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To assess how altitude training impacts force-velocity-power (F-V-P) profiling and muscular power and anaerobic capacity in elite badminton players in reference to intra- and inter-individual sex-based variability. Following a quasi-experimental design, 14 players (6 females, 8 males) from the French national badminton singles and doubles teams performed a 3-week 'living high-training high' camp at natural altitude (2320 m). F-V-P profile and Wingate anaerobic test were assessed Pre- and Post-intervention, using ANOVA repeated measures conventional statistics, with further estimation statistics to show the magnitude of the testing condition and visualize intra- and inter-individual responses. No significant interaction nor time effect (Pre- vs . Post-) was observed for any variables (all p  > 0.05), but a significant sex effect was observed for maximal theoretical velocity ( p  < 0.01), relative maximal theoretical power (P maxrel ) ( p  = 0.02) and relative F-V-P profile and for peak and mean power outputs (both p  < 0.001) during Wingate test. Pre-to-Post changes (from -11.0% to + 14.4%) did not significantly differ between sexes, except for P maxrel ( p  < 0.05) in favor of female athletes (+10.2% vs . -4.3% for male athletes). Hedge's g effect sizes (male minus female) revealed moderate and large effects for F-V-P profiling-derived variables. Mean conventional statistics did not reveal significant effect of altitude training, mainly due to high intra- and inter-variability across F-V-P profiling-derived variables and Wingate test. Substantial sex-based difference contributes to this variability, emphasizing the importance of individualized approach to enhance participant responsiveness to altitude training.

Background: No consensus exists on how to average data to optimize V ˙ O 2max assessment. Although the V ˙ O 2max value is reduced with larger averaging blocks, no mathematical procedure is available to account for the effect of the length of the averaging block on V ˙ O 2max. AIMS: To determine the effect that the number of breaths or seconds included in the averaging block has on the V ˙ O 2max value and its reproducibility and to develop correction equations to standardize V ˙ O 2max values obtained with different averaging strategies., Methods: Eighty-four subjects performed duplicate incremental tests to exhaustion (IE) in the cycle ergometer and/or treadmill using two metabolic carts (Vyntus and Vmax N29). Rolling breath averages and fixed time averages were calculated from breath-by-breath data from 6 to 60 breaths or seconds., Results: V ˙ O 2max decayed from 6 to 60 breath averages by 10% in low fit ( V ˙ O 2max  < 40 mL kg -1  min -1 ) and 6.7% in trained subjects. The V ˙ O 2max averaged from a similar number of breaths or seconds was highly concordant (CCC > 0.97). There was a linear-log relationship between the number of breaths or seconds in the averaging block and V ˙ O 2max (R 2  > 0.99, P < 0.001), and specific equations were developed to standardize V ˙ O 2max values to a fixed number of breaths or seconds. Reproducibility was higher in trained than low-fit subjects and not influenced by the averaging strategy, exercise mode, maximal respiratory rate, or IE protocol., Conclusions: The V ˙ O 2max decreases following a linear-log function with the number of breaths or seconds included in the averaging block and can be corrected with specific equations as those developed here., (© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

In obesity, leptin receptors (OBR) and leptin signaling in skeletal muscle are downregulated. To determine whether OBR and leptin signaling are upregulated with a severe energy deficit, 15 overweight men were assessed before the intervention (PRE), after 4 days of caloric restriction (3.2 kcal·kg body wt -1 ·day -1 ) in combination with prolonged exercise (CRE; 8 h walking + 45 min single-arm cranking/day) to induce an energy deficit of ~5,500 kcal/day, and following 3 days of control diet (isoenergetic) and reduced exercise (CD). During CRE, the diet consisted solely of whey protein ( n = 8) or sucrose ( n = 7; 0.8 g·kg body wt -1 ·day -1 ). Muscle biopsies were obtained from the exercised and the nonexercised deltoid muscles and from the vastus lateralis. From PRE to CRE, serum glucose, insulin, and leptin were reduced. OBR expression was augmented in all examined muscles associated with increased maximal fat oxidation. Compared with PRE, after CD, phospho-Tyr 1141 OBR, phospho-Tyr 985 OBR, JAK2, and phospho-Tyr 1007/1008 JAK2 protein expression were increased in all muscles, whereas STAT3 and phospho-Tyr 705 STAT3 were increased only in the arms. The expression of protein tyrosine phosphatase 1B (PTP1B) in skeletal muscle was increased by 18 and 45% after CRE and CD, respectively ( P < 0.05). Suppressor of cytokine signaling 3 (SOCS3) tended to increase in the legs and decrease in the arm muscles (ANOVA interaction: P < 0.05). Myosin heavy chain I isoform was associated with OBR protein expression ( r  = -0.75), phospho-Tyr 985 OBR ( r  = 0.88), and phospho-Tyr 705 STAT3/STAT3 ( r = 0.74). In summary, despite increased PTP1B expression, skeletal muscle OBR and signaling are upregulated by a severe energy deficit with greater response in the arm than in the legs likely due to SOCS3 upregulation in the leg muscles. NEW & NOTEWORTHY This study shows that the skeletal muscle leptin receptors and their corresponding signaling cascade are upregulated in response to a severe energy deficit, contributing to increase maximal fat oxidation. The responses are more prominent in the arm muscles than in the legs but partly blunted by whey protein ingestion and high volume of exercise. This occurs despite an increase of protein tyrosine phosphatase 1B protein expression, a known inhibitor of insulin and leptin signaling., (Copyright © 2017 the American Physiological Society.)

To determine the contribution of convective and diffusive limitations to V̇(O2peak) during exercise in humans, oxygen transport and haemodynamics were measured in 11 men (22 ± 2 years) during incremental (IE) and 30 s all-out cycling sprints (Wingate test, WgT), in normoxia (Nx, P(IO2): 143 mmHg) and hypoxia (Hyp, P(IO2): 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6-7% before both WgTs to left-shift the oxyhaemoglobin dissociation curve. Leg V̇(O2) was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O2 diffusing capacity (D(MO2)) was calculated. In the WgT mean power output, leg BF, leg O2 delivery and leg V̇(O2) were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05); however, peak WgT D(MO2) was higher in Hyp (51.5 ± 9.7) than Nx (20.5 ± 3.0 ml min(-1) mmHg(-1), P < 0.05). Despite a similar P(aO2) (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary P(O2) (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, D(MO2) and leg V̇(O2) were 12 and 14% higher, respectively, during WgT than IE in Hyp (both P < 0.05). D(MO2) was insensitive to COHb (COHb: 0.7 vs. 7%, in IE Hyp and WgT Hyp). At exhaustion, the Y equilibration index was well above 1.0 in both conditions, reflecting greater convective than diffusive limitation to the O2 transfer in both Nx and Hyp. In conclusion, muscle V̇(O2) during sprint exercise is not limited by O2 delivery, O2 offloading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O2 diffusing capacity., (© 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.)