Muscle metabolic responses during 16 hours of intermittent heavy exercise

2007 ◽  
Vol 85 (6) ◽  
pp. 634-645 ◽  
Author(s):  
H.J. Green ◽  
T.A. Duhamel ◽  
G.P. Holloway ◽  
J. Moule ◽  
J. Ouyang ◽  
...  

The alterations in muscle metabolism were investigated in response to repeated sessions of heavy intermittent exercise performed over 16 h. Tissue samples were extracted from the vastus lateralis muscle before (B) and after (A) 6 min of cycling at approximately 91% peak aerobic power at repetitions one (R1), two (R2), nine (R9), and sixteen (R16) in 13 untrained volunteers (peak aerobic power = 44.3 ± 0.66 mL·kg–1·min–1, mean ± SE). Metabolite content (mmol·(kg dry mass)–1) in homogenates at R1 indicated decreases (p < 0.05) in ATP (21.9 ± 0.62 vs. 17.7 ± 0.68) and phosphocreatine (80.3 ± 2.0 vs. 8.56 ± 1.5) and increases (p < 0.05) in inosine monophosphate (IMP, 0.077 ± 0.12 vs. 3.63 ± 0.85) and lactate (3.80 ± 0.57 vs. 84.6 ± 10.3). The content (µmol·(kg dry mass)–1) of calculated free ADP ([ADPf], 86.4 ± 5.5 vs. 1014 ± 237) and free AMP ([AMPf], 0.32 ± 0.03 vs. 78.4 ± 31) also increased (p < 0.05). No differences were observed between R1 and R2. By R9 and continuing to R16, pronounced reductions (p < 0.05) at A were observed in IMP (72.2%), [ADPf] (58.7%), [AMPf] (85.5%), and lactate (41.3%). The 16-hour protocol resulted in an 89.7% depletion (p < 0.05) of muscle glycogen. Repetition-dependent increases were also observed in oxygen consumption during exercise. It is concluded that repetitive heavy exercise results in less of a disturbance in phosphorylation potential, possibly as a result of increased mitochondrial respiration during the rest-to-work non-steady-state transition.

1996 ◽  
Vol 21 (4) ◽  
pp. 271-284 ◽  
Author(s):  
Paula S. Wendling ◽  
Sandra J. Peters ◽  
Lawrence L. Spriet ◽  
George J. F. Heigenhauser

The role of physiological elevations of plasma epinephrine concentration on muscle glycogenolysis during prolonged exercise was investigated. Eight healthy volunteers cycled for 90 min at 65% VO2max on two occasions; once with an infusion of epinephrine (EPI) and once without (control). Biopsy samples were taken from the vastus lateralis muscle both prior to and following exercise for the analysis of muscle glycogen. EPI infusion significantly elevated venous plasma EPI ~2.5-fold over control values throughout exercise (90 min: 5.78 ± 0.95 vs. 2.35 ± 0.49 nM). EPI infusion did not significantly alter net glycogenolysis as compared to control (310.0 ± 30.8 vs. 299.5 ± 41.1 mmol glucosyl units/kg dry mass). Venous concentrations of plasma FFA and whole blood glycerol were unaffected by EPI infusion. Whole blood glucose was significantly elevated during EPI infusion at 10, 30, 60 and 90 min of exercise compared to control values. Whole blood lactate was elevated to a greater extent during EPI infusion as compared to control at 10, 30, and 60 min of exercise. In conclusion, EPI infusion had no effect on muscle glycogenolysis and appeared to have little effect on adipose tissue lipolysis. The explanation for the elevation of blood lactate is unknown while the elevation in blood glucose suggests that EPI infusion potentiated liver glycogenolysis. Key words: muscle metabolism, plasma catecholamines, blood lactate, lipolysis, blood glucose


2007 ◽  
Vol 293 (2) ◽  
pp. E523-E530 ◽  
Author(s):  
H. J. Green ◽  
T. A. Duhamel ◽  
G. P. Holloway ◽  
J. W. Moule ◽  
J. Ouyang ◽  
...  

