Biomedical subjects

K Sahlin

Publications and source records attributed to K Sahlin.

At least 91 records · Page 5Linked to original sources

PubMed1986

Muscle ammonia and amino acid metabolism during dynamic exercise in man.

The effect of dynamic exercise on muscle and blood ammonia (NH3) and amino acid contents has been investigated. Eight healthy men cycled at 50% and 97% of maximal oxygen uptake for 10 min and 5.2 min (to fatigue), respectively. Biopsies (quadriceps femoris muscle), arterial and femoral venous blood samples were obtained at rest and during exercise. Muscle NH3 at rest and after submaximal exercise was (means +/- SE) 0.5 +/- 0.1 mmol/kg dry muscle (d.m.) and increased to 4.1 +/- 0.5 mmol/kg d.m. at fatigue (P less than 0.001). The total adenine nucleotide (TAN) pool (TAN = ATP + ADP + AMP) did not change after submaximal exercise but decreased significantly at fatigue (P less than 0.001). The decrease in TAN was similar to the increase in NH3. Muscle lactate was 3 +/- 1 mmol/kg d.m. at rest and increased to 104 +/- 5 mmol/kg d.m. at fatigue. Whole blood and plasma NH3 did not change significantly during submaximal but both increased significantly during maximal exercise (P less than 0.001). During maximal exercise the leg released 7,120 mumol/min of lactate, whereas only 89 mumol/min of NH3 were released. NH3 accumulation in muscle could buffer only 3% of the hydrogen ions released from lactate, and NH3 release could account for only 1% of the net hydrogen ion transport out of the cell. Muscle glutamine was constant throughout the study, whereas glutamate decreased and alanine increased during exercise (P less than 0.001). No significant changes in either arterial whole blood glutamine or glutamate were observed. Arterial plasma glutamine and glutamate concentrations, however, increased and decreased (P less than 0.001), respectively, during exercise. It is concluded that (1) muscle and blood NH3 levels increase only during strenuous exercise and (2) NH3 accumulation is of minor importance for regulating acid-base balance in body fluids during exercise.

Adult↗

PubMed1986

Redox state changes in human skeletal muscle after isometric contraction.

Subjects maintained an isometric contraction of the quadriceps femoris muscle at two-thirds maximal voluntary contraction (m.v.c.) force for 5 s (5.0 +/- 0.3 s; mean +/- S.E. of mean; n = 6) or until fatigue (52 +/- 4 s; n = 13). Muscle biopsies were obtained at rest, immediately after the contractions and also at 1 and 4 min of recovery after contraction to fatigue. In all subjects 5 s isometric contraction resulted in an increase of muscle NADH (0.084 +/- 0.012 at rest to 0.203 +/- 0.041 mmol/kg dry wt.) and a decrease of phosphocreatine (PC; change in concentration = -17.3 +/- 3.8 mmol/kg dry wt.). Glucose-6-phosphate concentration was more than doubled whereas lactate increased in only four of the six subjects. The two subjects who did not show any increase in lactate also had the lowest increase in NADH. At fatigue NADH increased to 0.226 +/- 0.032 mmol/kg dry wt. which was not significantly different from the value after 5 s contraction. Muscle PC was nearly depleted and lactate increased 12-fold above resting levels. The major part (65%) of the NADH increase at fatigue had reverted after 1 min recovery but only a slight further decrease occurred between 1 and 4 min of recovery. In relative terms the time course of the changes in muscle NADH during the first minute of recovery was similar to that of PC resynthesis, suggesting a common regulator such as O2 availability. In contrast to the delayed return of NADH concentration, PC resynthesis continued during the later part of the recovery period and PC concentration was almost fully restored after 4 min of recovery. It is concluded that muscle NADH is already maximally increased in the first seconds of muscle contraction at two-thirds m.v.c. Indirect evidence indicates that this increase reflects a reduction of the mitochondrial NAD-NADH redox couple. The rapid establishment of a reduced mitochondrial redox state at the start of muscle contraction will probably lead to a reduction of the redox state in the cytoplasm also and therefore be important for enhancing lactate formation.

