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Biomedical subjects

O J Heinonen

Publications and source records attributed to O J Heinonen.

At least 37 records · Page 2Linked to original sources
PubMed1999

Muscle creatine phosphate in gyrate atrophy of the choroid and retina with hyperornithinaemia--clues to pathogenesis.

BACKGROUND: In gyrate atrophy of the choroid and retina with hyperornithinaemia (GA), inherited deficiency of ornithine-o-aminotransferase leads to progressive fundus destruction and atrophy of type II skeletal muscle fibres. Because high ornithine concentrations inhibit creatine biosynthesis, the ensuing deficiency of high-energy creatine phosphate may mediate the pathogenesis. MATERIALS AND METHODS: Relative concentrations of inorganic phosphate (Pi), creatine phosphate (PCr) and ATP in resting calf muscle were recorded in 23 GA patients and 33 control subjects using 31P-magnetic resonance spectroscopy (MRS). Eight patients with autosomal recessive retinitis pigmentosa with matched control subjects constituted an additional reference group. RESULTS: The PCr/Pi and PCr/ATP ratios (means +/- SD) were lower for the GA patients than for healthy control subjects [4.66 +/- 0.37 vs. 9.75 +/- 2.17 (P < 0.0001) and 2.85 +/- 0.37 vs. 3.70 +/- 0.50 (P < 0.05) respectively]. In retinitis pigmentosa the respective values were 9.12 +/- 2.57 and 4.25 +/- 0.45. Age and stage of the disease had no effect. CONCLUSION: Muscle 31P-MRS spectra were markedly abnormal in all GA patients.

Adenosine Triphosphate↗
PubMed1999

Creatine corrects muscle 31P spectrum in gyrate atrophy with hyperornithinaemia.

BACKGROUND: Eye fundus destruction and type II muscle fiber atrophy in gyrate atrophy of the choroid and retina with hyperornithinaemia (GA) may be mediated by elevated ornithine concentrations which strongly inhibit creatine biosynthesis. This results in deficiency of creatine phosphate (PCr), a key intracellular energy source, as we have demonstrated in skeletal muscle of the patients by 31P magnetic resonance spectroscopy (31P MRS). MATERIALS AND METHODS: Possible correction of the relative PCr deficiency by long-term daily exogenous supplementation of creatine or its precursors was investigated in four GA patients receiving creatine and in five patients treated with guanidinoacetic acid-methionine combination. The relative PCr concentration, expressed as PCr/Pi (Pi; inorganic phosphate) or as PCr/ATP ratios, was compared with the values of untreated GA patients, and matched healthy volunteers. RESULTS: Muscle PCr/Pi ratios (mean +/- SD) of the untreated and creatine supplemented GA patients and controls were 4.9 +/- 1.4, 7.9 +/- 0.4 and 8.4 +/- 1.3. Guanidinoacetate-methionine combination was similarly effective (respective PCr/Pi ratios: 4.9 +/- 0.7, 6.3 +/- 1.1 and 10.7 +/- 2.8). CONCLUSION: Supplementation with creatine or creatine precursors almost normalised low muscle PCr/Pi ratios of patients with GA.

Adolescent↗
PubMed1996

Knee extension dynamometer: a new device for dynamic isokinetic magnetic resonance spectroscopy experiments.

In the present study we introduce a new device for exercise magnetic resonance spectroscopy (MRS). It operates in a standard whole-body scanner. Mechanical exertion unit allows maximal 10 degrees to 15 degrees short-arc knee extensions. The device operates hydraulically and is based on isokinetic movement. The force and work conducted are automatically controlled by the electronic control and computer unit. A small surface coil placed on the vastus medialis muscle allows the collection of spectra without interfering spectra from nearby resting muscles. The force used for the extensions can be followed simultaneously as a curve on the screen in the operator's room and the data is transferred to a personal computer for later analysis. Total work and fatigue percentage are also calculated by the device. It also allows the use of different isokinetic exercise protocols. The measurements of force proved reliable in repeat measurements using an isokinetic test device as a control. This device has been used clinically for over a year, is easy to operate, and offers reliable measurements. It is well suited to trials where muscle energy states versus time are followed since it allows noninvasive simultaneous quantification of muscle performance and collecting MRS spectra at rest, during exercise, and in the recovery phase.

