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Biomedical subjects

E Hultman

Publications and source records attributed to E Hultman.

At least 55 records · Page 3Linked to original sources
PubMed1995

Skeletal muscle pyruvate dehydrogenase activity during acetate infusion in humans.

Pyruvate dehydrogenase activity (PDHa), acetyl group, and citrate accumulation were examined in human skeletal muscle at rest and during cycling exercise while acetate was infused. Eight subjects received 400 mmol of sodium acetate (Ace) at a constant rate during 20 min of rest, 5 min of cycling at 40% maximal O2 uptake (VO2max) and 15 min of cycling at 80% VO2max. Two weeks later experiments were repeated while 400 mmol of sodium bicarbonate was infused in the control condition (CON). Ace infusion increased muscle acetyl-coenzyme A (acetyl-CoA), citrate, and acetylcarnitine. A decline in resting PDHa during 20 min of Ace infusion (0.37 +/- 0.08 vs. 0.16 +/- 0.03 mmol.min-1.kg wet wt-1) coincided with an elevation in the acetyl-CoA-to-free CoA ratio (acetyl-CoA/CoASH; 0.28 +/- 0.04 to 0.73 +/- 0.14). After 20 min of CON infusion, resting PDHa (0.32 +/- 0.06 mmol.min-1.kg wet wt-1) was similar to PDHa before Ace infusion. During exercise, acetyl-CoA, citrate, and acetyl-CoA/CoASH were further elevated, and the differences that existed at rest were resolved. PDHa increased to the same extent in Ace and CON, in which it was 44-47% transformed after 5 min at 40% VO2max and completely transformed after 15 min at 80% VO2max. At rest PDHa was regulated by variations in acetyl-CoA/CoASH secondary to enhanced acetate metabolism. Conversely, during exercise PDHa regulation appeared independent of variations in acetyl-CoA/CoASH. The resting data are consistent with a central role for PDHa and citrate in the regulation of the glucose-fatty acid cycle in skeletal muscle, as classically proposed. However, in the present study Ace infusion was not effective in perturbing the glucose-fatty acid cycle during exercise.

Acetates↗
PubMed1995

Exercise causes branched-chain oxoacid dehydrogenase dephosphorylation but not AMP deaminase binding.

The responses of AMP deaminase (AMPD) and branched-chain oxoacid dehydrogenase (BCOAD) to moderate (70% maximal O2 consumption for 90 min) followed by intense (90% maximal O2 consumption to exhaustion) cycling exercise were evaluated in the active skeletal muscle of human subjects (n = 8). The exercise conditions invoke different energy demands and ammonia production rates. Active muscle and plasma ammonia concentrations continuously increased throughout moderate exercise in the absence of significant inosine 5-monophosphate accumulation. The free activity of AMPD decreased during moderate exercise (by approximately 25-35%), whereas myosin-bound activity did not change. BCOAD was significantly dephosphorylated (activated) at 5 min and was continuously dephosphorylated during moderate exercise (to a maximum of approximately 21%). Ammonia accumulation rate increased dramatically during the higher intensity exercise accompanied by inosine monophosphate accumulation of approximately 2 mmol/kg dry muscle. The higher intensity exercise caused no further changes in AMPD activity distribution or BCOAD dephosphorylation. Resting muscle percent bound AMPD was notably higher than values previously reported for rat muscle. Increases in percent bound AMPD during exercise were the result of decreases in the sum of free and bound activities and not increases in bound activity. The results of this study do not support a role for myosin binding in the activation of AMPD in human skeletal muscle.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1995

Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance.

