scholarly journals Prior heavy exercise eliminates slow component and reduces efficiency during submaximal exercise in humans

2005 ◽  
Vol 564 (3) ◽  
pp. 765-773 ◽  
Author(s):  
K. Sahlin ◽  
J. B. Sørensen ◽  
L. B. Gladden ◽  
H. B. Rossiter ◽  
P. K. Pedersen
Keyword(s):  
Slow Component ◽  
Submaximal Exercise ◽  
Heavy Exercise ◽  
Exercise In Humans

Leg glucose uptake during maximal dynamic exercise in humans

1986 ◽  
Vol 251 (1) ◽  
pp. E65-E70 ◽  
Author(s):  
A. Katz ◽  
S. Broberg ◽  
K. Sahlin ◽  
J. Wahren
Keyword(s):  
Glucose Uptake ◽  
Glucose Utilization ◽  
Energy State ◽  
Submaximal Exercise ◽  
Dynamic Exercise ◽  
Heavy Exercise ◽  
The Mean ◽  
Muscle Biopsies ◽  
Exercise In Humans ◽  
Intracellular Glucose

Leg glucose uptake (LGU) during submaximal (50% maximal O2 uptake) and maximal dynamic exercise (97%) has been quantified from the product of the leg blood flow and the arterial minus femoral venous glucose concentration. Muscle biopsies were also obtained. During 15 min of submaximal exercise the mean LGU values ranged from 1.07 to 1.25 mmol/min, which demonstrates that LGU was stable under this condition. In contrast, during maximal exercise LGU increased continuously, reaching 2.38 +/- 0.22, 2.95 +/- 0.32, and 3.82 +/- 0.34 mmol/min after 2, 4, and 5.2 min (fatigue), respectively. The mean LGU was negatively related to the mean muscle phosphocreatine content (r = -1.00;P less than 0.01). Intracellular glucose-6-phosphate (G-6-P) and glucose were very low at rest and did not change significantly during submaximal exercise (P greater than 0.05). However, at fatigue G-6-P and glucose increased substantially and were both 8.5 mmol/kg dry muscle (P less than 0.001). These findings demonstrate that during heavy exercise glucose accumulates in the cell probably due to hexokinase inhibition by G-6-P, and thus the rate of glucose utilization appears to be lower than the rate of glucose uptake. It is suggested that 1) LGU during short-term exercise is dependent on the energy state of the muscle and 2) LGU is equal to leg glucose utilization during submaximal exercise but is in excess of utilization during heavy exercise.

scholarly journals The slow component of O 2 uptake is not accompanied by changes in muscle EMG during repeated bouts of heavy exercise in humans

2001 ◽  
Vol 531 (1) ◽  
pp. 245-256 ◽  
Author(s):  
Barry W. Scheuermann ◽  
Brian D. Hoelting ◽  
M. Larry Noble ◽  
Thomas J. Barstow
Keyword(s):  
Slow Component ◽  
Heavy Exercise ◽  
Exercise In Humans

scholarly journals Time required for the restoration of normal heavy exercise V̇o2 kinetics following prior heavy exercise

2006 ◽  
Vol 101 (5) ◽  
pp. 1320-1327 ◽  
Author(s):  
Mark Burnley ◽  
Jonathan H. Doust ◽  
Andrew M. Jones
Keyword(s):  
Blood Lactate ◽  
Priming Effect ◽  
Slow Component ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Heavy Exercise ◽  
Cycle Exercise ◽  
V̇o2 Kinetics ◽  
Time Required ◽  
Male Subjects

Prior heavy exercise markedly alters the O2 uptake (V̇o2) response to subsequent heavy exercise. However, the time required for V̇o2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the V̇o2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second V̇o2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary V̇o2 time constant (from 25.9 ± 4.7 s to 23.9 ± 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary V̇o2 amplitude (from 2.42 ± 0.39 to 2.53 ± 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the V̇o2 slow component (from 0.44 ± 0.13 to 0.21 ± 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20–45 min, but not after 60 min, of recovery. The increase in the primary V̇o2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 ± 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20–60 min of recovery. The priming effect of prior heavy exercise on the V̇o2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.

