Fernando Augusto Monteiro Saboia Pompeu

Athletes use hypoxic training methods to enhance their performance under altitude conditions. Comparative studies involving populations from low (500–2,000 m) and moderate (2,000–3,000 m) altitudes offer an opportunity to understand the mechanisms behind adaptations to hypoxia. The present study combined data from metabolomics analysis based on gas- and liquid-chromatography mass spectrometry (GC-MS and LC-MS) to compare plasma profiles from 80 adolescent athletes at moderate- or low altitudes. 161 metabolites were identified, including 84 elevated and 77 decreased in moderate-altitude adolescents compared to their low-altitude counterparts. Pathway analysis revealed that metabolites related to carbohydrates, amino acids, and lipid metabolism differed between groups. Lipid metabolism was significantly altered in moderate-altitude athletes, including pathways such as linolenic and linoleic acid, sphingolipid, and arachidonic acid, as well as processes involving the transfer of acetyl groups into mitochondria and fatty acid biosynthesis. Biomarker analysis looking for signatures of chronic adaptation to moderate altitude identified glycerol and 5-oxoproline metabolites amongst the variables with the strongest sensitivity and specificity. This study demonstrates differences in metabolic profiles between moderate- and low-altitude populations and highlights the potential of these differential metabolites and associated metabolic pathways to provide new insights into the mechanisms of adaptation to moderate altitude.

Maximal oxygen uptake (VO₂max) is a determining indicator for cardiorespiratory capacity in endurance athletes, and epigenetics is crucial in its levels and variability. This initial study examined a broad plasma miRNA profile of twenty-three trained elite endurance athletes with similar training volumes but different VO₂max in response to an acute maximal graded endurance test. Six were clustered as higher/lower levels based on their VO₂max (75.4 ± 0.9 and 60.1 ± 5.0 mL.kg⁻¹.min⁻¹). Plasma was obtained from athletes before and after the test and 15 ng of total RNA was extracted and detected using an SYBR-based 1113 miRNA RT-qPCR panel. A total of 51 miRNAs were differentially expressed among group comparisons. Relative amounts of miRNA showed a clustering behavior among groups regarding distinct performance/time points. Significantly expressed miRNAs were used to perform functional bioinformatic analysis (DIANA tools). Fatty acid metabolism pathways were strongly targeted for the significantly different miRNAs in all performance groups and time points (p < 0.001). Although this pathway does not solely determine endurance performance, their significant contribution is certainly achieved through the involvement of miRNAs. A highly genetically dependent gold standard variable for performance evaluation in a homogeneous group of elite athletes allowed genetic/epigenetic aspects related to fatty acid pathways to emerge.

An important epistemological problem has been faced by Exercise Physiologists. On one hand, one theory explains the fatigue through a ceiling effect of oxygen uptake. On the other hand, the new theory proposes that an encephalon mechanism would stop the effort before a catastrophic homeostasis failure. Many physiologists have looked for evidence to support their favourite theory even though the induction logic problem does not allow to prove whether truth is discovered; however, it is possible to prove that it does not occur. When some researchers fail to test their hypotheses, they use relativism to bring up their theories again. Noakes and his colleagues have based their theory on relativism, because it is impossible to refute by empirical observation. It also doesn't explain all phenomena that the oldest Hill's theory is able to explain. Noakes's theory isn't more accurate in its previsions. Noakes did not check whether the oxygen uptake plateau occurs in suitable tests to measure on the mouth what happens in the muscles. Finally, it doesn't propose new tests for the encephalon role during maximal effort, as that is expected in scientific work. For all of these reasons, it is possible to conclude there are no advantages in switching to the “Central Governor” theory.

