Endurance exercise training attenuates leucine oxidation and BCOAD activation during exercise in humans

2000 ◽  
Vol 278 (4) ◽  
pp. E580-E587 ◽  
Author(s):  
Scott McKenzie ◽  
Stuart M. Phillips ◽  
Sherry L. Carter ◽  
Stuart Lowther ◽  
Martin J. Gibala ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Citrate Synthase ◽  
Exercise Bout ◽  
Leucine Oxidation ◽  
Endurance Exercise Training ◽  
Exercise Training Program ◽  
Activated State ◽  
Branched Chain ◽  
Exercise In Humans

We studied the effects of a 38-day endurance exercise training program on leucine turnover and substrate metabolism during a 90-min exercise bout at 60% peak O2 consumption (V˙o 2 peak) in 6 males and 6 females. Subjects were studied at both the same absolute (ABS) and relative (REL) exercise intensities posttraining. Training resulted in a significant increase in whole bodyV˙o 2 peak and skeletal muscle citrate synthase (CS; P < 0.001), complex I-III ( P < 0.05), and total branched-chain 2-oxoacid dehydrogenase (BCOAD; P < 0.001) activities. Leucine oxidation increased during exercise for the pretraining trial (PRE, P < 0.001); however, there was no increase for either the ABS or REL posttraining trial. Leucine oxidation was significantly lower for females at all time points during rest and exercise ( P < 0.01). The percentage of BCOAD in the activated state was significantly increased after exercise for both the PRE and REL exercise trials, with the increase in PRE being greater ( P < 0.001) compared with REL ( P < 0.05). Females oxidized proportionately more lipid and less carbohydrate during exercise compared with males. In conclusion, we found that 38 days of endurance exercise training significantly attenuated both leucine oxidation and BCOAD activation during 90 min of endurance exercise at 60%V˙o 2 peak for both ABS and REL exercise intensities. Furthermore, females oxidize proportionately more lipid and less carbohydrate compared with males during endurance exercise.

Regional vascular resistance during exercise: role of cardiac afferents and exercise training

1990 ◽  
Vol 258 (3) ◽  
pp. H842-H847 ◽  
Author(s):  
S. E. DiCarlo ◽  
V. S. Bishop
Keyword(s):  
Exercise Training ◽  
Vascular Resistance ◽  
Endurance Exercise ◽  
Vagal Afferents ◽  
Inhibitory Influence ◽  
Endurance Exercise Training ◽  
Exercise Training Program ◽  
Before And After ◽  
Regional Vascular Resistance ◽  
Cardiac Afferents

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Adaptations in Mitochondrial Enzymatic Activity Occurs Independent of Genomic Dosage in Response to Aerobic Exercise Training and Deconditioning in Human Skeletal Muscle

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 237 ◽  
Author(s):  
Andreas Fritzen ◽  
Frank Thøgersen ◽  
Kasper Thybo ◽  
Christoffer Vissing ◽  
Thomas Krag ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Enzymatic Activity ◽  
Endurance Exercise ◽  
Complex I ◽  
Citrate Synthase ◽  
Knee Extensor ◽  
Mitochondrial Complex ◽  
Membrane Markers ◽  
Endurance Exercise Training

Mitochondrial DNA (mtDNA) replication is thought to be an integral part of exercise-training-induced mitochondrial adaptations. Thus, mtDNA level is often used as an index of mitochondrial adaptations in training studies. We investigated the hypothesis that endurance exercise training-induced mitochondrial enzymatic changes are independent of genomic dosage by studying mtDNA content in skeletal muscle in response to six weeks of knee-extensor exercise training followed by four weeks of deconditioning in one leg, comparing results to the contralateral untrained leg, in 10 healthy, untrained male volunteers. Findings were compared to citrate synthase activity, mitochondrial complex activities, and content of mitochondrial membrane markers (porin and cardiolipin). One-legged knee-extensor exercise increased endurance performance by 120%, which was accompanied by increases in power output and peak oxygen uptake of 49% and 33%, respectively (p < 0.01). Citrate synthase and mitochondrial respiratory chain complex I–IV activities were increased by 51% and 46–61%, respectively, in the trained leg (p < 0.001). Despite a substantial training-induced increase in mitochondrial activity of TCA and ETC enzymes, there was no change in mtDNA and mitochondrial inner and outer membrane markers (i.e. cardiolipin and porin). Conversely, deconditioning reduced endurance capacity by 41%, muscle citrate synthase activity by 32%, and mitochondrial complex I–IV activities by 29–36% (p < 0.05), without any change in mtDNA and porin and cardiolipin content in the previously trained leg. The findings demonstrate that the adaptations in mitochondrial enzymatic activity after aerobic endurance exercise training and the opposite effects of deconditioning are independent of changes in the number of mitochondrial genomes, and likely relate to changes in the rate of transcription of mtDNA.

