Non-oxidative Energy Supply Correlates with Lactate Transport and Removal in Trained Rowers

2020 ◽  
Vol 41 (13) ◽  
pp. 936-943
Author(s):  
Hugo Maciejewski ◽  
Muriel Bourdin ◽  
Léonard Féasson ◽  
Hervé Dubouchaud ◽  
Laurent André Messonnier
Keyword(s):  
Blood Lactate ◽  
Energy Supply ◽  
Citrate Synthase ◽  
Monocarboxylate Transporter ◽  
Oxygen Deficit ◽  
Muscle Lactate ◽  
Lactate Accumulation ◽  
Accumulated Oxygen Deficit ◽  
Lactate Removal ◽  
Exercise Muscle

AbstractThis study aimed to test if the non-oxidative energy supply (estimated by the accumulated oxygen deficit) is associated with an index of muscle lactate accumulation during exercise, muscle monocarboxylate transporter content and the lactate removal ability during recovery in well-trained rowers. Seventeen rowers completed a 3-min all-out exercise on rowing ergometer to estimate the accumulated oxygen deficit. Blood lactate samples were collected during the subsequent passive recovery to assess individual blood lactate curves, which were fitted to the bi-exponential time function: La(t)= [La](0)+A1·(1–e–γ 1 t)+A2·(1–e–γ 2 t), where the velocity constants γ1 and γ2 (min–1) denote the lactate exchange and removal abilities during recovery, respectively. The accumulated oxygen deficit was correlated with the net amount of lactate released from the previously active muscles (r =0.58, P<0.05), the monocarboxylate transporters MCT1 and MCT4 (r=0.63, P<0.05) and γ2 (r=0.55, P<0.05). γ2 and the lactate release rate at exercise completion were negatively correlated with citrate synthase activity. These findings suggest that the capacity to supply non-oxidative energy during supramaximal rowing exercise is associated with muscle lactate accumulation and transport, as well as lactate removal ability.

Lactate, ATP, and CP in working muscles during exhaustive exercise in man

1970 ◽  
Vol 29 (5) ◽  
pp. 598-602 ◽  
Author(s):  
Jan Karlsson ◽  
Bengt Saltin
Keyword(s):  
Blood Lactate ◽  
Muscle Tissue ◽  
Anaerobic Metabolism ◽  
Lactate Concentration ◽  
Oxygen Deficit ◽  
Bicycle Exercise ◽  
Muscle Lactate ◽  
Lactate Accumulation ◽  
Biopsy Specimens

The dynamics of lactate accumulation in working muscle was studied in three subjects performing maximal bicycle exercise of 2, 6, and 16 min duration. In separate experiments, the two longer maximal work periods were interrupted after 2 min and after 2 and 6 min, respectively. Biopsy specimens from the quadriceps femoris were obtained immediately after the work was terminated for determination of ATP, CP, glycogen, G-6-P and lactate. Blood lactate was also determined. The breakdown of the phosphagens (ATP and CP) was already maximal after 2 min of work in all experiments and averaged 2.7 and 3.6 mmole kg–1 wet muscle, respectively. The accumulation of lactate in the muscle and in the blood increased continuously until exhaustion and averaged in the muscle tissue both at the highest and medium loads 16.1 but was only 12.0 mmole kg–1 wet muscle at the lowest load. It is concluded that low ATP and CP stores in these experiments was not the reason for muscular fatigue. Further, if the muscle tissue lactate concentration was the reason for exhaustion on the two heaviest work loads another factor must be present to explain the exhaustion in the 16-min experiment. exhaustion; muscle metabolites; muscle lactate; blood lactate; anaerobic metabolism; oxygen deficit

Threshold for muscle lactate accumulation during progressive exercise

1989 ◽  
Vol 66 (6) ◽  
pp. 2710-2716 ◽  
Author(s):  
J. Chwalbinska-Moneta ◽  
R. A. Robergs ◽  
D. L. Costill ◽  
W. J. Fink
Keyword(s):  
Blood Lactate ◽  
Bicycle Ergometer ◽  
Exercise Tests ◽  
Muscle Lactate ◽  
Lactate Accumulation ◽  
Ergometer Exercise ◽  
Progressive Exercise ◽  
Blood Lactate Accumulation ◽  
Highly Correlated ◽  
The Relationship

The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the “below-OBLA” stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage; however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle glycogen repletion during active postexercise recovery

