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Biomedical subjects

B Quistorff

Publications and source records attributed to B Quistorff.

At least 19 recordsLinked to original sources
PubMed2003

31P-MRS characterization of sprint and endurance trained athletes.

Muscle metabolism and force production were studied in sprint trained runners, endurance trained runners and in untrained subjects, using 31P-MRS. 31P-spectra were obtained at a time resolution of 5 s during four maximal isometric contractions of 30-sec duration, interspersed by 60-sec recovery intervals. Resting CrP/ATP ratio averaged 3.3 +/- 0.3, with no difference among the three groups. The sprint trained subjects showed about 20 % larger contraction forces in contraction bouts 1 and 2 (p < 0.05). The groups differed with respect to CrP breakdown (p < 0.05), with sprinters demonstrating about 75 % breakdown in each contraction compared to about 60 % and 40 % for untrained and endurance trained subjects, respectively (p < 0.05). The endurance trained runners showed almost twice as fast CrP recovery (t 1/2 = 12.5 +/- 1.5) compared to sprint trained (t 1/2 = 22.5 +/- 2.53) and untrained subjects (t 1/2 = 26.4 +/- 2.8). From the initial rate of CrP resynthesis the rate of maximal aerobic ATP synthesis was estimated to 0.74 +/- 0.07, 0.73 +/- 0.10 and 0.33 +/- 0.07 mmol ATP x kg -1 wet muscle x sec -1 for sprint trained, endurance trained and untrained subjects, respectively. Only the sprint trained and the untrained subjects displayed a significant drop in pH and only during the first of the four contractions, about 0.2 and 0.1 pH units, respectively, indicating that only under those contractions was the glycolytic proton production larger than the proton consumption by the CK reaction. Also, in the first contraction the energy cost of contraction was higher for the sprinters compared to the two other groups. The simple 31P-MRS protocol used in the present study demonstrates marked differences in force production, aerobic as well as anaerobic muscle metabolism, clearly allowing differentiation between endurance trained, sprint trained and untrained subjects.

Adult↗
PubMed2002

Bicarbonate attenuates intracellular acidosis.

BACKGROUND: This study was prompted by concern that administration of bicarbonate for correction of lactate acidosis aggravates a low intracellular pH (pHi). In healthy subjects we evaluated skeletal muscle pHi using 31P-magnetic resonance spectroscopy during 5-minute rhythmic handgrip to provoke intracellular acidosis. METHODS: Subjects were randomized to treatment with bicarbonate or saline infused intravenously in a cross-over study design with 1 h between trials. RESULTS: In response to rhythmic handgrip, muscle venous O(2) hemoglobin saturation decreased from 51 +/- 4% to 36 +/- 2% and lactate increased from 1.0 +/- 0.1 to 4.9 +/- 0.5 mmol/l with a reduction in pH from 7.43 +/- 0.01-7.23 +/- 0.01 (P<0.05). pHi decreased from 7.06 +/- 0.02-6.36 +/- 0.08 (P<0.05). Infusion of bicarbonate increased the arterial blood concentration from 26 +/- 1 to 39 +/- 1 mmol/l (P<0.05). The arterial CO(2) partial pressure decreased from 5.6 +/- 0.2 to 5.2 +/- 0.3 kPa during rhythmic handgrip, whereas it increased to 5.9 +/- 0.2 kPa (P<0.05) during infusion of bicarbonate. Bicarbonate treatment also increased pH of arterial and venous blood (7.55 +/- 0.01 vs. 7.44 +/- 0.02 and 7.31 +/- 0.01 vs. 7.23 +/- 0.02, respectively; P<0.05). In the last min of rhythmic handgrip the decrease in pHi was attenuated by the administration of bicarbonate (6.60 +/- 0.11 vs. 6.40 +/- 0.12; P<0.05). CONCLUSION: During exercise-induced metabolic acidosis, intravenous administration of bicarbonate increased the buffering capacity of blood and attenuated the decrease in intracellular muscle pH, although there was a small increase in the arterial carbon dioxide pressure.

Acidosis↗
PubMed2001

Muscle heat production and anaerobic energy turnover during repeated intense dynamic exercise in humans.

