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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lactic acid is formed and accumulated in the muscle under conditions of high energy demand, rapid fluctuations of the energy requirement and insufficient supply of O2. During intense exercise sustained to fatigue muscle pH decreases to about 6.4-6.6. Force generation does not appear to be limited by the high H+ ion concentration per se but is more related to the PCr level. Phosphofructokinase may be inhibited by high H+ concentration but the inhibition is adequately overcome by increases in the activators AMP and ADP. A high concentration of H+ will decrease PCr by a direct effect on the creatine kinase equilibrium and indirectly by an increase in ADP. The effect of acidosis on glycolysis and on the PCr level will result in a decreased rate of ADP rephosphorylation, and it is suggested that ADP increases transiently above the steady-state level in the contracting muscle fibre. It is further suggested that the function of Na-K-ATPase is impaired by the increase of ADP resulting in an altered ionic balance over the muscle cell membrane. Muscle fatigue is thus considered to be due to an insufficient rate of ADP rephosphorylation resulting in a block in the activation process or in the excitation/contraction coupling.
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PMID:Muscle fatigue and lactic acid accumulation. 347 Oct 61

Fatigue--or decrease in force generation--is a reduction of simultaneously attached cross-bridges in the force generating state. Two processes are necessary for the force generation: Firstly Ca++ release from the sarcoplasmic reticulum to the sarcoplasm and the binding of Ca++ by the troponin molecule and secondly the turnover of myosin-actin cross-bridges. These processes require energy in at least three different ATPase reactions and can consequently be inhibited when ATP hydrolysis is decreased, i.e. when ATP content is to low or when the reaction products (ADP, Pi and H+) reach inhibiting levels or when muscle pH has decreased to values inhibiting actomyosin ATPase activity (22). Low pH will also decrease Ca++ release and Ca++ affinity by troponin (23). In isometric contraction the force is well preserved as long as ADP phosphorylation can be provided by both PCr degradation and anaerobic glycolysis. When the PCr store is exhausted the force starts to decline and if muscle activation is maintained the force will continue to decrease along with falling glycolytic rate. ADP phosphorylation rate decreases successively and ATP content falls with an at least transient increase in ADP. The ATP decrease, apart from the minor increase in ADP, is balanced by an equimolar increase in IMP. Lactate accumulation produces an increasing acidity with muscle pH values down to 6.25. Early changes in free ADP content cannot be excluded as reason for the initial decrease in force production followed by more pronounced inhibition of ATPase activity during continued contraction due to both substrate lack and product inhibition together with pH effect on the excitation--contraction mechanism. In dynamic exercise with supramaximum work intensity the relation between fatigue development and metabolism is similar. In prolonged dynamic exercise relying on oxidative metabolism without lactate formation the point of fatigue is reached when the glycogen store is exhausted. Again ADP phosphorylation rate is decreased when the energy substrate is changed from carbohydrate to fat with lower maximum rate of ATP resynthesis.
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PMID:Biochemistry of muscle fatigue. 396 54

Shock was elicited in anaesthetized dogs by maintaining a haemorrhagic hypotension of 4 kPa until 30 per cent spontaneous refusion, followed by total reinfusion. Functional residual capacity (FRC) and minute ventilation increased considerably similarly to our previous experiments. Lactate content in both the external intercostal and the biceps femoris muscles increased significantly in advanced shock. The expiratory external abdominal oblique muscle showed electromyographic signs of fatigue. At the height of the FRC changes tonic contraction of the external intercostal muscle could be demonstrated electron microscopically. This tonic contraction is the main factor in the large FRC rise in late shock forming the basis of a hitherto unknown vicious circle.
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PMID:Mechanism of functional residual capacity increase in haemorrhagic shock. 623 Aug 49

