Effect of prolonged exercise on muscle citrate concentration before and after endurance training in men

1993 ◽  
Vol 264 (2) ◽  
pp. E215-E220 ◽  
Author(s):  
A. R. Coggan ◽  
R. J. Spina ◽  
W. M. Kohrt ◽  
J. O. Holloszy

It has been hypothesized that endurance training reduces carbohydrate utilization during exercise via citrate-mediated inhibition of phosphofructokinase (PFK). To test this hypothesis, vastus lateralis muscle biopsy samples were obtained from eight men before and immediately (approximately 10 s) after 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake, both before and after 12 wk of endurance exercise training (3 days/wk running, 3 days/wk interval cycling). Training increased muscle citrate synthase (CS) activity from 3.69 +/- 0.48 (SE) to 5.30 +/- 0.42 mol.h-1.kg protein-1 and decreased the mean respiratory exchange ratio during exercise from 0.92 +/- 0.01 to 0.88 +/- 0.01 (both P < 0.001). Muscle citrate concentration at the end of exercise correlated significantly with CS activity (r = 0.70; P < 0.005) and was slightly but not significantly higher after training (0.80 +/- 0.19 vs. 0.54 +/- 0.19 mmol/kg dry wt; P = 0.16). Muscle glucose 6-phosphate (G-6-P) concentration at the end of exercise, however, was 31% lower in the trained state (1.17 +/- 0.10 vs. 1.66 +/- 0.27 mmol/kg dry wt; P < 0.05), in keeping with a 36% decrease in the amount of muscle glycogen utilized (133 +/- 22 vs. 209 +/- 19 mmol.kg dry wt-1.2 h-1; P < 0.01). The lower G-6-P concentration after training suggests that the training-induced reduction in carbohydrate utilization results from attenuation of flux before the PFK step in glycolysis and is not due to citrate-mediated inhibition of PFK.

2000 ◽  
Vol 278 (4) ◽  
pp. E571-E579 ◽  
Author(s):  
Hervé Dubouchaud ◽  
Gail E. Butterfield ◽  
Eugene E. Wolfel ◽  
Bryan C. Bergman ◽  
George A. Brooks

To evaluate the effects of endurance training on the expression of monocarboxylate transporters (MCT) in human vastus lateralis muscle, we compared the amounts of MCT1 and MCT4 in total muscle preparations (MU) and sarcolemma-enriched (SL) and mitochondria-enriched (MI) fractions before and after training. To determine if changes in muscle lactate release and oxidation were associated with training-induced changes in MCT expression, we correlated band densities in Western blots to lactate kinetics determined in vivo. Nine weeks of leg cycle endurance training [75% peak oxygen consumption (V˙o 2 peak)] increased muscle citrate synthase activity (+75%, P < 0.05) and percentage of type I myosin heavy chain (+50%, P < 0.05); percentage of MU lactate dehydrogenase-5 (M4) isozyme decreased (−12%, P < 0.05). MCT1 was detected in SL and MI fractions, and MCT4 was localized to the SL. Muscle MCT1 contents were consistent among subjects both before and after training; in contrast, MCT4 contents showed large interindividual variations. MCT1 amounts significantly increased in MU, SL, and MI after training (+90%, +60%, and +78%, respectively), whereas SL but not MU MCT4 content increased after training (+47%, P < 0.05). Mitochondrial MCT1 content was negatively correlated to net leg lactate release at rest ( r = −0.85, P < 0.02). Sarcolemmal MCT1 and MCT4 contents correlated positively to net leg lactate release at 5 min of exercise at 65%V˙o 2 peak ( r = 0.76, P < 0.03 and r = 0.86, P < 0.01, respectively). Results support the conclusions that 1) endurance training increases expression of MCT1 in muscle because of insertion of MCT1 into both sarcolemmal and mitochondrial membranes, 2) training has variable effects on sarcolemmal MCT4, and 3) both MCT1 and MCT4 participate in the cell-cell lactate shuttle, whereas MCT1 facilitates operation of the intracellular lactate shuttle.


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.


