Emma Roca

Inter-individual variability in right ventricle adaptation after an endurance race.

Background Right ventricle (RV) dysfunction has been described in athletes after endurance races. We aimed to understand and characterize the RV response to endurance exercise, the impact of individual variability and the effects of the amount of exercise. Methods and results Echocardiography was performed in 55 healthy adults at baseline and after a three-stage trail race: short (14 km; n = 17); medium (35 km; n = 21); and long (56 km; n = 17). Standard and speckle tracking echocardiographic assessment of the RV was performed with global and separate analysis of the RV basal (inflow) and apical regions. Although no change was observed in the short distance runners, the RV systolic deformation decreased significantly (p < 0.05) after both the medium length and long races (Δ% RV global strain −7.6 ± 20.1 and −8.7 ± 21.8, respectively) with significant RV dilatation (Δ% RV volume +10.6 ± 9.9 and +15.3 ± 12.8, respectively). The RV basal segment made a major contribution to stroke volume during exercise, showing larger increases in size and strain compared with the apex. Various patterns of RV adaptation to exercise, ranging from increases in both RV segmental strains and sizes to an insufficient increase in size and a decrease in strain, were identified; this individual variability was not correlated with prior training. Conclusion An acute RV impairment was demonstrated after a trail-running race and was related to the amount of exercise. A high inter-individual variability was observed. Differences in RV adaptation patterns were independent of prior training, suggesting the influence was due to other individual factors.

Exercise-Induced Hypoxaemia Developed at Sea-Level Influences Responses to Exercise at Moderate Altitude

Purpose The aim of this study was to investigate the impact of exercise-induced hypoxaemia (EIH) developed at sea-level on exercise responses at moderate acute altitude. Methods Twenty three subjects divided in three groups of individuals: highly trained with EIH (n = 7); highly trained without EIH (n = 8) and untrained participants (n = 8) performed two maximal incremental tests at sea-level and at 2,150 m. Haemoglobin O2 saturation (SpO2), heart rate, oxygen uptake (VO2) and several ventilatory parameters were measured continuously during the tests. Results EIH athletes had a drop in SpO2 from 99 ± 0.8% to 91 ± 1.2% from rest to maximal exercise at sea-level, while the other groups did not exhibit a similar decrease. EIH athletes had a greater decrease in VO2max at altitude compared to non-EIH and untrained groups (-22 ± 7.9%, -16 ± 5.3% and -13 ± 9.4%, respectively). At altitude, non-EIH athletes had a similar drop in SpO2 as EIH athletes (13 ± 0.8%) but greater than untrained participants (6 ± 1.0%). EIH athletes showed greater decrease in maximal heart rate than non-EIH athletes at altitude (8 ± 3.3 bpm and 5 ± 2.9 bpm, respectively). Conclusion EIH athletes demonstrated specific cardiorespiratory response to exercise at moderate altitude compared to non-EIH athletes with a higher decrease in VO2max certainly due to the lower ventilator and HRmax responses. Thus EIH phenomenon developed at sea-level negatively impact performance and cardiorespiratory responses at acute moderate altitude despite no potentiated O2 desaturation.

Sarcomere Disruptions of Slow Fiber Resulting From Mountain Ultramarathon

OBJECTIVE To investigate changes after a mountain ultramarathon (MUM) in the serum concentration of fast (FM) and slow (SM) myosin isoforms, which are fiber-type-specific sarcomere proteins. The changes were compared against creatine kinase (CK), a widely used fiber-sarcolemma-damage biomarker, and cardiac troponin I (cTnI), a widely used cardiac biomarker. METHODS Observational comparison of response in a single group of 8 endurance-trained amateur athletes. Time-related changes in serum levels of CK, cTnI, SM, and FM from competitors were analyzed before, 1 h after the MUM, and 24 and 48 h after the start of the MUM by 1-way ANOVA for repeated measures or Friedman and Wilcoxon tests. Pearson correlation coefficient was employed to examine associations between variables. RESULTS While SM was significantly (P = .009) increased in serum 24 h after the beginning of the MUM, FM and cTnI did not change significantly. Serum CK activity peak was observed 1 h after the MUM (P = .002). Moreover, serum peaks of CK and SM were highly correlated (r = .884, P = .004). CONCLUSIONS Since there is evidence of muscle damage after prolonged mountain running, the increase in SM serum concentration after a MUM could be indirect evidence of slow- (type I) fiber-specific sarcomere disruptions.

