Letizia Rasica

This study determined: (i) whether carbohydrates (CHO) supplementation had beneficial effects on endurance performance, as assessed by a time trial (TT) test, following exercise bouts within either the moderate‐ or heavy‐intensity exercise; and (ii) if above the recommended dose of CHO supplementation would impact endurance performance. Twelve recreationally trained males underwent: (i) a step‐ramp‐step test to estimate gas exchange threshold (GET) and maximal metabolic steady state (MMSS _est ); (ii) 9 randomized visits consisting of 3 different constant power output (PO) bouts: within the moderate‐ (120 min at 90% of GET [MOD]); lower portion of the heavy‐ (90 min at Δ20% between GET and MMSS _est [HVY ₁ ]); and higher portion of the heavy‐ (60 min at Δ80% between GET and MMSS _est [HVY ₂ ]) intensity domain under 3 different conditions (placebo, recommended 40 g/h CHO [R‐CHO], and high 90 g/h CHO [H‐CHO]) dose per intensity with a subsequent 4 km TT. The 4 km TT was improved ( p = 0.017) in the R‐CHO (8.3 ± 0.7 min) compared to placebo (8.6 ± 0.9 min) after HVY ₁ but not in the H‐CHO (8.5 ± 0.9 min) condition. In contrast, 4 km TT performance was not different after MOD (placebo = 8.8 ± 1.3 min; R‐CHO = 8.6 ± 1.1 min; H‐CHO = 8.6 ± 1.1; p = 0.589) or HVY ₂ (placebo = 8.8 ± 1.1 min; R‐CHO = 8.6 ± 0.9 min; H‐CHO = 8.7 ± 1.0; p = 0.465). In recreationally trained individuals, R‐CHO supplementation improved 4 km TT performance following exercise within the lower portion of the heavy‐intensity domains, but not following exercise in the moderate‐ or upper region of the heavy‐intensity domain. Additionally, above‐recommended CHO dose was no longer beneficial for performance regardless of the prior exercise intensity bout.

The study aimed to investigate the effects of sodium bicarbonate (NaHCO₃) intake with divergent verbal and visual information on constant load cycling time-to-task failure, conducted within the severe intensity domain. Fifteen recreational cyclists participated in a randomized double-blind, crossover study, ingesting NaHCO₃ or placebo (i.e., dextrose), but with divergent information about its likely influence (i.e., likely to induce ergogenic, inert, or harmful effects). Performance was evaluated using constant load cycling time to task failure trial at 115% of peak power output estimated during a ramp incremental exercise test. Data on blood lactate, blood acid–base balance, muscle electrical activity (EMG) through electromyography signal, and the twitch interpolation technique to assess neuromuscular indices were collected. Despite reduced peak force in the isometric maximal voluntary contraction and post-effort peripheral fatigue in all conditions (P < 0.001), neither time to task failure, EMG nor, blood acid–base balance differed between conditions (P > 0.05). Evaluation of effect sizes of all conditions suggested that informing participants that the supplement would be likely to have a positive effect (NaHCO₃/Ergogenic: 0.46; 0.15–0.74; Dextrose/Ergogenic: 0.45; 0.04–0.88) resulted in improved performance compared to control. Thus, NaHCO₃ ingestion consistently induced alkalosis, indicating that the physiological conditions to improve performance were present. Despite this, NaHCO₃ ingestion did not influence performance or indicators of neuromuscular fatigue. In contrast, effect size estimates indicate that participants performed better when informed that they were ingesting an ergogenic supplement. These findings suggest that the apparently ergogenic effect of NaHCO₃ may be due, at least in part, to a placebo effect.

