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Limitations to oxygen transport and utilization during sprint exercise in humans: evidence for a functional reserve in muscle O 2 diffusing capacity
Author(s) -
Calbet José A. L.,
LosaReyna José,
TorresPeralta Rafael,
Rasmussen Peter,
PonceGonzález Jesús Gustavo,
Sheel A. William,
la CalleHerrero Jaime,
GuadalupeGrau Amelia,
MoralesAlamo David,
Fuentes Teresa,
RodríguezGarcía Lorena,
Siebenmann Christoph,
Boushel Robert,
Lundby Carsten
Publication year - 2015
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp270408
Subject(s) - chemistry , oxygen , perfusion , vo2 max , oxygen transport , sprint , blood flow , hemodynamics , medicine , heart rate , blood pressure , physical therapy , organic chemistry
Key points Severe acute hypoxia reduces sprint performance. MuscleV ̇ O 2during 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. 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. During whole‐body incremental exercise to exhaustion in severe hypoxia, legV ̇ O 2is primarily dependent on convective O 2 delivery and less limited by diffusion constraints than previously thought. The kinetics of O 2 offloading from haemoglobin does not limitV ̇O 2 peakin hypoxia. Our results indicate that the limitation toV ̇ O 2during short sprints resides in mechanisms regulating mitochondrial respiration.Abstract To determine the contribution of convective and diffusive limitations toV ̇O 2 peakduring 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 I O 2: 143 mmHg) and hypoxia (Hyp, P I O 2: 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6–7% before both WgTs to left‐shift the oxyhaemoglobin dissociation curve. LegV ̇ O 2was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O 2 diffusing capacity ( D M O 2) was calculated. In the WgT mean power output, leg BF, leg O 2 delivery and legV ̇ O 2were 7, 5, 28 and 23% lower in Hyp than Nx ( P < 0.05); however, peak WgT D M O 2was 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 a O 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 M O 2and legV ̇ O 2were 12 and 14% higher, respectively, during WgT than IE in Hyp (both P < 0.05). D M O 2was 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 2during sprint exercise is not limited by O 2 delivery, O 2 offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O 2 diffusing capacity.