Early adaptations in blood substrates, metabolites, and hormones to prolonged exercise training in man

1991 ◽  
Vol 69 (8) ◽  
pp. 1222-1229 ◽  
Author(s):  
H. J. Green ◽  
S. Jones ◽  
M. Ball-Burnett ◽  
I. Fraser

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects ([Formula: see text], [Formula: see text]) for 10–12 days with each exercise session lasting for 2 h at an average intensity of 59% of [Formula: see text]. This training protocol resulted in reductions (p < 0.05) in blood lactate concentration (mM) at 15 min (2.96 ± 0.46 vs. 1.73 ± 0.23), 30 min (2.92 ± 0.46 vs. 1.70 ± 0.22), 60 min (2.96 ± 0.53 vs. 1.72 ± 0.29), and 90 min (2.58 ± 1.3 vs. 1.62 ± 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p < 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p < 0.05) were observed for blood β-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p < 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p < 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.Key words: exercise, training, blood metabolites, substrates, hormones.

2006 ◽  
Vol 101 (5) ◽  
pp. 1320-1327 ◽  
Author(s):  
Mark Burnley ◽  
Jonathan H. Doust ◽  
Andrew M. Jones

Prior heavy exercise markedly alters the O2 uptake (V̇o2) response to subsequent heavy exercise. However, the time required for V̇o2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the V̇o2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second V̇o2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary V̇o2 time constant (from 25.9 ± 4.7 s to 23.9 ± 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary V̇o2 amplitude (from 2.42 ± 0.39 to 2.53 ± 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the V̇o2 slow component (from 0.44 ± 0.13 to 0.21 ± 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20–45 min, but not after 60 min, of recovery. The increase in the primary V̇o2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 ± 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20–60 min of recovery. The priming effect of prior heavy exercise on the V̇o2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.


1993 ◽  
Vol 3 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Mikael Fogelholm ◽  
Inkeri Ruokonen ◽  
Juha T. Laakso ◽  
Timo Vuorimaa ◽  
Jaakko-Juhani Himberg

By means of a 5-week vitamin B-complex .supplementation, associations between indices of vitamin B1, B2, and B6, status (activation coefficients [AC] for erythrocyte transketolase, glutathione reductase, and aspartate aminotransferase) and exercise-induced blood lactate concentration were studied. Subjects, 42 physically active college students (18–32 yrs), were randomized into vitamin (n=22) and placebo (n=20) groups. Before the supplementation there were no differences in ACs or basal enzyme activities between the groups. The ACs were relatively high, suggesting marginal vitamin status. In the vitamin group, all three ACs were lower (p<0.0001) after supplementation: transketolase decreased from l. 16 (1.14–1.18) (mean and 95% confidence interval) to 1.08 (1.06–1.10); glutathione reductase decreased from 1.33 (1.28–1.39) to 1 .I4 (1.1 1–1.17); and aspartate aminotransferase decreased from 2.04 (1.94–2.14) to 1.73 (1.67–1.80). No changes were found after placebo. Despite improved indices of vitamin status, supplementation did not affect exercise-induced blood lactate concentration. Hence no association was found between ACs and blood lactate. It seems that marginally high ACs do not necessarily predict altered lactate metabolism.


1994 ◽  
Vol 76 (2) ◽  
pp. 846-852 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3′, 3′,5′-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3′,5′-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.


2020 ◽  
Vol 2020 ◽  
pp. 1-24
Author(s):  
David G. Levitt ◽  
Joseph E. Levitt ◽  
Michael D. Levitt

Blood lactate concentration predicts mortality in critically ill patients and is clinically used in the diagnosis, grading of severity, and monitoring response to therapy of septic shock. This paper summarizes available quantitative data to provide the first comprehensive description and critique of the accepted concepts of the physiology of lactate in health and shock, with particular emphasis on the controversy of whether lactate release is simply a manifestation of tissue hypoxia versus a purposeful transfer (“shuttle”) of lactate between tissues. Basic issues discussed include (1) effect of nonproductive lactate-pyruvate exchange that artifactually enhances flux measurements obtained with labeled lactate, (2) heterogeneous tissue oxygen partial pressure (Krogh model) and potential for unrecognized hypoxia that exists in all tissues, and (3) pathophysiology that distinguishes septic from other forms of shock. Our analysis suggests that due to exchange artifacts, the turnover rate of lactate and the lactate clearance are only about 60% of the values of 1.05 mmol/min/70 kg and 1.5 L/min/70 kg, respectively, determined from the standard tracer kinetics. Lactate turnover reflects lactate release primarily from muscle, gut, adipose, and erythrocytes and uptake by the liver and kidney, primarily for the purpose of energy production (TCA cycle) while the remainder is used for gluconeogenesis (Cori cycle). The well-studied physiology of exercise-induced hyperlactatemia demonstrates massive release from the contracting muscle accompanied by an increased lactate clearance that may occur in recovering nonexercising muscle as well as the liver. The very limited data on lactate kinetics in shock patients suggests that hyperlactatemia reflects both decreased clearance and increased production, possibly primarily in the gut. Our analysis of available data in health and shock suggests that the conventional concept of tissue hypoxia can account for most blood lactate findings and there is no need to implicate a purposeful production of lactate for export to other organs.


2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S374
Author(s):  
F J. Diaz ◽  
M R. Garcia ◽  
T Franco ◽  
G Monta??o ◽  
F Moreno ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Tong Zhao ◽  
Shenglong Le ◽  
Nils Freitag ◽  
Moritz Schumann ◽  
Xiuqiang Wang ◽  
...  