Sex differences in physiological responses to various stressors, including exercise, have been well documented. However, the specific impact of these differences on exposure to hypoxia, both at rest and during exercise, has remained underexplored. Many studies on the physiological responses to hypoxia have either excluded women or included only a limited number without analyzing sex-related differences. To address this gap, this comprehensive review conducted an extensive literature search to examine changes in physiological functions related to oxygen transport and consumption in hypoxic conditions. The review encompasses various aspects, including ventilatory responses, cardiovascular adjustments, hematological alterations, muscle metabolism shifts, and autonomic function modifications. Furthermore, it delves into the influence of sex hormones, which evolve throughout life, encompassing considerations related to the menstrual cycle and menopause. Among these physiological functions, the ventilatory response to exercise emerges as one of the most sex-sensitive factors that may modify reactions to hypoxia. While no significant sex-based differences were observed in cardiac hemodynamic changes during hypoxia, there is evidence of greater vascular reactivity in women, particularly at rest or when combined with exercise. Consequently, a diffusive mechanism appears to be implicated in sex-related variations in responses to hypoxia. Despite well-established sex disparities in hematological parameters, both acute and chronic hematological responses to hypoxia do not seem to differ significantly between sexes. However, it is important to note that these responses are sensitive to fluctuations in sex hormones, and further investigation is needed to elucidate the impact of the menstrual cycle and menopause on physiological responses to hypoxia.

Elbow flexors (EFs) and knee extensors (KEs) have shown differences in performance fatigability and recovery of neuromuscular function after isometric and isotonic single-joint fatiguing contractions. However, dynamic multi-joint movements are more representative of real-world activities. The aim of the study was to assess central and peripheral mechanisms of fatigability after either arm-cranking or cycling. Ten physically active men performed maximal incremental arm-cranking and cycling until task failure. Maximal voluntary isometric contraction (MVIC) and electrically evoked forces of both EF and KE were assessed before (PRE) and 1 (POST) and 20 (POST20) min after exercise. At POST, MVIC decreased similarly to 76 ± 8% and 81 ± 7% (both P < 0.001) of PRE for EF and KE, respectively. MVIC force remained lower than PRE at POST20 for both EF and KE (85 ± 8% vs. 95 ± 3% of PRE, P ≤ 0.033), having recovered less in EF than in KE (P = 0.003). Electrically evoked forces decreased similarly from PRE to POST in EF and KE (all P > 0.05). At POST20, the ratio of low-to-high frequency doublets was lower in EF than in KE (75 ± 13% vs. 85 ± 10% of PRE; P ≤ 0.034). Dynamic maximal incremental exercise acutely induced similar magnitudes of MVIC and evoked force loss in EF and KE. However, at POST20, impaired MVIC recovery and lower ratio of low-to-high frequency doublets in EF than in KE suggest the recovery of neuromuscular function after dynamic maximal exercises is specific to and dependent on changes within the muscles investigated.

Purpose High altitude results in lower barometric pressure and hence partial pressure of O₂ decrease can lead to several molecular and cellular changes, such as generation of reactive oxygen species (ROS). Electron Paramagnetic Resonance technique was adopted in the field, to evaluate the effects of acute and sub-acute hypobaric hypoxia (HH) on ROS production by micro-invasive method. Biological biomarkers, indicators of oxidative stress, renal function and inflammation were investigated too. Methods Fourteen lowlander subjects (mean age 27.3 ± 5.9 years) were exposed to HH at 3269 m s.l. ROS production, related oxidative damage to cellular components, systemic inflammatory response and renal function were determined through blood and urine profile performed at 1st, 2nd, 4th, 7th, and 14th days during sojourn. Results Kinetics of changes during HH exposition showed out significant (range p < 0.05–0.0001) increases that at max corresponds to 38% for ROS production rate, 140% for protein carbonyl, 44% for lipid peroxidation, 42% for DNA damage, 200% for inflammatory cytokines and modifications in renal function (assessed by neopterin concentration: 48%). Conversely, antioxidant capacity significantly (p < 0.0001) decreased − 17% at max. Conclusion This 14 days in-field study describes changes of oxidative-stress biomarkers during HH exposure in lowlanders. The results show an overproduction of ROS and consequent oxidative damage to protein, lipids and DNA with a decrease in antioxidant capacity and the involvement of inflammatory status and a transient renal dysfunction. Exposure at high altitude induces a hypoxic condition during acute and sub-acute phases accompanied by molecular adaptation mechanism indicating acclimatization.