1. The aim of the present study was to examine muscle heat production, oxygen uptake and anaerobic energy turnover throughout repeated intense exercise to test the hypotheses that (i) energy turnover is reduced when intense exercise is repeated and (ii) anaerobic energy production is diminished throughout repeated intense exercise. 2. Five subjects performed three 3 min intense one-legged knee-extensor exercise bouts (EX1, EX2 and EX3) at a power output of 65 +/- 5 W (mean +/- S.E.M.), separated by 6 min rest periods. Muscle, femoral arterial and venous temperatures were measured continuously during exercise for the determination of muscle heat production. In addition, thigh blood flow was measured and femoral arterial and venous blood were sampled frequently during exercise for the determination of muscle oxygen uptake. Anaerobic energy turnover was estimated as the difference between total energy turnover and aerobic energy turnover. 3. Prior to exercise, the temperature of the quadriceps muscle was passively elevated to 37.02 +/- 0.12 degrees C and it increased 0.97 +/- 0.08 degrees C during EX1, which was higher (P < 0.05) than during EX2 (0.79 +/- 0.05 degrees C) and EX3 (0.77 +/- 0.06 degrees C). In EX1 the rate of muscle heat accumulation was higher (P < 0.05) during the first 120 s compared to EX2 and EX3, whereas the rate of heat release to the blood was greater (P < 0.05) throughout EX2 and EX3 compared to EX1. The rate of heat production, determined as the sum of heat accumulation and release, was the same in EX1, EX2 and EX3, and it increased (P < 0.05) from 86 +/- 8 during the first 15 s to 157 +/- 7 J s(-1) during the last 15 s of EX1. 4. Oxygen extraction was higher during the first 60 s of EX2 and EX3 than in EX 1 and thigh oxygen uptake was elevated (P < 0.05) during the first 120 s of EX2 and throughout EX3 compared to EX1. The anaerobic energy production during the first 105 s of EX2 and 150 s of EX3 was lower (P < 0.05) than in EX1. 5. The present study demonstrates that when intense exercise is repeated muscle heat production is not changed, but muscle aerobic energy turnover is elevated and anaerobic energy production is reduced during the first minutes of exercise.

Adult↗
PubMed2001

Quantitative estimates of angiogenic and anti-angiogenic activity by laser Doppler flowmetry (LDF) and near infra-red spectroscopy (NIRS).

The use of laser Doppler flowmetry (LDF) and near-infra-red spectroscopy (NIRS) for non-invasive in vivo measurements of angiogenic and anti-angiogenic activity in nude mice was evaluated. Angiogenic foci were induced in the skin by implantation of slow release pellets containing 200 ng basic fibroblast growth factor (bFGF). LDF and NIRS recordings from induced foci were significantly higher than placebo implants (P<0.05) and controls (P<0.001), proving that LDF and NIRS provide measures of angiogenic activity. Correspondingly, by these methods, an anti-angiogenic activity was significantly demonstrated in bFGF-stimulated animals treated with either the specific anti-angiogenic compound TNP-470 (P<0.05) or the anti-inflammatory agent dexamethasone (P<0.001). We conclude that LDF and NIRS, alone or in combination, are useful non-invasive tools for early evaluation of angiogenic and anti-angiogenic activity in vivo.

Animals↗
PubMed2001

Reduced mitochondrial adenosine triphosphate synthesis in skeletal muscle in patients with Child-Pugh class B and C cirrhosis.

Patients with cirrhosis of the liver often complain of tiredness and a lack of strength at physical exercise. Other investigators have found that muscle strength, work capacity, and maximal oxygen consumption are reduced in cirrhosis. We hypothesized that mitochondrial maximal rate of ATP synthesis in skeletal muscle may be impaired in these patients. This was tested with (31)P nuclear magnetic resonance spectroscopy in anterior tibial muscle of cirrhotic patients and healthy controls at rest, during exercise, and subsequent recovery. In patients with Child-Pugh class B and C cirrhosis resting PCr/P(i) ratio (8.3 +/- 1.0; n = 7) was lower than in patients with Child-Pugh class A cirrhosis (12.1 +/- 2.1; n = 7) and controls (11. 7 +/- 1.1; n = 6; P =.03), while the resting P(i)/gammaATP ratio was higher in Child-Pugh class B and C patients (0.43, 0.30, and 0.27, respectively; P =.03). Maximal rate of mitochondrial adenosine triphosphate (ATP) synthesis (V(max)) as calculated from the initial rate of phosphocreatine (PCr) recovery after work was lower in Child-Pugh class B and C cirrhosis (0.189 mmol/L/s +/- 0.034) than in both Child-Pugh class A patients (0.402 mmol/L/s +/- 0.103) and controls (0.425 mmol/L/s +/- 0.064; P =.01). V(max) was significantly correlated to intracellular free [Mg(2+)] obtained from the (31)P nuclear magnetic resonance (NMR) spectra (P =.003). Insufficient oxygen delivery did not seem a likely cause of reduced ATP synthesis in the patients. These findings suggest either a decreased number of mitochondria in skeletal muscle of the cirrhotic patient in Child-Pugh class B and C or a defective mitochondrial function that could be related to low intracellular free [Mg(2+)].