Young rats were made iron deficient by feeding them a low-iron diet for 8 wk. Iron deficiency resulted in a 50% decrease in cytochrome c and cytochrome oxidase and a 26% decrease in mitochondrial glycerol-3-phosphate dehydrogenase activity in skeletal muscle. Respiratory capacity of muscle homogenates was reduced 55%. After 8 days of iron treatment, respiratory capacity, cytochrome c, cytochrome oxidase, and glycerol-3-phosphate dehydrogenase had returned 50% toward normal. Maximum O2 uptake of contracting hindlimb muscles averaged 8.5 mumol O2.min-1.g-1 in control, 4.3 mumol O2.min-1.g-1 in iron-deficient, and 6.2 mumol O2.min-1.g-1 in the 8-day-iron-repleted rats. Muscle fatigue during 10 min of stimulation was greater in the iron-deficient group. Lactate concentration in red muscle was higher in iron-deficient than in control rats after stimulation. The muscle fatigue and lactate responses returned 50% toward normal during 8 days of iron treatment. We conclude that iron deficiency results in a decrease in skeletal muscle capacity for aerobic metabolism and, by this mechanism, increases susceptibility to fatigue.
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PMID:Physiological and biochemical effects of iron deficiency on rat skeletal muscle. 626 4

Isolated extensor digitorum longus muscles from rat were exposed to atmospheres of 30% CO2 (high-CO2 muscles) or 6.5% CO2 (control muscles) in O2 for 95 min. Muscle contraction characteristics were studied before and after the incubation. Tetanic tension decreased in high-CO2 muscles to 55% of initial value but remained unchanged in control muscles. Relaxation time was prolonged in high-CO2 muscles but not in control muscles. Intracellular pH was 6.67 +/- 0.04 (SD) in high-CO2 muscles and 7.01 +/- 0.04 in control muscles. CO2-induced acidosis had a marked influence on the intermediary energy metabolism as shown by a fourfold increase of glucose 6-phosphate, a 14% increase of ADP, and a decrease of phosphocreatine to 44% of the control value. Lactate and pyruvate contents were unchanged. The observed metabolic changes can be explained by an effect of H+ on the activity of phosphofructokinase and on the creatine kinase equilibrium. It can be concluded that H+ concentration causes muscular fatigue. It is, however, uncertain whether this is an effect of increased H+ per se or by high-energy phosphate depletion induced by acidosis.
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PMID:Fatigue and phosphocreatine depletion during carbon dioxide-induced acidosis in rat muscle. 640 27

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 torque were used as indices for fatigue and recovery, respectively. Venous blood samples were collected repeatedly up to 8 min 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 contractions. Following recovery, peak torque averaged 70 (47-86%) of the initial value. Lactate concentration after the 50 contractions was 2.9 +/- 1.3 mmol X 1(-1) and the peak post exercise value averaged 8.7 +/- 2.1 mmol X 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.
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PMID:Recovery from short term intense exercise: its relation to capillary supply and blood lactate concentration. 668 37

The present study was designed to evaluate the effects of changes in glycogen concentrations on lactate accumulation in human skeletal muscle during a 1 min maximal muscle fatigue test (MFT). All subjects first performed the MFT during a control experiment. Four subjects then performed the MFT again 1 h after prolonged exercise. Seven other subjects performed the MFT again after a 3 day carbohydrate (CHO) poor diet and again after 4 additional days of a CHO rich diet. The m. vastus lateralis was biopsied prior to (for glycogen determinations) and immediately after (for lactate determinations) each performance of the MFT. High but similar lactate concentrations were observed (22.3 mmol x kg-1 w.w.) with normal and supernormal glycogen levels. Lactate was significantly reduced following both the prolonged exercise (to 7.0 mmol x kg-1 w.w.) and the CHO poor diet (to 16.8 mmol x kg-1 w.w.). Alterations in muscle strength and fatigue patterns were also observed from the dietary manipulations but they were neither commensurate with the changes in metabolite concentrations nor statistically significant.
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PMID:Lactate concentrations after short, maximal exercise at various glycogen levels. 730 8

