4.6 Article

Limitations to systemic and locomotor limb muscle oxygen delivery and uptake during maximal exercise in humans

Journal

JOURNAL OF PHYSIOLOGY-LONDON
Volume 566, Issue 1, Pages 273-285

Publisher

WILEY
DOI: 10.1113/jphysiol.2005.086025

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Reductions in systemic and locomotor limb muscle blood flow and O-2 delivery limit aerobic capacity in humans. To examine whether O-2 delivery limits both aerobic power and capacity, we first measured systemic haemodynamics, O-2 transport and O-2 uptake (<(V)over dot >(O2) during incremental and constant (372 +/- 11 W, 85% of peak power; mean +/- S.E.M.) cycling exercise to exhaustion (n = 8) and then measured systemic and leg haemodynamics and <(V)over dot > (O2) during incremental cycling and knee-extensor exercise in male subjects (n = 10). During incremental cycling, cardiac output <(Q)over dot > and systemic O-2 delivery increased linearly to 80% of peak power (r(2) = 0.998, P < 0.001) and then plateaued in parallel to a decline in stroke volume (SV) and an increase in central venous and mean arterial pressures (P < 0.05). In contrast, heart rate and <(V)over dot >(O2), increased linearly until exhaustion (r(2) = 0.993; P < 0.001) accompanying a rise in systemic O-2 extraction to 84 +/- 2%. In the exercising legs, blood flow and O-2 delivery levelled off at 73-88% of peak power, blunting leg <(V)over dot >(O2) per unit of work despite increasing 02 extraction. When blood flow increased linearly during one-legged knee-extensor exercise,<(V)over dot >(O2) per unit of work was unaltered on fatigue. During constant cycling, <(Q)over dot >, SV, systemic O-2 delivery and <(V)over dot >(O2) reached maximal values within similar to 5 min, but dropped before exhaustion (P < 0.05) despite increasing or stable central venous and mean arterial pressures. In both types of maximal cycling, the impaired systemic O-2 delivery was due to the decline or plateau in <(Q)over dot > because arterial O-2 content continued to increase. These results indicate that an inability of the circulatory system to sustain a linear increase in O-2 delivery to the locomotor muscles restrains aerobic power. The similar impairment in SV and O-2 delivery during incremental and constant load cycling provides evidence for a central limitation to aerobic power and capacity in humans.

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