Adenosine Triphosphate↗
PubMed2001

Aerobic metabolism of human quadriceps muscle: in vivo data parallel measurements on isolated mitochondria.

The aim of the present study was to examine whether parameters of isolated mitochondria could account for the in vivo maximum oxygen uptake (VO2max) of human skeletal muscle. VO2max and work performance of the quadriceps muscle of six volunteers were measured in the knee extensor model (range 10-18 mmol O2 x min(-1) x kg(-1) at work rates of 22-32 W/kg). Mitochondria were isolated from the same muscle at rest. Strong correlations were obtained between VO2max and a number of mitochondrial parameters (mitochondrial protein, cytochrome aa3, citrate synthase, and respiratory activities). The activities of citrate synthase, succinate dehydrogenase, and pyruvate dehydrogenase, measured in isolated mitochondria, corresponded to, respectively, 15, 3, and 1.1 times the rates calculated from VO2max. The respiratory chain activity also appeared sufficient. Fully coupled in vitro respiration, which is limited by the rate of ATP synthesis, could account for, at most, 60% of the VO2max. This might be due to systematic errors or to loose coupling of the mitochondrial respiration under intense exercise.

Adenosine Triphosphate↗
PubMed2001

Exercise intolerance in mitochondrial myopathy is not related to lactic acidosis.

In a double-blinded, placebo-controlled, crossover study in seven mitochondrial myopathy patients (MM), we investigated whether lowering of lactate with dichloroacetate (DCA) can improve exercise tolerance and oxidative capacity in MM. DCA lowered plasma lactate at rest and during exercise (from 10.5 +/- 2.0 to 5.0 +/- 1.6 mM; p = 0.005) but did not improve maximal work load or VO2 in cycle exercise or phosphorous magnetic resonance spectroscopy (31P-MRS)-assessed indices of muscle oxidative metabolism. This indicates that lactate acidosis is not the primary cause of exercise intolerance in MM.

Acidosis, Lactic↗
PubMed2000

[Effects of excessive isocaloric intake of either carbohydrate or fat on body composition, fat mass, de novo lipogenesis and energy expenditure in normal young men].

Ten pairs of normal young men were overfed by 5 MJ per day for 21 days with either a carbohydrate-rich or a fat-rich diet (C- and F-group). The two subjects of a pair were requested to follow each other throughout the day to ensure similar physical activity. The increase in body weight and fat mass were not significantly different between the C- and the F-group. Heat production during sleep did not change during overfeeding. The accumulated faecal loss of energy, dry matter, carbohydrate and protein was significantly higher in the C- than in the F-group. Hepatic de novo lipogenesis was 212 g per 21 days in the C-group and was too low to be determined in the F-group. Whole body de novo lipogenesis was positive in six of the ten subjects in the C-group (mean: 332 g per 21 days). It is concluded that the increase in body weight and fat mass during overfeeding of isocaloric amounts of diets rich in carbohydrate or in fat was not significantly different, and that surplus of carbohydrate seemed to be converted to fat both by hepatic and extrahepatic de novo lipogenesis.

Adipose Tissue↗
PubMed2000

Kinetic and functional characterization of 1,4-dideoxy-1, 4-imino-d-arabinitol: a potent inhibitor of glycogen phosphorylase with anti-hyperglyceamic effect in ob/ob mice.

