ECSS Paris 2023: OP-PN31
INTRODUCTION: At the Mexico City Olympics, ~3% of Beamon’s long jump record [1] and ~2–3% sprint/jump gains were due to altitude reducing air density and drag [2]. In this context, several studies have examined hypoxia’s effect on the force–velocity (F–V) profile. Feriche et al. [3] reported that real altitude (2320 m, hypobaric hypoxia) improved mean power and velocity, whereas equivalent normobaric hypoxia did not. Surprisingly, these gains occurred only at high loads (60–90 kg), where air density has the least impact. The authors suggested that these improvements could result from hypoxia per se, via increased recruitment of type-II muscle fibres, motor units and neuromuscular excitability. Although it is known that severe hypoxia (HH) (>3500 m) leads to mechanical alteration during high-intensity exercise not seen in moderate hypoxia (LH) (<2000 m) [4], the influence of hypoxia severity on F–V profile remains unknown. Therefore, this study aimed to examine the impact of different levels of normobaric hypoxia severity on the F–V relationship. METHODS: Using a single-blind design, 17 healthy trained participants (14 men, 3 women; 23.8±1.6 yr; 75.5±10.3 kg; 183±8 cm) completed three F–V profiling bench press test in normoxic control (CON, FiO₂ = 20.9%), low (LH, 2000 m, FiO₂ = 16.9%) and high normobaric hypoxia (HH, 3800 m, FiO₂ = 13.1%) in randomised order. After a standardised warm-up, heart rate and peripheral oxygen saturation (SpO₂) were measured. One-repetition maximum (1-RM) test was determined, followed by maximal-effort at six relative loads (0–80% 1-RM) to characterise the F–V profile. Maximal velocity, force, and power were recorded with an accelerometer (Myotest® Pro) on the bar. RESULTS: The quality of the F–V relationships was controlled using mean R² (0.97–0.98) and the range covered (79%) for each condition (CON, LH, and HH). SpO₂ was significantly lower only in HH (87.1±5.4%) compared to CON (95.8±1.8%) (p < .001) and LH (94.0±1.7%) (p = 0.004). No significant differences were observed between the three conditions for F–V profile variables, with only trivial percentage differences between CON and LH/HH in theoretical maximal force (−0.0% and +0.7%), theoretical maximal velocity (+2.4% and +1.2%) and theoretical maximal power (+1.7% and +1.0%). CONCLUSION: The severity of acute normobaric hypoxia exposure did not influence the bench press F–V profile. These results confirm that the gains in velocity and power under hypobaric hypoxia are likely induced by the reduced air density and not hypoxia per se in such short-duration exercise. By showing that the relationship between force and velocity remain unchanged, this study has practical application for resistance training in hypoxia usually performed in severe normobaric hypoxia [5]. REFERENCES 1. Frohlich C, 1985, American Journal of Physics; 2. Hamlin MJ, 2015, Int J Sports Physiol Perform; 3. Feriche B, 2014, PLOS ONE; 4. Brocherie F, 2016, Med Sci Sports Exerc; 5. Scott BR, 2014, Sports Med.
Read CV Yohan ROUSSEECSS Paris 2023: OP-PN31
INTRODUCTION: Ageing is associated with progressive decline in muscle function yet the underlying metabolic alterations remain incompletely understood. 31P-NMR spectroscopy provides a non-invasive method to assess in vivo skeletal muscle oxidative metabolism through phosphocreatine (PCr) recovery kinetics (1). In the present study, we comparatively assessed muscle oxidative metabolism in physically active young and elderly adults during a maximum voluntary intermittent and isometric contractions (1.5/0.5 s work rest) exercise (MVIIC) under two oxygen conditions i.e. normoxia and simulated hypoxia. METHODS: Healthy and active (Leisure Score Index >25) participants matched on body-weight and physical activity (young n=13; elderly n=9) completed two randomized exercise sessions: normoxia (FiO2=20.9%) and hypoxia (FiO2=13.0%). Quadriceps 31P NMR spectra were acquired at 3T (TR=1.5 s) during a standardized rest (2 min), exercise (12 s, MVIIC), passive recovery (6 min) protocol. High-energy phosphate metabolites (PCr, Pi, ATP) and pH changes were continuously assessed during each session. Recognized indices of oxidative metabolism as PCr recovery time constant (tau), initial recovery rate (Vi) and theoretical maximal rate of oxidative ATP production (Vmax) were computed. RESULTS: No significant effect of oxygen Condition nor AgeXCondition interactions were observed for any metabolic variable throughout sessions. No Age effect was