Effect of endurance training on muscle TCA cycle metabolism during exercise in humans

2004 ◽  
Vol 97 (2) ◽  
pp. 579-584 ◽  
Author(s):  
Krista R. Howarth ◽  
Paul J. LeBlanc ◽  
George J. F. Heigenhauser ◽  
Martin J. Gibala
Keyword(s):  
Oxygen Uptake ◽  
Endurance Training ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Tca Cycle ◽  
Peak Oxygen Uptake ◽  
Endurance Capacity ◽  
Exercise Induced ◽  
Cycle Endurance ◽  
Pretraining Trial

We tested the theory that links the capacity to perform prolonged exercise with the size of the muscle tricarboxylic acid (TCA) cycle intermediate (TCAI) pool. We hypothesized that endurance training would attenuate the exercise-induced increase in TCAI concentration ([TCAI]); however, the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22 ± 1 yr) cycled at ∼80% of initial peak oxygen uptake before and after 7 wk of training (1 h/day, 5 days/wk). Biopsies (vastus lateralis) were obtained during both trials at rest, after 5 min, and at the point of exhaustion during the pretraining trial (42 ± 6 min). A biopsy was also obtained at the end of exercise during the posttraining trial (91 ± 6 min). In addition to improved performance, training increased ( P < 0.05) peak oxygen uptake and citrate synthase maximal activity. The sum of four measured TCAI was similar between trials at rest but lower after 5 min of exercise posttraining [2.7 ± 0.2 vs. 4.3 ± 0.2 mmol/kg dry wt ( P < 0.05)]. There was a clear dissociation between [TCAI] and endurance capacity because the [TCAI] at the point of exhaustion during the pretraining trial was not different between trials (posttraining: 2.9 ± 0.2 vs. pretraining: 3.5 ± 0.2 mmol/kg dry wt), and yet cycle endurance time more than doubled in the posttraining trial. Training also attenuated the exercise-induced decrease in glutamate concentration (posttraining: 4.5 ± 0.7 vs. pretraining: 7.7 ± 0.6 mmol/kg dry wt) and increase in alanine concentration (posttraining: 3.3 ± 0.2 vs. pretraining: 5.6 ± 0.3 mmol/kg dry wt; P < 0.05), which is consistent with reduced carbon flux through alanine aminotransferase. We conclude that, after aerobic training, cycle endurance capacity is not limited by a decrease in muscle [TCAI].

scholarly journals Endurance Training Improves Oxygen Uptake and Endurance Capacity in Patients With Moderate to Severe Valvular Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Karin Vonbank ◽  
Daniel Haubenberger ◽  
Raphael Rosenhek ◽  
Matthias Schneider ◽  
Stefan Aschauer ◽  
...  
Keyword(s):  
Heart Disease ◽  
Oxygen Uptake ◽  
Endurance Training ◽  
Valvular Heart Disease ◽  
Cardiopulmonary Exercise Testing ◽  
Peak Oxygen Uptake ◽  
Endurance Capacity ◽  
Working Capacity ◽  
Endurance Test ◽  
Cardiopulmonary Exercise

Aim: Peak oxygen uptake (peakVO2) is one of the strongest predictors of survival in patients with valvular heart disease. The purpose of this study was to determine whether endurance training improves peakVO2 and endurance capacity in patients with moderate-severe aortic and mitral valve disease.Methods: 30 patients with moderate-severe valvular heart disease were randomly assigned to 12 weeks of endurance training (TG) (n = 16) or standard care (SC) (n = 14). PeakVO2 and maximum working capacity (Wattmax) were assessed by cardiopulmonary exercise testing, as well as submaximal endurance test at 80% of peakVO2 at baseline and after 12 weeks.Results: There was a significant improvement in peakVO2 from 27.2 ± 5.9 ml/kg to 30.4 ± 6.3 ml/kg (P &lt; 0.001) in TG compared to the SC (peakVO2 from 24.6 ± 4.4 to 24.7 ± 3.8) and in the Wattmax from 151.8 ± 41.0 Watt to 171.2 ± 49.7 Watt in the TG compared to the SC (152.9 ± 35.6 Watt to 149.2 ± 28.4 Watt). The endurance capacity increased significantly from 17.0 ± 9.4 min to 32.8 ± 16.8 min (p = 0.003) in the TG compared to the SC (11.7 ± 6.2 min to 11.2 ± 7.6 min). The heart rate during the endurance test decreased in the TG from 154 ± 14 b/min to 142 ± 20 b/min for the same workload. No changes could be seen in the SC.Conclusion: Endurance training in patients with moderate to severe valvular heart disease increased significantly the peakVO2 as well as the endurance capacity.