This study investigated the effects of a 16-h protocol of heavy intermittent exercise on the intrinsic activity and protein and isoform content of skeletal muscle Na+-K+-ATPase. The protocol consisted of 6 min of exercise performed once per hour at ∼91% peak aerobic power (V̇o2 peak) with tissue sampling from vastus lateralis before (B) and immediately after repetitions 1 (R1), 2 (R2), 9 (R9), and 16 (R16). Eleven untrained volunteers with a V̇o2 peak of 44.3 ± 2.3 ml·kg−1·min−1 participated in the study. Maximal Na+-K+-ATPase activity ( Vmax, in nmol·mg protein−1·h−1) as measured by the 3- O-methylfluorescein K+-stimulated phosphatase assay was reduced ( P < 0.05) by ∼15% with exercise regardless of the number of repetitions performed. In addition, Vmax at R9 and R16 was lower ( P < 0.05) than at R1 and R2. Vanadate-facilitated [3H]ouabain determination of Na+-K+-ATPase content (maximum binding capacity, pmol/g wet wt), although unaltered by exercise, increased ( P < 0.05) 8.3% by R9 with no further increase observed at R16. Assessment of relative changes in isoform abundance measured at B as determined by quantitative immunoblotting showed a 26% increase ( P < 0.05) in the α2-isoform by R2 and a 29% increase in α3 by R9. At R16, β3 was lower ( P < 0.05) than at R2 and R9. No changes were observed in α1, β1, or β2. It is concluded that repeated sessions of heavy exercise, although resulting in increases in the α2- and α3-isoforms and decreases in β3-isoform, also result in depression in maximal catalytic activity.


2011 ◽  
Vol 36 (6) ◽  
pp. 904-912 ◽  
Author(s):  
Howard J. Green ◽  
Margaret Burnett ◽  
Helen Kollias ◽  
Jing Ouyang ◽  
Ian Smith ◽  
...  

This study investigated the hypothesis that adaptations would occur in the sarcoplasmic reticulum in vastus lateralis soon after the onset of aerobic-based training consistent with reduced Ca2+-cycling potential. Tissue samples were extracted prior to (0 days) and following 3 and 6 days of cycling performed for 2 h at 60%–65% of peak aerobic power (VO2peak) in untrained males (VO2peak = 47 ± 2.3 mL·kg–1·min–1; mean ± SE, n = 6) and assessed for changes (nmol·mg protein–1·min–1) in maximal Ca2+-ATPase activity (Vmax), Ca2+-uptake, and Ca2+-release (phase 1 and phase 2) as well as the sarcoplasmic (endoplasmic) reticulum Ca2+-ATPase (SERCA) isoforms. Training resulted in reductions (p < 0.05) in SERCA1a at 6 days (–14%) but not at 3 days. For SERCA2a, reductions (p < 0.05) were also noted only at 6 days (–7%). For Vmax, depressions (p < 0.05) were found at 6 days (172 ± 11) but not at 3 days (176 ± 13; p < 0.10) compared with 0 days (192 ± 11). These changes were accompanied by a lower (p < 0.05) Ca2+-uptake at both 3 days (–39%) and 6 days (–48%). A similar pattern was found for phase 1 Ca2+-release with reductions (p < 0.05) of 37% observed at 6 days and 23% (p = 0.21) at 3 days of training, respectively. In a related study using the same training protocol and participant characteristics, microphotometric determinations of Vmax indicated reductions (p < 0.05) in type I at 3 days (–27%) and at 6 days (–34%) and in type IIA fibres at 6 days (–17%). It is concluded that in response to aerobic-based training, sarcoplasmic reticulum Ca2+-cycling potential is reduced by adaptations that occur soon after training onset.