Adult↗

PubMed1986

Muscle ammonia metabolism during isometric contraction in humans.

The changes in ammonia (NH3) and amino acid contents in human skeletal muscle during isometric exercise (2/3 maximal voluntary contraction force) to fatigue have been investigated. Biopsies from musculus quadriceps femoris were obtained at rest, fatigue, and 1 and 4 min recovery. Muscle NH3 (n = 9) increased from 1.3 +/- 0.3 (mean +/- SE) mmol/kg dry muscle (dm) at rest to 3.6 +/- 0.6 at fatigue (P less than 0.01) and remained elevated during recovery, whereas the lactate increase after contraction decreased rapidly during recovery. Total adenine nucleotide (TAN) content decreased from 28.7 +/- 0.5 mmol/kg dm at rest to 25.1 +/- 0.6 at fatigue (P less than 0.001). Muscle glutamine did not change after contraction (P greater than 0.05), whereas glutamate decreased (P less than 0.001), and alanine increased (P less than 0.001). In vivo AMP deaminase activity (measured by the rate of TAN decrease) was positively correlated with the percentage of fast-twitch fibers (r = 0.92; P less than 0.001) and the ATP turnover rate (r = 0.75; P less than 0.001) but was not related to the muscle lactate content (r = 0.27; P greater than 0.05). Phosphocreatine decreased to 6.1 +/- 0.7 mmol/kg dm (range = 1-11) after contraction. It is concluded that during exercise activation of AMP deaminase in vivo occurs when a high ATP turnover rate is coupled with a low phosphocreatine level, muscle pH is of minor importance for direct activation of AMP deaminase in vivo, and increases in NH3 do not have an important influence on glycolysis.

AMP Deaminase↗

PubMed1986

Leg glucose uptake during maximal dynamic exercise in humans.

Leg glucose uptake (LGU) during submaximal (50% maximal O2 uptake) and maximal dynamic exercise (97%) has been quantified from the product of the leg blood flow and the arterial minus femoral venous glucose concentration. Muscle biopsies were also obtained. During 15 min of submaximal exercise the mean LGU values ranged from 1.07 to 1.25 mmol/min, which demonstrates that LGU was stable under this condition. In contrast, during maximal exercise LGU increased continuously, reaching 2.38 +/- 0.22, 2.95 +/- 0.32, and 3.82 +/- 0.34 mmol/min after 2, 4, and 5.2 min (fatigue), respectively. The mean LGU was negatively related to the mean muscle phosphocreatine content (r = -1.00;P less than 0.01). Intracellular glucose-6-phosphate (G-6-P) and glucose were very low at rest and did not change significantly during submaximal exercise (P greater than 0.05). However, at fatigue G-6-P and glucose increased substantially and were both 8.5 mmol/kg dry muscle (P less than 0.001). These findings demonstrate that during heavy exercise glucose accumulates in the cell probably due to hexokinase inhibition by G-6-P, and thus the rate of glucose utilization appears to be lower than the rate of glucose uptake. It is suggested that 1) LGU during short-term exercise is dependent on the energy state of the muscle and 2) LGU is equal to leg glucose utilization during submaximal exercise but is in excess of utilization during heavy exercise.

Adult↗

PubMed1986

Muscle ATP turnover rate during isometric contraction in humans.

ATP turnover and glycolytic rates during isometric contraction in humans have been investigated. Subjects contracted the knee extensor muscles at two-thirds maximal voluntary force to fatigue (mean +/- SE, 53 +/- 4 s). Biopsies were obtained before and after exercise and analyzed for high-energy phosphates and glycogenolytic-glycolytic intermediates. Total ATP turnover was 190 +/- 7 mmol/kg dry muscle, whereas the average turnover rate was 3.7 +/- 0.2 mmol . kg dry muscle-1 . S-1. The average ATP turnover rate was positively correlated with the percentage of fast-twitch fibers in the postexercise biopsy (r = 0.71; P less than 0.05) and negatively correlated with contraction duration to fatigue (r = -0.88; P less than 0.05). At fatigue, phosphocreatine ranged from 1 to 11 mmol/kg dry muscle (86-99% depletion of value at rest), whereas lactate ranged from 59 to 101. The mean glycolytic rate was 0.83 +/- 0.05 mmol . kg dry muscle-1 . S-1 and was positively correlated with the rate of glucose 6-phosphate accumulation (r = 0.83; P less than 0.05). It is concluded that a major determinant of the ATP turnover rate is the muscle fiber composition, which is probably explained by a higher turnover rate in fast-twitch fibers; fatigue is more closely related to a low phosphocreatine content than to a high lactate content; and the increase in prephosphofructokinase intermediates is important for stimulating glycolysis during contraction.