BACKGROUND: Cardiac creatine levels are depressed in chronic heart failure. Oral supplementation of creatine to healthy volunteers has been shown to increase physical performance. AIM: To evaluate the effects of creatine supplementation on ejection fraction, symptom-limited physical endurance and skeletal muscle strength in patients with chronic heart failure. METHODS: With a double-blind, placebo-controlled design 17 patients (age 43-70 years, ejection fraction < 40) were supplemented with creatine 20 g daily for 10 days. Before and on the last day of supplementation ejection fraction was determined by radionuclide angiography as was symptom-limited 1-legged knee extensor and 2-legged exercise performance on the cycle ergometer. Muscle strength as unilateral concentric knee extensor performance (peak torque, Nm at 180 degrees/s) was also evaluated. Skeletal muscle biopsies were taken for the determination of energy-rich phosphagens. RESULTS: Ejection fraction at rest and at work did not change. Performance before creatine supplementation did not differ between placebo and creatine groups. While no change was seen in the placebo group compared to baseline, creatine supplementation increased skeletal muscle total creatine and creatine phosphate by 17 +/- 4% (P < 0.05) and 12 +/- 4% (P < 0.05), respectively. Increments were seen only in patients with < 140 mmol total creatine/kg d.w. (P < 0.05). One-legged performance (21%, P < 0.05), 2-legged performance (10%, P < 0.05), and peak torque, Nm (5%, P < 0.05) increased. Both peak torque and 1-legged performance increased linearly with increased skeletal muscle phosphocreatine (P < 0.05). The increments in 1-legged, 2-legged and peak torque were significant compared to the placebo group, (P < 0.05). CONCLUSIONS: One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.

Administration, Oral↗
PubMed1994

The metabolic responses of human type I and II muscle fibres during maximal treadmill sprinting.

1. Muscle biopsy samples were obtained from the vastus lateralis of six healthy volunteers before and after 30 s of treadmill sprinting. A portion of each biopsy sample was used for mixed-fibre metabolite analysis. Single fibres were dissected from the remaining portion of each biopsy and were used for ATP, phosphocreatine (PCr) and glycogen determination. 2. Before exercise, PCr and glycogen contents were higher in type II fibres (79.3 +/- 2.7 and 472 +/- 35 mmol (kg dry matter (DM)-1, respectively) compared with type I fibres (71.3 +/- 3.0 mmol (kg DM)-1, P < 0.01 and 375 +/- 25 mmol (kg DM)-1, P < 0.001, respectively). 3. Peak power output was 885 +/- 66 W and declined by 65 +/- 3% during exercise. Phosphocreatine and glycogen degradation in type II fibres during exercise (74.3 +/- 2.5 and 126.3 +/- 15.8 mmol (kg DM)-1, respectively) was greater than the corresponding degradation in type I fibres (59.1 +/- 2.9 mmol (kg DM)-1, P < 0.001 and 77.0 +/- 14.3 mmol (kg DM)-1, P < 0.01, respectively). The decline in ATP during exercise was similar when comparing fibre types (P > 0.05). 4. Compared with previous studies involving similar durations of maximal cycling exercise, isokinetic knee extension and intermittent isometric contraction, the rates of substrate utilization recorded in type I fibres were extremely high, being close to the rapid rates observed in this fibre type during intense contraction with limb blood flow occluded.

Adenosine Triphosphate↗
PubMed1994

Effect of oral creatine supplementation on skeletal muscle phosphocreatine resynthesis.

Biopsy samples were obtained from the vastus lateralis muscle of eight subjects after 0, 20, 60, and 120 s of recovery from intense electrically evoked isometric contraction. Later (10 days), the same procedures were performed using the other leg, but subjects ingested 20 g creatine (Cr)/day for the preceding 5 days. Muscle ATP, phosphocreatine (PCr), free Cr, and lactate concentrations were measured, and total Cr was calculated as the sum of PCr and free Cr concentrations. In five of the eight subjects, Cr ingestion substantially increased muscle total Cr concentration (mean 29 +/- 3 mmol/kg dry matter, 25 +/- 3%; range 19-35 mmol/kg dry matter, 15-32%) and PCr resynthesis during recovery (mean 19 +/- 4 mmol/kg dry matter, 35 +/- 6%; range 11-28 mmol/kg dry matter, 23-53%). In the remaining three subjects, Cr ingestion had little effect on muscle total Cr concentration, producing increases of 8-9 mmol/kg dry matter (5-7%), and did not increase PCr resynthesis. The data suggest that a dietary-induced increase in muscle total Cr concentration can increase PCr resynthesis during the 2nd min of recovery from intense contraction.

