7 DO METABOLIC ADAPTATIONS TO SUBMAXIMAL EXERCISE FOLLOWING SHORT TERM TRAINING OCCUR DURING THE NON-STEADY STATE PHASE?

1993 ◽  
Vol 25 (Supplement) ◽  
pp. S2
Author(s):  
H. J. Green ◽  
J. Cadefau ◽  
R. Cuss?? ◽  
M. Ball-Barnett ◽  
S. Grant ◽  
...  
Keyword(s):  
Steady State ◽  
Submaximal Exercise ◽  
Short Term ◽  
Metabolic Adaptations

Metabolic adaptations to short-term training are expressed early in submaximal exercise

1995 ◽  
Vol 73 (4) ◽  
pp. 474-482 ◽  
Author(s):  
H. J. Green ◽  
M. Ball-Burnett ◽  
G. Jamieson ◽  
J. Cadefau ◽  
R. Cussó
Keyword(s):  
Steady State ◽  
Metabolic Control ◽  
Vastus Lateralis ◽  
Lactate Concentration ◽  
Muscle Metabolism ◽  
Dry Weight ◽  
Submaximal Exercise ◽  
Short Term ◽  
Oxidative Potential ◽  
Metabolic Adaptations

In previous studies we have been able to demonstrate tighter metabolic control of muscle metabolism during prolonged steady-state exercise 5 to 6 days after the initiation of training and well before changes in oxidative potential. To examine whether the metabolic adaptations are manifested during the non-steady-state adjustment to submaximal exercise, 11 male subjects ([Formula: see text] peak, 45 ± 2.4 mL∙kg−1∙min−1, [Formula: see text]) performed 98 min of cycle exercise at 67% of [Formula: see text] peak prior to and following 3 to 4 days of training for 2 h per day. Analysis of lactate concentration (mmol/kg dry weight) in samples rapidly extracted from vastus lateralis indicated reductions (p < 0.05) of 44% at 3 min (42.1 ± 7.1 vs. 23.6 ± 7.7), 29% at 15 min (35.4 ± 6.4 vs. 25.0 ± 6.0), and 32% at 98 min (22.9 ± 6.9 vs. 15.6 ± 3.2) with training. Training also resulted in higher phosphocreatine and lower creatine and Pi values that were not specific to any exercise time point. In addition, [Formula: see text] was not altered either during the non-steady state or during the steady-state phases of exercise. These results suggest that at least part of the tightening of the metabolic control and the apparent reduction in glycogenolysis and glycolysis in response to short-term training occurs during the adjustment phase to steady-state exercise.Key words: training, metabolic control, nonsteady state.

Validation of On-line Respiration Meter and its Applications by Computer Simulation

1992 ◽  
Vol 26 (5-6) ◽  
pp. 1355-1363 ◽  
Author(s):  
C-W. Kim ◽  
H. Spanjers ◽  
A. Klapwijk
Keyword(s):  
Steady State ◽  
Activated Sludge ◽  
Respiration Rate ◽  
Oxygen Demand ◽  
Operating Conditions ◽  
Mass Balances ◽  
Short Term ◽  
Respiration Rates ◽  
On Line ◽  
Made In

An on-line respiration meter is presented to monitor three types of respiration rates of activated sludge and to calculate effluent and influent short term biochemical oxygen demand (BODst) in the continuous activated sludge process. This work is to verify if the calculated BODst is reliable and the assumptions made in the course of developing the proposed procedure were acceptable. A mathematical model and a dynamic simulation program are written for an activated sludge model plant along with the respiration meter based on mass balances of BODst and DO. The simulation results show that the three types of respiration rate reach steady state within 15 minutes under reasonable operating conditions. As long as the respiration rate reaches steady state the proposed procedure calculates the respiration rate that is equal to the simulated. Under constant and dynamic BODst loading, the proposed procedure is capable of calculating the effluent and influent BODst with reasonable accuracy.

scholarly journals Pharmacokinetic Interactions of Maraviroc with Darunavir-Ritonavir, Etravirine, and Etravirine-Darunavir-Ritonavir in Healthy Volunteers: Results of Two Drug Interaction Trials

2011 ◽  
Vol 55 (5) ◽  
pp. 2290-2296 ◽  
Author(s):  
Thomas N. Kakuda ◽  
Samantha Abel ◽  
John Davis ◽  
Julia Hamlin ◽  
Monika Schöller-Gyüre ◽  
...  
Keyword(s):  
Steady State ◽  
Healthy Volunteers ◽  
Potent Inhibitor ◽  
Cytochrome P450 3A ◽  
Short Term ◽  
Two Phase ◽  
Time Curve ◽  
Safety Issues ◽  
Concentration Time ◽  
Crossover Studies