The effects of 1,4-dideoxy-1,4-imino-d-arabinitol (DAB) were investigated on preparations of glycogen phosphorylase (GP) and in C57BL6J (ob/ob) mice by (13)C NMR in vivo. Independent of the phosphorylation state or the mammalian species or tissue from which GP was derived, DAB inhibited GP with K(i)-values of approximately 400 nM. The mode of inhibition was uncompetitive or noncompetitive, with respect to glycogen and P(i), respectively. The effects of glucose and caffeine on the inhibitory effect of DAB were investigated. Taken together, these data suggest that DAB defines a novel mechanism of action. Intraperitoneal treatment with DAB (a total of 105 mg/kg in seven doses) for 210 min inhibited glucagon-stimulated glycogenolysis in obese and lean mice. Thus, liver glycogen levels were 361 +/- 19 and 228 +/- 19 micromol glucosyl units/g with DAB plus glucagon in lean and obese mice, respectively, compared to 115 +/- 24 and 37 +/- 8 micromol glucosyl units/g liver with glucagon only. Moreover, with glucagon only end-point blood glucose levels were at 29 +/- 2 and 17.5 +/- 2 mM in obese and lean mice, respectively, compared to 17.5 +/- 1 and 12 +/- 1 mM with glucagon plus DAB. In conclusion, DAB is a novel and potent inhibitor of GP with an apparently distinct mechanism of action. Further, DAB inhibited the hepatic glycogen breakdown in vivo and displayed an accompanying anti-hyperglycemic effect, which was most pronounced in obese mice. The data suggest that inhibition of GP may offer a therapeutic principle in Type 2 diabetes.

Animals↗
PubMed2000

Heat production in human skeletal muscle at the onset of intense dynamic exercise.

1. We hypothesised that heat production of human skeletal muscle at a given high power output would gradually increase as heat liberation per mole of ATP produced rises when energy is derived from oxidation compared to phosphocreatine (PCr) breakdown and glycogenolysis. 2. Five young volunteers performed 180 s of intense dynamic knee-extensor exercise ( approximately 80 W) while estimates of muscle heat production, power output, oxygen uptake, lactate release, lactate accumulation and ATP and PCr hydrolysis were made. Heat production was determined continuously by (i) measuring heat storage in the contracting muscles, (ii) measuring heat removal to the body core by the circulation, and (iii) estimating heat transfer to the skin by convection and conductance as well as to the body core by lymph drainage. 3. The rate of heat storage in knee-extensor muscles was highest during the first 45 s of exercise (70-80 J s-1) and declined gradually to 14 +/- 10 J s-1 at 180 s. 4. The rate of heat removal by blood was negligible during the first 10 s of exercise, rising gradually to 112 +/- 14 J s-1 at 180 s. The estimated rate of heat release to skin and heat removal via lymph flow was < 2 J s-1 during the first 5 s and increased progressively to 24 +/- 1 J s-1 at 180 s. The rate of heat production increased significantly throughout exercise, being 107 % higher at 180 s compared to the initial 5 s, with half of the increase occurring during the first 38 s, while power output remained essentially constant. 5. The contribution of muscle oxygen uptake and net lactate release to total energy turnover increased curvilinearly from 32 % and 2 %, respectively, during the first 30 s to 86 % and 8 %, respectively, during the last 30 s of exercise. The combined energy contribution from net ATP hydrolysis, net PCr hydrolysis and muscle lactate accumulation is estimated to decline from 37 % to 3 % comparing the same time intervals. 6. The magnitude and rate of elevation in heat production by human skeletal muscle during exercise in vivo could be the result of the enhanced heat liberation during ATP production when aerobic metabolism gradually becomes dominant after PCr and glycogenolysis have initially provided most of the energy.

Adenosine Triphosphate↗
PubMed2000

Lactate, glucose and O2 uptake in human brain during recovery from maximal exercise.

