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Limitations to systemic and locomotor limb muscle oxygen delivery and uptake during maximal exercise in humans
Author(s) -
Mortensen Stefan P.,
Dawson Ellen A.,
Yoshiga Chie C.,
Dalsgaard Mads K.,
Damsgaard Rasmus,
Secher Niels H.,
GonzálezAlonso José
Publication year - 2005
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/jphysiol.2005.086025
Subject(s) - hemodynamics , oxygen delivery , heart rate , cardiology , stroke volume , medicine , blood flow , cycling , cardiac output , vo2 max , vascular resistance , anesthesia , blood pressure , chemistry , oxygen , organic chemistry , archaeology , history
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 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 during incremental cycling and knee‐extensor exercise in male subjects ( n = 10). During incremental cycling, cardiac output 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 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 per unit of work despite increasing O 2 extraction. When blood flow increased linearly during one‐legged knee‐extensor exercise, per unit of work was unaltered on fatigue. During constant cycling, , SV, systemic O 2 delivery and reached maximal values within ∼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 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.