1999 ◽  
Vol 87 (6) ◽  
pp. 2244-2252 ◽  
Author(s):  
Michael J. McKenna ◽  
Judith Morton ◽  
Steve E. Selig ◽  
Rodney J. Snow

This study investigated creatine supplementation (CrS) effects on muscle total creatine (TCr), creatine phosphate (CrP), and intermittent sprinting performance by using a design incorporating the time course of the initial increase and subsequent washout period of muscle TCr. Two groups of seven volunteers ingested either creatine [Cr; 6 × (5 g Cr-H2O + 5 g dextrose)/day)] or a placebo (6 × 5 g dextrose/day) over 5 days. Five 10-s maximal cycle ergometer sprints with rest intervals of 180, 50, 20, and 20 s and a resting vastus lateralis biopsy were conducted before and 0, 2, and 4 wk after placebo or CrS. Resting muscle TCr, CrP, and Cr were unchanged after the placebo but were increased ( P < 0.05) at 0 [by 22.9 ± 4.2, 8.9 ± 1.9, and 14.0 ± 3.3 (SE) mmol/kg dry mass, respectively] and 2 but not 4 wk after CrS. An apparent placebo main effect of increased peak power and cumulative work was found after placebo and CrS, but no treatment (CrS) main effect was found on either variable. Thus, despite the rise and washout of muscle TCr and CrP, maximal intermittent sprinting performance was unchanged by CrS.


1993 ◽  
Vol 264 (6) ◽  
pp. C1538-C1541 ◽  
Author(s):  
H. J. Green ◽  
E. R. Chin ◽  
M. Ball-Burnett ◽  
D. Ranney

To investigate the effect of short-term training on Na(+)-K(+)-adenosine triphosphatase (ATPase) concentration in skeletal muscle and on plasma K+ homeostasis during exercise, 9 subjects performed cycle exercise for 2 h per day for 6 consecutive days at 65% of maximal aerobic power (VO2 max). Na(+)-K(+)-ATPase concentration determined from biopsies obtained from the vastus lateralis muscle using the [3H]ouabain-binding technique increased 13.6% (P < 0.05) as a result of the training (339 +/- 16 vs. 385 +/- 19 pmol/g wet wt, means +/- SE). Increases in Na(+)-K(+)-ATPase concentration were accompanied by a small but significant increase in VO2 max (3.36 +/- 0.16 vs. 3.58 +/- 0.13 l/min). The increase in arterialized plasma K+ concentration and plasma K+ content determined during continuous exercise at three different intensities (60, 79, and 94% VO2 max) was depressed (P < 0.05) following training. These results indicate that not only is training capable of inducing an upregulation in sarcolemmal Na(+)-K(+)-ATPase concentration in humans, but provided that the exercise is of sufficient intensity and duration, the upregulation can occur within the first week of training. Moreover, our findings are consistent with the notion that the increase in Na(+)-K(+)-ATPase pump concentration attenuates the loss of K+ from the working muscle.


1990 ◽  
Vol 68 (7) ◽  
pp. 856-862 ◽  
Author(s):  
H. Meng ◽  
G. N. Pierce

Our knowledge of the effects of exercise on the heart is limited by the predominant use of rats as an animal model. The rabbit has many advantages over the rat as an animal model to study. However, little work has characterized its capacity to exercise. The purposes of the present study were to determine if the rabbit could (i) learn to run on a motor-driven treadmill at relatively high speeds using different exercise protocols, and (ii) characterize the various physiological and metabolic responses of the rabbit to acute bouts of exercise. We found that female New Zealand white rabbits had the capacity to run continuously on the treadmill for up to 21 min at 20 m/min until exhausted. Continuous, endurance-type exercise resulted in significant elevations in body temperature, heart rate, and plasma lactate levels. Plasma triglyceride concentration decreased as a function of this type of running whereas plasma glucose levels were unchanged. Twenty-four hours after a bout of running, plasma creatine phosphokinase activity was significantly elevated. The rabbits also had the capacity to learn to run using an intermittent, higher speed protocol. These physically untrained animals could achieve speeds of up to 70 m/min for 10 bouts of 15 s run/30 s rest. Their metabolic and physiological responses to this protocol were similar to those of continuous running with the following exceptions. The decrease in plasma triglyceride was less marked and the increase in plasma lactate was greater after intermittent exercise. Glycogen content of the rabbit vastus lateralis muscle was also significantly depleted after exhaustive, intermittent exercise. Our results demonstrate that rabbits can learn to run using different exercise protocols on a treadmill and, therefore, could serve as an appropriate model in which to study exercise conditioning. Their ability to run at extremely high speeds and withstand relatively intense exercise bouts will be particularly useful in future investigations of the cardiovascular adaptations of the rabbit to exercise training.Key words: exercise, rabbit, treadmill running, lactate, glycogen.


