Decreased glucose turnover after short-term training is unaccompanied by changes in muscle oxidative potential

1995 ◽  
Vol 269 (2) ◽  
pp. E222-E230 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. A. Tarnopolsky ◽  
S. M. Grant

This study investigated the hypothesis that training-induced reductions in exercise blood glucose utilization can occur independently of increases in muscle mitochondrial potential. To induce a training adaptation, eight active participants (23 +/- 1 yr, 80.6 +/- 3.7 kg, mean +/- SE) with a maximal oxygen consumption (VO2max) of 45.5 +/- 2.4 ml.kg-1.min-1, cycled at 59% VO2max for 2 h per day for 10 consecutive days. Measurements of blood glucose appearance (Ra) and disappearance (Rd), using a primed continuous infusion of [6,6-2H2]glucose, were made during 90 min of cycle exercise (59% VO2max) performance before and after training. Training resulted in a 25% decrease (P < 0.01) in mean glucose Ra during exercise (43.0 +/- 3.7 to 34.4 +/- 2.8 mumol.kg-1.min-1). Since blood glucose concentration was not different between training conditions, glucose metabolic clearance rate was also depressed (P < 0.05). Exercise-induced glycogen depletion in vastus lateralis muscle was reduced (P < 0.05) with training. Calculation of carbohydrate and fat oxidation based on the respiratory exchange ratio supported a shift toward greater preference for fat. Because training did not elicit changes in the maximal activities of citrate synthase and malate dehydrogenase, two enzymes of the citric acid cycle, it would appear that increases in mitochondrial potential are not necessary for the adaptations that occurred.

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.


1996 ◽  
Vol 270 (2) ◽  
pp. E265-E272 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. A. Tarnopolsky ◽  
G. J. Heigenhauser ◽  
S. M. Grant

We investigated the hypothesis that a program of prolonged endurance training, previously shown to decrease metabolic perturbations to acute exercise within 5 days of training, would result in greater metabolic adaptations after a longer training duration. Seven healthy male volunteers [O2 consumption = 3.52 +/- 0.20 (SE) l/min] engaged in a training program consisting of 2 h of cycle exercise at 59% of pretraining peak O2 consumption (VO2peak) 5-6 times/wk. Responses to a 90-min submaximal exercise challenge were assessed pretraining (PRE) and after 5 and 31 days of training. On the basis of biopsies obtained from the vastus lateralis muscle, it was found that, after 5 days of training, muscle lactate concentration, phosphocreatine (PCr) hydrolysis, and glycogen depletion were reduced vs. PRE (all P < 0.01). Further training (26 days) showed that, at 31 days, the reduction in PCr and the accumulation of muscle lactate was even less than at 5 days (P < 0.01). Muscle oxidative potential, estimated from the maximal activity of succinate dehydrogenase, was increased only after 31 days of training (+41%; P < 0.01). In addition, VO2peak was only increased (10%) by 31 days (P < 0.05). The results show that a period of short-term training results in many characteristic training adaptations but that these adaptations occurred before increases in mitochondrial potential. However, a further period of training resulted in further adaptations in muscle metabolism and muscle phosphorylation potential, which were linked to the increase in muscle mitochondrial capacity.


1991 ◽  
Vol 70 (5) ◽  
pp. 2032-2038 ◽  
Author(s):  
H. J. Green ◽  
S. Jones ◽  
M. E. Ball-Burnett ◽  
D. Smith ◽  
J. Livesey ◽  
...  

A short-term training program involving 2 h of daily exercise at 59% of peak O2 uptake (VO2max) repeated for 10-12 consecutive days was employed to determine the significance of adaptations in energy metabolic potential on alterations in energy metabolism and substrate utilization in working muscle. The initial VO2max determined before training on the eight male subjects was 53.0 +/- 2.0 (SE) ml.kg-1.min-1. Analysis of samples obtained by needle biopsy from the vastus lateralis muscle before exercise (0 min) and at 15, 60, and 99 min of exercise indicated that on the average training resulted (P less than 0.05) in a 6.5% higher concentration of creatine phosphate, a 9.9% lower concentration of creatine, and a 39% lower concentration of lactate. Training had no effect on ATP concentration. These adaptations were also accompanied by a reduction in the utilization in glycogen such that by the end of exercise glycogen concentration was 47.1% higher in the trained muscle. Analysis of the maximal activities of representative enzymes of different metabolic pathways and segments indicated no change in potential in the citric acid cycle (succinate dehydrogenase, citrate synthase), beta-oxidation (3-hydroxyacyl CoA dehydrogenase), glucose phosphorylation (hexokinase), or potential for glycogenolysis (phosphorylase) and glycolysis (pyruvate kinase, phosphofructokinase, alpha-glycerophosphate dehydrogenase, lactate dehydrogenase). With the exception of increases in the capillary-to-fiber area ratio in type IIa fibers, no change was found in any fiber type (types I, IIa, and IIb) for area, number of capillaries, capillary-to-fiber area ratio, or oxidative potential with training.(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 73 (5) ◽  
pp. 1873-1880 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
J. P. Kirwan ◽  
D. M. Bier ◽  
...  