ABSTRACTThe effects of darunavir-ritonavir at 600 and 100 mg twice daily (b.i.d.) alone, 200 mg of etravirine b.i.d. alone, or 600 and 100 mg of darunavir-ritonavir b.i.d. with 200 mg etravirine b.i.d. at steady state on the steady-state pharmacokinetics of maraviroc, and vice versa, in healthy volunteers were investigated in two phase I, randomized, two-period crossover studies. Safety and tolerability were also assessed. Coadministration of 150 mg maraviroc b.i.d. with darunavir-ritonavir increased the area under the plasma concentration-time curve from 0 to 12 h (AUC12) for maraviroc 4.05-fold relative to 150 mg of maraviroc b.i.d. alone. Coadministration of 300 mg maraviroc b.i.d. with etravirine decreased the maraviroc AUC12by 53% relative to 300 mg maraviroc b.i.d. alone. Coadministration of 150 mg maraviroc b.i.d. with etravirine-darunavir-ritonavir increased the maraviroc AUC123.10-fold relative to 150 mg maraviroc b.i.d. alone. Maraviroc did not significantly affect the pharmacokinetics of etravirine, darunavir, or ritonavir. Short-term coadministration of maraviroc with darunavir-ritonavir, etravirine, or both was generally well tolerated, with no safety issues reported in either trial. Maraviroc can be coadministered with darunavir-ritonavir, etravirine, or etravirine-darunavir-ritonavir. Maraviroc should be dosed at 600 mg b.i.d. with etravirine in the absence of a potent inhibitor of cytochrome P450 3A (CYP3A) (i.e., a boosted protease inhibitor) or at 150 mg b.i.d. when coadministered with darunavir-ritonavir with or without etravirine.

scholarly journals High-resistance training and muscle metabolism during prolonged exercise

1999 ◽  
Vol 276 (3) ◽  
pp. E489-E496 ◽  
Author(s):  
C. Goreham ◽  
H. J. Green ◽  
M. Ball-Burnett ◽  
D. Ranney
Keyword(s):  
Resistance Training ◽  
High Resistance ◽  
Metabolic Response ◽  
Muscle Metabolism ◽  
Submaximal Exercise ◽  
Oxidative Potential ◽  
Cross Sectional ◽  
Metabolic Adaptations ◽  
Before And After ◽  
Rate Of Oxygen Consumption

To investigate the hypothesis that changes in muscle submaximal exercise metabolism would occur as a result of fiber hypertrophy, induced by high-resistance training (HRT), active but untrained males (age 20 ± 0.7 yr; mean ± SE) performed lower-limb weight training 3 days/wk for 12 wk using three sets of 6–8 repetitions maximal (RM)/day. Muscle metabolism was examined at different stages of training (4, 7, and 12 wk) using a two-stage continuous cycle test performed at the same absolute power output and duration (56.4 ± 2.9 min) and representing 57 and 72% of pretraining peak aerobic power (V˙o 2 peak). Compared with pretraining, at the end of exercise, HRT resulted in a higher ( P < 0.05) phosphocreatine (PCr; 27.4 ± 6.7 vs. 38.0 ± 1.9 mmol/kg dry wt), a lower lactate (38.9 ± 8.5 vs. 24.4 ± 6.1 mmol/kg dry wt), and a higher ( P < 0.05) glycogen content (132 ± 11 vs. 181 ± 7.5 mmol glucosyl units/kg dry wt). The percent change from rest before and after training was 63 and 50% for PCr, 676 and 410% for lactate, and 60 and 43% for glycogen, respectively. These adaptations, which were observed only at 72%V˙o 2 peak, occurred by 4 wk of training in the case of PCr and glycogen and before any changes in fiber cross-sectional area, capillarization, or oxidative potential. Fiber hypertrophy, observed at 7 and 12 wk of training, failed to potentiate the metabolic response. No effect of HRT was found onV˙o 2 peak with training (41.2 ± 2.9 vs. 41.0 ± 2.1 ml ⋅ kg−1 ⋅ min−1) or on the steady-state, submaximal exercise rate of oxygen consumption. It is concluded that the HRT results in muscle metabolic adaptations that occur independently of fiber hypertrophy.

scholarly journals Impact of Nitrite Therapy on Change in Steady State Submaximal Exercise in Older

2018 ◽  
Vol 50 (5S) ◽  
pp. 35
Author(s):  
Kelly Allsup ◽  
Rachel Eleazu ◽  
Nancy W. Glynn ◽  
Jessica M. Shultz ◽  
James Kostra ◽  
...  
Keyword(s):  
Steady State ◽  
Submaximal Exercise

Reassessment of primed constant-infusion tracer method to measure urea kinetics

1987 ◽  
Vol 252 (4) ◽  
pp. E557-E564 ◽  
Author(s):  
F. Jahoor ◽  
R. R. Wolfe
Keyword(s):  
Steady State ◽  
Constant Infusion ◽  
Dependent Manner ◽  
Tracer Technique ◽  
Tracer Method ◽  
Priming Dose ◽  
Short Term ◽  
Urea Production ◽  
Urea Kinetics ◽  
Dose Dependent