2009 ◽  
Vol 297 (5) ◽  
pp. R1383-R1391 ◽  
Author(s):  
H. J. Green ◽  
E. Bombardier ◽  
M. E. Burnett ◽  
I. C. Smith ◽  
S. M. Tupling ◽  
...  

In this study, we investigated the hypothesis that the metabolic adaptations observed during steady-state exercise soon after the onset of training would be displayed during the nonsteady period of moderate exercise and would occur in the absence of increases in peak aerobic power (V̇o2peak) and in muscle oxidative potential. Nine untrained males [age = 20.8 ± 0.70 (SE) yr] performed a cycle task at 62% V̇o2peak before (Pre-T) and after (Post-T) training for 2 h/day for 5 days at task intensity. Tissue samples extracted from the vastus lateralis at 0 min (before exercise) and at 10, 60, and 180 s of exercise, indicated that at Pre-T, reductions ( P < 0.05) in phosphocreatine and increases ( P < 0.05) in creatine, inorganic phosphate, calculated free ADP, and free AMP occurred at 60 and 180 s but not at 10 s. At Post-T, the concentrations of all metabolites were blunted ( P < 0.05) at 60 s. Training also reduced ( P < 0.05) the increase in lactate and the lactate-to-pyruvate ratio observed during exercise at Pre-T. These adaptations occurred in the absence of change in V̇o2peak (47.8 ± 1.7 vs. 49.2 ± 1.7 ml·kg−1·min−1) and in the activities (mol·kg protein−1·h−1) of succinic dehydrogenase (3.48 ± 0.21 vs. 3.77 ± 0.35) and citrate synthase (7.48 ± 0.61 vs. 8.52 ± 0.65) but not cytochrome oxidase (70.8 ± 5.1 vs. 79.6 ± 6.6 U/g protein; P < 0.05). It is concluded that the tighter metabolic control observed following short-term training is initially expressed during the nonsteady state, probably as a result of increases in oxidative phosphorylation that is not dependent on changes in V̇o2peak while the role of oxidative potential remains uncertain.


2000 ◽  
Vol 88 (2) ◽  
pp. 634-640 ◽  
Author(s):  
Howard Green ◽  
Brian Roy ◽  
Susan Grant ◽  
Margaret Burnett ◽  
Russ Tupling ◽  
...  

To investigate the hypothesis that acclimatization to altitude would result in a downregulation in muscle Na+-K+-ATPase pump concentration, tissue samples were obtained from the vastus lateralis muscle of six volunteers (5 males and 1 female), ranging in age from 24 to 35 yr, both before and within 3 days after a 21-day expedition to the summit of Mount Denali, Alaska (6,194 m). Na+-K+-ATPase, measured by the [3H]ouabain-binding technique, decreased by 13.8% [348 ± 12 vs. 300 ± 7.6 (SE) pmol/g wet wt; P< 0.05]. No changes were found in the maximal activities (mol ⋅ kg protein− 1 ⋅ h− 1) of the mitochondrial enzymes, succinic dehydrogenase (3.63 ± 0.20 vs. 3.25 ± 0.23), citrate synthase (4.76 ± 0.44 vs. 4.94 ± 0.44), and malate dehydrogenase (12.6 ± 1.8 vs. 12.7 ± 1.2). Similarly, the expedition had no effect on any of the histochemical properties examined, namely fiber-type distribution (types I, IIA, IIB, IC, IIC, IIAB), area, capillarization, and succinic dehydrogenase activity. Peak aerobic power (52.3 ± 2.1 vs. 50.6 ± 1.9 ml ⋅ kg− 1 ⋅ min− 1) and body mass (76.9 ± 3.7 vs. 75.5 ± 2.9 kg) were also unaffected. We concluded that acclimatization to altitude results in a downregulation in muscle Na+-K+-ATPase pump concentration, which occurs without changes in oxidative potential and other fiber-type histochemical properties.