Ergometry↗
PubMed1996

Carnitine and physical exercise.

Carnitine plays a central role in fatty acid (FA) metabolism. It transports long-chain fatty acids into mitochondria for beta-oxidation. Carnitine also modulates the metabolism of coenzyme-A (CoA). It is not surprising that the use of supplementary carnitine to improve physical performance has become widespread in recent years, although there is no unequivocal support to this practice. However, critical reflections and current scientific-based knowledge are important because the implications of reduced or increased carnitine concentrations in vivo are not thoroughly understood. Several rationales have been forwarded in support of the potential ergogenic effects of oral carnitine supplementation. However, the following arguments derived from established scientific observations may be forwarded: (i) carnitine supplementation neither enhances FA oxidation in vivo or spares glycogen or postpones fatigue during exercise. Carnitine supplementation does not unequivocally improve performance of athletes; (ii) carnitine supplementation does not reduce body fat or help to lose weight; (iii) in vivo pyruvate dehydrogenase complex (PDC) is fully active already after a few seconds of intense exercise. Carnitine supplementation induces no further activation of PDC in vivo; (iv) despite an increased acetyl-CoA/free CoA ratio, PDC is not depressed during exercise in vivo and therefore supplementary carnitine has no effect on lactate accumulation; (v) carnitine supplementation per se does not affect the maximal oxygen uptake (VO2max); (vi) during exercise there is a redistribution of free carnitine and acylcarnitines in the muscle but there is no loss of total carnitine. Athletes are not at risk for carnitine deficiency and do not have an increased need for carnitine. Although there are some theoretical points favouring potential ergogenic effects of carnitine supplementation, there is currently no scientific basis for healthy individuals or athletes to use carnitine supplementation to improve exercise performance.

Animals↗
PubMed1994

[Not Available].

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Letter↗
PubMed1994

Different alterations in the insulin-stimulated glucose uptake in the athlete's heart and skeletal muscle.

Physical training increases skeletal muscle insulin sensitivity. Since training also causes functional and structural changes in the myocardium, we compared glucose uptake rates in the heart and skeletal muscles of trained and untrained individuals. Seven male endurance athletes (VO2max 72 +/- 2 ml/kg/min) and seven sedentary subjects matched for characteristics other than VO2max (43 +/- 2 ml/kg/min) were studied. Whole body glucose uptake was determined with a 2-h euglycemic hyperinsulinemic clamp, and regional glucose uptake in femoral and arm muscles, and myocardium using 18F-fluoro-2-deoxy-D-glucose and positron emission tomography. Glucose uptake in the athletes was increased by 68% in whole body (P < 0.0001), by 99% in the femoral muscles (P < 0.01), and by 62% in arm muscles (P = 0.06), but it was decreased by 33% in the heart muscle (P < 0.05) as compared with the sedentary subjects. The total glucose uptake rate in the heart was similar in the athletes and control subjects. Left ventricular mass in the athletes was 79% greater (P < 0.001) and the meridional wall stress smaller (P < 0.001) as estimated by echocardiography. VO2max correlated directly with left ventricular mass (r = 0.87, P < 0.001) and inversely with left ventricular wall stress (r = -0.86, P < 0.001). Myocardial glucose uptake correlated directly with the rate-pressure product (r = 0.75, P < 0.02) and inversely with left ventricular mass (r = -0.60, P < 0.05) or with the whole body glucose disposal (r = -0.68, P < 0.01). Thus, in athletes, (a) insulin-stimulated glucose uptake is enhanced in the whole body and skeletal muscles, (b) whereas myocardial glucose uptake per muscle mass is reduced possibly due to decreased wall stress and energy requirements or the use of alternative fuels, or both.

Adult↗
PubMed1994

Moderate carnitine depletion and long-chain fatty acid oxidation, exercise capacity, and nitrogen balance in the rat.