Affected pathways and transcriptional regulators in gene expression response to an ultra-marathon trail: Global and independent activity approaches

Gene expression (GE) analyses on blood samples from marathon and half-marathon runners have reported significant impacts on the immune and inflammatory systems. An ultra-marathon trail (UMT) represents a greater effort due to its more testing conditions. For the first time, we report the genome-wide GE profiling in a group of 16 runners participating in an 82 km UMT competition. We quantified their differential GE profile before and after the race using HuGene2.0st microarrays (Affymetrix Inc., California, US). The results obtained were decomposed by means of an independent component analysis (ICA) targeting independent expression modes. We observed significant differences in the expression levels of 5,084 protein coding genes resulting in an overrepresentation of 14% of the human biological pathways from the Kyoto Encyclopedia of Genes and Genomes database. These were mainly clustered on terms related with protein synthesis repression, altered immune system and infectious diseases related mechanisms. In a second analysis, 27 out of the 196 transcriptional regulators (TRs) included in the Open Regulatory Annotation database were overrepresented. Among these TRs, we identified transcription factors from the hypoxia-inducible factors (HIF) family EPAS1 (p< 0.01) and HIF1A (p<0.001), and others jointly described in the gluconeogenesis program such as HNF4 (p< 0.001), EGR1 (p<0.001), CEBPA (p< 0.001) and a highly specific TR, YY1 (p<0.01). The five independent components, obtained from ICA, further revealed a down-regulation of 10 genes distributed in the complex I, III and V from the electron transport chain. This mitochondrial activity reduction is compatible with HIF-1 system activation. The vascular endothelial growth factor (VEGF) pathway, known to be regulated by HIF, also emerged (p<0.05). Additionally, and related to the brain rewarding circuit, the endocannabinoid signalling pathway was overrepresented (p<0.05).

Pulmonary vascular function and aerobic exercise capacity at moderate altitude

Purpose There has been suggestion that a greater “pulmonary vascular reserve” defined by a low pulmonary vascular resistance (PVR) and a high lung diffusing capacity (DL) allow for a superior aerobic exercise capacity. How pulmonary vascular reserve might affect exercise capacity at moderate altitude is not known. Methods Thirty-eight healthy subjects underwent an exercise stress echocardiography of the pulmonary circulation, combined with measurements of DL for nitric oxide (NO) and carbon monoxide (CO) and a cardiopulmonary exercise test at sea level and at an altitude of 2250 m. Results At rest, moderate altitude decreased arterial oxygen content (CaO2) from 19.1 ± 1.6 to 18.4 ± 1.7 mL·dL−1, P < 0.001, and slightly increased PVR, DLNO, and DLCO. Exercise at moderate altitude was associated with decreases in maximum O2 uptake (V˙O2max), from 51 ± 9 to 43 ± 8 mL·kg−1⋅min−1, P < 0.001, and CaO2 to 16.5 ± 1.7 mL·dL−1, P < 0.001, but no different cardiac output, PVR, and pulmonary vascular distensibility. DLNO was inversely correlated to the ventilatory equivalent of CO2 (V˙E/V˙CO2) at sea level and at moderate altitude. Independent determinants of V˙O2max as determined by a multivariable analysis were the slope of mean pulmonary artery pressure–cardiac output relationship, resting stroke volume, and resting DLNO at sea level as well as at moderate altitude. The magnitude of the decrease in V˙O2max at moderate altitude was independently predicted by more pronounced exercise-induced decrease in CaO2 at moderate altitude. Conclusion Aerobic exercise capacity is similarly modulated by pulmonary vascular reserve at moderate altitude and at sea level. Decreased aerobic exercise capacity at moderate altitude is mainly explained by exercise-induced decrease in arterial oxygenation.