1990 ◽  
Vol 68 (3) ◽  
pp. 990-996 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
D. M. Bier ◽  
J. O. Holloszy

To assess the effects of endurance training on plasma glucose kinetics during moderate-intensity exercise in men, seven men were studied before and after 12 wk of strenuous exercise training (3 days/wk running, 3 days/wk cycling). After priming of the glucose and bicarbonate pools, [U-13C] glucose was infused continuously during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2) to determine glucose turnover and oxidation. Training increased cycle ergometer peak VO2 by 23% and decreased the respiratory exchange ratio during the final 30 min of exercise from 0.89 +/- 0.01 to 0.85 +/- 0.01 (SE) (P less than 0.001). Plasma glucose turnover during exercise decreased from 44.6 +/- 3.5 mumol.kg fat-free mass (FFM)-1.min-1 before training to 31.5 +/- 4.3 after training (P less than 0.001), whereas plasma glucose clearance (i.e., rate of disappearance/plasma glucose concentration) fell from 9.5 +/- 0.6 to 6.4 +/- 0.8 ml.kg FFM-1.min-1 (P less than 0.001). Oxidation of plasma-derived glucose, which accounted for approximately 90% of plasma glucose disappearance in both the untrained and trained states, decreased from 41.1 +/- 3.4 mumol.kg FFM-1.min-1 before training to 27.7 +/- 4.8 after training (P less than 0.001). This decrease could account for roughly one-half of the total reduction in the amount of carbohydrate utilized during the final 30 min of exercise in the trained compared with the untrained state.


1993 ◽  
Vol 75 (1) ◽  
pp. 70-75 ◽  
Author(s):  
A. R. Coggan ◽  
D. L. Habash ◽  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
C. L. Kien

Endurance training reduces the rate of CO2 release (i.e., VCO2) during submaximal exercise, which has been interpreted to indicate a reduction in carbohydrate oxidation. However, decreased ventilation, decreased buffering of lactate, and/or increased fixation of CO2 could also account for a lower VCO2 after training. We therefore used a primed continuous infusion of NaH13CO3 to determine the whole body rate of appearance of CO2 (RaCO2) in seven men during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2peak) before and after endurance training. RaCO2 is independent of the above-described factors affecting VCO2 but may overestimate net CO2 production due to pyruvate carboxylation and subsequent isotopic exchange in the tricarboxylic acid cycle. Training consisted of cycling at 75–100% VO2peak for 45–90 min/day, 6 days/wk, for 12 wk and increased VO2peak by 28% (P < 0.001). VCO2 during submaximal exercise was reduced from 86.8 +/- 3.7 to 76.2 +/- 4.2 mmol/min, whereas RaCO2 fell from 88.9 +/- 4.0 to 76.4 +/- 4.4 mmol/min (both P < 0.001). VCO2 and RaCO2 were highly correlated in the untrained (r = 0.98, P < 0.001) and trained (r = 0.99, P < 0.001) states, as were individual changes in VCO2 and RaCO2 with training (r = 0.88, P < 0.01). These results support the hypothesis that endurance training decreases CO2 production during exercise. The magnitude and direction of this change cannot be explained by reported training-induced alterations in amino acid oxidation, indicating that it must be the result of a decrease in carbohydrate oxidation and an increase in fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)


2016 ◽  
Vol 32 (6) ◽  
pp. 593-598 ◽  
Author(s):  
Igor Ramathur Telles Jesus ◽  
Roger Gomes Tavares Mello ◽  
Jurandir Nadal

During muscle fatigue analysis some standard indexes are calculated from the surface electromyogram (EMG) as root mean square value (RMS), mean (Fmean), and median power frequency (Fmedian). However, these parameters present limitations and principal component analysis (PCA) appears to be an adequate alternative. In this context, we propose two indexes based on PCA to enhance the quantitative muscle fatigue analysis during cyclical contractions. Signals of vastus lateralis muscle were collected during a maximal exercise test. Twenty-four subjects performed the test starting at 12.5 W power output with increments of 12.5 W⋅min–1, maintaining cadence of 50 rpm until voluntary exhaustion. The epochs of myoelectric activation were identified and used to estimate the power spectra. PCA was then applied to the power spectra of each subject. The standard (ST) and Euclidean (ED) distances were employed to estimate the alteration occurred due to fatigue. For comparison, the standard indexes were calculated. ST, ED, and RMS value were adequate for muscle fatigue analysis. Among these parameters, ST was more sensitive with higher effect size. Moreover, the Fmean and Fmedian were not sensitive to fatigue. The proposed method based on PCA of EMG in frequency domain allowed producing fatigue indexes suitable for cyclical contractions.