Carnitine plays a central role in lipid metabolism by transporting long-chain fatty acids into the mitochondria for beta-oxidation. Reduction of carnitine concentration does not automatically imply that functional carnitine deficiency exists with direct consequences on energy metabolism. In our experimental model, we reduced tissue concentrations of carnitine to levels that are comparable to those in patients with various metabolic disorders with secondary carnitine deficiency and did a study on the in vivo effects of moderate carnitine depletion on palmitate oxidation, exercise capacity, and nitrogen balance. Thirty rats were divided into a carnitine-depleted group (group I) and pair-fed controls (group II). Carnitine depletion resulting in a 48% reduction of tissue carnitine concentrations was induced by feeding ad libitum a carnitine-free oral diet consisting of parenteral nutrition solutions. Palmitate oxidation was measured by collecting expired 14CO2 after an intraperitoneal injection of [1-14C]palmitate, and exercise capacity was determined by having the rats swim to exhaustion. Despite the 48% depletion of carnitine in serum, muscle, and liver, there were no differences in cumulative palmitate oxidation in 3 h (group I, 40 +/- 7%; group II, 37 +/- 9% of injected activity), swimming time to exhaustion (group I, 8.1 +/- 2.8 h; group II, 7.7 +/- 3.6 h), or nitrogen balance (group I, 1.1 +/- 0.5 g of nitrogen/kg/d; group II, 1.2 +/- 0.5 g of nitrogen/kg/d). We conclude that carnitine depletion of 48% has no effect on palmitate oxidation, exercise capacity, or nitrogen balance in the rats studied.

Animals↗
PubMed1993

Effects of endurance training on hormonal responses to prolonged physical exercise in males.

The effect of several years' endurance training on hormonal changes during acute prolonged physical exercise was studied. In trial I, 13 cross-country skiers were studied before and after a 75-km ski race and 3 weeks later on a control day. In trial II, 10 trained and 8 untrained subjects bicycled for 4 h on the road with as high a performance level as possible. Venous blood samples were taken in both trials before and after the exercise. In trial I, serum concentrations of luteinizing hormone (p < 0.01) and follicle-stimulating hormone (FSH, p < 0.001) decreased more from morning to afternoon samples, and cortisol (p < 0.001) and growth hormone (GH, p < 0.001) increased more during the ski race when compared to the control day. Serum testosterone decreased during the ski race (p < 0.01) but not on the control day. In trial II, a group difference was seen in serum FSH levels which was higher in the trained than untrained subjects at all three time points (F = 4.66, p = 0.046). A significant trial-group interaction (p = 0.020) was seen in GH, the GH being lower before exercise and higher 2 h after exercise in the untrained subjects. There was a significant group contrast between pre- and post-exercise samples in testosterone (p = 0.021) and cortisol (p = 0.022). In conclusion, the higher basal FSH concentration in the trained versus untrained subjects may be a sign of compensated hypogonadism due to intensive chronic training or it may be due to dysfunction of Sertoli cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of carnitine loading on long-chain fatty acid oxidation, maximal exercise capacity, and nitrogen balance.

Carnitine has a potential effect on exercise capacity due to its role in the transport of long-chain fatty acids into the mitochondria for beta-oxidation, the export of acyl-coenzyme A compounds from mitochondria and the activation of branched-chain amino acid oxidation in the muscle. We studied the effect of carnitine supplementation on palmitate oxidation, maximal exercise capacity and nitrogen balance in rats. Daily carnitine supplementation (500 mg.kg-1 body mass for 6 weeks) was given to 30 rats, 15 of which were on an otherwise carnitine-free diet (group I) and 15 pair-fed with a conventional pellet diet (group II). A control group (group III, n = 6) was fed ad libitum the pellet diet. Palmitate oxidation was measured by collecting 14CO2 after an intraperitoneal injection of [1-14C]palmitate and exercise capacity by swimming to exhaustion. After carnitine supplementation carnitine concentrations in serum were supranormal [group I, total 150.8 (SD 48.5), free 78.9 (SD 18.4); group II, total 170.9 (SD 27.9), free 115.8 (SD 24.6) mumol.l-1] and liver carnitine concentrations were normal in both groups [group I, total 1.6 (SD 0.3), free 1.2 (SD 0.2); group II, total 1.3 (SD 0.3), free 0.9 (SD 0.2) mumol.g-1 dry mass]. In muscle carnitine concentrations were normal in group I [total 3.8 (SD 1.2), free 3.2 (SD 1.0) mumol.g-1 dry mass] and increased in group II [total 6.6 (SD 0.5), free 4.9 (SD 0.9) mumol.g-1 dry mass].(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Effect of food restriction on tissue carnitine concentration in rats.