Effects of glycogen depletion and work load on postexercise O2 consumption and blood lactate

1979 ◽  
Vol 47 (3) ◽  
pp. 514-521 ◽  
Author(s):  
S. S. Segal ◽  
G. A. Brooks
Keyword(s):  
Blood Lactate ◽  
Slow Component ◽  
Minute Ventilation ◽  
Co2 Flux ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Co2 Production ◽  
O2 Consumption ◽  
Glycogen Depletion ◽  
Heavy Exercise

To study a possible relationship between blood lactate and O2 consumption (VO2) after exercise, 11 male subjects exercised on a bicycle ergometer at moderate and heavy work loads in both normal glycogen and glycogen-depleted states. At rest, glycogen depletion resulted in significantly lowered blood glucose and lactate concentrations, CO2 production (VCO2), respiratory exchange ratio (R), and minute ventilation (VE). With the exception of glucose, these variables changed more in response to heavy exercise (HE: 2 min at a mean of 1,750 kg.m/min) than to moderate exercise (ME: 2 min at a mean of 1,000 kg.m/min). At either work load, VCO2, R, and lactate showed consistently greater responses in the normal glycogen state. The slope of the initial component of the postexercise VO2 curve was unaffected by either work load or lactate. Although the slope of the slow component of the postexercise VO2 curve became significantly more negative after HE, it was unaffected by the level of lactate. These results are inconsistent with the hypothesis of a “lactacid O2 debt.” Exercise intensity was the predominant factor influencing the magnitude and kinetics of postexercise VO2. Glycogen depletion resulted in lower VCO2, R, and blood lactate, but higher VE during heavy exercise. The results suggest that factors, in addition to CO2 flux to the lungs, influence VE during exercise.

Pulmonary oxygen uptake kinetics

2017 ◽  
Author(s):  
Alan R Barker ◽  
Neil Armstrong
Keyword(s):  
Oxygen Uptake ◽  
Oxidative Phosphorylation ◽  
Children And Adolescents ◽  
Phase Ii ◽  
Slow Component ◽  
Moderate Intensity ◽  
Heavy Exercise ◽  
Moderate Intensity Exercise ◽  
Pulmonary Oxygen Uptake ◽  
Age Related

The pulmonary oxygen uptake (pV̇O2) kinetic response to exercise provides valuable non-invasive insight into the control of oxidative phosphorylation and determinants of exercise tolerance in children and adolescents. Few methodologically robust studies have investigated pV̇O2 kinetics in children and adolescents, but age- and sex-related differences have been identified. There is a clear age-related slowing of phase II pV̇O2 kinetics during heavy and very heavy exercise, with a trend showing during moderate intensity exercise. During heavy and very heavy exercise the oxygen cost is higher for phase II and the pV̇O2 component is truncated in children. Sex-related differences occur during heavy, but not moderate, intensity exercise, with boys having faster phase II pV̇O2 kinetics and a smaller pV̇O2 slow component compared to girls. The mechanisms underlying these differences are likely related to changes in phosphate feedback controllers of oxidative phosphorylation, muscle oxygen delivery, and/or muscle fibre recruitment strategies.

Comparison of oxygen uptake kinetics during knee extension and cycle exercise

2005 ◽  
Vol 288 (1) ◽  
pp. R212-R220 ◽  
Author(s):  
Shunsaku Koga ◽  
David C. Poole ◽  
Tomoyuki Shiojiri ◽  
Narihiko Kondo ◽  
Yoshiyuki Fukuba ◽  
...  
Keyword(s):  
Blood Flow ◽  
Time Constant ◽  
Phase Ii ◽  
Slow Component ◽  
Muscle Blood Flow ◽  
Knee Extension ◽  
Primary Component ◽  
Heavy Exercise ◽  
Muscle Energetics ◽  
Kinetics Of

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 (pV̇o2) kinetics and 2) to characterize the muscle blood flow, muscle V̇o2 (mV̇o2), and pV̇o2 kinetics during KE to investigate the rate-limiting factor(s) of pV̇o2 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 pV̇o2 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 mV̇o2 at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pV̇o2 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 mV̇o2 during heavy KE [25.8 ± 9.0 s (SD)] was not significantly different from that of the phase II pV̇o2. Moreover, the slow component of pV̇o2 evident for the heavy KE reflected the gradual increase in mV̇o2. The initial LBF kinetics after onset of KE were significantly faster than the phase II pV̇o2 kinetics (moderate: time constant LBF = 8.0 ± 3.5 s, pV̇o2 = 32.7 ± 5.6 s, P < 0.05; heavy: LBF = 9.7 ± 2.0 s, pV̇o2 = 29.9 ± 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pV̇o2. 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 pV̇o2, consistent with an intramuscular limitation to V̇o2 kinetics, i.e., a microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia.

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