ECSS Paris 2023: CP-PN17
INTRODUCTION: Heat acclimatization and hypoxic training have improved aerobic capacity and endurance performance, potentially linked to enhanced fat oxidation capacity. Evidence from diseased or obese populations suggests that environmental adaptations can increase fat oxidation as an energy source. However, there is limited research on the metabolic responses of elite athletes. This study aimed to assess the impact of heat acclimatization and hypoxic training on fat oxidation capacity in competitive athletes, exploring potential factors that contribute to improvements in aerobic capacity. METHODS: Eight elite male modern pentathletes participated in a four-week aerobic endurance training program under three different environmental conditions: control (CON group; 23°C, RH45%, FiO2=20.9%), hot (HOT group; 35°C, RH70%, FiO2=20.9%), and hypoxia (HYP group; 23°C, RH45%, FiO2=15.6%). Incremental exercise tests were performed before and after the training in both the control and respective specialized environments. Gas exchange data were collected to assess aerobic capacity, while indirect calorimetry was used to determine fat oxidation rates, which were plotted as a function of exercise intensity. A SIN model was employed to determine the intensity (Fatmax) causing maximal fat oxidation (MFO), and the models three independent variables, dilation (d), symmetry (s), and translation (t), were used to characterize the dynamics of fat oxidation. A two-way repeated measures ANOVA was used to assess the effects of environmental conditions and training factors, with statistical significance set at α = 0.05. Data are presented as mean ± SD. RESULTS: In the control environment, after the training, the HOT group exhibited a significant increase in absolute V̇O2 (4322.6 ± 651.64 vs. 4560.75 ± 722.64 ml/min, p=0.003). Both the HOT (626.44 ± 75.58 vs. 722.50 ± 49.79 s, p=0.006) and HYP (573.83 ± 51.77 vs. 683.75 ± 76.15 s, p=0.002) groups showed significant increases in VT2@Time after training. Additionally, both HOT (0.65 ± 0.14 vs. 0.78 ± 0.13 g/min, p=0.015) and HYP (0.63 ± 0.17 vs. 0.79 ± 0.18 g/min, p=0.004) groups demonstrated increased MFO after training. The HOT group also exhibited an increase in Fatmax (30.46 ± 3.61 vs. 35.76 ± 5.12 ml/min·kg, p=0.005). Both HOT (-0.74 ± 0.28 vs. -0.45 ± 0.16, p=0.003) and HYP groups (-0.79 ± 0.27 vs. -0.51 ± 0.12, p=0.003) showed significant increases in d under the control environment, with the HOT group also showing an increase in d under hot environment (-0.74 ± 0.28 vs. -0.45 ± 0.16, p=0.013) after training. CONCLUSION: Four weeks of hypoxic and heat acclimatization training can enhance aerobic metabolic capacity in competitive athletes under normal conditions, accompanied by improvements in fat oxidation curve dilation and increased fat oxidation capacity. Additionally, heat acclimatization training has similar beneficial effects on fat oxidation capacity during exercise in hot environments.
Read CV Jun QiuECSS Paris 2023: CP-PN17
INTRODUCTION: The aim of this study was to investigate the effectiveness of thermal strategies on recovery rate after exercise induced delayed onset of muscle soreness. METHODS: The study used a randomized, parallel group design (N=40 with 10 in each group) over four consecutive test days. Participants performed a single bout of eccentric knee extensions, with baseline and post maximal voluntary contraction (MVC) measurements on a isokinetic dynamometer (HUMAC NORM), followed by a thermal recovery strategy: hot water immersion (HWI;30 min at 42 °C), cold water immersion (CWI;15 min at 9 °C), hot air immersion (HAI; 30 min at 30°C, 30% RH) or control (CON: 30 min at 18 °C, 30% RH). Recovery rate of strength (via MVC), and pain and muscle soreness (via visual analogue scales) was monitored over 72hr (pre exercise, post exercise, post therapy, 24hrs, 48hrs, and 72hrs after therapy). Venous blood samples were collected each session to analyse Inflammatory marker Interleukin 6 (IL-6), heat shock proteins (HSP72), and Creatine Kinase Muscle-Muscle isoenzyme (CKMM). RESULTS: HWI returned 85 and 89% of strength back to baseline MVC values at 48hr (284.30±22.04N vs 243.70±25.33; p= 0.356) and 72hrs (284.30±22.04N vs 256.00 ± 26.12; p= 0.801) respectively. CON and HAI returned 88% and 89% of strength back to baseline MVC values at 72hrs (303.70±22.04N vs 268.50±26.12N; p= 0.314, and 299.70±22.04N vs 268.70±26.12N; p= 