scholarly journals PlanHab: hypoxia exaggerates the bed-rest-induced reduction in peak oxygen uptake during upright cycle ergometry

2016 ◽  
Vol 311 (2) ◽  
pp. H453-H464 ◽  
Author(s):  
Michail E. Keramidas ◽  
Roger Kölegård ◽  
Igor B. Mekjavic ◽  
Ola Eiken
Keyword(s):  
Oxygen Uptake ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Vastus Lateralis ◽  
Bed Rest ◽  
Peak Oxygen Uptake ◽  
Cycle Ergometry ◽  
Vastus Lateralis Muscle ◽  
Before And After ◽  
Exercise Induced

The study examined the effects of hypoxia and horizontal bed rest, separately and in combination, on peak oxygen uptake (V̇o2 peak) during upright cycle ergometry. Ten male lowlanders underwent three 21-day confinement periods in a counterbalanced order: 1) normoxic bed rest [NBR; partial pressure of inspired O2(PiO2) = 133.1 ± 0.3 mmHg]; 2) hypoxic bed rest (HBR; PiO2= 90.0 ± 0.4 mmHg), and 3) hypoxic ambulation (HAMB; PiO2= 90.0 ± 0.4 mmHg). Before and after each confinement, subjects performed two incremental-load trials to exhaustion, while inspiring either room air (AIR), or a hypoxic gas (HYPO; PiO2= 90.0 ± 0.4 mmHg). Changes in regional oxygenation of the vastus lateralis muscle and the frontal cerebral cortex were monitored with near-infrared spectroscopy. Cardiac output (CO) was recorded using a bioimpedance method. The AIR V̇o2 peakwas decreased by both HBR (∼13.5%; P ≤ 0.001) and NBR (∼8.6%; P ≤ 0.001), with greater drop after HBR ( P = 0.01). The HYPO V̇o2 peakwas also reduced by HBR (−9.7%; P ≤ 0.001) and NBR (−6.1%; P ≤ 0.001). Peak CO was lower after both bed-rest interventions, and especially after HBR (HBR: ∼13%, NBR: ∼7%; P ≤ 0.05). Exercise-induced alterations in muscle and cerebral oxygenation were blunted in a similar manner after both bed-rest confinements. No changes were observed in HAMB. Hence, the bed-rest-induced decrease in V̇o2 peakwas exaggerated by hypoxia, most likely due to a reduction in convective O2transport, as indicated by the lower peak values of CO.

Green tea extract supplementation does not hamper endurance-training adaptation but improves antioxidant capacity in sedentary men

2015 ◽  
Vol 40 (10) ◽  
pp. 990-996 ◽  
Author(s):  
Yu-Chi Kuo ◽  
Jung-Charng Lin ◽  
Jeffrey R. Bernard ◽  
Yi-Hung Liao
Keyword(s):  
Oxygen Uptake ◽  
Antioxidant Capacity ◽  
Endurance Training ◽  
Green Tea ◽  
Acute Exercise ◽  
Green Tea Extract ◽  
Placebo Control ◽  
Endurance Capacity ◽  
Exercise Induced ◽  
Tea Extract