Adenosine Triphosphate↗

PubMed1986

Muscle fatigue and lactic acid accumulation.

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.

Adenosine Triphosphate↗

PubMed1985

NADH in human skeletal muscle during short-term intense exercise.

The influence of high-intensity bicycle exercise on the redox level and lactate accumulation in skeletal muscle (m. quadriceps femoris) of man has been investigated. Six subjects exercised to exhaustion at a load corresponding to 100% VO2max. Muscle content of NADH, determined by the bioluminescence technique, increased from (means +/- SEM) 0.089 +/- 0.007 mmol/kg dry wt. at rest to 0.190 +/- 0.031 after 2 min of exercise (P less than 0.05) and to 0.213 +/- 0.021 at exhaustion (P less than 0.05). Values after 2 min exercise and at exhaustion were not statistically different (P greater than 0.05). Muscle lactate was increased 13-fold after 2 min of exercise and 22-fold at exhaustion as compared to the resting value. After 10 min recovery NADH was restored back to the pre-exercise level whereas muscle lactate was still elevated. The increase of muscle NADH during exercise is in contrast to earlier studies on isolated animal muscles, where an oxidation of NADH was observed during contractions. The difference might be due to the experimental model (isolated muscle vs. in vivo) or to the analytical method (qualitative data by reflectance fluorimetri from the surface of intact muscle vs. quantitative data from muscle extracts). Calculations of the cytosolic NADH concentration from the lactate dehydrogenase equilibrium show that 95% or more of the NADH is confined to the mitochondrial compartment. The observed increase of muscle NADH therefore imply that the redox potential of the mitochondria is decreased during intense exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

The effect of long-term circulatory occlusion on pH and energy metabolism of the quadriceps muscle in man.

The effect of up to 2.5 h circulatory occlusion on muscle pH and energy metabolism of the quadriceps muscle was studied in 13 patients operated on for an inveterate knee injury. Muscle samples were taken by the percutaneous needle biopsy technique at different times during the arterial occlusion and after restoration of circulation. Energy was provided by a complete utilization of phosphocreatine and by a low rate of glycolysis during 2 h of occlusion. The ATP level remained unchanged throughout the occlusion period. Muscle pH decreased from 7.0-7.1 to about 6.8 after 2 h occlusion. Muscle pH was essentially normalized within 20 min after restoration of the blood flow.

Adenosine Triphosphate↗

PubMed1985

Induction and treatment of metabolic acidosis: a study of pH changes in porcine skeletal muscle and cerebrospinal fluid.

Metabolic acidosis was induced in 18 piglets of Swedish native breed by prolonged iv infusion of lactic acid, which decreased both blood and muscle pH. A two- to three-fold increase in muscle lactate content was related to the decrease in muscle pH. Treatment of the induced metabolic acidosis with either sodium bicarbonate or a tris buffer mixture re-established normal or near-normal arterial pH, but PaCO2 remained elevated after sodium bicarbonate infusion. The pH in muscle and cerebrospinal fluid (CSF) normalized only in the group treated with the tris buffer mixture. Thus, the tris buffer mixture was more effective than traditional sodium bicarbonate in correcting the acid-base disturbance in the CSF and the muscle intracellular compartment.

Acidosis↗

PubMed1985

Activation of glycogen phosphorylase by electrical stimulation of isolated fast-twitch and slow-twitch muscles from rat.