Purpose: On level, the metabolic cost (C) of backward running is higher than forward running probably due to a lower elastic energy recoil. On positive gradient, the ability to store and release elastic energy is impaired in forward running. We studied running on level and on gradient to test the hypothesis that the higher metabolic cost and lower efficiency in backward than forward running was due to the impairment in the elastic energy utilisation. Methods: Eight subjects ran forward and backward on a treadmill on level and on gradient (from 0 to + 25%, with 5% step). The mechanical work, computed from kinematic data, C and efficiency (the ratio between total mechanical work and C) were calculated in each condition. Results: Backward running C was higher than forward running at each condition (on average + 35%) and increased linearly with gradient. Total mechanical work was higher in forward running only at the steepest gradients, thus efficiency was lower in backward running at each gradient. Conclusion: Efficiency decreased by increasing gradient in both running modalities highlighting the impairment in the elastic contribution on positive gradient. The lower efficiency values calculated in backward running in all conditions pointed out that backward running was performed with an almost inelastic rebound; thus, muscles performed most of the mechanical work with a high metabolic cost. These new backward running C data permit, by applying the recently introduced ‘equivalent slope’ concept for running acceleration, to obtain the predictive equation of metabolic power during level backward running acceleration.

Key points: Increased plasma nitrite concentrations may have beneficial effects on skeletal muscle function. The physiological basis explaining these observations has not been clearly defined and it may involve positive effects on muscle contraction force, microvascular O₂ delivery and skeletal muscle oxidative metabolism. In the isolated canine gastrocnemius model, we evaluated the effects of acute nitrite infusion on muscle force and skeletal muscle oxidative metabolism. Under hypoxic conditions, but in the presence of normal convective O₂ delivery, an elevated plasma nitrite concentration affects neither muscle force, nor muscle contractile economy. In accordance with previous results suggesting limited or no effects of nitrate/nitrite administrations in highly oxidative and highly perfused muscle, our data suggest that neither mitochondrial respiration, nor muscle force generation are affected by acute increased concentrations of NO precursors in hypoxia. Contrasting findings have been reported concerning the effects of augmented nitric oxide (NO) on skeletal muscle force production and oxygen consumption (). The present study examined skeletal muscle mitochondrial respiration and contractile economy in an isolated muscle preparation during hypoxia (but normal convective O₂ delivery) with nitrite infusion. Isolated canine gastrocnemius muscles in situ (n = 8) were studied during 3 min of electrically stimulated isometric tetanic contractions corresponding to ∼35% of . During contractions, sodium nitrite (NITRITE) or sodium chloride (SALINE) was infused into the popliteal artery. was calculated from the Fick principle. Experiments were carried out in hypoxia ( = 0.12), whereas convective O₂ delivery was maintained at normal levels under both conditions by pump‐driven blood flow (). Muscle biopsies were taken and mitochondrial respiration was evaluated by respirometry. Nitrite infusion significantly increased both nitrite and nitrate concentrations in plasma. No differences in force were observed between conditions. was not significantly different between NITRITE (6.1 ± 1.8 mL100 g⁻¹ min⁻¹) and SALINE (6.2 ± 1.8 mL 100 g⁻¹ min⁻¹), even after being ‘normalized’ per unit of developed force (muscle contractile economy). No differences between conditions were found for maximal ADP‐stimulated mitochondrial respiration (both for complex I and complex II), leak respiration and oxidative phosphorylation coupling. In conclusion, in the absence of changes in convective O₂ delivery, muscle force, muscle contractile economy and mitochondrial respiration were not affected by acute infusion of nitrite. The previously reported positive effects of elevated plasma nitrite concentrations are presumably mediated by the increased microvascular O₂ availability.