1987 ◽  
Vol 253 (3) ◽  
pp. E305-E311 ◽  
Author(s):  
E. M. Peters Futre ◽  
T. D. Noakes ◽  
R. I. Raine ◽  
S. E. Terblanche
Keyword(s):  
Blood Lactate ◽  
Muscle Glycogen ◽  
High Intensity ◽  
Active Recovery ◽  
Muscle Lactate ◽  
Glycogen Resynthesis ◽  
Passive Recovery ◽  
Lactate Removal ◽  
Glycogen Repletion ◽  
Lactate Levels

High-intensity intermittent bicycle exercise was used to deplete muscle glycogen levels by 70% and elevate blood lactate levels to greater than 13.0 mmol/l. Thereafter subjects either cycled with one leg for 45 min followed by 45 min of passive recovery (partially active recovery) or rested for 90 min (passive recovery). During the first 45 min of partially active recovery 1) blood lactate (P less than 0.05) and pH levels (P less than 0.05) returned more rapidly to preexercise values than during passive recovery, 2) the rate of net glycogen resynthesis (0.28 mumol . g-1 . min-1) was the same in both legs, and 3) muscle lactate levels were significantly lower (P less than 0.05) in the passive than in the active leg. Thereafter the rate of net muscle glycogen resynthesis was unchanged (0.26 mumol . g-1 . min-1) and lactate removal could theoretically account for only 18% of the glycogen resynthesized. Overall, the rate of muscle glycogen resynthesis and muscle lactate removal was not different from that measured during passive recovery. After high-intensity exercise 1) glycogen repletion is not impeded by light exercise, and 2) blood glucose is an important substrate for glycogen resynthesis.

scholarly journals Relationships between maximal muscle oxidative capacity and blood lactate removal after supramaximal exercise and fatigue indexes in humans

2004 ◽  
Vol 97 (6) ◽  
pp. 2132-2138 ◽  
Author(s):  
C. Thomas ◽  
P. Sirvent ◽  
S. Perrey ◽  
E. Raynaud ◽  
J. Mercier
Keyword(s):  
Blood Lactate ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Slow Phase ◽  
Vastus Lateralis Muscle ◽  
Supramaximal Exercise ◽  
Muscle Oxidative Capacity ◽  
S Cycling ◽  
Lactate Removal

The present study investigated whether blood lactate removal after supramaximal exercise and fatigue indexes measured during continuous and intermittent supramaximal exercises are related to the maximal muscle oxidative capacity in humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (γ2), which denoted the blood lactate removal ability. Fatigue indexes were calculated during all-out (FIAO) and repeated 10-s cycling sprints (FISprint). Biopsies were taken from the vastus lateralis muscle, and maximal ADP-stimulated mitochondrial respiration ( Vmax) was evaluated in an oxygraph cell on saponin-permeabilized muscle fibers with pyruvate + malate and glutamate + malate as substrates. Significant relationships were found between γ2 and pyruvate + malate Vmax ( r = 0.60, P < 0.05), γ2 and glutamate + malate Vmax ( r = 0.66, P < 0.01), and γ2 and citrate synthase activity ( r = 0.76, P < 0.01). In addition, γ2, glutamate + malate Vmax, and pyruvate + malate Vmax were related to FIAO (γ2 − FIAO: r = 0.85; P < 0.01; glutamate + malate Vmax − FIAO: r = 0.70, P < 0.01; and pyruvate + malate Vmax − FIAO: r = 0.63, P < 0.01) and FISprint (γ2 − FISprint: r = 0.74, P < 0.01; glutamate + malate Vmax − FISprint: r = 0.64, P < 0.01; and pyruvate + malate Vmax − FISprint: r = 0.46, P < 0.01). In conclusion, these results suggested that the maximal muscle oxidative capacity was related to blood lactate removal ability after a 1-min all-out test. Moreover, maximal muscle oxidative capacity and blood lactate removal ability were associated with the delay in the fatigue observed during continuous and intermittent supramaximal exercises in well-trained subjects.