The purpose of this study was to investigate the effect of green tea extract (GTE) supplementation combined with endurance training on endurance capacity and performance in sedentary men. Forty untrained men (age: 20 ± 1 years) participated in this study. Subjects were assigned to 1 of 4 treatments: (i) placebo-control (CTRL), (ii) GTE, (iii) endurance training (Ex), and (iv) endurance training with GTE (ExGTE). During the 4-week intervention, exercise training was prescribed as 75% oxygen uptake reserve for three 20-min sessions per week, and either GTE (250 mg/day) or placebo was provided. Endurance capacity, malondialdehyde (MDA), total antioxidant status (TAS), and creatine kinase (CK) were examined. Ex and ExGTE but not GTE improved exhaustive-run time (Ex: +8.2%, p = 0.031; ExGTE: +14.3%, p < 0.001); in addition, Ex and ExGTE significantly increased maximal oxygen uptake by ∼14% (p = 0.041) and ∼17% (p = 0.017) above the values of the CTRL group, respectively. Both Ex and ExGTE significantly decreased the increase of CK by ∼11%–32% below that of CTRL following an exhaustive run (Ex: p = 0.007; ExGTE: p = 0.001). Moreover, TAS levels increased by ∼11% in ExGTE after training (p = 0.040), and GTE, Ex, and ExGTE markedly attenuated exercise-induced MDA production (p = 0.01, p = 0.005, p = 0.011, respectively). In conclusion, this investigation demonstrated that daily ingestion of GTE during endurance training does not impair improvements in endurance capacity. Moreover, endurance training combined with GTE not only increases antioxidant capacity without attenuating endurance training adaptations, but also further attenuates acute exercise-induced CK release.

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans

2005 ◽  
Vol 98 (6) ◽  
pp. 1985-1990 ◽  
Author(s):  
Kirsten A. Burgomaster ◽  
Scott C. Hughes ◽  
George J. F. Heigenhauser ◽  
Suzanne N. Bradwell ◽  
Martin J. Gibala
Keyword(s):  
Citrate Synthase ◽  
Training Session ◽  
Interval Training ◽  
Maximal Activity ◽  
Work Capacity ◽  
Control Group ◽  
Endurance Capacity ◽  
Sprint Interval Training ◽  
Oxidative Potential ◽  
Cycle Endurance

Parra et al. ( Acta Physiol. Scand 169: 157–165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change “anaerobic” work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (V̇o2 peak), no study has examined the effect of SIT on “aerobic” exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1–2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at ∼80% V̇o2 peak. Eight recreationally active subjects [age = 22 ± 1 yr; V̇o2 peak = 45 ± 3 ml·kg−1·min−1 (mean ± SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven “all-out” 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 ± 1.0 vs. 4.0 ± 0.7 mmol·kg protein−1·h−1) and resting muscle glycogen content increased by 26% (614 ± 39 vs. 489 ± 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 ± 11 vs. 26 ± 5 min; P < 0.05), despite no change in V̇o2 peak. The coefficient of variation for the cycle test was 12.0%, and a control group ( n = 8) showed no change in performance when tested ∼2 wk apart without SIT. We conclude that short sprint interval training (∼15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.

Plasma glucose kinetics during exercise in subjects with high and low lactate thresholds

1992 ◽  
Vol 73 (5) ◽  
pp. 1873-1880 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
J. P. Kirwan ◽  
D. M. Bier ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Plasma Glucose ◽  
Glucose Oxidation ◽  
Citrate Synthase ◽  
Metabolic Response ◽  
Vastus Lateralis ◽  
Cycle Ergometer ◽  
Vastus Lateralis Muscle ◽  
Respiratory Capacity ◽  
Group A

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.