The purpose of this study was to test the hypothesis that the rate of plasma glucose oxidation during exercise is inversely related to muscle respiratory capacity. To this end, 14 subjects were studied: in 7 of these subjects, the blood lactate threshold (LT) occurred at a relatively high intensity [i.e., at 65 +/- 2% of peak cycle ergometer oxygen uptake (VO2 peak)], whereas in the other 7 subjects, LT occurred at a relatively low intensity (i.e., at 45 +/- 2% of VO2 peak). VO2peak did not differ between the two groups, but citrate synthase activity in the vastus lateralis muscle was 53% higher (P < 0.05) in the high LT group. A primed continuous infusion of [U-13C]glucose was used to quantify rates of glucose appearance (Ra), disappearance (Rd), and oxidation (R(ox)) during 90 min of exercise at 55% VO2peak. Although both absolute and relative rates of oxygen uptake during exercise were similar in the two groups, mean Ra and Rd were 17% lower (P < 0.001) in the high LT group, and mean R(ox) was 25% lower (21.0 +/- 2.6 vs. 27.9 +/- 2.6 mumol.min-1.kg-1; P < 0.001). The percentage of total energy derived from glucose oxidation was inversely related to muscle citrate synthase activity (r = -0.85; P < 0.01). These data support the concept that skeletal muscle respiratory capacity has a major role in determining the metabolic response to submaximal exercise.


1995 ◽  
Vol 269 (6) ◽  
pp. H1949-H1954 ◽  
Author(s):  
R. M. McAllister ◽  
M. D. Delp ◽  
K. A. Thayer ◽  
M. H. Laughlin

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.


2018 ◽  
Vol 125 (5) ◽  
pp. 1636-1645 ◽  
Author(s):  
Kevin J. Gries ◽  
Ulrika Raue ◽  
Ryan K. Perkins ◽  
Kaleen M. Lavin ◽  
Brittany S. Overstreet ◽  
...  

The purpose of this study was to examine the effects of aerobic lifelong exercise (LLE) on maximum oxygen consumption (V̇o2max) and skeletal muscle metabolic fitness in trained women ( n = 7, 72 ± 2 yr) and men ( n = 21, 74 ± 1 yr) and compare them to old, healthy nonexercisers (OH; women: n = 10, 75 ± 1 yr; men: n = 10, 75 ± 1 yr) and young exercisers (YE; women: n = 10, 25 ± 1 yr; men: n = 10, 25 ± 1 yr). LLE men were further subdivided based on intensity of lifelong exercise and competitive status into performance (LLE-P, n = 14) and fitness (LLE-F, n = 7). On average, LLE exercised 5 day/wk for 7 h/wk over the past 52 ± 1 yr. Each subject performed a maximal cycle test to assess V̇o2maxand had a vastus lateralis muscle biopsy to examine capillarization and metabolic enzymes [citrate synthase, β-hydroxyacyl-CoA dehydrogenase (β-HAD), and glycogen phosphorylase]. V̇o2maxhad a hierarchical pattern (YE > LLE > OH, P < 0.05) for women (44 ± 2 > 26 ± 2 > 18 ± 1 ml·kg−1·min−1) and men (53 ± 3 > 34 ± 1 > 22 ± 1 ml·kg−1·min−1) and was greater ( P < 0.05) in LLE-P (38 ± 1 ml·kg−1·min−1) than LLE-F (27 ± 2 ml·kg−1·min−1). LLE men regardless of intensity and women had similar capillarization and aerobic enzyme activity (citrate synthase and β-HAD) as YE, which were 20%–90% greater ( P < 0.05) than OH. In summary, these data show a substantial V̇o2maxbenefit with LLE that tracked similarly between the sexes, with further enhancement in performance-trained men. For skeletal muscle, 50+ years of aerobic exercise fully preserved capillarization and aerobic enzymes, regardless of intensity. These data suggest that skeletal muscle metabolic fitness may be easier to maintain with lifelong aerobic exercise than more central aspects of the cardiovascular system.NEW & NOTEWORTHY Lifelong exercise (LLE) is a relatively new and evolving area of study with information especially limited in women and individuals with varying exercise intensity habits. These data show a substantial maximal oxygen consumption benefit with LLE that tracked similarly between the sexes. Our findings contribute to the very limited skeletal muscle biopsy data from LLE women (>70 yr), and similar to men, revealed a preserved metabolic phenotype comparable to young exercisers.


