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Am J Physiol Regul Integr Comp Physiol 288: R212-R220, 2005. First published August 26, 2004; doi:10.1152/ajpregu.00147.2004
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ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Comparison of oxygen uptake kinetics during knee extension and cycle exercise

Shunsaku Koga,1 David C. Poole,2 Tomoyuki Shiojiri,3 Narihiko Kondo,4 Yoshiyuki Fukuba,5 Akira Miura,5 and Thomas J. Barstow2

1Applied Physiology Laboratory, Kobe Design University, Kobe; 3Yokohama City University, Yokohama; 4Kobe University, Kobe; 5Hiroshima Women's University, Hiroshima, Japan; and 2Department of Kinesiology, Kansas State University, Manhattan, Kansas

Submitted 8 March 2004 ; accepted in final form 18 August 2004

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O2 uptake (pO2) kinetics and 2) to characterize the muscle blood flow, muscle O2 (mO2), and pO2 kinetics during KE to investigate the rate-limiting factor(s) of pO2 on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pO2 during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mO2 at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pO2 for both moderate and heavy exercise was higher during KE (~12 ml·W–1·min–1) compared with CE (~10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mO2 during heavy KE [25.8 ± 9.0 s (SD)] was not significantly different from that of the phase II pO2. Moreover, the slow component of pO2 evident for the heavy KE reflected the gradual increase in mO2. The initial LBF kinetics after onset of KE were significantly faster than the phase II pO2 kinetics (moderate: time constant LBF = 8.0 ± 3.5 s, pO2 = 32.7 ± 5.6 s, P < 0.05; heavy: LBF = 9.7 ± 2.0 s, pO2 = 29.9 ± 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pO2. These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pO2, consistent with an intramuscular limitation to O2 kinetics, i.e., a microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia.

pulmonary oxygen uptake kinetics; muscle oxygen consumption; muscle blood flow


Address for reprint requests and other correspondence: S. Koga, Applied Physiology Laboratory, Kobe Design Univ., 8-1-1 Gakuennishi-machi, Nishi-ku, Kobe 651-2196, Japan (E-mail: s-koga{at}kobe-du.ac.jp)




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