Footstrike is the major cause of hemolysis during running

2003 ◽  
Vol 94 (1) ◽  
pp. 38-42 ◽  
Author(s):  
R. D. Telford ◽  
G. J. Sly ◽  
A. G. Hahn ◽  
R. B. Cunningham ◽  
C. Bryant ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Random Order ◽  
Peak Oxygen Uptake ◽  
Red Cell ◽  
Free Hemoglobin ◽  
Serum Haptoglobin ◽  
Total Hemoglobin ◽  
Exercise Induced

There is a wide body of literature reporting red cell hemolysis as occurring after various forms of exercise. Whereas the trauma associated with footstrike is thought to be the major cause of hemolysis after running, its significance compared with hemolysis that results from other circulatory stresses on the red blood cell has not been thoroughly addressed. To investigate the significance of footstrike, we measured the degree of hemolysis after 1 h of running. To control for the potential effects of oxidative and circulatory stresses on the red blood cell, the same subjects cycled for 1 h at equivalent oxygen uptake. Our subjects were 10 male triathletes, who each completed two separate 1-h sessions of running and cycling at 75% peak oxygen uptake, which were performed in random order 1 wk apart. Plasma free hemoglobin and serum haptoglobin concentrations were measured as indicators of hemolysis. We also measured methemoglobin as a percentage of total hemoglobin immediately postexercise as an indicator of red cell oxidative stress. Plasma free hemoglobin increased after both running ( P < 0.01) and cycling ( P < 0.01), but the increase was fourfold greater after running ( P < 0.01). This was reflected by a significant fall in haptoglobin 1 h after the running trials, whereas no significant changes occurred after cycling at any sample point. Methemoglobin increased twofold after both running and cycling ( P < 0.01), with no significant differences between modes of exercise. The present data indicate that, whereas general circulatory trauma to the red blood cells associated with 1 h of exercise at 75% maximal oxygen uptake may result in some exercise-induced hemolysis, footstrike is the major contributor to hemolysis during running.

Muscle metabolism during prolonged exercise in humans: influence of carbohydrate availability

1999 ◽  
Vol 87 (3) ◽  
pp. 1083-1086 ◽  
Author(s):  
G. McConell ◽  
R. J. Snow ◽  
J. Proietto ◽  
M. Hargreaves
Keyword(s):  
Oxygen Uptake ◽  
Vastus Lateralis ◽  
Time To Exhaustion ◽  
Endurance Capacity ◽  
Vastus Lateralis Muscle ◽  
Double Blind ◽  
Muscle Lactate ◽  
Carbohydrate Ingestion ◽  
Inosine Monophosphate ◽  
Muscle Energy

Eight endurance-trained men cycled to volitional exhaustion at 69 ± 1% peak oxygen uptake on two occasions to examine the effect of carbohydrate supplementation during exercise on muscle energy metabolism. Subjects ingested an 8% carbohydrate solution (CHO trial) or a sweet placebo (Con trial) in a double-blind, randomized order, with vastus lateralis muscle biopsies ( n = 7) obtained before and immediately after exercise. No differences in oxygen uptake, heart rate, or respiratory exchange ratio during exercise were observed between the trials. Exercise time to exhaustion was increased by ∼30% when carbohydrate was ingested [199 ± 21 vs. 152 ± 9 (SE) min, P < 0.05]. Plasma glucose and insulin levels during exercise were higher and plasma free fatty acids lower in the CHO trial. No differences between trials were observed in the decreases in muscle glycogen and phosphocreatine or the increases in muscle lactate due to exercise. Muscle ATP levels were not altered by exercise in either trial. There was a small but significant increase in muscle inosine monophosphate levels at the point of exhaustion in both trials, and despite the subjects in CHO trial cycling 47 min longer, their muscle inosine monophosphate level was significantly lower than in the Con trial (CHO: 0.16 ± 0.08, Con: 0.23 ± 0.09 mmol/kg dry muscle). These data suggest that carbohydrate ingestion may increase endurance capacity, at least in part, by improving muscle energy balance.