It is unclear how athletes regulate their performance prior and during exercise when deceptive methods are applied. Therefore, the aim of this study was to test if time manipulation can influence pacing strategy and running performance. Ten recreationally active subjects were informed they would complete four 60-min time trials only with time feedback. The first session was a familiarization trial (60-min), and in the following three sessions, the time feedback was modified: normal chronometer (NC—60 min.), 10% faster (Faster chronometer—FC—54 min.), and 10% slower (slower chronometer—SC—66 min.). Total distance was different between conditions, while average of total speed, Heart Rate, oxygen consumption, and Rate of Perceived Exertion were similar (p > 0.05). A slow start pacing strategy was adopted in all conditions and did not differ between conditions when averaged across the session; however, when analyzing the first and final 10 min of the session, differences were found between conditions. Finally, the observed time was an important determinant of the regulation of exercise intensity, because, although the pacing strategy adopted in all conditions was regulated according to previous exercise information, adjustments were made in the initial (NC) and final (FC) phases of the trials.

Purpose: High cardiorespiratory capacity is a key determinant of human performance and life expectancy; however, the underlying mechanisms are not fully understood. The objective of this pilot study was to investigate biochemical signatures of endurance-performance athletes using high-resolution nontargeted metabolomics. Methods: Elite long-distance runners with similar training and anthropometrical records were studied. After athletes’ maximal oxygen consumption () was measured, they were divided into 2 groups: low (−1·min⁻¹, n = 7) and high (>75 mL·kg⁻¹·min⁻¹, n = 7). Plasma was collected under basal conditions after 12 hours of fasting and after a maximal exercise test (nonfasted) and analyzed by high-resolution LC–MS. Multivariate and univariate statistics were applied. Results: A total of 167 compounds were putatively identified with an LC–MS-based metabolomics pipeline. Partial least-squares discriminant analysis showed a clear separation between groups. Significant variations in metabolites highlighted group differences in diverse metabolic pathways, including lipids, vitamins, amino acids, purine, histidine, xenobiotics, and others, either under basal condition or after the maximal exercise test. Conclusions: Taken together, the metabolic alterations revealed in the study affect cellular energy use and availability, oxidative stress management, muscle damage, central nervous system signaling metabolites, nutrients, and compound bioavailability, providing new insights into metabolic alterations associated with exercise and cardiorespiratory fitness levels in trained athletes.

MicroRNA Profile and Adaptive Response to Exercise Training: A Review ^* These authors contributed equally to this work.

Professor Robergs recently raised issues based on Popper’s philosophy about the Central Governor Model (CGM), whereby he concluded that the CGM is not a true scientific theory. Thus, he started his paper with Popper’s demarcation criterion and finished this showing several ad hoc hypotheses that changed the CGM.1

Ethanol (ET) is a substance that modulates the Central Nervous System (CNS). Frequently, ET intake occurs combined with energy drinks, which contain taurine (TA), an important amino acid found in the body (i.e brain and muscles). Although TA administration has been used in the improvement of physical performance, the impact of TA, ET and exercise remains unknown. This study aimed to analyze the acute effect of 6g of Taurine (TA), 0.6 mL∙kg^-1 of Ethanol (ET), and Taurine combined with Ethanol (TA+ET) ingestion on the electrocortical activity before and after a moderate intensity exercise in 9 subjects, 5 women (counterbalanced experimental design). In each of the 4 treatments (Placebo—PL, TA, ET and TA+ET), electroencephalography (EEG) tests were conducted in order to analyze changes in absolute beta power (ABP) in the frontal lobe in 3 moments: baseline (before ingestion), peak (before exercise) and post-exercise. In the PL treatment, the frontal areas showed decrease in ABP after exercise. However, in the ET+TA treatment, ABP values were greater after exercise, except for Fp1. The ET treatment had no effect on the Superior Frontal Gyrus area (F3, Fz and F4) and ABP decreased after exercise in Fp1 and Fp2. In the TA treatment, ABP increased after exercise, while it decreased at the peak moment in most of the frontal regions, except for Fp1, F3 and Fz. We concluded that after a moderate intensity exercise, a decrease in cortical activity occurs in placebo treatment. Moreover, we found a inhibitory effect of TA on cortical activity before exercise and a increased in cortical activity after exercise. A small ET dose is not enough to alter ABP in all regions of the frontal cortex and, in combination with TA, it showed an increase in the frontal cortex activity at the post-exercise moment.