Purpose: To assess the effect of chronic exercise training on blood lactate metabolism at rest (i.e., basal lactate concentrations) and during exercise (i.e., blood lactate concentration at a fixed load, load at a fixed blood lactate concentration, and load at the individual blood lactate threshold) among patients with type 2 diabetes mellitus (T2DM).Methods: PubMed (MedLine), Embase, Web of Science, and Scopus were searched. Randomized controlled trials, non-randomized controlled trials, and case-control studies using chronic exercise training (i.e., 4 weeks) and that assessed blood lactate concentrations at rest and during exercise in T2DM patients were included.Results: Thirteen studies were eligible for the systematic review, while 12 studies with 312 participants were included into the meta-analysis. In the pre-to-post intervention meta-analysis, chronic exercise training had no significant effect on changes in basal blood lactate concentrations (standardized mean difference (SMD) = −0.20; 95% CI, −0.55 to 0.16; p = 0.28), and the results were similar when comparing the effect of intervention and control groups. Furthermore, blood lactate concentration at a fixed load significantly decreased (SMD = −0.73; 95% CI, −1.17 to −0.29; p = 0.001), while load at a fixed blood lactate concentration increased (SMD = 0.40; 95% CI, 0.07 to 0.72; p = 0.02) after chronic exercise training. No change was observed in load at the individual blood lactate threshold (SMD = 0.28; 95% CI, −0.14 to 0.71; p = 0.20).Conclusion: Chronic exercise training does not statistically affect basal blood lactate concentrations; however, it may decrease the blood lactate concentrations during exercise, indicating improvements of physical performance capacity which is beneficial for T2DM patients' health in general. Why chronic exercise training did not affect basal blood lactate concentrations needs further investigation.


2015 ◽  
Vol 308 (11) ◽  
pp. H1434-H1442 ◽  
Author(s):  
Clark T. Holdsworth ◽  
Steven W. Copp ◽  
Scott K. Ferguson ◽  
Gabrielle E. Sims ◽  
David C. Poole ◽  
...  

The ATP-sensitive K+ (KATP) channel is part of a class of inward rectifier K+ channels that can link local O2 availability to vasomotor tone across exercise-induced metabolic transients. The present investigation tested the hypothesis that if KATP channels are crucial to exercise hyperemia, then inhibition via glibenclamide (GLI) would lower hindlimb skeletal muscle blood flow (BF) and vascular conductance during treadmill exercise. In 27 adult male Sprague-Dawley rats, mean arterial pressure, blood lactate concentration, and hindlimb muscle BF (radiolabeled microspheres) were determined at rest ( n = 6) and during exercise ( n = 6–8, 20, 40, and 60 m/min, 5% incline, i.e., ∼60–100% maximal O2 uptake) under control and GLI conditions (5 mg/kg intra-arterial). At rest and during exercise, mean arterial pressure was higher (rest: 17 ± 3%, 20 m/min: 5 ± 1%, 40 m/min: 5 ± 2%, and 60 m/min: 5 ± 1%, P < 0.05) with GLI. Hindlimb muscle BF (20 m/min: 16 ± 7%, 40 m/min: 30 ± 9%, and 60 m/min: 20 ± 8%) and vascular conductance (20 m/min: 20 ± 7%, 40 m/min: 33 ± 8%, and 60 m/min: 24 ± 8%) were lower with GLI during exercise at 20, 40, and 60 m/min, respectively ( P < 0.05 for all) but not at rest. Within locomotory muscles, there was a greater fractional reduction present in muscles comprised predominantly of type I and type IIa fibers at all exercise speeds ( P < 0.05). Additionally, blood lactate concentration was 106 ± 29% and 44 ± 15% higher during exercise with GLI at 20 and 40 m/min, respectively ( P < 0.05). That KATP channel inhibition reduces hindlimb muscle BF during exercise in rats supports the obligatory contribution of KATP channels in large muscle mass exercise-induced hyperemia.


2020 ◽  
Vol 19 (1) ◽  
pp. 32
Author(s):  
Gustavo Taques Marczynski ◽  
Luís Carlos Zattar Coelho ◽  
Leonardo Emmanuel De Medeiros Lima ◽  
Rodrigo Pereira Da Silva ◽  
Dilmar Pinto Guedes Jr ◽  
...  

The aim of this study was to analyze the influence of two velocities of execution relative to blood lactate concentration in strength training exercise until the momentary concentric failure. Fifteen men (29.1 ± 5.9 years), trained, participated in the experiment. The volunteers performed three bench press sessions, with an interval of 48 hours between them. At the first session, individuals determined loads through the 10-12 RMs test. In the following two sessions, three series with 90 seconds of interval were performed, in the second session slow execution speed (cadence 3030) and later in the third session fast speed (cadence 1010). For statistical analysis, the Student-T test was used for an independent sample study and considered the value of probability (p) ≤ 0.05 statistically significant. By comparing the number of repetitions and time under tension of the two runs, all series compared to the first presented significant reductions (p < 0.05). The total work volume was higher with the fast speed (p < 0.05). The study revealed that rapid velocities (cadence 1010) present a higher concentration of blood lactate when compared to slow runs (cadence 3030). The blood lactate concentration, in maximum repetitions, is affected by the speed of execution.Keywords: resistance training, cadence, blood lactate.


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