Time-course of recovery of peak oxygen uptake after exercise-induced muscle damage

2015 ◽  
Vol 216 ◽  
pp. 70-77 ◽  
Author(s):  
Christopher D. Black ◽  
Alexander R. Gonglach ◽  
Robert E. Hight ◽  
Jessica B. Renfroe
Keyword(s):  
Oxygen Uptake ◽  
Muscle Damage ◽  
Time Course ◽  
Peak Oxygen Uptake ◽  
Exercise Induced

Effects of endurance training and captivity on activity metabolism of lizards

1987 ◽  
Vol 252 (3) ◽  
pp. R450-R456 ◽  
Author(s):  
T. Garland ◽  
P. L. Else ◽  
A. J. Hulbert ◽  
P. Tap
Keyword(s):  
Endurance Training ◽  
Citrate Synthase ◽  
Standard Metabolic Rate ◽  
Thigh Muscle ◽  
Evolutionary Significance ◽  
Endurance Capacity ◽  
Adaptive Responses ◽  
Liver Mass ◽  
Sedentary Group ◽  
In Captivity

Two groups of Amphibolurus nuchalis, an Australian agamid lizard, were maintained in captivity for 8 wk. The “trained” group was given submaximal exercise at 1 km/h on a motorized treadmill, 30 min/day, 5 days/wk; the treadmill was inclined 10% for the last 5 wk. The “sedentary” group was not exercised. Endurance capacity did not change significantly in either group, but sprint speed decreased in trained lizards. The sedentary group exhibited significant decreases in maximal O2 consumption, standard metabolic rate, and heart mass, but an increase in liver mass. Trained lizards exhibited significant decreases in heart and thigh muscle masses, but significant increases in liver mass, hematocrit, liver pyruvate kinase, and heart citrate synthase activities. It is concluded that the adaptive response to endurance training, typical of mammals, does not generally occur in lizards. Moreover, levels of chronic activity that would elicit adaptive responses in mammals may be excessive for lizards and may induce pathological effects in joints and skeletal muscle. The ecological and evolutionary significance of these conclusions is discussed.

scholarly journals Nicotinamide Riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise

2020 ◽  
Author(s):  
Ben Stocks ◽  
Stephen P. Ashcroft ◽  
Sophie Joanisse ◽  
Yasir S. Elhassan ◽  
Gareth G. Lavery ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Exercise ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Endurance Capacity ◽  
Similar Response ◽  
Transcriptional Responses ◽  
Nicotinamide Riboside ◽  
Exercise Induced

AbstractOral supplementation of the NAD+ precursor Nicotinamide Riboside (NR) has been reported to increase Sirtuin (SIRT) signalling, mitochondrial biogenesis and endurance capacity in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study aimed to assess the effect of 7-day NR supplementation on exercise-induced transduction and transcriptional responses in skeletal muscle of young, healthy, recreationally active human volunteers. In a double-blinded, randomised, counter-balanced, crossover design, eight male participants (age: 23 ± 4 years, VO2peak: 46.5 ± 4.4 mL·kg-1·min-1) received one week of NR or cellulose placebo (PLA) supplementation (1000 mg·d-1) before performing one hour of cycling at 60% Wmax. Muscle biopsies were collected prior to supplementation and pre-, immediately and three-hours post-exercise from the medial vastus lateralis, whilst venous blood samples were collected throughout the trial. Global acetylation, auto-PARylation of PARP1, acetylation of p53Lys382 and MnSODLys122 were unaffected by NR supplementation or exercise. Exercise led to an increase in AMPKThr172 (1.6-fold), and ACCSer79 (4-fold) phosphorylation, in addition to an increase in PGC-1α (∼5-fold) and PDK4 (∼10-fold) mRNA expression, however NR had no additional effect on this response. There was also no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Finally, NR supplementation blunted the exercise induced activation of skeletal muscle NNMT mRNA expression, but had no effect on mRNA expression of NMRK1, NAMPT or NMNAT1, which were not significantly affected by NR supplementation or exercise. In summary, one week of NR supplementation does not augment skeletal muscle signal transduction pathways implicated in mitochondrial adaptation to endurance exercise.

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