The influence of muscle contraction, induced by electrical stimulation, on the activity of glycogen phosphorylase, the contents of high-energy phosphates, hexose-monophosphates and lactate have been studied in isolated extensor digitorum longus (EDL) and soleus muscles from rats. The activity of phosphorylase a + b was about nine times higher in fast twitch muscles (EDL) than in slow-twitch soleus and remained unchanged during the stimulation. A pronounced increase of phosphorylase a occurred during the stimulation in EDL muscle. Stimulation with a frequency of 50 Hz for 10 s and 2 Hz for 90 s resulted in a 44-fold and five-fold increase in phosphorylase a, respectively. In contrast, stimulation of soleus muscle resulted in only a minor increase of phosphorylase a. The rate of glycogenolysis increased in both muscles during the stimulation but the increase was four to five times higher in the EDL than in soleus muscle. The content of phosphocreatine (PCr) before stimulation was much higher in EDL than in soleus but similar after the stimulation. This resulted in a three- to four-fold higher release of inorganic phosphate (Pi) in EDL than in soleus during contraction. Pi has previously been shown to be present in a limiting amount for the activity of phosphorylase and the increase during contraction is of importance for increasing the glycogenolytic rate. It is concluded that the higher glycogenolytic capacity in fast-twitch muscles compared to slow-twitch muscles is due to: (1) higher content of phosphorylase a + b, (2) higher degree of transformation of the enzyme into the a form during contraction, and (3) higher content of PCr, which liberates a large amount of Pi during contraction.

Animals↗

PubMed1985

Effect of beta-adrenoceptor blockade on H+ and K+ flux in exercising humans.

The effect of beta-adrenoceptor blockade (beta B) on muscle release and uptake of H+ and K+ in humans during maximal exercise has been investigated. Eight volunteers cycled intermittently at power outputs corresponding to 100% of maximal O2 uptake. Prior to exercise either propranolol (beta B) or saline (control) was infused into the femoral vein. Arterial and femoral venous blood samples were drawn at rest, during exercise, and during 30-min recovery. Peak arterial blood values for K+, lactic acid (LA), and base deficit (BD) (mean +/- SE) were respectively 5.5 +/- 0.1, 9.5 +/- 0.6, and 11.7 +/- 0.9 mmol/l during beta B and 5.1 +/- 0.1, 8.3 +/- 0.6, and 10.3 +/- 1.0 for control (P less than 0.05). The release of K+ from the working leg did not differ between treatments during exercise, but K+ uptake during late recovery (5-30 min) was slightly lower during beta B. Thus the higher arterial K+ levels during exercise (beta B) cannot be attributed to greater release by active muscle but are likely due to decreased K+ uptake by noncontracting muscle. Arterial-femoral venous differences for LA and BD did not differ significantly between treatments. Additionally LA exchange across the leg was similar to H+ exchange (arterial-femoral venous differences for BD) under all conditions. During early recovery (1-5 min), regardless of experimental treatment, BD levels iin arterial blood were higher than LA (P less than 0.05). These elevated BD levels may be due to unequal removal rates between LA and H+ equivalents by nonexercised tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Intracellular pH and electrolytes in human skeletal muscle during adrenaline and insulin infusions.

There is evidence that both beta-adrenergic stimulation and insulin are of importance in controlling intracellular pH. Therefore we have investigated the influence of intravenous infusion of adrenaline or insulin glucose (euglycaemic clamp) on pH and electrolyte composition in resting skeletal muscle (m. quadriceps femoris) and arterial blood in six healthy subjects. A decrease in the arterial potassium concentration was observed during infusion of adrenaline and is in conformity with previous studies. Both adrenaline and insulin infusions resulted in an increased lactate content of muscle and blood, indicating an enhanced glycolysis. The intracellular concentrations of K+, Na+, Mg2+ and H+, however, remained unchanged during the adrenaline infusions as well as during infusions of insulin. It is concluded that increasing the plasma adrenaline and insulin concentrations to levels well above the physiological range (adrenaline) or in the upper physiological range (insulin) does not affect the concentrations of electrolytes and hydrogen ions in resting human muscle to any appreciable extent.

