Of this study was to evaluate the effects of short-term nitrate supplementation on endurance performance in subjects with different levels of aerobic fitness. Methods Twenty-one subjects (mean age, 22.7 ± 1.8 yr) with different aerobic fitness level (V˙O2peak value ranging from 28.2 to 81.7 mL·kg−1·min−1) participated in a crossover double-blind placebo-controlled study. Subjects were tested after 6 d of supplementation with either 0.5 l per day of nitrate (5.5 mmol)-containing water (NITR) or nitrate-free water (PLA). Participants performed an incremental running test until exhaustion and four repetitions of 6-min submaximal (approximately 80% of gas exchange threshold) constant load exercise on a motorized treadmill. Moreover, subjects performed a 3-km running time trial on the field. Results After NITR, a negative correlation between reduction of O2 cost of submaximal exercise and individual aerobic fitness level was observed (r2 = 0.80; P < 0.0001). A significant inverse correlation was also found between aerobic fitness level and improvement in performance for 3-km time trial after NITR (r2 = 0.76; P < 0.0001). Additionally, subjects responded differently to dietary nitrate supplementation according to aerobic fitness level with higher-fit subjects showing a lower increase in plasma [NO3−] (r2 = 0.86; P < 0.0001) and [NO2−] (r2 = 0.75; P < 0.0001). Conclusions The results of the present study suggest that the individual aerobic fitness level affects the ergogenic benefits induced by dietary nitrate supplementation. The optimal nitrate loading regimen required to elevate plasma [NO2−] and to enhance performance in elite athletes is different from that of low-fit subjects and requires further studies....

Despite the growing interest in the role of reactive oxygen species (ROS) in health and disease, reliable quantitative noninvasive methods for the assessment of oxidative stress in humans are still lacking. EPR technique, coupled to a specific spin probe (CMH: 1-hydroxy-3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine) is here presented as the method of choice to gain a direct measurement of ROS in biological fluids and tissues. The study aimed at demonstrating that, differently from currently available “a posteriori” assays of ROS-induced damage by means of biomolecules (e.g., proteins and lipids) spin-trapping EPR provides direct evidence of the “instantaneous” presence of radical species in the sample and, as signal areas are proportional to the number of excited electron spins, lead to absolute concentration levels. Using a recently developed bench top continuous wave system (e-scan EPR scanner, Bruker) dealing with very low ROS concentration levels in small (50 μL) samples, we successfully monitored rapid ROS production changes in peripheral blood of athletes after controlled exercise and sedentary subjects after antioxidant supplementation. The correlation between EPR results and data obtained by various enzymatic assays (e.g., protein carbonyls and thiobarbituric acid reactive substances) was determined too. Synthetically, our method allows reliable, quick, noninvasive quantitative determination of ROS in human peripheral blood.

The growing interest in the role of Reactive Oxygen Species (ROS) and in the assessment of oxidative stress in health and disease clashes with the lack of consensus on reliable quantitative noninvasive methods applicable. The study aimed at demonstrating that a recently developed Electron Paramagnetic Resonance microinvasive method provides direct evidence of the “instantaneous” presence of ROS returning absolute concentration levels that correlate with “a posteriori” assays of ROS-induced damage by means of biomarkers. The reliability of the choice to measure ROS production rate in human capillary blood rather than in plasma was tested (step I). A significant (P<0.01) linear relationship between EPR data collected on capillary blood versus venous blood (R2=0.95), plasma (R2=0.82), and erythrocytes (R2=0.73) was found. Then (step II) ROS production changes of various subjects’ categories, young versus old and healthy versus pathological at rest condition, were found significantly different (range 0.0001–0.05Plevel). The comparison of the results with antioxidant capacity and oxidative damage biomarkers concentrations showed that all changes indicating increased oxidative stress are directly related to ROS production increase. Therefore, the adopted method may be an automated technique for a lot of routine in clinical trials.

Purpose: Aerobic exercise prescription is often based on a linear relationship between pulmonary oxygen consumption (V˙O₂) and heart rate (HR). The aim of the present study was to test the hypothesis that during constant work rate (CWR) exercises at different intensities, the slow component of HR kinetics occurs at lower work rate and is more pronounced that the slow component of V˙O₂kinetics.Methods: Seventeen male (age, 27 ± 4 yr) subjects performed on a cycle ergometer an incremental exercise to voluntary exhaustion and several CWR exercises: 1) moderate CWR exercises, below gas exchange threshold (GET); 2) heavy CWR exercise, at 45% of the difference between GET and V˙O₂peak (Δ); 3) severe CWR exercise, at 95% of Δ; 4) “HR_CLAMPED” exercise in which work rate was continuously adjusted to maintain a constant HR, slightly higher than that determined at GET. Breath-by-breath V˙O₂, HR, and other variables were determined.Results: In moderate CWR exercises, no slow component of V˙O₂kinetics was observed, whereas a slow component with a relative amplitude (with respect to the total response) of 24.8 ± 11.0% was observed for HR kinetics. During heavy CWR exercise, the relative amplitude of the HR slow component was more pronounced than that for V˙O₂(31.6 ± 11.2% and 23.3 ± 9.0%, respectively). During HR_CLAMPED, the decrease in work rate (~14%) needed to maintain a constant HR was associated with a decreased V˙O₂(~10%).Conclusions: The HR slow component occurred at a lower work rate and was more pronounced than the V˙O₂slow component. Exercise prescriptions at specific HR values, when carried out for periods longer than a few minutes, could lead to premature fatigue.

Several months after mild acute SARS-CoV-2 infection, a substantial proportion of patients present persisting, and often debilitating, symptoms and sequelae. These patients show reduced quality of life due to exercise intolerance, muscle weakness, and fatigue. The present study supports the hypothesis that “peripheral” impairments at skeletal muscle level, namely, reduced mitochondrial function and markers of mitochondrial biogenesis, are major determinants of exercise intolerance and fatigue, “central” phenomena at respiratory, and cardiac level being less relevant.

Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA; body mass 102.6 ± 7.3 kg, mean ± SD) and 11 controls (CTRL; body mass 77.8 ± 6.0 kg). Pulmonary O₂ uptake (V̇o₂) and vastus lateralis muscle fractional O₂ extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross-sectional area, volume (determined by magnetic resonance imaging), and strength were greater in RTA vs. CTRL (by ∼40%, ∼33%, and ∼20%, respectively). V̇o_2peak during CE was higher in RTA vs. CTRL (4.05 ± 0.64 vs. 3.56 ± 0.30 l/min); no difference between groups was observed during KE. The O₂ cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE), V̇o₂ peak was lower (by 15–20%) in RTA vs. CTRL. Vastus lateralis fractional O₂ extraction was lower in RTA vs. CTRL at all work rates, during both CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.7 ± 23.7 pmol O₂·s⁻¹·mg⁻¹ ww) vs. CTRL (35.7 ± 10.2 pmol O₂·s⁻¹·mg⁻¹ ww) and a tighter coupling of oxidative phosphorylation. In RTA, the greater muscle mass and maximal force and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O₂ diffusion. The net results are an enhanced whole body oxidative function at peak exercise and unchanged efficiency and O₂ cost at submaximal exercise, despite a much greater body mass.