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Key pointsr At the end of an incremental exercise to exhaustion a large functional reserve remains in the muscles to generate power, even at levels far above the power output at which task failure occurs, regardless of the inspiratory O 2 pressure during the incremental exercise.r Exhaustion (task failure) is not due to lactate accumulation and the associated muscle acidification; neither the aerobic energy pathways nor the glycolysis are blocked at exhaustion.r Muscle lactate accumulation may actually facilitate early recovery after exhaustive exercise even under ischaemic conditions. r Although the maximal rate of ATP provision is markedly reduced at task failure, the resynthesis capacity remaining exceeds the rate of ATP consumption, indicating that task failure during an incremental exercise to exhaustion depends more on central than peripheral mechanisms.Abstract To determine the mechanisms causing task failure during incremental exercise to exhaustion (IE), sprint performance (10 s all-out isokinetic) and muscle metabolites were measured before (control) and immediately after IE in normoxia (P IO 2 : 143 mmHg) and hypoxia (P IO 2 : 73 mmHg) in 22 men (22 ± 3 years). After IE, subjects recovered for either 10 or 60 s, with open circulation or bilateral leg occlusion (300 mmHg) in random order. This was followed by a 10 s sprint with open circulation. Post-IE peak power output (W peak ) was higher than the power output reached at exhaustion during IE (P < 0.05). After 10 and 60 s recovery in normoxia, W peak was reduced by 38 ± 9 and 22 ± 10% without occlusion, and 61 ± 8 and 47 ± 10% with occlusion (P < 0.05). Following 10 s occlusion, W peak was 20% higher in hypoxia than normoxia (P < 0.05), despite similar muscle lactate accumulation ([La]) and phosphocreatine and ATP reduction. Sprint performance and anaerobic ATP resynthesis were greater after 60 s compared with 10 s occlusions, despite the higher [La] and [H + ] after 60 s compared with 10 s occlusion recovery (P < 0.05). The mean rate of ATP turnover during the 60 s occlusion was 0.180 ± 0.133 mmol (kg wet wt) −1 s −1 , i.e. equivalent to 32% of leg peak O 2 uptake (the energy expended by the ion pumps). A greater degree of recovery is achieved, however, without occlusion. In conclusion, during incremental exercise task failure is not due to metabolite accumulation or lack of energy resources. Anaerobic metabolism, despite the accumulation of lactate and H + , facilitates early Abbreviations Cr, creatine; d.w., dry weight; F IO2 , inspired oxygen fraction; HR, heart rate; HR peak , peak heart rate; Hyp, hypoxia; IE, incremental exercise to exhaustion; La, lactate; Mb, myoglobin; Nx, normoxia; PCr, phosphocreatine; P ETCO2 , end-tidal CO 2 pressure; P ETO2 , end-tidal O 2 pressure; P IO2 , partial pressure of inspired O 2 ; RER, respiratory exchange ratio; S pO2 , haemoglobin oxygen saturation measured by pulse-oximetry; TOI, tissue oxygenation index;V CO2 , CO 2 production;V CO2peak , peak CO 2 production;V E , minute ventilation;V O2 , O 2 consumpt...

Cerebral blood flow (CBF) is regulated to secure brain O delivery while simultaneously avoiding hyperperfusion; however, both requisites may conflict during sprint exercise. To determine whether brain O delivery or CBF is prioritized, young men performed sprint exercise in normoxia and hypoxia (PO = 73 mmHg). During the sprints, cardiac output increased to ∼22 L min, mean arterial pressure to ∼131 mmHg and peak systolic blood pressure ranged between 200 and 304 mmHg. Middle-cerebral artery velocity (MCAv) increased to peak values (∼16%) after 7.5 s and decreased to pre-exercise values towards the end of the sprint. When the sprints in normoxia were preceded by a reduced PCO, CBF and frontal lobe oxygenation decreased in parallel ( r = 0.93, P < 0.01). In hypoxia, MCAv was increased by 25%, due to a 26% greater vascular conductance, despite 4-6 mmHg lower PaCO in hypoxia than normoxia. This vasodilation fully accounted for the 22 % lower CaO in hypoxia, leading to a similar brain O delivery during the sprints regardless of PO. In conclusion, when a conflict exists between preserving brain O delivery or restraining CBF to avoid potential damage by an elevated perfusion pressure, the priority is given to brain O delivery.

