TY - JOUR
T1 - Elevated baseline work rate slows pulmonary oxygen uptake kinetics and decreases critical power during upright cycle exercise
AU - Goulding, R.P.
AU - Roche, D.M.
AU - Marwood, S.
PY - 2018/7/1
Y1 - 2018/7/1
N2 - © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.Critical power is a fundamental parameter defining high-intensity exercise tolerance, and is related to the phase II time constant of pulmonary oxygen uptake kinetics ((Formula presented.)). Whether this relationship is causative is presently unclear. This study determined the impact of raised baseline work rate, which increases (Formula presented.), on critical power during upright cycle exercise. Critical power was determined via four constant-power exercise tests to exhaustion in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a baseline work rate of 90% of the gas exchange threshold (M→S). During these exercise transitions, (Formula presented.) and the time constant of muscle deoxyhemoglobin kinetics (τ[HHb + Mb]) (the latter via near-infrared spectroscopy) were determined. In M→S, critical power was lower (M→S = 203 ± 44 W vs. U→S = 213 ± 45 W, P = 0.011) and (Formula presented.) was greater (M→S = 51 ± 14 sec vs. U→S = 34 ± 16 sec, P = 0.002) when compared with U→S. Additionally, τ[HHb + Mb] was greater in M→S compared with U→S (M→S = 28 ± 7 sec vs. U→S = 14 ± 7 sec, P = 0.007). The increase in (Formula presented.) and concomitant reduction in critical power in M→S compared with U→S suggests a causal relationship between these two parameters. However, that τ[HHb + Mb] was greater in M→S exculpates reduced oxygen availability as being a confounding factor. These data therefore provide the first experimental evidence that (Formula presented.) is an independent determinant of critical power. Keywords critical power, exercise tolerance, oxygen uptake kinetics, power-duration relationship, muscle deoxyhemoglobin kinetics, work-to-work exercise.
AB - © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.Critical power is a fundamental parameter defining high-intensity exercise tolerance, and is related to the phase II time constant of pulmonary oxygen uptake kinetics ((Formula presented.)). Whether this relationship is causative is presently unclear. This study determined the impact of raised baseline work rate, which increases (Formula presented.), on critical power during upright cycle exercise. Critical power was determined via four constant-power exercise tests to exhaustion in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a baseline work rate of 90% of the gas exchange threshold (M→S). During these exercise transitions, (Formula presented.) and the time constant of muscle deoxyhemoglobin kinetics (τ[HHb + Mb]) (the latter via near-infrared spectroscopy) were determined. In M→S, critical power was lower (M→S = 203 ± 44 W vs. U→S = 213 ± 45 W, P = 0.011) and (Formula presented.) was greater (M→S = 51 ± 14 sec vs. U→S = 34 ± 16 sec, P = 0.002) when compared with U→S. Additionally, τ[HHb + Mb] was greater in M→S compared with U→S (M→S = 28 ± 7 sec vs. U→S = 14 ± 7 sec, P = 0.007). The increase in (Formula presented.) and concomitant reduction in critical power in M→S compared with U→S suggests a causal relationship between these two parameters. However, that τ[HHb + Mb] was greater in M→S exculpates reduced oxygen availability as being a confounding factor. These data therefore provide the first experimental evidence that (Formula presented.) is an independent determinant of critical power. Keywords critical power, exercise tolerance, oxygen uptake kinetics, power-duration relationship, muscle deoxyhemoglobin kinetics, work-to-work exercise.
U2 - 10.14814/phy2.13802
DO - 10.14814/phy2.13802
M3 - Article
SN - 2051-817X
VL - 6
JO - Physiological Reports
JF - Physiological Reports
IS - 14
M1 - e13802
ER -