-2017-31814 ), and the Eunice Kennedy Shriver National Insti- tute of Child Health and Human Development of the National Institutes of Health under award number K12HD073945