1993 ◽  
Vol 75 (1) ◽  
pp. 49-54 ◽  
Author(s):  
A. J. Young ◽  
M. N. Sawka ◽  
M. D. Quigley ◽  
B. S. Cadarette ◽  
P. D. Neufer ◽  
...  

This investigation studied the importance of the rise in body temperature during exercise for aerobic capacity adaptations produced by endurance training. The approach used was to compare training effects produced by subjects exercising in hot (35 degrees C) water vs. cold (20 degrees C) water. Hot water was used to potentiate, and cold water to blunt, the rise in body temperature during exercise. Eighteen young men trained by cycle-ergometer exercise at 60% of maximal oxygen uptake (VO2max) while immersed to the neck in either hot (HWT, n = 9) or cold (CWT, n = 9) water for 60 min, 5 days/wk, for 8 wk. Before and after training, VO2max, erythrocyte volume, plasma volume, and vastus lateralis citrate synthase activity were measured. Training increased (P < 0.01) VO2max by 13%, with no difference between HWT and CWT in the magnitude of the effect. Erythrocyte volume increased 4% (P < 0.01) with training, with no difference between HWT and CWT in the magnitude of the effect. Plasma volume remained unchanged by training in both the HWT and CWT groups. Last, vastus lateralis citrate synthase activity increased by 38% with training, but there was no difference between HWT and CWT in the training effect. Thus, exercise-induced body temperature elevations are not an important stimulus for the aerobic adaptations to moderate-intensity endurance training.


1992 ◽  
Vol 73 (6) ◽  
pp. 2517-2523 ◽  
Author(s):  
G. Grimby ◽  
A. Aniansson ◽  
M. Hedberg ◽  
G. B. Henning ◽  
U. Grangard ◽  
...  

Nine men, 78–84 yr of age, participated in a dynamometer training program 2–3 times/wk, totaling 25 sessions, using voluntary maximal isometric, concentric, and eccentric right knee–extension actions (30 and 180 degrees/s). Measurements of muscle strength with a Kin-Com dynamometer and simultaneous electromyograms (EMG) were performed of both sides before and after the training period. Muscle biopsies were taken from the right vastus lateralis muscle. The total quadriceps cross-sectional area was measured with computerized tomography. Training led to an increase in maximal torque for concentric (10% at 30 degrees/s) and eccentric (13–19%) actions in the trained leg. The EMG activity increased at maximal eccentric activities. The total cross-sectional quadriceps area of the trained leg increased by 3%, but no changes were recorded in muscle fiber areas in these subjects, who already had large mean fiber areas (5.15 microns 2 x 10(3)). The fatigue index measured from 50 consecutive concentric contractions at 180 degrees/s decreased and the citrate synthase activity increased in all but one subject. The results demonstrate that increased neural activation accompanies an increase in muscle strength at least during eccentric action in already rather active elderly men and that muscle endurance may also be improved with training.


2014 ◽  
Vol 307 (9) ◽  
pp. R1101-R1114 ◽  
Author(s):  
Jerzy A. Zoladz ◽  
Bruno Grassi ◽  
Joanna Majerczak ◽  
Zbigniew Szkutnik ◽  
Michal Korostyński ◽  
...  

The effect of prolonged endurance training on the pulmonary V̇o2 on- and off-kinetics in humans, in relation to muscle mitochondria biogenesis, is investigated. Eleven untrained physically active men (means ± SD: age 22.4 ± 1.5 years, V̇o2peak 3,187 ± 479 ml/min) performed endurance cycling training (4 sessions per week) lasting 20 wk. Training shortened τp of the pulmonary V̇o2 on-kinetics during moderate-intensity cycling by ∼19% from 28.3 ± 5.2 to 23.0 ± 4.0 s ( P = 0.005). τp of the pulmonary V̇o2 off-kinetics decreased by ∼11% from 33.7 ± 7.2 to 30.0 ± 6.6 ( P = 0.02). Training increased (in vastus lateralis muscle) mitochondrial DNA copy number in relation to nuclear DNA (mtDNA/nDNA) (+53%) ( P = 0.014), maximal citrate synthase (CS) activity (+38%), and CS protein content (+38%) ( P = 0.004), whereas maximal cytochrome c oxidase (COX) activity after training tended to be only slightly (+5%) elevated ( P = 0.08). By applying to the experimental data, our computer model of oxidative phosphorylation (OXPHOS) and using metabolic control analysis, we argue that COX activity is a much better measure of OXPHOS intensity than CS activity. According to the model, in the present study a training-induced increase in OXPHOS activity accounted for about 0–10% of the decrease in τp of muscle and pulmonary V̇o2 for the on-transient, whereas the remaining 90–100% is caused by an increase in each-step parallel activation of OXPHOS.