0.563 respectively). Whereas, CWI MVC values were still 25% higher than baseline at 72hrs (279.10±22.04N vs 218.80±26.12N; p=0.005). There was no significant difference in the recovery of pain or muscle soreness between groups over time (P >0.05). CKMM increased from baseline to post-exercise in all groups (p < 0.05). However, HWI caused a significant decrease in CKMM in comparison to other groups over time (p < 0.05). HSP72 increased significantly after HWI and HAI (1.36±0.11 vs 1.81±0.14 mg/ml and 1.36±0.11 to 1.6±0.14 mg/ml; p = 0.001), while CWI caused a significant decrease (1.36±0.11 vs 0.87±0.10 mg/ml; p = 0.001), with no change in CON (1.21±0.01; p = 0.671). Quadriceps muscle temperature increased with HWI (36.57±1.2 °C vs 38.83±1.3 °C; p= 0.005) and decreased with HAI (37.05±0.5 °C vs 34±1.7 °C; p= 0.05) and CON (36.61±0.9 °C vs 34.78±2.2 °C; p= 0.012). There was no significant difference in HAI (36.05±0.9 °C vs 36.27±0.5 °C; p = 0.444). HWI reduced IL6 after 48 hours (0.54±0.02 vs 0.56±0.02 pg/ml; p = 0.096), whereas CWI reduced after 72 hours (0.61±0.04 vs 0.61±0.03 pg/ml; p = 0.953). CONCLUSION: Hot water immersion was the most effective thermal therapy for returning baseline strength. This was related to the physiological stimulus that hot water immersion caused on the body (elevation in muscle temperature and heat shock protein 70) and associated upregulation of inflammation (IL6) and low circulating markers of muscle damage (CK-MM) compared to other therapies. Therefore, hot water immersion should be favored for recovery of strength.
Read CV Freya BayneECSS Paris 2023: CP-PN17
INTRODUCTION: Ice slurry ingestion prior to exercise can expand the heat storage window whilst improving tolerance to rising core temperature (Tcore) [1] and blunting the sweating response [2]. Alternatively, sodium citrate (SC) supplementation has been shown to promote water retention and subsequently induce hyperhydration [3]. Both offer potential value as pre-race strategies to mitigate thermal strain experienced by motorsport driver-athletes who race in thermally resistant clothing that renders evaporative heat loss largely ineffective, thus exacerbating thermal strain in high temperature cockpit conditions [4]. The current study aimed to determine the effects of ice slurry ingestion and SC supplementation alone or in combination on thermoregulatory mechanisms during exposure to a hot environment in a motorsport-simulated environment. METHODS: Four healthy, non-heat acclimated participants (24±2years, 71.8±13.9kg) completed four trials in a double-blind randomised cross-over design. Participants ingested 300mg/kg BM of SC or placebo with 25 mL/kg BM of room temperature water 150 min before a driving simulation, both with and without 10g/kg BM ice slurry consumed in the final 30 min. Simulated driving was conducted in an environmental chamber at 35 °C and 30 % humidity whilst wearing a full-body fire-retardant suit, racing overalls, gloves, boots, balaclava and helmet. Changes in Tcore (∆Tcore) and plasma volume (∆PV) were assessed pre- and post-30 min ice slurry stage. Whole-body sweat rate (WBSR), back local sweat rate area under the curve (LSR AUC), ∆Tcore and ∆PV were measured across 60 min of simulated driving conditions. RESULTS: There was a significant condition effect for change in Tcore (∆Tcore) during the 30 min slurry ingestion period (F(3,8) = 9.023,P<0.05). Ice slurry ingestion significantly reduced Tcore in both conditions compared with the no slurry + placebo condition (P<0.05) but not compared to no slurry + SC (P=0.06). There were condition effects for ∆Tcore during the 60 min simulated driving (P=0.05) but no interaction effects were observed (P>0.05). There were no condition effects for WBSR (P=0.90), back LSR AUC (P=0.11) and thermosensitivity derived from LSR AUC relative to ∆Tcore (P=0.09) during the simulated driving. There was also no significant condition effect for ∆PV between baseline and post-hyperhydration (P=0.44), pre- and post-chamber (P=0.69) and baseline to post-chamber (P=0.14). CONCLUSION: Ice slurry ingestion reduced Tcore prior to simulated driving in the heat. These preliminary data demonstrate potential uses for motor racing athletes. [1] Jay & Morris, 2018, Sports Med; [2] Siegel et al, 2010, Med Sci Sports Exerc; [3] Siegler et al, 2021, Int jour sport nutr and exerc metab;[4] Reid & Lightfoot, 2019, Med Sci Sports Exerc
Read CV Joe PageECSS Paris 2023: CP-PN17