1993 ◽  
Vol 75 (4) ◽  
pp. 1502-1506 ◽  
Author(s):  
T. P. Rooney ◽  
Z. V. Kendrick ◽  
J. Carlson ◽  
G. S. Ellis ◽  
B. Matakevich ◽  
...  

The effect of 17 beta-estradiol 3-benzoate (10 micrograms.01 ml of sunflower oil-1 x 100 g body wt-1) on the temporal pattern of exercise-induced tissue glycogen depletion and tissue lipid availability during submaximal treadmill running was determined in male rats. Animal were administered estradiol or oil for 5 days and were then time matched for motorized treadmill running for 30, 60, 90, or 120 min. Significant depletion of liver, soleus muscle, and red and white vastus lateralis muscle tissue glycogen occurred in oil-administered animals run between 30 and 120 min. The greatest extent of tissue glycogen depletion occurred during the first 30 min of exercise with the rate of glycogen depletion slowing between 30 and 120 min of exercise. Administration of estradiol attenuated the temporal pattern of glycogen depletion in both liver and muscle tissues. Significant depletion of red and white vastus glycogen of estradiol-administered animals did not occur until 90 and 120 min of exercise, respectively. Administration of estradiol significantly increased resting plasma free fatty acids and red and white vastus triacylglycerol content. These data indicate that estradiol administration for 5 days resulted in significant glycogen sparing of liver and muscle tissues during submaximal treadmill running for up to 120 min by altering the temporal pattern of glycogen depletion of male rats secondary to an estradiol-mediated increase in availability of lipid substrate during exercise.


1999 ◽  
Vol 277 (1) ◽  
pp. E39-E48 ◽  
Author(s):  
H. Green ◽  
S. Grant ◽  
E. Bombardier ◽  
D. Ranney

To investigate the hypothesis that training-induced increases in muscle mitochondrial potential are not obligatory to metabolic adaptations observed during submaximal exercise, regardless of peak aerobic power (V˙o 2 peak) of the subjects, a short-term training study was utilized. Two groups of untrained male subjects ( n = 7/group), one with a high (HI) and the other with a low (LO)V˙o 2 peak(means ± SE; 51.4 ± 0.90 vs. 41.0 ± 1.3 ml ⋅ kg−1 ⋅ min−1; P< 0.05), cycled for 2 h/day at 66–69% ofV˙o 2 peak for 6 days. Muscle tissue was extracted from vastus lateralis at 0, 3, and 30 min of standardized cycle exercise before training (0 days) and after 3 and 6 days of training and analyzed for metabolic and enzymatic changes. During exercise after 3 days of training in the combined HI + LO group, higher ( P < 0.05) concentrations (mmol/kg dry wt) of phosphocreatine (40.5 ± 3.4 vs. 52.2 ± 4.2) and lower ( P < 0.05) concentrations of Pi (61.5 ± 4.4 vs. 53.3 ± 4.4), inosine monophosphate (0.520 ± 0.19 vs. 0.151 ± 0.05), and lactate (37.9 ± 5.5 vs. 22.8 ± 4.8) were observed. These changes were also accompanied by reduced levels of calculated free ADP, AMP, and Pi. All adaptations were fully expressed by 3 min of exercise and by 3 days of training and were independent of initialV˙o 2 peak levels. Moreover, maximal activity of citrate synthase, a measure of mitochondrial capacity, was only increased with 6 days of training (5.71 ± 0.29 vs. 7.18 ± 0.37 mol ⋅ kg protein−1 ⋅ h−1; P < 0.05). These results demonstrate that metabolic adaptations to prolonged exercise occur within the first 3 days of training and during the non-steady-state period. Moreover, neither time course nor magnitude of metabolic adaptations appears to depend on increases in mitochondrial potential or on initial aerobic power.