The validity of the primed constant-infusion tracer technique to make short-term measurements of urea production rates (Ra) in humans in a physiological steady state and during disruption of steady state was evaluated. Four subjects received a primed constant infusion (P/I = 560 min) of [13C]urea for 8 h. A plateau in urea enrichment was reached after 2 h and maintained throughout. When [13C]- and [18O]urea were simultaneously infused into four subjects at P/I ratios of 560:1 and 360:1, respectively, both tracers reached plateau enrichment at the same time (2-4 h). The enrichment at plateau was a function of the infusion rate rather than the priming dose, and calculated urea Ra was the same with either prime. In five additional experiments the technique responded acutely to a physiological perturbation (alanine infusion) in a dose-dependent manner. The results confirm that this technique is appropriate for short-term measurements of urea Ra, and the requirement for accuracy in estimating the priming dose is not impractically stringent.

VO2 kinetics of constant-load exercise following bed-rest-induced deconditioning

1984 ◽  
Vol 57 (5) ◽  
pp. 1545-1550 ◽  
Author(s):  
V. A. Convertino ◽  
D. J. Goldwater ◽  
H. Sandler
Keyword(s):  
Steady State ◽  
Supine Position ◽  
Bed Rest ◽  
Constant Load ◽  
Submaximal Exercise ◽  
Delayed Response ◽  
Total Recovery ◽  
Vo2 Kinetics ◽  
O2 Deficit ◽  
Constant Load Exercise

The purpose of this study was to determine the effects of bed-rest-induced deconditioning on changes in O2 uptake (VO2) kinetics, O2 deficit, steady-state VO2, and recovery VO2 during the performance of constant-load exercise. Five male subjects (36–40 yr) underwent 7 days of continuous bed rest (BR) in the head-down (-6 degrees) position. Two days before (pre) and the day after (post) BR each subject performed one submaximal exercise test in the supine and one in the upright position consisting of 5 min of rest, 5 min of cycle ergometer exercise at 700 kg.m/min, and 10 min of recovery from exercise. VO2 was measured continuously in all tests from 2-liter aliquot gas samples collected every 30 s. Following BR steady-state VO2 was unchanged in supine and upright exercise. In the supine position BR did not change total exercise VO2, O2 deficit, or total recovery VO2. However, compared with pre-BR, total exercise VO2 decreased (P less than 0.05) from 7.41 +/- 0.11 to 7.23 +/- 0.17 liters, O2 deficit increased (P less than 0.05) from 1.15 +/- 0.05 to 1.41 +/- 0.07 liters, and total recovery VO2 increased (P less than 0.05) from 5.17 +/- 0.11 to 5.47 +/- 0.17 liters during the post-BR upright test. Despite the ability to attain similar steady-state VO2 within 5 min, bed-rest-induced deconditioning resulted in a reduction of total VO2 capacity and an increase in the O2 deficit during submaximal constant-load exercise. This change in VO2 kinetics is found only with exercise in the upright rather than supine position implicating orthostatic mechanisms in the delayed response to submaximal exercise.

Metabolic adrenergic changes during submaximal exercise and in the recovery period in man

1979 ◽  
Vol 47 (4) ◽  
pp. 701-705 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
M. H. Mayet ◽  
R. Flandrois
Keyword(s):  
Recovery Period ◽  
Submaximal Exercise ◽  
Short Term ◽  
Lipid Mobilization ◽  
Healthy Men ◽  
Muscular Work ◽  
Urinary Levels ◽  
Postexercise Recovery ◽  
Vanilmandelic Acid

The urinary excretion of dihydroxyphenylalanine (DOPA), catecholamines (CA) [dopamine (DA), norepinephrine (NE), and epinephrine (e)], their 3-O-methylated derivatives [3-O-methyldopamine (3-MT), normetanephrine (NMN), and metanephrine (MN)], and their deaminated metabolites [dihydroxyphenylacetic acid (DOPAC) and vanilmandelic acid (VMA)] was studied in six healthy men, at rest during short-term (15 min) or exhaustive submaximal exercise, and in the 2-h postexercise recovery period. During short-term exercise only NE and VMA excretions increased, whereas in postexercise period only DA output was enhanced. Exhaustive muscular work induced a rise in NE and E excretion during the test, and an increase in DA, NE, and NMN urinary levels during postexercise recovery, while the output of deaminated metabolites was unaltered. It is concluded that both release and synthesis of CA are stimulated by submaximal exercise, which induces, in addition to NE, a specific release of DA. A possible role of NE in lipid mobilization during recovery from exhaustive muscular work is evoked. The origin and role of released DA are also discussed.

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