Key pointsr Severe acute hypoxia reduces sprint performance. r MuscleV O 2 during sprint exercise in normoxia is not limited by O 2 delivery, O 2 offloading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle of young healthy men.r A large functional reserve in muscle O 2 diffusing capacity exists and remains available at exhaustion during exercise in normoxia; this functional reserve is recruited during exercise in hypoxia.r During whole-body incremental exercise to exhaustion in severe hypoxia, legV O 2 is primarily dependent on convective O 2 delivery and less limited by diffusion constraints than previously thought.r The kinetics of O 2 offloading from haemoglobin does not limitV O 2 peak in hypoxia. r Our results indicate that the limitation toV O 2 during short sprints resides in mechanisms regulating mitochondrial respiration.Abstract To determine the contribution of convective and diffusive limitations toV O 2 peak 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 IO 2 : 143 mmHg) and hypoxia (Hyp, P IO 2 : 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6-7% before both WgTs to left-shift the oxyhaemoglobin dissociation curve. Leġ V O 2 was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O 2 diffusing capacity (D MO 2 ) was calculated. In the WgT mean power output, leg BF, leg O 2 delivery and legV O 2 were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05); however, peak WgT D MO 2 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 aO 2 (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary P O 2 (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, D MO 2 and legV O 2 were 12 and 14% higher, respectively, during WgT than IE in Hyp (both P < 0.05). D MO 2 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 O 2 transfer in both Nx and Hyp. In conclusion, muscleV O 2 during sprint exercise is not limited by O 2 delivery, O 2 offloading from haemoglobin or structure-dependent diffusion constraints in

Background No consensus exists on how to average data to optimize trueV˙O2max assessment. Although the trueV˙O2max 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 trueV˙O2max. Aims To determine the effect that the number of breaths or seconds included in the averaging block has on the trueV˙O2max value and its reproducibility and to develop correction equations to standardize trueV˙O2max 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 trueV˙O2max decayed from 6 to 60 breath averages by 10% in low fit (trueV˙O2max < 40 mL kg−1 min−1) and 6.7% in trained subjects. The trueV˙O2max 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 trueV˙O2max (R2 > 0.99, P < 0.001), and specific equations were developed to standardize trueV˙O2max 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 trueV˙O2max 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.

The loss of fat-free mass (FFM) caused by very-low-calorie diets (VLCD) can be attenuated by exercise. The aim of this study was to determine the role played by exercise and dietary protein content in preserving the lean mass and performance of exercised and non-exercised muscles, during a short period of extreme energy deficit (~23 MJ deficit/day). Fifteen overweight men underwent three consecutive experimental phases: baseline assessment (PRE), followed by 4 days of caloric restriction and exercise (CRE) and then 3 days on a control diet combined with reduced exercise (CD). During CRE, the participants ingested a VLCD and performed 45 min of one-arm cranking followed by 8 h walking each day. The VLCD consisted of 0.8 g/kg body weight/day of either whey protein (PRO, n = 8) or sucrose (SU, n = 7). FFM was reduced after CRE (P < 0.001), with the legs and the exercised arm losing proportionally less FFM than the control arm [57% (P < 0.05) and 29% (P = 0.05), respectively]. Performance during leg pedaling, as reflected by the peak oxygen uptake and power output (Wpeak), was reduced after CRE by 15 and 12%, respectively (P < 0.05), and recovered only partially after CD. The deterioration of cycling performance was more pronounced in the whey protein than sucrose group (P < 0.05). Wpeak during arm cranking was unchanged in the control arm, but improved in the contralateral arm by arm cranking. There was a linear relationship between the reduction in whole-body FFM between PRE and CRE and the changes in the cortisol/free testosterone ratio (C/FT), serum isoleucine, leucine, tryptophan, valine, BCAA, and EAA (r = −0.54 to −0.71, respectively, P < 0.05). C/FT tended to be higher in the PRO than the SU group following CRE (P = 0.06). In conclusion, concomitant low-intensity exercise such as walking or arm cranking even during an extreme energy deficit results in remarkable preservation of lean mass. The intake of proteins alone may be associated with greater cortisol/free testosterone ratio and is not better than the ingestion of only carbohydrates for preserving FFM and muscle performance in interventions of short duration.

Torres-Peralta, Rafael, José Losa-Reyna, Miriam González-Izal, Ismael Perez-Suarez, Jaime Calle-Herrero, Mikel Izquierdo, and José A.L. Calbet. Muscle activation during exercise in severe acute hypoxia: Role of absolute and relative intensity. High Alt Med Biol 15:472-482, 2014.-The aim of this study was to determine the influence of severe acute hypoxia on muscle activation during whole body dynamic exercise. Eleven young men performed four incremental cycle ergometer tests to exhaustion breathing normoxic (F I o 2 = 0.21, two tests) or hypoxic gas (F I o 2 = 0.108, two tests). Surface electromyography (EMG) activities of rectus femoris (RF), vastus medialis (VL), vastus lateralis (VL), and biceps femoris (BF) were recorded. The two normoxic and the two hypoxic tests were averaged to reduce EMG variability. Peak Vo 2 was 34% lower in hypoxia than in normoxia ( p < 0.05). The EMG root mean square (RMS) increased with exercise intensity in all muscles ( p < 0.05), with greater effect in hypoxia than in normoxia in the RF and VM ( p < 0.05), and a similar trend in VL ( p = 0.10). At the same relative intensity, the RMS was greater in normoxia than in hypoxia in RF, VL, and BF ( p < 0.05), with a similar trend in VM ( p = 0.08). Median frequency increased with exercise intensity ( p < 0.05), and was higher in hypoxia than in normoxia in VL ( p < 0.05). Muscle contraction burst duration increased with exercise intensity in VM and VL ( p < 0.05), without clear effects of F I o 2 . No significant F I o 2 effects on frequency domain indices were observed when compared at the same relative intensity. In conclusion, muscle activation during whole body exercise increases almost linearly with exercise intensity, following a muscle-specific pattern, which is adjusted depending on the F I o 2 and the relative intensity of exercise. Both VL and VM are increasingly involved in power output generation with the increase of intensity and the reduction in F I o 2 .

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·day) 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 ( = 8) or sucrose ( = 7; 0.8 g·kg body wt·day). 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-TyrOBR, phospho-TyrOBR, JAK2, and phospho-TyrJAK2 protein expression were increased in all muscles, whereas STAT3 and phospho-TyrSTAT3 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 ( < 0.05). Suppressor of cytokine signaling 3 (SOCS3) tended to increase in the legs and decrease in the arm muscles (ANOVA interaction: < 0.05). Myosin heavy chain I isoform was associated with OBR protein expression ( = -0.75), phospho-TyrOBR ( = 0.88), and phospho-TyrSTAT3/STAT3 ( = 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. 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.