Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2020.06.18.159269

Dose-response modelling of total haemoglobin mass to hypoxic dose in elite speed skaters

Vinogradov, M.·Zelenkova, I.
View original source ↗Export metadata ↓

Abstract

The aim of the present study is the modelling of the total haemoglobin mass responses in altitude environment with the dose-response model in elite endurance athletes and comparison different existing approaches in the quantification of hypoxic dose.Data from seven healthy elite endurance athletes specialised in middle distance speed skating participated in the study: six males (24±1.8 years, 182 ±0.3 cm, 84 ±1.5 kg, BMI 23.2±0.6 kg/m2, 59.3±1.5 ml/kg/min) and one female (21 years, 164 cm, 56 kg, BMI 17.1 kg/m2, 59.9 ml/kg/min). Data were collected during a 3-month training period which included two training camps (14 +14 days) at sea level and two training camps (21+21 days) at altitude of 1224 m and 1850 m above sea level. Total haemoglobin mass (tHb-mass) were measured before the start of the season (baseline) and before and after each training camp (seven measurements) using an optimized CO-rebreathing method, training loads and oxygen saturation at altitude were measured and hypoxic dose were calculated.Mean total haemoglobin mass for the male group at the base line were 1067±83 g, before the training camp 1 were 1095±82 g, after TC1 1113±105 g, before the training camp 2 (TC2) 1107±88 g, after TC2 1138±104 g. For the female athlete at the base line were 570 g, after TC1 564 g, after TC2 582 g.The increase of tHb-mass after TC2 were 3,25% and were significant (p<0,005). Mean hypoxic dose for the male group TC1 were %·h (98%) 1078±157, %·h (95%) 79±57, and km.h 473±1 and at TC2 were %·h(98%) 1586±585, %·h (95%) 422±182, and km.h 893±18 and were different from TC1 (p<0,05) for %·h (95%) and km.h methods. For the female athlete hypoxic dose at TC1 were %·h (98%) 970, %·h (95%) 32, and km.h 470 and at TC2 were %·h(98%) 1587, %·h (95%) 289, and km.h 900.The relationship between hypoxic dose and haematological response was analysed with a non-linear model. The magnitude of the increase of the total haemoglobin mass were investigated using simulation procedures based upon individual responses to the hypoxic dose. We introduced a measurement error to the list square method as a way of avoiding overfitting problem. Dose-response mathematical model between hypoxic dose and total haemoglobin mass was developed. Modelled total haemoglobin mass was within measurement error range. This model is suitable for the computer simulations. The individual response to hypoxic dose due to model data was different. Maximal values in total haemoglobin mass that can be achieved by male athletes according to the model was 1321.9 ± 32 g. The model predicted that (τ) erythrocyte life span is 73.8 ± 9.0 days. Moreover, highest value of individual tHb-mass increase after returning to the sea level according to the model was16.3 ±0.7 days.The model developed in the current study describes the time course of total haemoglobin mass during altitude exposure and post-altitude decline in elite speed skaters.Competing Interest StatementThe authors have declared no competing interest.View Full Text

Explore related subjects

physiologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Vinogradov, M., Zelenkova, I.. 2020-06-18. Dose-response modelling of total haemoglobin mass to hypoxic dose in elite speed skaters. https://doi.org/10.1101/2020.06.18.159269

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

IBD-Derived Colonic Fibroblasts Exhibit an Osteopontin-Enriched Secretome, and Osteopontin Restrains Human Colonic Organoid Maturation