Adult↗

PubMed1984

Influence of glucose and fructose ingestion on the capacity for long-term exercise in well-trained men.

The aim of the present study was to examine the influence of glucose and fructose ingestion on the capacity to perform prolonged heavy exercise. Eight well-trained healthy volunteers exercised on a bicycle ergometer at 68 +/- 3% of their VO2 max until exhaustion, on three occasions, with 8-day intervals. During the exercise they ingested either glucose (250 ml, 7%), fructose (250 ml, 7%) or water (250 ml) every 20 min in a double-blind randomized study design. Arterial blood samples were collected at rest and during exercise for the determination of substrates and hormones. Muscle glycogen content (m. quadriceps femoris) was measured before and after exercise. The duration of exercise lengthened with repeated exercise (3rd test: 136 +/- 13 min v. 1st test: 110 +/- 12 min, P less than 0.01). Corrected for the sequence effect, total work time until exhaustion was significantly longer with glucose (137 +/- 13 min) than with either fructose (114 +/- 12 min) or water (116 +/- 13 min) (both P less than 0.01). When glucose or fructose was ingested, the arterial plasma glucose concentration was maintained at the normoglycaemic level; with water ingestion, plasma glucose values fell during exercise in seven subjects and remained at the resting level in the eighth subject. The muscle glycogen concentration was 467 +/- 29 mmol kg d.w.-1 at rest and fell to approximately half the initial value at exhaustion. In the subgroup of seven subjects in whom glucose values decreased with water intake, the mean rate of glycogen degradation was significantly lower (P less than 0.05) with the ingestion of glucose (1.3 +/- 0.4 mmol kg d.w.-1 min-1) as compared to fructose (2.1 +/- 0.5 mmol kg d.w.-1 min-1) or water (2.3 +/- 0.5 mmol kg d.w.-1 min-1). Intermittent glucose ingestion (3 X 17.5 g h-1) during prolonged, heavy bicycle exercise postpones exhaustion and exerts a glycogen-conserving effect in the working muscles. In contrast, fructose ingestion during exercise maintains the glucose concentration at the basal level but fails to influence either muscle glycogen degradation or endurance performance.

Adult↗

PubMed1984

Buffer capacity and lactate accumulation in skeletal muscle of trained and untrained men.

Buffer capacity (beta) of skeletal muscle has been determined in trained (n = 7) and in sedentary subjects (n = 8). The trained subjects were active in ball games where a high degree of anaerobic energy utilization is required. Percentage fibre type occurrence in the thigh muscle was not significantly different in the two groups. However, there was a tendency towards a higher proportion of type I (slow-twitch) fibres (61.5 +/- 11.6% vs. 50.2 +/- 12.5%) and a lower proportion of type IIB fibres (2.1 +/- 3.5% vs 14.1 +/- 16.3%) in the trained subjects. The proportion of the cross-sectional area of the muscle biopsies that was made up of type I or type II fibres was not different in the two groups. All subjects performed an isometric contraction of the knee extensors to fatigue at 61% of their maximal voluntary contraction force. Muscle biopsies were taken from the quadriceps femoris muscle at rest and immediately after contraction. The buffer capacity of muscle was calculated from: beta = (Muscle lactate (work)-Muscle lactate (rest)/(Muscle pH (rest)-Muscle pH (work)). A higher buffer capacity (p less than 0.05) was observed in the trained subjects (beta = 194 +/- 30 mmol X pH-1 X kg-1 dry wt.) compared to the sedentary group (beta = 164 +/- 20) (mean +/- SD). An unexpected finding was that muscle lactate after contraction to fatigue was lower (30%, p less than 0.01) and muscle pH was higher (6.80 +/- 0.06 vs. 6.61 +/- 0.12, p less than 0.01) in the trained subjects than in the sedentary controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1983

Quantitative estimation of anaerobic and oxidative energy metabolism and contraction characteristics in intact human skeletal muscle in response to electrical stimulation.