Administration, Oral↗
PubMed1994

Plasma volume and ion regulation during exercise after low- and high-carbohydrate diets.

This study compared plasma volume (PV) and ion regulation during prolonged exercise in control vs. glycogen-depleted (GD) conditions, with emphasis on the initial minutes of exercise. In two trials separated by 1-2 wk, four adult males cycled at 75% of peak oxygen consumption (VO2) until exhaustion (50 +/- 7 min for GD) or until the GD exhaustion time in the control trial. Blood was sampled from catheters placed in the brachial artery and retrograde in the femoral vein (fv). Arterial PV decreased rapidly and by 15 min PV was 83% (control) and 88% (GD) of initial. The decrease in PV was accompanied by a net osmotic flux of water from plasma and inactive tissues to contracting muscles. The significantly greater decrease in PV in control compared with GD was associated with a higher muscle lactate content (Lac-; 36 vs. 17 mumol/g dry wt, respectively). Increases in plasma [Cl-] and [Na+] were less than predicted from decreased PV, indicating net loss of these ions from the plasma compartment. Increases in arterial and fv [K+] were 50% greater than could be accounted for by decreased PV, corresponding with increased arterial and fv plasma K+ contents. The rapid net release of K+ and Lac- from contracting muscle during the first few minutes of exercise in both trials was abolished (control) or reversed (GD) within 15 min of beginning exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Nutritional status, muscle composition and plasma and muscle free amino acids in renal transplant patients.

To investigate the effects of renal transplantation (Rtx) on the nutritional status, muscle composition and the plasma and muscle free amino acid (AA) pattern, three groups of altogether 30 renal transplant patients (group I n = 10; 46 +/- 14 [SD] days after Trx), (group II n = 10; 13 +/- 2 months after Rtx) and (group III n = 10; 9 +/- 2 years after Rtx) underwent anthropometric measurements, blood sampling and percutaneous muscle biopsy. The immunosuppressive therapy consisted of prednisolone, azathioprine and cyclosporine-A. The results were compared with data from age-matched healthy subjects. Renal function was impaired in groups I, II and III. Serum albumin was decreased in groups I and II. The patients of group II had an increased percentage of body fat, triceps and subscapular skin folds and total sum of skinfolds. In group I the ratio alkaline-soluble protein (ASP) to DNA, which is a sensitive index of protein depletion on the cellular level, was decreased. Muscle magnesium content was decreased whereas the muscle DNA, sodium and chloride contents were increased. The mean plasma concentration of most essential AA (EAA) was essentially normal except phenylalanine which was increased in groups I and II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Influence of oral creatine supplementation of muscle torque during repeated bouts of maximal voluntary exercise in man.

1. The present experiment was undertaken to investigate the influence of oral creatine supplementation, shown previously to increase the total creatine content of human skeletal muscle (Harris RC, Soderlund K, Hultman E. Clin Sci 1992; 83: 367-74), on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise. 2. Twelve subjects undertook five bouts of 30 maximal voluntary isokinetic contractions, interspersed with 1 min recovery periods, before and after 5 days of placebo (4 x 6 g of glucose/day, n = 6) or creatine (4 x 5 g of creatine plus 1 g of glucose/day, n = 6) oral supplementation. Muscle torque production and plasma ammonia and blood lactate accumulation were measured during and after exercise on each treatment. 3. No difference was seen when comparing muscle peak torque production during exercise before and after placebo ingestion. After creatine ingestion, muscle peak torque production was greater in all subjects during the final 10 contractions of exercise bout 1 (P < 0.05), throughout the whole of exercise bouts 2 (P < 0.01), 3 (P < 0.05) and 4 (P = 0.057) and during contractions 11-20 of the final exercise bout (P < 0.05), when compared with the corresponding measurements made before creatine ingestion. Plasma ammonia accumulation was lower during and after exercise after creatine ingestion. No differences were found when comparing blood lactate levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Energy metabolism in single human muscle fibres during intermittent contraction with occluded circulation.