The impact of moderate altitude on exercise metabolism in recreational sportsmen: a nuclear magnetic resonance metabolomic approach

Although it is known that altitude impairs performance in endurance sports, there is no consensus on the involvement of energy substrates in this process. The objective of the present study was to determine whether the metabolomic pathways used during endurance exercise differ according to whether the effort is performed at sea level or at moderate altitude (at the same exercise intensity, using proton nuclear magnetic resonance, 1H NMR). Twenty subjects performed two 60-min endurance exercise tests at sea level and at 2150 m at identical relative intensity on a cycle ergometer. Blood plasma was obtained from venous blood samples drawn before and after exercise. 1H NMR spectral analysis was then performed on the plasma samples. A multivariate statistical technique was applied to the NMR data. The respective relative intensities of the sea level and altitude endurance tests were essentially the same when expressed as a percentage of the maximal oxygen uptake measured during the corresponding incremental maximal exercise test. Lipid use was similar at sea level and at altitude. In the plasma, levels of glucose, glutamine, alanine, and branched-chain amino acids had decreased after exercise at altitude but not after exercise at sea level. The decrease in plasma glucose and free amino acid levels observed after exercise at altitude indicated that increased involvement of the protein pathway was necessary but not sufficient for the maintenance of glycaemia. Metabolomics is a powerful means of gaining insight into the metabolic changes induced by exercise at altitude.

Assessment of Heart Rate Variability during an Endurance Mountain Trail Race by Multi-Scale Entropy Analysis

The aim of the study was to analyze heart rate variability (HRV) response to high-intensity exercise during a 35-km mountain trail race and to ascertain whether fitness level could influence autonomic nervous system (ANS) modulation. Time-domain, frequency-domain, and multi-scale entropy (MSE) indexes were calculated for eleven mountain-trail runners who completed the race. Many changes were observed, mostly related to exercise load and fatigue. These changes were characterized by increased mean values and standard deviations of the normal-to-normal intervals associated with sympathetic activity, and by decreased differences between successive intervals related to parasympathetic activity. Normalized low frequency (LF) power suggested that ANS modulation varied greatly during the race and between individuals. Normalized high frequency (HF) power, associated with parasympathetic activity, varied considerably over the race, and tended to decrease at the final stages, whereas changes in the LF/HF ratio corresponded to intervals with varying exercise load. MSE indexes, related to system complexity, indicated the existence of many interactions between the heart and its neurological control mechanism. The time-domain, frequency-domain, and MSE indexes were also able to discriminate faster from slower runners, mainly in the more difficult and in the final stages of the race. These findings suggest the use of HRV analysis to study cardiac function mechanisms in endurance sports.

Training-induced gene expression plasticity in cardiac function and neural regulation for ultra-trail runners

This study aims to assess the gene regulatory response from a group of 16 athletes and to observe the plasticity induced by their training regime on the gene expression response after their participation in an 82km race. Blood samples for differential gene expression (DGE) were collected before and after this effort from two groups of runners with different training regimes: elite and active. Analyses only focused on genes annotated as related to cardiac function (CF) and neural regulation (NR) from the KEGG PATHWAY Database. Thus, 13 pathways were considered accounting for a total of 629 genes. Training regime modulated the response to exercise based on a list of 18 ranked genes with significant DGE for elite runners while remained statistically insignificant for active athletes. UQCR11, COX7C and COX4I1 genes, related to mitochondrial respiratory chain, were down-regulated which may indicate mitochondrial function impairment in cardiac muscle. Increased expression levels were obtained for PIK3R2, PLCG2, IRAK3 genes from the positive signaling cascades of neurotrophins pathway, which may reveal an improved heart rate control thanks to a better cardiac sympathetic innervation.