The metabolic activity of the brain has not been evaluated during physical exercise. In six volunteers substrate uptake by the brain was determined during graded exercise and recovery from maximal exercise by measuring the arterial-internal jugular venous concentration differences(a-v differences). The a-v difference for lactate increased from 0.02 +/- 0.08 mmol l-1 at rest to 0.39 +/- 0. 13 mmol l-1 during exercise and remained positive during 30 min of recovery (P < 0.05). The a-v difference for glucose (0.55 +/- 0.06 mmol l-1 at rest) did not change significantly during exercise, but during the initial 5 min of recovery it increased to 0.83 +/- 0.10 mmol l-1 (P < 0.05). The O2 a-v difference at rest of 3.11 +/- 0.30 mmol l-1 remained stable during exercise, then increased during the initial 5 min of recovery (3.77 +/- 0.52 mmol l-1) and remained high during the subsequent 30 min recovery period (3.62 +/- 0.64 mmol l-1; P < 0.05). Thus the O2/glucose uptake ratio did not change during exercise (pre-exercise 5.95 +/- 0.68; post-exercise 6.02 +/- 1.39) but decreased to 4.93 +/- 0.99 during the initial 5 min of recovery (P < 0.05). When lactate uptake was included, the resting O2/carbohydrate uptake ratio of 5.84 +/- 0.73 was reduced to 4.42 +/- 0.25 during exercise and decreased further during the recovery phase (to 3.79 +/- 0.30; P < 0.05). In contrast, in the resting and immobilised rat, lactate infusion to a level similar to that obtained during maximal exercise in humans did not affect the a-v difference for lactate. The large carbohydrate uptake by the brain during recovery from maximal exercise suggests that brain glycogen metabolism is important in the transition from rest to exercise, since this would explain the significant post-exercise decrease in the O2/carbohydrate uptake ratio.

Adult↗
PubMed2000

Effects of oral D-tagatose, a stereoisomer of D-fructose, on liver metabolism in man as examined by 31P-magnetic resonance spectroscopy.

D-tagatose, which is a stereoisomer of D-fructose, is phosphorylated to D-tagatose-1-phosphate by fructokinase in the liver. Because of a slow degradation rate of D-tagatose-1-phosphate, this substance may accumulate, and ingested D-tagatose may therefore cause a longer lasting reduction in inorganic phosphate (Pi) and adenosine triphosphate (ATP) levels in the liver compared with D-fructose. Similar to what is seen in patients with hereditary fructose intolerance, this may increase purine nucleotide degradation and thereby increase uric acid production. The effect of 30 g D-tagatose or D-fructose administered orally on ketohexose-1-phosphates, ATP, and Pi levels in the liver was studied by 31P-magnetic resonance spectroscopy (PMRS) in 5 young male volunteers. Blood and urine were collected to detect a possible increased uric acid production. A peak at 5.2 ppm assigned as D-tagatose-1-phosphate equivalent to about 1 mmol/L was found in the spectrum within 30 minutes after D-tagatose was administered in all subjects. Concomitantly, ATP was reduced by about 12% (P < .05). Both effects had vanished after 150 minutes. Serum uric acid concentration was increased by 17% 50 minutes after D-tagatose (P < .05) and did not reach baseline level when the experiment was terminated 230 minutes after the load. Although renal fractional extraction of uric acid decreased by approximately 12%, this could not explain the acute hyperuricemic effect of D-tagatose. No changes in 31PMRS spectra or serum uric acid concentration were found after D-fructose. These results suggest that a moderate intake of D-tagatose may affect liver metabolism by phosphate trapping despite the fact that the sugar may only be incompletely absorbed in the gut.

Adenosine Triphosphate↗
PubMed2000

Effects of isoenergetic overfeeding of either carbohydrate or fat in young men.

Ten pairs of normal men were overfed by 5 MJ/d for 21 d with either a carbohydrate-rich or a fat-rich diet (C- and F-group). The two subjects in each pair were requested to follow each other throughout the day to ensure similar physical activity and were otherwise allowed to maintain normal daily life. The increase in body weight, fat free mass and fat mass showed great variation, the mean increases being 1.5 kg, 0.6 kg and 0.9 kg respectively. No significant differences between the C- and F-group were observed. Heat production during sleep did not change during overfeeding. The RQ during sleep was 0.86 and 0.78 in the C- and F-group respectively. The accumulated faecal loss of energy, DM, carbohydrate and protein was significantly higher in the C- compared with the F-group (30, 44, 69 and 51% higher respectively), whereas the fat loss was the same in the two groups. N balance was not different between the C- and F-group and was positive. Fractional contribution from hepatic de novo lipogenesis, as measured by mass isotopomer distribution analysis after administration of [1-(13)C]acetate, was 0.20 and 0.03 in the C-group and the F-group respectively. Absolute hepatic de novo lipogenesis in the C-group was on average 211 g per 21 d. Whole-body de novo lipogenesis, as obtained by the difference between fat mass increase and dietary fat available for storage, was positive in six of the ten subjects in the C-group (mean 332 (SEM 191)g per 21 d). The change in plasma leptin concentration was positively correlated with the change in fat mass. Thus, fat storage during overfeeding of isoenergetic amounts of diets rich in carbohydrate or in fat was not significantly different, and carbohydrates seemed to be converted to fat by both hepatic and extrahepatic lipogenesis.