1. Glycogenolysis in type I and II muscle fibres was investigated in five healthy volunteers during electrical stimulation of the quadriceps muscle group with blood flow occluded. 2. The quadriceps femoris muscles were stimulated intermittently (1.6 s stimulation, 1.6 s rest) at a frequency of 50 Hz for 64 s and isometric contraction force was recorded. Muscle biopsies were obtained at rest prior to and immediately after stimulation. Single muscle fibres were dissected free and were identified as type I and II fibres. ATP, phosphocreatine (PCr) and glycogen contents were measured luminometrically and enzymatically in single fibres and mixed fibre muscle. 3. Electrical stimulation resulted in a marked decline in contraction force and near total depletion of PCr in both fibre types. The ATP turnover rate (P < 0.05) and the magnitude of the decline in ATP (P < 0.05) were greater in type II fibres. Prior to stimulation the muscle glycogen content was 32% higher in type II fibres compared with type I fibres (P < 0.01). During stimulation the rate of glycogenolysis in type II fibres (4.32 +/- 0.54 mmol (kg dry matter (DM)-1 s-1 was twofold greater than the rate in type I fibres (2.05 +/- 0.70 mmol (kg DM)-1 s-1, P < 0.05). 4. The data suggest that the relatively higher rate of glycogenolysis observed in type I fibres during intermittent electrical stimulation with occluded circulation (2.05 +/- 0.70 mmol (kg DM)-1 s-1), when compared with the corresponding rate recorded during intense contraction with circulation intact (0.18 +/- 0.14 mmol (kg DM)-1 s-1, P < 0.05), may result from an accelerated ATP turnover rate in this fibre type increasing the cellular concentrations of free AMP and inosine 5'-monophosphate (IMP), which are known activators of glycogen phosphorylase. 5. The similarity in the rate of type II fibre glycogenolysis during contraction with circulatory occlusion (4.32 +/- 0.54 mmol (kg DM)-1 s-1), when compared with the corresponding rate recorded during non-occluded circulation (3.54 +/- 0.53 mmol (kg DM)-1 s-1, P > 0.05), is in agreement with the suggestion that glycogenolysis in this fibre type is already occurring at a near-maximal rate with circulation intact.

Adult↗
PubMed1993

Pyruvate dehydrogenase activity and acetyl group accumulation during exercise after different diets.

Pyruvate dehydrogenase activity (PDHa) and acetyl group accumulation were examined in human skeletal muscle at rest and during exercise after different diets. Five males cycled at 75% of maximal O2 uptake (VO2 max) to exhaustion after consuming a low-carbohydrate diet (LCD) for 3 days and again 1-2 wk later for the same duration after consuming a high-carbohydrate diet (HCD) for 3 days. Resting PDHa was lower after a LCD (0.20 +/- 0.04 vs. 0.69 +/- 0.05 mmol.min-1.kg wet wt-1; P < 0.05) and coincided with a greater intramuscular acetyl-CoA-to-CoASH ratio, acetyl-CoA content, and acetylcarnitine content. PDHa increased during exercise in both conditions but at a lower rate in the LCD condition compared with the HCD condition (1.46 +/- 0.25 vs. 2.65 +/- 0.23 mmol.min-1.kg wet wt-1 at 16 min and 1.88 +/- 0.20 vs. 3.11 +/- 0.14 at the end of exercise; P < 0.05). During exercise muscle acetyl-CoA and acetylcarnitine content and the acetyl-CoA-to-CoASH ratio decreased in the LCD condition but increased in the HCD condition. Under resting conditions PDHa was influenced by the availability of fat or carbohydrate fuels acting through changes in the acetyl-CoA-to-CoASH ratio. However, during exercise the activation of PDHa occurred independent of changes in the acetyl-CoA-to-CoASH ratio, suggesting that other factors are more important.