Anaerobic Capacity: A Maximal Anaerobic Running Test Versus the Maximal Accumulated Oxygen Deficit

1996 ◽  
Vol 21 (1) ◽  
pp. 35-47 ◽  
Author(s):  
Neil S. Maxwell ◽  
Myra A. Nimmo
Keyword(s):  
Blood Lactate ◽  
Intermittent Exercise ◽  
Anaerobic Capacity ◽  
Capillary Blood ◽  
Treadmill Running ◽  
Oxygen Deficit ◽  
Blood Samples ◽  
Significant Difference ◽  
Accumulated Oxygen Deficit ◽  
Exercise Treadmill

The present investigation evaluates a maximal anaerobic running test (MART) against the maximal accumulated oxygen deficit (MAOD) for the determination of anaerobic capacity. Essentially, this involved comparing 18 male students performing two randomly assigned supramaximal runs to exhaustion on separate days. Post warm-up and 1, 3, and 6 min postexercise capillary blood samples were taken during both tests for plasma blood lactate (BLa) determination. In the MART only, blood ammonia (BNH3) concentration was measured, while capillary blood samples were additionally taken after every second sprint for BLa determination. Anaerobic capacity, measured as oxygen equivalents in the MART protocol, averaged 112.2 ± 5.2 ml∙kg−1∙min−1. Oxygen deficit, representing the anaerobic capacity in the MAOD test, was an average of 74.6 ± 7.3 ml∙kg−1. There was a significant correlation between the MART and MAOD (r =.83, p <.001). BLa values obtained over time in the two tests showed no significant difference, nor was there any difference in the peak BLa recorded. Peak BNH3 concentration recorded was significantly increased from resting levels at exhaustion during the MART. Key words: supramaximal intermittent exercise, treadmill running performance, blood lactate, ammonia

Effects of hyperoxia on skeletal muscle carbohydrate metabolism during transient and steady-state exercise

2005 ◽  
Vol 98 (1) ◽  
pp. 250-256 ◽  
Author(s):  
Trent Stellingwerff ◽  
Lee Glazier ◽  
Matthew J. Watt ◽  
Paul J. LeBlanc ◽  
George J. F. Heigenhauser ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Blood Lactate ◽  
Active Form ◽  
Carbohydrate Oxidation ◽  
Muscle Lactate ◽  
Carbohydrate Utilization ◽  
Lactate Accumulation ◽  
Substrate Phosphorylation ◽  
Blood Lactate Accumulation

This study compared the effects of inspiring either a hyperoxic (60% O2) or normoxic gas (21% O2) while cycling at 70% peak O2 uptake on 1) the ATP derived from substrate phosphorylation during the initial minute of exercise, as estimated from phosphocreatine degradation and lactate accumulation, and 2) the reliance on carbohydrate utilization and oxidation during steady-state cycling, as estimated from net muscle glycogen use and the activity of pyruvate dehydrogenase (PDH) in the active form (PDHa), respectively. We hypothesized that 60% O2 would decrease substrate phosphorylation at the onset of exercise and that it would not affect steady-state exercise PDH activity, and therefore muscle carbohydrate oxidation would be unaltered. Ten active male subjects cycled for 15 min on two occasions while inspiring 21% or 60% O2, balance N2. Blood was obtained throughout and skeletal muscle biopsies were sampled at rest and 1 and 15 min of exercise in each trial. The ATP derived from substrate-level phosphorylation during the initial minute of exercise was unaffected by hyperoxia (21%: 52.2 ± 11.1; 60%: 54.0 ± 9.5 mmol ATP/kg dry wt). Net glycogen breakdown during 15 min of cycling was reduced during the 60% O2 trial vs. 21% O2 (192.7 ± 25.3 vs. 138.6 ± 16.8 mmol glycosyl units/kg dry wt). Hyperoxia had no effect on PDHa, because it was similar to the 21% O2 trial at rest and during exercise (21%: 2.20 ± 0.26; 60%: 2.25 ± 0.30 mmol·kg wet wt−1·min−1). Blood lactate was lower (6.4 ± 1.0 vs. 8.9 ± 1.0 mM) at 15 min of exercise and net muscle lactate accumulation was reduced from 1 to 15 min of exercise in the 60% O2 trial compared with 21% (8.6 ± 5.1 vs. 27.3 ± 5.8 mmol/kg dry wt). We concluded that O2 availability did not limit oxidative phosphorylation in the initial minute of the normoxic trial, because substrate phosphorylation was unaffected by hyperoxia. Muscle glycogenolysis was reduced by hyperoxia during steady-state exercise, but carbohydrate oxidation (PDHa) was unaffected. This closer match between pyruvate production and oxidation during hyperoxia resulted in decreased muscle and blood lactate accumulation. The mechanism responsible for the decreased muscle glycogenolysis during hyperoxia in the present study is not clear.

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