The main aims of this study were to determine the accuracy of the portable metabolic cart K5 by comparison with a stationary metabolic cart (Vyntus CPX), to check on the validity of Vyntus CPX using a butane combustion test, and to assess the reliability of K5 during prolonged walks in the field. For validation, measurements were consecutively performed tests with both devices at rest and during submaximal exercise (bicycling) at low (60 W) and moderate intensities (130–160 W) in 16 volunteers. For the reliability study, 14 subjects were measured two times during prolonged walks (13 km, at 5 km/h), with the K5 set in mixing chamber (Mix) mode. Vyntus measured the stoichiometric RQ of butane combustion with high accuracy (error <1.6%) and precision (CV <0.5%), at VO2 values between 0.788 and 6.395 L/min. At rest and 60 W, there was good agreement between Vyntus and K5 (breath-by-breath, B×B) in VO2, VCO2, RER, and energy expenditure, while in Mix mode the K5 overestimated VO2 by 13.4 and 5.8%, respectively. Compared to Vyntus, at moderate intensity the K5 in B×B mode underestimated VO2, VCO2, and energy expenditure by 6.6, 6.9, and 6.6%, respectively. However, at this intensity there was an excellent agreement between methods in RER and fat oxidation. In Mix mode, K5 overestimated VO2 by 5.8 and 4.8%, at 60 W and the higher intensity, respectively. The K5 had excellent reliability during the field tests. Total energy expenditure per Km was determined with a CV for repeated measurements of 4.5% (CI: 3.2–6.9%) and a concordance correlation coefficient of 0.91, similar to the variability in VO2. This high reproducibility was explained by the low variation of FEO2 measurements, which had a CV of 0.9% (CI: 0.7–1.5%) combined with a slightly greater variability of FECO2, VE, VCO2, and RER. In conclusion, the K5 is an excellent portable metabolic cart which is almost as accurate as a state-of-art stationary metabolic cart, capable of measuring precisely energy expenditure in the field, showing a reliable performance during more than 2 h of continuous work. At high intensities, the mixing-chamber mode is more accurate than the B×B mode.

In vitro and in vivo studies described the myokine IL-15 and its receptor IL-15Rα as anabolic/anti-atrophy agents, however, the protein expression of IL-15Rα has not been measured in human skeletal muscle and data regarding IL-15 expression remain inconclusive. The purpose of the study was to determine serum and skeletal muscle IL-15 and IL-15Rα responses to resistance exercise session and to analyze their association with myofibrillar protein synthesis (MPS). Fourteen participants performed a bilateral leg resistance exercise composed of four sets of leg press and four sets of knee extension at 75% 1RM to task failure. Muscle biopsies were obtained at rest, 0, 4 and 24 hours post-exercise and blood samples at rest, mid-exercise, 0, 0.3, 1, 2, 4 and 24 hours post-exercise. Serum IL-15 was increased by ~5.3-fold immediately post-exercise, while serum IL-15Rα decreased ~75% over 1 hour post-exercise (P<.001). Skeletal muscle IL-15Rα mRNA and protein expression were increased at 4 hours post-exercise by ~2-fold (P<.001) and ~1.3-fold above rest (P=.020), respectively. At 24 hours post-exercise, IL-15 (P=.003) and IL-15Rα mRNAs increased by ~2-fold (P=.002). Myofibrillar fractional synthetic rate between 0-4 hours was associated with IL-15Rα mRNA at rest (r=.662, P=.019), 4 hours (r=.612, P=.029), and 24 hours post-exercise (r=.627, P=.029). Finally, the muscle IL-15Rα protein up-regulation was related to Leg press 1RM (r=.688, P=.003) and total weight lifted (r=.628, P=.009). In conclusion, IL-15/IL-15Rα signaling pathway is activated in skeletal muscle in response to a session of resistance exercise.