2004 ◽  
Vol 97 (6) ◽  
pp. 2132-2138 ◽  
Author(s):  
C. Thomas ◽  
P. Sirvent ◽  
S. Perrey ◽  
E. Raynaud ◽  
J. Mercier

The present study investigated whether blood lactate removal after supramaximal exercise and fatigue indexes measured during continuous and intermittent supramaximal exercises are related to the maximal muscle oxidative capacity in humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (γ2), which denoted the blood lactate removal ability. Fatigue indexes were calculated during all-out (FIAO) and repeated 10-s cycling sprints (FISprint). Biopsies were taken from the vastus lateralis muscle, and maximal ADP-stimulated mitochondrial respiration ( Vmax) was evaluated in an oxygraph cell on saponin-permeabilized muscle fibers with pyruvate + malate and glutamate + malate as substrates. Significant relationships were found between γ2 and pyruvate + malate Vmax ( r = 0.60, P < 0.05), γ2 and glutamate + malate Vmax ( r = 0.66, P < 0.01), and γ2 and citrate synthase activity ( r = 0.76, P < 0.01). In addition, γ2, glutamate + malate Vmax, and pyruvate + malate Vmax were related to FIAO (γ2 − FIAO: r = 0.85; P < 0.01; glutamate + malate Vmax − FIAO: r = 0.70, P < 0.01; and pyruvate + malate Vmax − FIAO: r = 0.63, P < 0.01) and FISprint (γ2 − FISprint: r = 0.74, P < 0.01; glutamate + malate Vmax − FISprint: r = 0.64, P < 0.01; and pyruvate + malate Vmax − FISprint: r = 0.46, P < 0.01). In conclusion, these results suggested that the maximal muscle oxidative capacity was related to blood lactate removal ability after a 1-min all-out test. Moreover, maximal muscle oxidative capacity and blood lactate removal ability were associated with the delay in the fatigue observed during continuous and intermittent supramaximal exercises in well-trained subjects.


2011 ◽  
Vol 110 (1) ◽  
pp. 236-245 ◽  
Author(s):  
Karen Van Proeyen ◽  
Karolina Szlufcik ◽  
Henri Nielens ◽  
Monique Ramaekers ◽  
Peter Hespel

Training with limited carbohydrate availability can stimulate adaptations in muscle cells to facilitate energy production via fat oxidation. Here we investigated the effect of consistent training in the fasted state, vs. training in the fed state, on muscle metabolism and substrate selection during fasted exercise. Twenty young male volunteers participated in a 6-wk endurance training program (1–1.5 h cycling at ∼70% V̇o2max, 4 days/wk) while receiving isocaloric carbohydrate-rich diets. Half of the subjects trained in the fasted state (F; n = 10), while the others ingested ample carbohydrates before (∼160 g) and during (1 g·kg body wt−1·h−1) the training sessions (CHO; n = 10). The training similarly increased V̇o2max (+9%) and performance in a 60-min simulated time trial (+8%) in both groups ( P < 0.01). Metabolic measurements were made during a 2-h constant-load exercise bout in the fasted state at ∼65% pretraining V̇o2max. In F, exercise-induced intramyocellular lipid (IMCL) breakdown was enhanced in type I fibers ( P < 0.05) and tended to be increased in type IIa fibers ( P = 0.07). Training did not affect IMCL breakdown in CHO. In addition, F (+21%) increased the exercise intensity corresponding to the maximal rate of fat oxidation more than did CHO (+6%) ( P < 0.05). Furthermore, maximal citrate synthase (+47%) and β-hydroxyacyl coenzyme A dehydrogenase (+34%) activity was significantly upregulated in F ( P < 0.05) but not in CHO. Also, only F prevented the development exercise-induced drop in blood glucose concentration ( P < 0.05). In conclusion, F is more effective than CHO to increase muscular oxidative capacity and at the same time enhances exercise-induced net IMCL degradation. In addition, F but not CHO prevented drop of blood glucose concentration during fasting exercise.


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