Acetyl Coenzyme A↗
PubMed1993

Regulation of fat-carbohydrate interaction in skeletal muscle during intense aerobic cycling.

Six male subjects received either a saline (control) or Intralipid infusion during 30 min rest and 15 min cycling at 85% maximal O2 uptake (VO2max) to examine the regulation of fat-carbohydrate interaction (glucose-fatty acid cycle) in skeletal muscle. Muscle biopsies were sampled immediately before and at 3 and 15 min of exercise in both trials. A muscle biopsy was also taken at -30 min rest in the Intralipid trial. Intralipid infusion significantly elevated plasma free fatty acids above control during rest (0.21 +/- 0.04 to 0.94 +/- 0.09 mM) and exercise (5 min: 1.27 +/- 0.15 mM; 15 min: 1.42 +/- 0.13 mM). Muscle glycogen degradation was significantly lower in the Intralipid trial (109.7 +/- 29.3 vs. 194.7 +/- 32.1 mmol/kg dry muscle). Muscle lactate accumulation after 15 min was similar in both trials (control, 60.7 +/- 12.2 and Intralipid, 60.9 +/- 12.4 mmol/kg dry muscle). Muscle citrate increased at rest during Intralipid (0.32 +/- 0.06 to 0.58 +/- 0.06 mmol/kg dry muscle) but was not different between trials at 3 min (control, 0.73 +/- 0.07 and Intralipid, 0.68 +/- 0.06 mmol/kg dry muscle) and 15 min of cycling. Resting acetyl-CoA was unaffected by Intralipid and increased similarly in both trials at 3 min of cycling (control, 59.0 +/- 10.3 and Intralipid, 50.7 +/- 13.6 mumol/kg dry muscle) and remained unchanged at 15 min. Pyruvate dehydrogenase activity increased five- to sevenfold during exercise and was similar in both trials (15 min: control, 2.42 +/- 0.30 and Intralipid, 2.79 +/- 0.41 mmol.min-1 x kg wet wt-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetyl Coenzyme A↗
PubMed1993

PDC activity and acetyl group accumulation in skeletal muscle during isometric contraction.

The activity of pyruvate dehydrogenase complex (PDC) was studied in the human quadriceps femoris muscle during isometric contraction induced by intermittent electrical stimulation at 20 Hz. Muscle biopsy samples were obtained at rest and after 10, 20, and 46 contractions. The active form of PDC (PDCa) increased from a mean value of 26% of the total PDC at rest to mean values of 46, 78, and 80%, respectively. Muscle biopsy samples were also obtained at rest, after 46 contractions with limb blood flow intact or occluded, and after 2 min of oxidative recovery. In another experiment, muscle biopsy samples were obtained at rest, after 10 min of resting ischemia, and after 46 contractions with limb blood flow occluded. The transformation of PDC to PDCa was nearly complete, regardless of whether the blood flow was intact or occluded. However, the accumulation of acetyl groups observed during stimulation with intact blood flow was abolished when the blood flow was occluded. The absence of NADH oxidation during anoxia had no effect on the contraction-induced transformation of PDC to PDCa, but it inhibited the flux through the enzyme reaction.

Acetyl Coenzyme A↗
PubMed1992

Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation.