1987 ◽  
Vol 63 (5) ◽  
pp. 1719-1724 ◽  
Author(s):  
R. L. Moore ◽  
E. M. Thacker ◽  
G. A. Kelley ◽  
T. I. Musch ◽  
L. I. Sinoway ◽  
...  

Human subjects participated in a training/detraining paradigm which consisted of 7 wk of intense endurance training followed by 3 wk of inactivity. In previously sedentary subjects, training produced a 23.9 +/- 7.2% increase in maximal aerobic power (V02max) (group S). Detraining did not affect group S V02max. In previously trained subjects (group T), the training/detraining paradigm did not affect V02max. In group S, training produced an increase in vastus lateralis muscle citrate synthase (CS) activities (nmol.mg protein-1. min-1) from 67.1 +/- 14.5 to 106.9 +/- 22.0. Detraining produced a decrease in CS activity to 80 +/- 14.6. In group T, pretraining CS activity (139.5 +/- 14.9) did not change in response to training. Detraining, however, produced a decrease in CS activity (121.5 +/- 7.8 to 66.8 +/- 5.9). Group S respiratory exchange ratios obtained during submaximal exercise at 60% V02max (R60) decreased in response to training (1.00 +/- 0.02 to 0.87 +/- 0.02) and increased (0.96 +/- 0.02) after detraining. Group T R60 (0.91 +/- 0.01) was not affected by training but increased (0.89 +/- 0.02 to 0.95 +/- 0.02) after detraining. R60 was correlated to changes in CS activity but was unrelated to changes in V02max. These data support the hypothesis that the mitochondrial content of working skeletal muscle is an important determinant of substrate utilization during submaximal exercise.


1982 ◽  
Vol 63 (1) ◽  
pp. 87-92 ◽  
Author(s):  
G. R. Ward ◽  
J. R. Sutton ◽  
N. L. Jones ◽  
C. J. Toews

1. The activity of pyruvate dehydrogenase in its active and inactive forms was measured in biopsy samples obtained from the vastus lateralis muscle of healthy subjects before and after exercise. 2. At rest, 40 ± 4% (mean ± sem) of the enzyme was in the active form. 3. After progressive aerobic exercise to exhaustion (n = 5), 88 ± 2·3% was in the active form. 4. After intermittent supramaximal short-term exercise (1 min exercise, 3 min rest) to exhaustion (n = 6), 60 ± 2·2% was in the active form. 5. After isometric maximal exercise of 65 ± 3·6 s duration (n = 3), only 39 ± 1% of the enzyme was in the active form. 6. Muscle glycogen depletion was greatest with intermittent exercise and least with isometric maximal exercise; in contrast, the increase in muscle lactate was least with progressive exercise (1·3 to 9·4 μmol/g), intermediate in intermittent maximal exercise (1·2 to 13·1 μmol/g) and greatest after isometric exercise (1·8 to 17·6 μmol/g). There were no significant differences between the three studies in the changes in lactate/pyruvate ratios. 7. In three subjects who exercised with one leg, activation of the enzyme was twice as great in the exercised as in the inactive leg. 8. The ratio of active to total enzyme in biopsies of resting muscle was greater in four well-trained athletes than in four untrained control subjects (70% compared with 41% respectively). 9. The activation of pyruvate dehydrogenase appears to play an important part in regulating the use of glycogen and glucose during exercise in man.


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