Diaphragm strips from young rats (45--60 g) about 0.3 mm thick were fatigued by tetanic stimulation at a train repetition rate of 2 HZ for 3 min. The isometric tension developed was measured during fatigue and recovery in solutions containing 25, 10, or 2 mM bicarbonate at both 37 and 30 degrees C. Tension fell during fatigue to between 20 and 30% of the initial value and this was not significantly influenced by external bicarbonate concentration or temperature over the range considered. Recovery of tension was complete and rapid (t1/2 < 1 min) in 25 mM bicarbonate at both temperatures. In 10 and 2 mM bicarbonate recovery was slowed (t1/2 3.5 and 7 min, respectively, at 30 degrees C, 1.6 and 4.5 min at 37 degrees C) and incomplete (85 and 72% at 30 degrees C, 82 and 61% at 37 degrees C). Muscle creatine phosphate fell during fatigue but was completely restored within 4 min at 30 degrees C in either 2 or 25 mM HCO3. Lactate increased less in muscles fatigued in 2 mM HCO3 and fell at a slower rate during recovery. The results seem to exclude intracellular creatine phosphate concentration as a major determinant in recovery. The evidence suggests that external bicarbonate can affect the recovery of tension following fatigue by altering intracellular acid-base balance.
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PMID:The effect of bicarbonate concentration on fatigue and recovery in isolated rat diaphragm muscle. 742 82

The purpose of this work was to examine the effect of the lactate ion on the fatigue process in working muscle independent of muscle [H+]. L-(+)-lactate was infused, at a pH that did not change arterial pH, into the blood perfusing an isolated, in situ dog gastrocnemius (N = 5) working at a submaximal intensity (isometric contractions at 2 Hz) and compared with control (C) conditions without lactate infusion. Each muscle was stimulated to work for two 60-min periods (separated by 45 min rest), consisting of three 20-min time periods with either the high arterial lactate condition (high [La]) or C condition sequentially ordered within each 60-min work period. Blood flow and O2 delivery were held constant between the C and high [La] conditions. Arterial and venous blood measurements and muscle biopsies were taken (7 biopsies from each condition) during each condition. Lactate infusion significantly increased arterial [La] (C = 4.2 +/- 0.2 mM vs high [La] = 14.4 +/- 0.2; mean +/- SE) and muscle [La] (C = 8.1 +/- 0.8 mM w.w. vs high [La] = 12.0 +/- 1.4) while arterial and muscle pH were unchanged between conditions. Muscle tension development was significantly reduced (C = 94 +/- 2 N.100 g-1 vs high [La] = 80 +/- 3) during lactate infusion and muscle O2 uptake changed proportionally with tension. These findings support an effect of the lactate anion on tension development which is independent of pH.
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PMID:Increased [lactate] in working dog muscle reduces tension development independent of pH. 775 64

Because cocaine causes a rapid sympathetic response and central euphoria, we tested whether it would improve endurance or alter carbohydrate metabolism during high-intensity activity. Thirty male rats (10 animals/group) were injected intraperitoneally with either saline (S) or one of two doses of cocaine-HCl (12.5 (C-1) or 20.0 (C-2) mg.kg-1 b.w.). Ten minutes later they began gradually running on a rodent treadmill. Within 2 min they were running at 56 m.min-1 until fatigued. The run time to exhaustion (mean +/- SE) for C-2 (569 +/- 97 s) was less than S (859 +/- 71) and C-1 (923 +/- 65) (P < 0.05) and 25% shorter (marginally insignificant) than a pretreatment run (754 +/- 67 s) (P > 0.05). Plasma lactate concentrations at exhaustion were 4.0 +/- 0.5 (S), 7.3 +/- 1.1 (C-1), and 13.9 +/- 2.5 (C-2) mmol (P < 0.05, S vs C-2). Lactate concentrations in white vastus muscle were also elevated by C (4.7 +/- 0.6 (S), 8.1 +/- 1.3 (C-1), and 15.0 +/- 3.7 (C-2) mumol.g-1, (P < 0.05, S vs C-2)], which correlated with the reduction in glycogen content in both C groups (9.9 +/- 2.3 (C-2), 10.3 +/- 1.2 (C-1), vs 33.9 +/- 2.0 (S) mumol.g-1]. These results show that, in spite of its purported stimulatory effect, cocaine treatment (20 mg.kg-1) immediately prior to intense exercise causes accelerated glycogen degradation and lactate accumulation in white vastus muscle during exercise and premature fatigue.
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PMID:Effects of cocaine on glycogen metabolism and endurance during high intensity exercise. 805 9


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