Effect of high-intensity exercise training on lactate/H+ transport capacity in human skeletal muscle (original) (raw)
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Effect of high-intensity exercise training on lactate/H+ transport capacity in human skeletal muscle
American Journal of Physiology-Endocrinology and Metabolism, 1999
The present study examined the effect of high-intensity exercise training on muscle sarcolemmal lactate/H+ transport and the monocarboxylate transporters (MCT1 and MCT4) as well as lactate and H+ release during intense exercise in humans. One-legged knee-extensor exercise training was performed for 8 wk, and biopsies were obtained from untrained and trained vastus lateralis muscle. The rate of lactate/H+ transport determined in sarcolemmal giant vesicles was 12% higher ( P < 0.05) in the trained than in untrained muscle ( n = 7). The content of MCT1 and MCT4 protein was also higher (76 and 32%, respectively; n = 4) in trained muscle. Release of lactate and H+ from the quadriceps muscle at the end of intense exhaustive knee-extensor exercise was similar in the trained and untrained leg, although the estimated muscle intracellular-to-interstitial gradients of lactate and H+ were lower ( P < 0.05) in the trained than in the untrained muscle. The present data show that intense exe...
Effect of high-intensity intermittent training on lactate and H+ release from human skeletal muscle
AJP: Endocrinology and Metabolism, 2003
The study investigated the effect of training on lactate and H + release from human skeletal muscle during one-legged knee-extensor exercise. Six subjects were tested after 7-8 weeks of training (fifteen 1-min bouts at ∼150 % of thigh VO 2max per day). Blood samples, blood flow, and muscle biopsies were obtained during and after a 30-W exercise bout and an incremental test to exhaustion of both trained (T-leg) and untrained (UT-leg) leg. Peak blood-flow was 16 % higher in T-leg than in UT-leg. In the 30-W test venous lactate and lactate release were lower in T-leg compared to UT-leg. In the incremental test time to fatigue was 10.6±0.7 and 8.2±0.7 min in T-leg and UT-leg (P<0.05). At exhaustion venous blood lactate was 10.7±0.4 and 8.0±0.9 mmol l -1 in T-leg and UT-leg (P<0.05), and lactate release was 19.4±3.6 and 10.6±2.0 mmol min -1 (P<0.05). H + release at exhaustion was higher in T-leg than in UT-leg. Muscle lactate content was 59.0±15.1 and 96.5 ± 14.5 mmol kg -1 dry weight in T-leg and UT-leg, and muscle pH was 6.82±0.05 and 6.69±0.04 in T-leg and UT-leg (P = 0.06). The membrane contents of the monocarboxylate transporters MCT1 and MCT4 and the Na + /H + exchanger were 115±5 (P<0.05), 111±11 and 116±6 % (P<0.05), respectively, in T-leg compared to UT-leg. The reason for the training-induced increase in peak lactate and H + release during exercise is a combination of an increased density of the lactate and H + transporting systems, an improved blood flow and blood flow distribution, as well as an increased systemic lactate and H + clearance.
Lactate and H+ effluxes from human skeletal muscles during intense, dynamic exercise
The Journal of Physiology, 1993
Lactate and H+ efflux from skeletal muscles were studied with the one-legged knee extension model under conditions in which blood flow, arterial lactate and the muscle-blood lactate concentration gradient were altered. Subjects exercised one leg twice to exhaustion (EXI, EX2), separated by a 10 min recovery and a period of intense intermittent exercise. After 1 h of recovery the exercise protocol was repeated with the other leg. Low-intensity exercise was performed with one leg during the recovery periods, while the other leg was passive during its recovery periods. 2. Prior to, and immediately after, EXI and EX2 and then 3 and 10 min after EXI, a biopsy was taken from the vastus lateralis of the exercised leg for lactate, pH, muscle water and fibre-type determinations. Measurements of leg blood flow and venous-arterial differences for lactate (whole blood and plasma), pH, partial pressure of CO2 (PC02) haemoglobin, saturation and base excess (BE) were performed at the end of exercise and regularly during the recovery period after EX1. 