1. The present study was undertaken to test whether creatine given as a supplement to normal subjects was absorbed, and if continued resulted in an increase in the total creatine pool in muscle. An additional effect of exercise upon uptake into muscle was also investigated. 2. Low doses (1g of creatine monohydrate or less in water) produced only a modest rise in the plasma creatine concentration, whereas 5g resulted in a mean peak after 1h of 795 (SD 104) mumol/l in three subjects weighing 76-87 kg. Repeated dosing with 5g every 2h sustained the plasma concentration at around 1000 mumol/l. A single 5g dose corresponds to the creatine content of 1.1 kg of fresh, uncooked steak. 3. Supplementation with 5g of creatine monohydrate, four or six times a day for 2 or more days resulted in a significant increase in the total creatine content of the quadriceps femoris muscle measured in 17 subjects. This was greatest in subjects with a low initial total creatine content and the effect was to raise the content in these subjects closer to the upper limit of the normal range. In some the increase was as much as 50%. 4. Uptake into muscle was greatest during the first 2 days of supplementation accounting for 32% of the dose administered in three subjects receiving 6 x 5g of creatine monohydrate/day. In these subjects renal excretion was 40, 61 and 68% of the creatine dose over the first 3 days. Approximately 20% or more of the creatine taken up was measured as phosphocreatine. No changes were apparent in the muscle ATP content.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Bacteriology, drug stability and exchange of percutaneous delivery systems and antibacterial filters in long-term intrathecal infusion of opioid drugs and bupivacaine in "refractory" pain.

OBJECTIVE: To provide a basis for recommendations on the exchange of containers (syringes and cassettes) and antibacterial filters, and for choice of administration device in patients with "refractory" pain treated with long-term percutaneous intrathecal (IT) infusions of opioid (morphine or buprenorphine) and bupivacaine mixtures. DESIGN: Prospective, cohort, nonrandomized control trial-case series, with consecutive sample, no standard criterion, and cost-benefit analysis. SETTING: Tertiary care center, institutional practice as well as hospitalized and ambulatory care. PATIENTS: Eighty-nine (51 women and 38 men); 81 with malignant pain and 8 with benign "refractory" pain. INTERVENTIONS: (a) The chemical stability of the drugs in the containers during 30 days. (b) The results of bacteriologic culture of the residual volumes of the analgesic mixtures from used and reused (1-16 times) syringes (n = 135) and cassettes (n = 258), and of 5 ml of sterile isotonic saline filtered through the used Millipore filters (n = 149). The bacteriologic samples from the 89 patients were taken after 1-40 (median = 7), 1-86 (median = 20), and 5-78 (median = 31) days of IT treatment, respectively. MAIN OUTCOME MEASURES: Chemical stability: buprenorphine and bupivacaine concentrations-liquid chromatography; morphine concentrations--gas chromatography. Bacteriologic cultures: standard laboratory procedures. The hypothesis (repeated use of the infusion systems and their exchange once a month does not significantly affect drug concentrations or increase the infection risk) was elaborated before data collection began. RESULTS: The bupivacaine-opioid mixtures were found to be chemically stable within 3-10% of the original doses up to 30 days. Seventeen cultures (from five syringes, six cassettes, and six filters) in 13 patients (having no signs of meningeal infection) were found to be colonized with Staphylococcus aureus (n = 4), coagulase negative staphylococci (n = 7), viridans streptococci (n = 3), Neisseria sp (n = 4), Corynebacterium sp (n = 4), Enterobacter sp (n = 2), Klebsiella sp (n = 3), gram-negative bacilli (n = 1), and yeasts (n = 2). The place of IT treatment, its duration, and patient-related infection risk factors (age; malignancy; diabetes; presence of a colostomy, pyelostomy, or indwelling urinary catheter; and the presence and location of infection foci) were not related to the results of the cultures. However, 9 of the 17 positive cultures came from patients with skin ulcers, a notable incidence. The positive cultures had no connection with the cultured item, its in-use duration, the number of times of reuse, the analgesic drugs used, their concentrations or the presence of preservatives (sodium metabisulfite and sodium edetate), or the antiseptic agent (70% ethanol or 0.5% chlorhexidine gluconate) used during bacteriologic sampling. The bacterial growth was sparse in 14 and massive in 3 of the 17 positive cultures. One item (filter) from one patient with meningitis was sterile. CONCLUSIONS: In our population, exchange of the infusion systems when they are empty (within 1 month) and of the antibacterial filters once a month does not appear to affect the concentrations of, or increase the infection risk from, the opioid-bupivacaine mixtures. The risk of bacterial contamination/colonization of the syringes from syringe drivers does not seem to be higher than that of cassettes from external portable pumps.

