scholarly journals Gluconeogenesis and hepatic glycogenolysis during exercise at the lactate threshold

2013 ◽  
Vol 114 (3) ◽  
pp. 297-306 ◽  
Author(s):  
Chi-An W. Emhoff ◽  
Laurent A. Messonnier ◽  
Michael A. Horning ◽  
Jill A. Fattor ◽  
Thomas J. Carlson ◽  
...  

Because the maintenance of glycemia is essential during prolonged exercise, we examined the effects of endurance training, exercise intensity, and plasma lactate concentration ([lactate]) on gluconeogenesis (GNG) and hepatic glycogenolysis (GLY) in fasted men exercising at, and just below, the lactate threshold (LT), where GNG precursor lactate availability is high. Twelve healthy men (6 untrained, 6 trained) completed 60 min of constant-load exercise at power outputs corresponding to their individual LT. Trained subjects completed two additional 60-min sessions of constant-load exercise: one at 10% below the LT workload (LT-10%), and the other with a lactate clamp (LT-10%+LC) to match the [lactate] of the LT trial. Flux rates were determined by primed continuous infusion of [6,6-2H2]glucose, [3-13C]lactate, and [13C]bicarbonate tracers during 90 min of rest and 60 min of cycling. Exercise at LT corresponded to 67.6 ± 1.3 and 74.8 ± 1.7% peak O2 consumption in the untrained and trained subjects, respectively ( P < 0.05). Relative exercise intensity was matched between the untrained group at LT and the trained group at LT-10%, and [lactate] during exercise was matched in the LT and LT-10%+LC trials via exogenous lactate infusion. Glucose kinetics (rate of appearance, rate of disposal, and metabolic clearance rate) were augmented with the lactate clamp. GNG was decreased in the trained subjects exercising at LT and LT-10% compared with the untrained subjects, but increasing [lactate] in the LT-10%+LC trial significantly increased GNG (4.4 ± 0.9 mg·kg−1·min−1) compared with its corresponding control (1.7 ± 0.4 mg·kg−1·min−1, P < 0.05). Hepatic GLY was higher in the trained than untrained subjects, but not significantly different across conditions. We conclude that GNG plays an essential role in maintaining total glucose production during exercise in fasted men, regardless of training state. However, endurance training increases the ability to achieve a higher relative exercise intensity and absolute power output at the LT without a significant decrease in GNG. Furthermore, raising systemic precursor substrate availability increases GNG during exercise, but not at rest.

2013 ◽  
Vol 114 (11) ◽  
pp. 1593-1602 ◽  
Author(s):  
Laurent A. Messonnier ◽  
Chi-An W. Emhoff ◽  
Jill A. Fattor ◽  
Michael A. Horning ◽  
Thomas J. Carlson ◽  
...  

To understand the meaning of the lactate threshold (LT) and to test the hypothesis that endurance training augments lactate kinetics [i.e., rates of appearance and disposal (Ra and Rd, respectively, mg·kg−1·min−1) and metabolic clearance rate (MCR, ml·kg−1·min−1)], we studied six untrained (UT) and six trained (T) subjects during 60-min exercise bouts at power outputs (PO) eliciting the LT. Trained subjects performed two additional exercise bouts at a PO 10% lower (LT-10%), one of which involved a lactate clamp (LC) to match blood lactate concentration ([lactate]b) to that achieved during the LT trial. At LT, lactate Ra was higher in T (24.1 ± 2.7) than in UT (14.6 ± 2.4; P < 0.05) subjects, but Ra was not different between UT and T when relative exercise intensities were matched (UT-LT vs. T-LT-10%, 67% V̇o2max). At LT, MCR in T (62.5 ± 5.0) subjects was 34% higher than in UT (46.5 ± 7.0; P < 0.05), and a reduction in PO resulted in a significant increase in MCR by 46% (LT-10%, 91.5 ± 14.9, P < 0.05). At matched relative exercise intensities (67% V̇o2max), MCR in T subjects was 97% higher than in UT ( P < 0.05). During the LC trial, MCR in T subjects was 64% higher than in UT ( P < 0.05), in whom %V̇o2max and [lactate]b were similar. We conclude that 1) lactate MCR reaches an apex below the LT, 2) LT corresponds to a limitation in MCR, and 3) endurance training augments capacities for lactate production, disposal and clearance.


1998 ◽  
Vol 8 (1) ◽  
pp. 60-69 ◽  
Author(s):  
Kristen L. Heck ◽  
Jeffrey A. Potteiger ◽  
Karen L. Nau ◽  
Jan M. Schroeder

We examined the effects of sodium bicarbonate ingestion on the VO2 slow component during constant-load exercise. Twelve physically active males performed two 30-min cycling trials at an intensity above the lactate threshold. Subjects ingested either sodium bicarbonate (BIC) or placebo (PLC) in a randomized. counterbalanced order. Arterialized capillary blood samples were analyzed for pH, bicarbonate concentration ([HCO3−), and lactate concentration ([La]). Expired gas samples were analyzed for oxygen consumption (VO2). The VO2 slow component was defined as the change in VO2 from Minutes 3 and 4 to Minutes 28 and 29. Values for pH and [HCO3−] were significantly higher for BIC compared to PLC. There was no significant difference in [La] between conditions. For both conditions there was a significant time effect for VO2 during exercise: however, no significant difference was observed between BIC and PLC. While extracellular acid-base measures were altered during the BIC trial, sodium bicarbonate ingestion did not attenuate the VO2 slow component during constant-load exercise.


