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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...

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