Adolescent↗
PubMed1992

Energy metabolism in type I and type II human muscle fibres during short term electrical stimulation at different frequencies.

The degradation of adenosine triphosphate, phosphocreatine and glycogen was determined in type I and type II fibres of the human quadriceps femoris muscle during intermittent electrical stimulation at 20 and 50 Hz, (1.6 seconds stimulation, 1.6 seconds rest). Seven healthy volunteers took part in the study. Muscle biopsy samples were obtained at rest and after 10 and 20 seconds of stimulation (six and 12 contractions, respectively). The resting contents of adenosine triphosphate, phosphocreatine and glycogen were all higher (P less than 0.05) in type II fibres compared to type I fibres. By the end of stimulation, whole muscle force production had declined to 84 and 77% of the initial force at 20 and 50 Hz, respectively. The phosphocreatine degradation rate for 10 and 20 seconds of stimulation was greater in type II fibres (P less than 0.05) compared to type I fibers at both 20 and 50 Hz. The rates of glycogenolysis after 20 seconds stimulation in type II fibres were 3.18 +/- 1.1 and 6.31 +/- 1.39 mmol glycosyl units kg-1 s-1. The corresponding rates in type I fibres were 0.46 +/- 0.73 and 0.60 +/- 0.39 mmol glycosyl units kg-1 s-1, which were not significantly different from zero. It is hypothesized that the decline in whole muscle force observed during electrical stimulation may be a consequence of the rapid loss of PCr stores in type II fibres.

Adenosine Triphosphate↗
PubMed1992

Effects of fat availability on acetyl-CoA and acetylcarnitine metabolism in rat skeletal muscle.

This study was designed to examine the effects of stimulation and fat availability on the contents of acetyl coenzyme A (acetyl-CoA), free CoA (CoASH), acetylcarnitine, and free carnitine in the oxidative fiber types of rat skeletal muscle. Hindlimb muscles were perfused with no exogenous free fatty acids (FFA) or high FFA (0.93 +/- 0.03 mM) for 10 min at rest and during isometric, tetanic stimulation. Soleus (SOL) and red gastrocnemius (RG) muscles were sampled prior to perfusion and following rest perfusion and 1 and 5 min of stimulation. The SOL muscle contains predominantly slow oxidative (SO) fibers and the RG contains 56% fast oxidative-glycolytic (FOG) and 35% SO fibers. O2 uptake and tetanic tension production were similar in the fat-free and high FFA treatments. Rest perfusion with high FFA increased acetyl-CoA from 14.6 +/- 1.0 to 20.1 +/- 2.5 nmol/g dry muscle (dm) and acetylcarnitine from 0.12 +/- 0.01 to 0.78 +/- 0.18 mumol/g dm in the RG, while fat-free perfusion had no effect. The SOL results were similar as high FFA increased acetyl-CoA from 7.7 +/- 1.0 to 14.2 +/- 3.1 nmol/g dm and acetylcarnitine from 0.14 +/- 0.02 to 0.49 +/- 0.09 mumol/g dm. Stimulation increased acetyl-CoA and acetylcarnitine to values above rest in SOL and RG in both treatments and removed all fat-free and high-fat differences. The decreases in CoASH and free carnitine were reciprocal to the increases in acetyl-CoA and acetylcarnitine at all time points in both muscles such that total CoA and carnitine were constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetyl Coenzyme A↗