3. The lactate release was linearly related (r = 0-96; P < 0-05) to the muscle lactate gradient over a range of muscle lactate from 0 to 45 mmol (kg wet wt)-1. The muscle lactate transport was evaluated from the net femoral venous-arterial differences (V-Adiff) for lactate. This rose with increases in the muscle lactate gradients, but as the gradient reached higher levels the V-Adiff lactate responded less than at smaller gradients. Thus, the lactate transport over the muscle membrane appears to be partly saturated at high muscle lactate concentrations. 4. The percentage of slow twitch (% ST) fibres was inversely related to the muscle lactate gradient, but it was not correlated to the lactate release at the end of the exercises. In spite of a significantly higher blood flow during active recovery, the lactate release was the same whether the leg was resting or performed low-intensity exercise in the recovery periods. In several other conditions the muscle lactate and H+ gradients would have predicted that the V-Adiff lactate would have been greater than it actually was. Thus, a variety of factors affect muscle lactate transport, including arterial lactate concentration, muscle perfusion, muscle contraction pattern and muscle morphology. 5. The muscle and femoral venous pH declined during EXI to 6-73 and 7 14-7 15, MS 1198 5 PHY 462 116 J. BANGSBO AND OTHERS respectively, and they increased to resting levels during 10 min of either passive or active recovery. The ratio between proton release and lactate efflux was estimated from the BE difference across the muscle, adjusted for changes in reduced haemoglobin. This was 1-4-1P6 at the end of each exercise and remained greater than unity during recovery. Thus, proton release appears to be faster than the lactate efflux both during exercise and recovery.
Active muscle and whole body lactate kinetics after endurance training in men
Journal of Applied Physiology, 1999
We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate]a) during continuous exercise by decreasing net lactate release (L˙) and appearance rates (Ra) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O2consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 2 peak, same relative intensity (RLT)]. Nine men (27.4 ± 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75%V˙o 2 peak. Compared with the 65%V˙o 2 peakpretraining condition (4.75 ± 0.4 mM), [lactate]a decreased at ABT (41%) and RLT (21%) ( P < 0.05). L˙ decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that 1) active skeletal muscle is not solely responsible for elevated [lactate]a; and 2) training increases leg lactat...
Journal of Applied Physiology, 1999
The effect of a single bout of exhaustive exercise on muscle lactate transport capacity was studied in rat skeletal muscle sarcolemmal (SL) vesicles. Rats were assigned to a control (C) group ( n = 14) or an acutely exercised (E) group ( n = 20). Exercise consisted of treadmill running (25 m/min, 10% grade) to exhaustion. SL vesicles purified from C and E rats were sealed because of sensitivity to osmotic forces. The time course of 1 mM lactate uptake in zero- trans conditions showed that the equilibrium level in the E group was significantly lower than in the C group ( P < 0.05). The initial rate of 1 mM lactate uptake decreased significantly from 2.44 ± 0.22 to 1.03 ± 0.08 nmol ⋅ min−1 ⋅ mg protein−1( P < 0.05) after exercise, whereas that of 50 mM lactate uptake did not differ significantly between the two groups. For 100 mM external lactate concentration ([lactate]), exhaustive exercise increased initial rates of lactate uptake (219.6 ± 36.3 to 465.4 ± 80.2 nmol ⋅ min−1 ⋅ ...
AJP: Regulatory, Integrative and Comparative Physiology, 2006
This study examined the effect of two different intense exercise training regimens on skeletal muscle ion transport systems, performance, and metabolic response to exercise. Thirteen subjects performed either sprint training [ST; 6-s sprints ( n = 6)], or speed endurance training [SET; 30-s runs ∼130% V̇o2 max, n = 7]. Training in the SET group provoked higher ( P < 0.05) plasma K+ levels and muscle lactate/H+ accumulation. Only in the SET group was the amount of the Na+/H+ exchanger isoform 1 (31%) and Na+-K+-ATPase isoform α2 (68%) elevated ( P < 0.05) after training. Both groups had higher ( P < 0.05) levels of Na+-K+-ATPase β1-isoform and monocarboxylate transporter 1 (MCT1), but no change in MCT4 and Na+-K+-ATPase α1-isoform. Both groups had greater ( P < 0.05) accumulation of lactate during exhaustive exercise and higher ( P < 0.05) rates of muscle lactate decrease after exercise. The ST group improved ( P < 0.05) sprint performance, whereas the SET group ele...
