ECSS Paris 2023: CP-PN01
INTRODUCTION: It has been largely acknowledged that the vastus lateralis (VL) deoxygenation (HHb) measured by near-infrared spectroscopy (NIRS) during a maximal incremental test on an ergocycle typically displays a linear increase followed by a break point (BP) above the maximal aerobic capacity (MAP) [1,2]. However, the onset of BP varies substantially across individuals [1,3,4] while the corresponding physiological accounting factors remain poorly understood. In the present study, we aimed to better characterize the BP using a combined lactate, muscle (time-domain NIRS) and systemic oxygenation analysis. We hypothesized that different BP profiles could be distinguished based on this whole set of measurements. METHODS: 13 trained male cyclists (19.7±0.9 years, V̇O₂max: 63.0±5.2 mL·min-1·kg-1) performed an incremental test to exhaustion (100 W + 25 W·2min-1). Both VL (time-domain NIRS) and systemic oxygenation (gas exchange analysis) were continuously monitored. First and second ventilatory thresholds (VT1, VT2) were determined using the Beaver method [5]. Capillary blood was sampled 2 min post-exercise to determine the maximal lactate concentration ([La]max). HHb kinetics were modelled using a double-linear regression resulting in 2 segments (S1, S2). BP intensity and slopes of S1 and S2 were determined. Statistical comparisons were performed using Mann-Whitney U tests. RESULTS: All subjects displayed a biphasic muscle oxygenation profile with 2 distinct patterns: 8 subjects (G1) displayed a deoxygenation acceleration (slope of S2 > slope of S1) after the BP whereas the remaining 5 subjects (G2) displayed a deoxygenation attenuation (slope of S2 < slope of S1). Of interest, BP occurred significantly earlier in G1 (70.08 ± 11.40 vs. 95.10 ± 9.20 % of MAP, p = 0.006). In addition, a higher power (300 ± 26.73 vs. 260 ± 13.69 W, p = 0.012) and a larger V̇O₂ (86.04 ± 2.53 vs. 80.93 ± 2.66 expressed %V̇O₂max, p = 0.016) at VT2 were quantified in G1. The MAP (350 ± 26.73 vs 300 ± 17.68 W, p = 0.007) was also larger. V̇O₂max (63.80 ± 6.16 vs. 60.52 ± 4.70 mL·min-1·kg-1, p = 0.21) and [La]max (10.32 ± 2.87 vs. 10.47 ± 1.83 mmol.L-1, p = 0.51) did not differ between groups. CONCLUSION: Combined muscle and systemic oxygenation measurements allow to distinguish two HHb patterns in the VL. The first profile was related to the occurrence of an early BP followed by an accelerated deoxygenation, while for the second profile, BP was delayed and followed by decelerated deoxygenation. The first profile was associated with a higher power output and V̇O₂ at VT2, as well as a larger MAP, despite similar V̇O₂max and [La]max between groups. These results suggest a potentially optimized peripheral efficiency in G1 which could be linked to a training effect. This inter-individual variability in peripheral O₂ extraction should be further documented in a larger amount of subjects. References [1] Boone & al., 2016 [2] Ianetta & al., 2017 [3] Ferreira & al., 2006 [4] Rupp & al., 2007 [5] Beaver & al., 1986
Read CV Alyssia BernabeuECSS Paris 2023: CP-PN01
INTRODUCTION: Angiotensin-Converting Enzyme 2 (ACE2) drives the protective ACE2/Ang-(1-7)/MasR axis, balancing tissue homeostasis against RAS-mediated stress. Simultaneously, ACE2 acts as a critical molecular gateway for viral entry, yet the mechanisms governing its acute regulation in skeletal muscle remain undefined. We hypothesised that exercise upregulates this gateway via redox-sensitive signalling mediated by NADPH oxidase 2 (NOX2) and Xanthine Oxidase (XO). To test this, we utilised post-exercise ischaemia (Isch) to amplify metabolic stress and polyphenol blockade to demonstrate causality. METHODS: Thirty-six men participated in two independent experiments involving incremental cycling to exhaustion (Exh) immediately followed by unilateral Isch (300 mmHg). Study I (n=11; crossover) examined severe hypoxia (PIO2:73mmHg) vs. normoxia. Study II (n=25; parallel design) investigated mechanistic blockade using Zynamite®-PX (140mg mangiferin/quercetin) vs Placebo administered every 8h for 48h prior to exercise. Vastus lateralis biopsies were collected at Rest (Pre), Exh (unilateral), and 60s post-exercise (Isch vs. perfused leg (Perf); Study I). Western blotting assessed RAS (ACE2/ACE1/AT1R/AT2R), TMPRSS2 and redox markers (NOX2/XO). Stats: RM/Mixed ANOVA, t-tests and Linear Mixed Models (LMM). RESULTS: Exh triggered a rapid upregulation of ACE2 (2.8-fold; p=0.01) and TMPRSS2 (1.6-fold; p<0.001) concurrent with NOX2 activation (p-p47phox: 2.9-fold; p=0.003) and XO increase (3.9-fold). Classical RAS components (ACE1, AT1R) remained unaltered, while AT2R decreased (-13%; p=0.03). In Study I, Isch maintained elevated ACE2/TMPRSS2 and increased further XO/NOX2, whereas Perf allowed rapid recovery (ACE2: -67% vs Isch; p=0.01). Crucially (Study II), Zynamite®-PX blunted the Exh-induced NOX2/XO response and abolished ACE2 upregulation (Time×Treat: p=0.02). ACE2 abundance strongly correlated with TMPRSS2 (R²c=0.71) and NOX2 activation (R²c=0.96) in mixed models. CONCLUSION: These novel data demonstrate, for the first time in humans, that the viral entry protein ACE2 is dynamically regulated by acute exercise via a redox-sensitive mechanism (NOX2/XO). The finding that polyphenol blockade abolishes this response identifies cellular redox state as a primary "switch" for ACE2 expression. Consequently, while exercise promotes metabolic health, the acute oxidative stress of exhaustive effort may transiently open molecular windows for viral susceptibility, a process modifiable via specific antioxidant strategies. PID2021-125354OB-C21/AEI/10.13039/501100011033/FEDER, EU; CSD (EXP_75097); (SD-24/03, ID 877) CUCIC. AGS: Catalina Ruiz postdoctoral (CUCIC-GOBCAN and ESF)
Read CV EDUARDO GARCÍA GONZÁLEZECSS Paris 2023: CP-PN01
INTRODUCTION: Much attention has been paid to the use of caffeine as a pre-workout supplement to improve athletic performance during acute bout of resistance exercise session (1). However, it is unclear whether pre-exercise caffeine ingestion subsequently affects exercise-induced muscle damage (EIMD) accompanied by reduced muscle functionality (e.g., force loss) for several days, because few studies have focused on post-exercise decreases in muscle force, as the reliable EIMD marker (2). Since higher eccentric exercise loads lead to greater EIMD (3), caffeine’s ergogenic effects may exacerbate EIMD by increasing eccentric loads during exercise. Here, this study examined the impact of pre-exercise caffeine ingestion on EIMD (i.e., reduced torque) after eccentric exercise, while focusing on the changes in eccentric loads induced by caffeine's ergogenic effects during exercise. METHODS: In double-blind, crossover trials, fifteen healthy young men ingested 6 mg/kg caffeine/placebo, followed by an eccentric exercise at 30–120° of knee angles: 100-times isokinetic eccentric maximal voluntary knee extensions in STUDY 1 (i.e., caffeine can change eccentric load) and 100-times isoload (fixed at 120% of concentric 1RM) eccentric leg extensions in STUDY 2 (i.e., caffeine cannot change eccentric load). In STUDY 1, torque-time integral (TTI) and angle-specific torque were calculated during the exercise as exercise performance. Maximal voluntary isometric torques (MVITs) of the knee extensors were evaluated at 24 and 48 h after the exercise as an indirect EIMD marker. The linear mixed-effects model and type III ANOVA were applied to detect the impact of caffeine on post-exercise MVITs. Repeated measures correlations were used to analyze relationships between eccentric load during exercise and EIMD in STUDY 1. RESULTS: In STUDY 1, caffeine significantly increased Total TTI (p=0.001) and torque during exercise than placebo, regardless of knee angle (p<0.001). However, caffeine produced lower post-exercise MVITs at 24 and 48 h than placebo (p<0.001). Conversely, there were no significant differences in post-exercise MVITs between conditions in STUDY 2 (p=0.242), emphasizing that the greatly reduced torque was derived from the caffeine-induced increase in eccentric load. In STUDY 1, post-exercise MVIT was negatively correlated with total TTI (r=-0.53, p=0.034) and torque at 90–120° knee angles (r=-0.54, p=0.034) but not at <90° knee angles (r=-0.34 to -0.06, p>0.05). CONCLUSION: Pre-exercise caffeine ingestion increases EIMD (greater torque reduction) for several days after eccentric exercise by increased eccentric load as caffeine’s ergogenic effect. Furthermore, increased eccentric loads at a long muscle length may particularly contribute to caffeine-induced greater EIMD. We should consider the potential impact for greater EIMD when using caffeine as a pre-workout supplement for resistance exercise. 1. Grgic. Sports Med. 2021 2. Matsumura et al. PharmaNutrition. 2026 3. Chen et al. J Appl Physiol. 2007
Read CV Teppei MatsumuraECSS Paris 2023: CP-PN01