The effect of feeding different amounts of a standard laboratory pellet diet on tissue carnitine concentration was studied in four groups of rats. Group I was fed ad libitum, whereas food intake was restricted to 25, 20, and 15g protein/kg body weight/day in group II, III, and IV, respectively. The intake of food, protein, energy and carnitine was constant and adjusted to actual body weight in groups 2-4. Six weeks food restriction had no effect on muscle carnitine. Restricted diet caused lowered concentrations of carnitine in serum (group I, fed ad libitum, total 95.0 +/- 13.8, free 80.2 +/- 2.7; group II total 78.4 +/- 8.4, free 56.9 +/- 4.7; group III total 81.7 +/- 8.8, free 66.0 +/- 8.8; and group IV total 73.8 +/- 8.7, free 59.5 +/- 7.6 micromol/l) and urinary carnitine excretion (group I, total 7.1 +/- 3.3, free 6.3 +/- 3.1; group II, total 2.5 +/- 0.7, free 2.2 +/- 0.7; group III, total 1.9 +/- 0.8, free 1.6 +/- 0.8; and group IV, total 1.3 +/- 0.4 free 1.1 +/- 0.3 micromol/day). In contrast, the liver carnitine tended to increase when dietary intake was reduced (group I total 1.1 +/- 0.1, free 1.0 +/- 0.1; group II total 1.5 +/- 0.2, free 1.4 +/- 0.2; group III total 1.3 +/- 0.1, free 1.1 +/- 0.1; and group IV total 1.5 +/- 0.2, free 1.4 +/- 0.2 micromol/g dry wt). The highest liver carnitine concentrations were observed during the lowest dietary intake when also the serum and urine carnitine were lowest. We conclude that the amount of food intake has a direct impact on carnitine concentrations in the liver, serum, and urine while muscle carnitine concentration remains relatively stable despite wide variations in food intake.

Journal Article↗
PubMed1991

Experimental carnitine depletion in rats.

We studied tissue carnitine concentrations after long-term peroral feeding with carnitine-free parenteral nutrient solutions in rats. Group I (n = 22) was fed perorally for 6 weeks with the carnitine free experimental diet. The control group (group II, n = 22) was pair-fed a standard laboratory pellet diet containing carnitine 60 nmol/g. The carnitine free experimental diet caused approximately 50% depletion of carnitine in serum, muscle, and liver while the concentrations in the pair-fed rats were normal. The free and total carnitine concentrations in serum were 25.5 +/- 7.8 and 32.9 +/- 9.3 micromol/l (group I), and 69.3 +/- 13.7 and 84.1 +/- 16.5 micromol/l (group II, p < 0.001), in muscle 2.1 +/- 0.3 and 2.3 +/- 0.4 micromol/g dry weight (group I), and 3.8 +/- 0.6 and 4.3 +/- 0.8 micromol/g dry weight (group II, p < 0.001), and in liver 0.5 +/- 0.1 and 0.6 +/- 0.1 micromol/g dry weight (group I), and 1.2 +/- 0.1 and 1.3 +/- 0.1 micromol/g dry weight (group II p < 0.001). Daily supplementation of the experimental liquid diet with I-carnitine caused normal tissue carnitine concentrations, indicating the exclusion of dietary carnitine as the cause of carnitine depletion. We conclude that in rats carnitine depletion in serum, muscle, and liver can be induced by prolonged peroral feeding with carnitine free diet.

Journal Article↗