1998 ◽  
Vol 274 (1) ◽  
pp. E23-E28 ◽  
Author(s):  
Réjean Drouin ◽  
Carole Lavoie ◽  
Josée Bourque ◽  
Francine Ducros ◽  
Danielle Poisson ◽  
...  

This study was designed to characterize the impact of endurance training on the hepatic response to glucagon. We measured the effect of glucagon on hepatic glucose production (HGP) in resting trained ( n = 8) and untrained ( n = 8) healthy male subjects (maximal rate of O2 consumption: 65.9 ± 1.6 vs. 46.8 ± 0.6 ml O2 ⋅ kg−1 ⋅ min−1, respectively, P < 0.001). Endogenous insulin and glucagon were suppressed by somatostatin (somatotropin release-inhibiting hormone) infusion (450 μg/h) over 4 h. Insulin (0.15 mU ⋅ kg−1 ⋅ min−1) was infused throughout the study, and glucagon (1.5 ng ⋅ kg−1 ⋅ min−1) was infused over the last 2 h. During the latter period, plasma glucagon and insulin remained constant at 138.2 ± 3.1 vs. 145.3 ± 2.1 ng/l and at 95.5 ± 4.5 vs. 96.2 ± 1.9 pmol/l in trained and untrained subjects, respectively. Plasma glucose increased and peaked at 11.4 ± 1.1 mmol/l in trained subjects and at 8.9 ± 0.8 mmol/l in untrained subjects ( P < 0.001). During glucagon stimulation, the mean increase in HGP area under the curve was 15.8 ± 2.8 mol ⋅ kg−1 ⋅ min−1in trained subjects compared with 7.4 ± 1.6 mol ⋅ kg−1 ⋅ min−1in untrained subjects ( P < 0.01) over the first hour and declined to 6.8 ± 2.8 and 4.9 ± 1.4 mol ⋅ kg−1 ⋅ min−1during the second hour. In conclusion, these observations indicate that endurance training is associated with an increase in HGP in response to physiological levels of glucagon, thus suggesting an increase in hepatic glucagon sensitivity.


1986 ◽  
Vol 60 (3) ◽  
pp. 777-781 ◽  
Author(s):  
J. Simon ◽  
J. L. Young ◽  
D. K. Blood ◽  
K. R. Segal ◽  
R. B. Case ◽  
...  

Six trained male cyclists and six untrained sedentary men were studied to determine whether the plasma lactate threshold (PLT) and ventilation threshold (VT) occur at the same work rate in both fit and unfit populations. The PLT was determined from a marked increase in plasma lactate concentration ([La]) and VT from a nonlinear increase in expired minute ventilation (VE) during incremental leg-cycling tests; work rate was increased 30 W every 2 min until volitional exhaustion. The trained subjects' mean VO2 max (63.8 ml O2 X kg-1 X min-1) and VT (65.8% VO2 max) were significantly higher (P less than 0.05) than the untrained subjects' mean VO2max (35.5 ml O2 X kg-1 X min-1) and VT (51.4% VO2 max). The trained subjects' mean PLT (68.8% VO2 max) and VT did not differ significantly, but the untrained subjects' mean PLT (61.6% VO2 max) was significantly higher than their VT. The trained subjects' mean peak [La] (10.5 mmol X l-1) did not differ significantly from the untrained subjects' mean peak [La] (11.5 mmol X l-1). However, the time of appearance of the peak [La] during passive recovery was inversely related to VO2 max. These results suggest that variance in lactate diffusion and/or removal processes between the trained and untrained subjects may account in part for the different relationships between the VT and PLT in each population.


2011 ◽  
Vol 6 (1) ◽  
pp. 8-24 ◽  
Author(s):  
Ralph Beneke ◽  
Renate M. Leithäuser ◽  
Oliver Ochentel

A link between lactate and muscular exercise was seen already more than 200 years ago. The blood lactate concentration (BLC) is sensitive to changes in exercise intensity and duration. Multiple BLC threshold concepts define different points on the BLC power curve during various tests with increasing power (INCP). The INCP test results are affected by the increase in power over time. The maximal lactate steady state (MLSS) is measured during a series of prolonged constant power (CP) tests. It detects the highest aerobic power without metabolic energy from continuing net lactate production, which is usually sustainable for 30 to 60 min. BLC threshold and MLSS power are highly correlated with the maximum aerobic power and athletic endurance performance. The idea that training at threshold intensity is particularly effective has no evidence. Three BLC-orientated intensity domains have been established: (1) training up to an intensity at which the BLC clearly exceeds resting BLC, light- and moderate-intensity training focusing on active regeneration or high-volume endurance training (Intensity < Threshold); (2) heavy endurance training at work rates up to MLSS intensity (Threshold ≤ Intensity ≤ MLSS); and (3) severe exercise intensity training between MLSS and maximum oxygen uptake intensity mostly organized as interval and tempo work (Intensity > MLSS). High-performance endurance athletes combining very high training volume with high aerobic power dedicate 70 to 90% of their training to intensity domain 1 (Intensity < Threshold) in order to keep glycogen homeostasis within sustainable limits.


PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10491
Author(s):  
Anna Gawedzka ◽  
Marcin Grandys ◽  
Krzysztof Duda ◽  
Justyna Zapart-Bukowska ◽  
Jerzy A. Zoladz ◽  
...  

Background Branched-chain amino acids (BCAA) i.e., leucine (Leu), isoleucine (Ile) and valine (Val) are important amino acids, which metabolism play a role in maintaining system energy homeostasis at rest and during exercise. As recently shown lowering of circulating BCAA level improves insulin sensitivity and cardiac metabolic health. However, little is known concerning the impact of a single bout of incremental exercise and physical training on the changes in blood BCAA. The present study aimed to determine the impact of a gradually increasing exercise intensity—up to maximal oxygen uptake (VO2max) on the changes of the plasma BCAA [∑BCAA]pl, before and after 5-weeks of moderate-intensity endurance training (ET). Methods Ten healthy young, untrained men performed an incremental cycling exercise test up to exhaustion to reach VO2max, before and after ET. Results We have found that exercise of low-to-moderate intensity (up to ∼50% of VO2max lasting about 12 min) had no significant effect on the [∑BCAA]pl, however the exercise of higher intensity (above 70% of VO2max lasting about 10 min) resulted in a pronounced decrease (p < 0.05) in [∑BCAA]pl. The lowering of plasma BCAA when performing exercise of higher intensity was preceded by a significant increase in plasma lactate concentration, showing that a significant attenuation of BCAA during incremental exercise coincides with exercise-induced acceleration of glycogen utilization. In addition, endurance training, which significantly increased power generating capabilities at VO2max (p = 0.004) had no significant impact on the changes of [∑BCAA]pl during this incremental exercise. Conclusion We have concluded that an exercise of moderate intensity of relatively short duration generally has no effect on the [∑BCAA]pl in young, healthy men, whereas significant decrease in [∑BCAA]pl occurs when performing exercise in heavy-intensity domain. The impact of exercise intensity on the plasma BCAA concentration seems to be especially important for patients with cardiometabolic risk undertaken cardiac rehabilitation or recreational activity.


2021 ◽  
Vol 9 (18) ◽  
Author(s):  
Ian R. Villanueva ◽  
John C. Campbell ◽  
Serena M. Medina ◽  
Theresa M. Jorgensen ◽  
Shannon L. Wilson ◽  
...  

Author(s):  
Madison M Fullerton ◽  
Louis Passfield ◽  
Martin J. MacInnis ◽  
Danilo Iannetta ◽  
Juan M Murias

Prior constant-load exercise performed for 30-min at or above maximal lactate steady state (MLSSp) significantly impairs subsequent time-to-task failure (TTF) compared with TTF performed without prior exercise. We tested the hypothesis that TTF would decrease in relation to the intensity and the duration of prior exercise compared to a baseline TTF trial. Eleven individuals (6 men, 5 women, 28 ± 8 yrs) completed the following tests on a cycle ergometer (randomly assigned after MLSSp was determined): i) a ramp-incremental test, ii) a baseline TTF trial performed at 80% of peak power (TTFb), iii) five 30-min constant-PO rides at 5% below lactate threshold (LT-5%), halfway between LT and MLSSp (Delta50), 5% below MLSSp (MLSS-5%), MLSSp, and 5% above MLSSp (MLSS+5%), and iv) 15- and 45-min rides at MLSSp (MLSS15 and MLSS45, respectively). Each condition was immediately followed by a TTF trial at 80% of peak power. Compared to TTFb (330 ± 52s), there was 8.0 ± 24.1, 23.6 ± 20.2, 41.0 ± 14.8, 52.2 ± 18.9, and 75.4 ± 7.4% reduction in TTF following LT-5%, Delta50, MLSS-5%, MLSSp, and MLSS+5%, respectively. Following MLSS15 and MLSS45 there were 29.0 ± 20.1 and 69.4 ± 19.6% reductions in TTF, respectively (P <0.05). It is concluded that TTF is reduced following prior exercise of varying duration at MLSSp and at submaximal intensities below MLSS. Novelty: •Prior constant-PO exercise, performed at intensities below MLSSp, reduces subsequent TTF performance. •Subsequent TTF performance is reduced in a linear fashion following an increase in the duration of constant-PO exercise at MLSSp.


1997 ◽  
Vol 82 (4) ◽  
pp. 1360-1369 ◽  
Author(s):  
Anne L. Friedlander ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Melvin J. Huie ◽  
George A. Brooks

Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (V˙o 2 peak)] and two posttraining trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra (4.63 ± 0.25), Rd (4.65 ± 0.24), Rox (3.77 ± 0.43), and Rd E (15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Rox was lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.


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