identified during the exercise phase exercise phase (p=0.654 for PCr, p=0.173 for pH, p=0.771 for Pi). Although the initial rate of PCr recovery in the recovery phase was significantly larger in elderly (tau=22.6+/-4.8 s; Vi=0.43+/-0.16 mmol/s,) as compared to young subjects (tau=29.7+/-8.7 s; Vi=0.32+/-0.09 mmol/s, p=0.035 and p=0.050, respectively), Vmax was similar in both groups (0.80+/-0.25 mmol/s vs 0.85+/-0.24 mmol/s, p=0.625), regardless of oxygen Condition. CONCLUSION: This 31P-NMR study indicated paradoxical findings in healthy, physically active elderly individuals. On the contrary to what has been reported so far in highly aerobic exercise (2), PCr consumption and acidosis were not increased in older subjects after a short high-intensity intermittent exercise. In our case, exercise is likely to be highly ischemic given the frequency and high intramuscular pressure with MVIIC. Hypoxic conditions would not then be expected to create an additional oxygen delivery limitation. In this context, the whole set of oxidative indices indicated a preserved aerobic function in older subjects compared to matched active young adults (2). The preserved Vmax suggests that the mitochondrial function of our elderly group is unchanged likely because of preserved physical activity (3). These results challenge the traditional interpretations of aging-related metabolic decline. REFERENCES: 1. Conley KE et al. J Appl Physiol. 2000;89(5):1937-44. 2. Layec G et al. Age (Dordr). 2013;35(4):1183-92. 3. Layec G et al. J Physiol. 2018;596:5337-9.
Read CV Josep Rebull BarreraECSS Paris 2023: OP-PN31
INTRODUCTION: Combining repeated high-intensity exercise with hypoxia has gained attention given its potential to induce greater physiological adaptations [1]. However, reduced inspired oxygen fraction constrains oxygen transport from air to muscle mitochondria, potentially limiting exercise capacity. Neuromuscular fatigue under hypoxia may involve both peripheral (active muscle) and central (central nervous system) mechanismhttps://sport-science.org/index.php/submission-2026/abstract-submission/how-to-submits [2]. Therefore, the aim of the present study was to examine active muscle (vastus lateralis) and cerebral (prefrontal cortex) oxygenation during repeated maximal cycling in hypoxia and normoxia using near-infrared spectroscopy. We hypothesized that larger hypoxia-related performance decrements would correspond with lower muscle and cerebral oxygenation levels. METHODS: Ten male middle-distance runners (age: 20±1 years; 800 m season best: 113.3±3.9 s) completed a repeated Wingate protocol under hypoxia (inspired oxygen fraction: 0.145) and normoxia using a randomized crossover design. The exercise protocol involved four 30-second all-out cycling bouts at maximal cadence. The exercise intensity was set to 7.5% of body weight for the first bout and progressively reduced to 6.5%, 5.5%, and 4.5% to maintain maximal effort. Each bout was separated by 4-minute of unloaded pedaling at 50 rpm (0 watts). RESULTS: Average mean power output across the four sets was ~4% higher in normoxia (474±24 W) than in hypoxia (455±24 W, P=0.007). During exercise, hypoxia elicited greater muscle deoxygenation and total hemoglobin in the vastus lateralis, alongside lower tissue oxygen saturation in both the vastus lateralis and prefrontal cortex (all P<0.05). During the 4-min recovery periods, muscle and cerebral reoxygenation were greater in normoxia than hypoxia (P=0.055 and P<0.001, respectively). Reductions in power output under hypoxia correlated with increased cerebral deoxygenation during exercise (r=-0.452, P=0.011) and recovery (r=0.440, P=0.046), whereas those marginally correlated with increased muscle de- (r=-0.268, P=0.145) and re-oxygenation (r=0.413, P=0.063). CONCLUSION: These results suggest that individuals with smaller reductions in cerebral oxygenation during exercise and recovery are better able to maintain repeated high-intensity exercise performance., which was supported by a previous finding, showing that limited oxygen availability decreased central motor drive, thereby limiting performance in hypoxia [3]. Cerebral oxygenation responses appear to be a key determinant of repeated high-intensity exercise performance in hypoxia. References [1] Girard et al. (2020) Front Sports Act Living, 2, 26. doi:10.3389/fspor.2020.00026 [2] Fan and Kayser. (2016) High Alt Med Biol, 17(2):72-84. [3] Amann et al. (2007) J Physiol, 581: 389-403.
Read CV Masahiro HoriuchiECSS Paris 2023: OP-PN31