A set up for electrical stimulation of the human quadriceps femoris muscle and registration of tension is described. Normal values for the frequency-tension relations and relaxation time are presented. There was no relationship between contraction characteristics and fibre type distribution. Muscle tissue was sampled after electrical stimulation by percutaneous biopsy technique. Phosphocreatine (PCr) decreased during a 75 s isometric contraction from 76 mmol per kg dry muscle down to a mean value of 9 mmol. Lactate increased during the same time period from 5 mmol per kg dry muscle to 100 mmol. At end of contraction there was a rapid resynthesis of PCr with a half time of about 20 s while the lactate content decreased slowly. The relaxation time of the muscle was prolonged from 38 ms, in non-fatigued muscle, to 128 ms after 75 s of isometric contraction. The relaxation time was normalized after the contraction at the same rate as the resynthesis of PCr. It is proposed that the relationship between PCr and lactate of contracting muscle can be used as an index of glycolytic capacity and that the rate of resynthesis of PCr after contraction is a measure of oxidative capacity. Relaxation time measurements alone may be used as a non-invasive estimation of the oxidative capacity.

Adenosine Diphosphate↗

PubMed1983

NADH and NADPH in human skeletal muscle at rest and during ischaemia.

A method for determining the content of NADH and NADPH in biopsy specimens from human skeletal muscle is described. It is based on the bioluminescent technique, utilizing oxidoreductases specific for NADH and NADPH, respectively. Muscle samples were taken from the lateral portion of the quadriceps muscle in the basal state and following local circulatory occlusion. In resting human skeletal muscle, the content of NADH was 91 +/- 6 mumol/kg dry muscle (mean +/- SE, n = 11) and the NAD/NADH ratio was 18.8 +/- 1.3. The content of NADPH determined in four subjects was 108 +/- 2 mumol/kg dry muscle. After 5 min of circulatory occlusion, NADH had risen about 100% and a further increase was found after 10 and 20 min, to a plateau about 150% above the basal value. The muscle content of NADPH also increased but to a minor extent (about 30% above the basal value). The changes in muscle lactate after 5 and 10 min occlusion were not uniform between subjects but an increase was obtained in all subjects after 20 min occlusion. No relation was found between the ratios pyruvate/lactate and NAD/NADH and the latter ratio was smaller than the estimated value, calculated from the LDH equilibrium in the cytoplasm. The results indicate that the major part of NADH in muscle tissue is confined to the mitochondrial compartment. It is concluded that measurement of NADH provides information primarily about the mitochondrial redox state rather than the cytosolic and that changes in NADH precede lactate formation and thus are a more sensitive index of tissue hypoxia than increases in lactate.

Adult↗

PubMed1983

Acidotic depression of cyclic AMP accumulation and phosphorylase b to a transformation in skeletal muscle of man.

Intravenous infusion of adrenaline was performed in three healthy subjects on two occasions. In one case subjects performed a maximal isometric contraction before infusion. Biopsies were taken from the quadriceps femoris muscle before and after infusion for 0.5 and 2 min, and analysed for muscle pH, cyclic AMP, metabolites and activities of glycogen phosphorylase and synthetase. Isometric contraction resulted in a decrease of muscle pH to 6.60 (normal value at rest 7.0-7.1). By this experimental procedure the effect of adrenaline infusion could be studied on a muscle with normal pH and one with low pH. Cyclic AMP increased from 3 to about 9.5 mumol per kg dry weight after 0.5 min of adrenaline infusion. When isometric contraction preceded the infusion, cyclic AMP increased more slowly and was about 5.5 mumol per kg dry weight after the same time of infusion. Phosphorylase a constituted about 22% of total phosphorylase in resting muscle but increased rapidly to 80% after 0.5 min infusion. When exercise preceded infusion phosphorylase a decreased and was still lower after 2 min infusion. The results can be explained by inhibition of adenylcyclase and phosphorylase b kinase at low muscle pH.

Acid-Base Equilibrium↗

PubMed1983

Fatigue and phosphocreatine depletion during carbon dioxide-induced acidosis in rat muscle.

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.

Acidosis↗