Journal of Applied Physiology, 2004
The present study investigated whether muscular monocarboxylate transporter (MCT) 1 and 4 contents are related to the blood lactate removal after supramaximal exercise, fatigue indexes measured during different supramaximal exercises, and muscle oxidative parameters in 15 humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A bi-exponential time function was then used to determine the velocity constant of the slow phase ( 2), which denoted the blood lactate removal ability. Fatigue indexes were calculated during 1-min all-out (FIAO) and repeated 10-s (FISprint) cycling sprints. Biopsies were taken from the vastus lateralis muscle. MCT1 and MCT4 contents were quantified by Western blots, and maximal muscle oxidative capacity (Vmax ) was evaluated with pyruvate + malate and glutamate + malate as substrates. The results showed that the blood lactate removal ability (i.e., 2)) after a 1-min all-out test was significantly related to MCT1 content (r=0.70, P <0.01) but not to MCT4 (r=0.50, P >0.05). However, greater MCT1 and MCT4 contents were negatively related with a reduction of blood lactate concentration at the end of 1-min allout exercise (r =-0.56, and r= -0.61, P < 0.05, respectively). Among skeletal muscle oxidative indexes, we only found a relationship between MCT1 and glutamate + malate Vmax (r = 0.63, P < 0.05). Furthermore, MCT1 content, but not MCT4, was inversely related to FIAO (r =-0.54, P < 0.05) and FISprint (r r =0.58, P <0.05). We concluded that skeletal muscle MCT1 expression was associated with the velocity constant of net blood lactate removal after a 1-min all-out test and with the fatigue indexes.
European Journal of Applied Physiology and Occupational Physiology, 1996
We investigated the role of the forearm skeletal muscles in the removal of lactate during repeated periods of short-term intensive leg exercise, i.e. a forcevelocity (FV) test known to induce a marked accumulation of lactate in the blood. The leg FV test was performed by seven untrained male subjects. Arterial and venous blood samples for determination of arterial ([la-]a) and venous ([la-]v) plasma lactate concentrations were concomitantly taken at rest before the test, during the FV test at the end of each period of intensive exercise just before the 5-min between-sprint recovery period, and after the completion of the test at 2, 4, 6, 8, 10, 15, and 20 min of the final recovery. The arteriovenous difference in concentration for plasma lactate ([-la-]a-v) was determined for each blood sample. During the test, [la-]a and [la-]v increased significantly (P < 0.001; P < 0.001) with significantly higher values for [la-la (P < 0.001). At the onset of the test, [la-]a-v became positive and increased up to a braking force of 6 kg, correlating significantly with [la-]a (r = 0.61, P < 0.001) with power (r = 0.58, P < 0.001) during the test. At the end of the test, [la-]a, [la-]v and [-la-]a-v decreased (P < 0.001; P < 0.001; P < 0.001 respectively) but were still higher than the basal values after 20-min of passive recovery. In conclusion, forearm skeletal muscles would seem to have been involved in the removal of lactate from the blood during the leg FV test, with an increase in lactate uptake proportional to the increase in plasma lactate concentration and power.
European Journal of Applied Physiology and Occupational Physiology, 1983
Muscle force recovery from short term intense exercise was examined in 16 physically active men. They performed 50 consecutive maximal voluntary knee extensions. Following a 40-s rest period five additional maximal contractions were executed. The decrease in torque during the 50 contractions and the peak torque during the five contractions relative to initial torqffe were used as indices for fatigue and recovery, respectively. Venous blood samples were collected repeatedly up to 8 rain post exercise for subsequent lactate analyses. Muscle biopsies were obtained from m. vastus lateralis and analysed for fiber type composition, fiber area, and capillary density. Peak torque decreased 67 (range 47-82%) as a result of the repeated contractionsT Following recovery, peak torque averaged 70 (47-86%) of the initial value. Lactate concentration after the 50 contractions was 2.9 + 1.3 mmol 9 1-1 and the peak post exercise value averaged 8.7 + 2.1 mmol. 1-1. Fatigue and recovery respectively were correlated with capillary density (r =-0.71 and 0.69) but not with fiber type distribution. A relationship was demonstrated between capillary density and post exercise/peak post exercise blood lactate concentration (r = 0.64). Based on the present findings it is suggested that lactate elimination from the exercising muscle is partly dependent upon the capillary supply and subsequently influences the rate of muscle force recovery.
Lactate accumulation, proton buffering, and pH change in ischemically exercising muscle
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2005
The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and Pi, a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NADϩ needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.