Background: Intestinal fibroblasts are extensively remodeled in inflammatory bowel disease (IBD), yet the soluble stromal signals that directly influence epithelial maturation remain incompletely understood. We examined whether fibroblasts derived from inflamed IBD colon display an osteopontin (OPN; SPP1)-enriched secretory phenotype and whether extracellular OPN directly modifies non-neoplastic human colonic epithelium. Methods: Conditioned media from 5 noninflamed-associated fibroblast (NAF) and 4 inflammatory-associated fibroblast (IAF) cultures were analyzed in the validated multi-donor cytokine-array matrix, with orthogonal SPP1 RT-qPCR validation in a complementary fibroblast cohort. Recombinant OPN was then tested in human colonic organoids from 3 donors using donor-resolved molecular and functional analyses under standard, fibroblast-conditioned, and WNT-modified culture conditions. Donor identity defined biological replication. Results: OPN showed the strongest positive rank-based separation between IAF and NAF cultures: all 4 IAF values were higher than all 5 NAF values (Cliff's delta=1.00; exact Mann-Whitney P=0.0159; median ratio=3.64; Benjamini-Hochberg q=.19). Fibroblast RT-qPCR showed approximately 10-fold higher mean SPP1 expression in IAF than NAF cultures (P<.05). In organoids, OPN consistently reduced KRT20, FABP1, CA2, and MUC2 from Day 5 to Day 9. SOX9, HES1, and NOTCH1 increased at Day 9, whereas LGR5 and ALDH provided no evidence of canonical stem-cell expansion. Organoid-area and EdU responses were modest and donor dependent. Conclusions: IBD-derived colonic fibroblasts can display an OPN-enriched secretory phenotype. In human colonic organoids, OPN is sufficient to impair epithelial maturation, whereas its effects on growth and proliferation are variable and depend on the surrounding niche.

physiology↗
bioRxiv2026

A multiscale analysis of liver lobule fibrosis and its impact on drug propagation and metabolism - a DLA approach

Employing DLA methods, this paper explores the self-assembly of collagen fibers and resulting fibrosis at three scales up to the scale of regular lobule models. This allows a mechanistic exploration of the effects of collagen on drug transport (flow and diffusion) and metabolism. In addition, this method permits an analysis of fiber growth characteristics. First, variations of the DLA method of Parkinson et al (1994) will be used to generate multiple explicit collagen microfibril self-assembly using DLA particles in one dimension using cubic grid blocks of (4 mm)3 in a 240 x 20 x 20 grid model. The second stage will be to assess the consequences of various densities of these fibers in three dimensions on flow reductions at a higher scale. Here we utilize DLA methods in cubic grid blocks of (80 nm)3 to mimic 3D collagen self-assembly of fibrils. We then apply a pressure gradient or specified flow rates across a spatially gridded version of these models to quantify flow effects. This region represents a local zone of liver tissue affected by fibrosis. Analytic models of fibrotic effects on flow are employed for comparison. A third stage explores the implications of fibrosis in a liver lobule model using multiple grid blocks of size 3200 mm to represent the lobule tissue. Here, a continuum model of fiber density is employed, based on the previous two scales. The model also includes the effects of additional grid blocks representing sinusoidal flow paths found in the lobule. We contrast and quantify drug propagation and metabolism of molecular dissolved versus nanoparticle delivery vehicles in fibrotic media, achieved by upscaling explicit collagen distributions to appropriate average values.

physiology↗
bioRxiv2026

Pulmonary pressure load shapes right ventricular molecular remodelling in dilated cardiomyopathy

Right ventricular (RV) adaptation to pulmonary hypertension determines outcome in dilated cardiomyopathy (DCM), but the molecular mechanisms of the transition to decompensation remain unclear. We analysed RV tissue from explanted hearts of patients with end-stage DCM using single-nucleus RNA sequencing (n=21), mass spectrometry and Olink Reveal proteomics (both n=44), and integrated these molecular profiles with echocardiographic and right-heart catheterisation measures to identify molecular correlates of RV dysfunction. Mean pulmonary arterial pressure was the dominant correlate of RV transcriptional remodelling, particularly in cardiomyocytes, where higher pressure was associated with contractile remodelling, autophagy, vesicle trafficking and glucose metabolism. In contrast, RV decompensation was characterised by immune activation and reduced oxidative phosphorylation exclusively at the proteomic level. Integrative multi-omics factor analysis (MOFA) further identified fibrosis as the dominant molecular program shared across transcriptomic and proteomic layers. Together, these findings indicate molecular adaptation to pressure load and tissue fibrosis during progression towards RV failure.

physiology↗