scholarly journals Perilipin 5 is dispensable for normal substrate metabolism and in the adaptation of skeletal muscle to exercise training

2016 ◽  
Vol 311 (1) ◽  
pp. E128-E137 ◽  
Author(s):  
Ruzaidi A. M. Mohktar ◽  
Magda K. Montgomery ◽  
Robyn M. Murphy ◽  
Matthew J. Watt
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Submaximal Exercise ◽  
Substrate Metabolism ◽  
Endurance Exercise Training ◽  
Perilipin 5

Cytoplasmic lipid droplets provide a reservoir for triglyceride storage and are a central hub for fatty acid trafficking in cells. The protein perilipin 5 (PLIN5) is highly expressed in oxidative tissues such as skeletal muscle and regulates lipid metabolism by coordinating the trafficking and the reversible interactions of effector proteins at the lipid droplet. PLIN5 may also regulate mitochondrial function, although this remains unsubstantiated. Hence, the aims of this study were to examine the role of PLIN5 in the regulation of skeletal muscle substrate metabolism during acute exercise and to determine whether PLIN5 is required for the metabolic adaptations and enhancement in exercise tolerance following endurance exercise training. Using muscle-specific Plin5 knockout mice ( Plin5 MKO), we show that PLIN5 is dispensable for normal substrate metabolism during exercise, as reflected by levels of blood metabolites and rates of glycogen and triglyceride depletion that were indistinguishable from control (lox/lox) mice. Plin5 MKO mice exhibited a functional impairment in their response to endurance exercise training, as reflected by reduced maximal running capacity (20%) and reduced time to fatigue during prolonged submaximal exercise (15%). The reduction in exercise performance was not accompanied by alterations in carbohydrate and fatty acid metabolism during submaximal exercise. Similarly, mitochondrial capacity (mtDNA, respiratory complex proteins, citrate synthase activity) and mitochondrial function (oxygen consumption rate in muscle fiber bundles) were not different between lox/lox and Plin5 MKO mice. Thus, PLIN5 is dispensable for normal substrate metabolism during exercise and is not required to promote mitochondrial biogenesis or enhance the cellular adaptations to endurance exercise training.

scholarly journals Role of intrinsic aerobic capacity and ventilator-induced diaphragm dysfunction

2015 ◽  
Vol 118 (7) ◽  
pp. 849-857 ◽  
Author(s):  
Kurt J. Sollanek ◽  
Ashley J. Smuder ◽  
Michael P. Wiggs ◽  
Aaron B. Morton ◽  
Lauren G. Koch ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Aerobic Capacity ◽  
Citrate Synthase ◽  
Contractile Function ◽  
Prolonged Mechanical Ventilation ◽  
Diaphragm Muscle ◽  
Oxidative Enzymes ◽  
Diaphragm Dysfunction ◽  
Endurance Exercise Training

Prolonged mechanical ventilation (MV) leads to rapid diaphragmatic atrophy and contractile dysfunction, which is collectively termed “ventilator-induced diaphragm dysfunction” (VIDD). Interestingly, endurance exercise training prior to MV has been shown to protect against VIDD. Further, recent evidence reveals that sedentary animals selectively bred to possess a high aerobic capacity possess a similar skeletal muscle phenotype to muscles from endurance trained animals. Therefore, we tested the hypothesis that animals with a high intrinsic aerobic capacity would naturally be afforded protection against VIDD. To this end, animals were selectively bred over 33 generations to create two divergent strains, differing in aerobic capacity: high-capacity runners (HCR) and low-capacity runners (LCR). Both groups of animals were subjected to 12 h of MV and compared with nonventilated control animals within the same strains. As expected, contrasted to LCR animals, the diaphragm muscle from the HCR animals contained higher levels of oxidative enzymes (e.g., citrate synthase) and antioxidant enzymes (e.g., superoxide dismutase and catalase). Nonetheless, compared with nonventilated controls, prolonged MV resulted in significant diaphragmatic atrophy and impaired diaphragm contractile function in both the HCR and LCR animals, and the magnitude of VIDD did not differ between strains. In conclusion, these data demonstrate that possession of a high intrinsic aerobic capacity alone does not afford protection against VIDD. Importantly, these results suggest that endurance exercise training differentially alters the diaphragm phenotype to resist VIDD. Interestingly, levels of heat shock protein 72 did not differ between strains, thus potentially representing an important area of difference between animals with intrinsically high aerobic capacity and exercise-trained animals.

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