1995 ◽  
Vol 268 (3) ◽  
pp. E375-E383 ◽  
Author(s):  
A. R. Coggan ◽  
S. C. Swanson ◽  
L. A. Mendenhall ◽  
D. L. Habash ◽  
C. L. Kien

In humans, endurance training markedly reduces the rate of hepatic glucose production during exercise. To determine whether this is due to a reduction in glycogenolysis, in gluconeogenesis, or in both processes, six men were studied at rest and during 2 h of cycle ergometer exercise at 60% pretraining peak O2 consumption (VO2peak), both before and after completion of a strenuous endurance training program (cycling at 75-100% VO2peak for 45-90 min/day, 6 days/wk for 12 wk). The overall rate of glucose appearance (Ra) was determined using a primed continuous infusion of [6,6-2H]glucose, whereas the rate of gluconeogenesis (Rgng) was estimated from the incorporation of 13C into glucose (via pyruvate carboxylase) from simultaneously infused [13C]bicarbonate. Training did not affect glucose kinetics at rest but reduced the average Ra during exercise by 42% [from 36.8 +/- 3.8 to 21.5 +/- 3.6 (SE) mumol.min-1.kg-1; P < 0.001]. This decrease appeared to be mostly due to a reduction in hepatic glycogenolysis. However, the estimated Rgng during exercise also decreased significantly (P < 0.001) with training, falling from 7.5 +/- 1.6 mumol.min-1.kg-1 (23 +/- 3% of total Ra) before training to 3.1 +/- 0.6 mumol.min-1.kg-1 (14 +/- 3% of total Ra) after training. These training-induced adaptations in hepatic glucose metabolism were associated with an attenuated hormonal response to exercise (i.e., higher insulin and lower glucagon, norepinephrine, and epinephrine concentrations) as well as a reduced availability of gluconeogenic precursors (i.e., lower lactate and glycerol concentrations). We conclude that endurance training reduces both hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men.


1990 ◽  
Vol 68 (1) ◽  
pp. 260-270 ◽  
Author(s):  
D. G. Sale ◽  
J. D. MacDougall ◽  
I. Jacobs ◽  
S. Garner

To assess the effects of concurrent strength (S) and endurance (E) training on S and E development, one group (4 young men and 4 young women) trained one leg for S and the other leg for S and E (S+E). A second group (4 men, 4 women) trained one leg for E and the other leg for E and S (E+S). E training consisted of five 3-min bouts on a cycle ergometer at a power output corresponding to that requiring 90-100% of oxygen uptake during maximal exercise (VO2 max). S training consisted of six sets of 15-20 repetitions with the heaviest possible weight on a leg press (combined hip and knee extension) weight machine. Training was done 3 days/wk for 22 wk. Needle biopsy samples from vastus lateralis were taken before and after training and were examined for histochemical, biochemical, and ultrastructural adaptations. The nominal S and E training programs were “hybrids”, having more similarities as training stimuli than differences; thus S made increases (P less than 0.05) similar to those of S+E in E-related measures of VO2max (S, S+E: 8%, 8%), repetitions with the pretraining maximal single leg press lift [1 repetition maximum (RM)] (27%, 24%), and percent of slow-twitch fibers (15%, 8%); and S made significant, although smaller, increases in repetitions with 80% 1 RM (81%, 152%) and citrate synthase (CS) activity (22%, 51%). Similarly, E increased knee extensor area [computed tomography (CT) scans] as much as E+S (14%, 21%) and made significant, although smaller, increases in leg press 1 RM (20%, 34%) and thigh girth (3.4%, 4.8%). When a presumably stronger stimulus for an adaptation was added to a weaker one, some additive effects occurred (i.e., increases in 1 RM and thigh girth that were greater in E+S than E; increases in CS activity and repetitions with 80% 1 RM that were greater in S+E than S). When a weaker, although effective, stimulus was added to a stronger one, addition generally did not occur. Concurrent S and E training did not interfere with S or E development in comparison to S or E training alone.


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