Adipose Tissue↗
PubMed1999

Kinetics of lactate and pyruvate transport in cultured rat myotubes.

Skeletal muscle transport of lactate and pyruvate was studied in primary cultures of rat myotubes, applying the pH-sensitive fluorescent indicator 2', 7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. The initial rate of decrease in intracellular pH (pHi) upon lactate or pyruvate incubation was used to determine total transport (carrier mediated and diffusion). Both lactate and pyruvate transport could be inhibited by a combination of 0.5 mM 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid, 5 mM mersalyl and 10 mM alpha-cyano-4-hydroxycinnamate. The kinetic parameters, Km and Vmax, for carrier-mediated transport of lactate were 9.9+/-1.1 mM and 0. 69+/-0.02 mmol l-1 s-1, respectively. For pyruvate, Km and Vmax were 4.4+/-1.3 mM and 0.30+/-0.05 mmol l-1 s-1, respectively. The diffusion component of the total transport was 0.0040+/-0.0005[S] (n=4) and 0.0048+/-0.0003[S] (n=4) for lactate and pyruvate, respectively. Furthermore, it was observed that the two monocarboxylate transporter isoforms present in mature skeletal muscles, MCT1 and MCT4 (formerly called MCT3 (M.C. Wilson, V.N. Jackson, C. Heddle, N.T. Price, H. Pilegaard, C. Juel, A. Bonen, I. Montgomery, O.F. Hutter, A.P. Halestrap, Lactic acid efflux from white skeletal muscle is catalyzed by the monocarboxylate transporter isoform MCT3, J. Biol. Chem. 273 (1998) 15920-15926)), were also expressed in primary culture of myotubes.

Animals↗
PubMed1999

High expression of MHC I in the tibialis anterior muscle of a paraplegic patient.

A long-term paraplegic man presented exclusively (>99%) myosin heavy chain I (MHC I) in the tibialis anterior muscle (TA). This was coupled to a slow speed of contraction, a high resistance to fatigue, and a rapid resynthesis of phosphocreatine after an electrically evoked fatiguing contraction when compared with the TA muscles of 9 other paraplegic individuals. In contrast, the MHC composition of his vastus lateralis, gastrocnemius, and soleus muscles was that expected of a muscle from a spinal cord injured individual. This information may be of clinical importance in terms of the expected morphological and functional adaptations of skeletal muscle to different types of electrical stimulation therapy.

Electromyography↗
PubMed1999

Decreased skeletal muscle capillary density is related to higher serum levels of low-density lipoprotein cholesterol and apolipoprotein B in men.

The relationships between skeletal muscle morphology, particularly muscle fiber capillary density, and serum lipid profiles were evaluated in 25 non-obese men aged 18 to 36 years (body mass index [BMI], 22.7 +/- 2.5 kg/m2; body fat, 13.6% +/- 4.0%, maximal oxygen uptake [VO2max], 46.2 < or = 6.3 mL/kg/min). Skeletal muscle samples were taken from the vastus lateralis using the needle-biopsy method. The fiber types (I, IIa, and IIx) and their percent distribution, the indices of capillary density, and the diffusion index expressed as the cross-sectional area occupied by one capillary were determined. Blood samples were drawn from the antecubital vein after a 12-hour fast. Based on Pearson's correlation analysis, the number of capillaries around type IIx fiber correlated inversely with the serum level of low-density lipoprotein cholesterol ([LDL-C] r = -.50, P < .05). The number of capillaries per fiber (cap/fiber ratio), number of capillaries per area (cap/mm2), and capillaries around each fiber type correlated inversely with the serum level of apolipoprotein B ([apo B] r = -.40 to -.54, P < .05 to .01). Further, the diffusion index for each fiber type correlated positively with LDL-C and apo B (r = .42 to .50, P < .05 to .01). Among 14 subjects in whom high-density lipoprotein cholesterol (HDL-C) subfractions were analyzed, a positive correlation was found between cap/mm2 and HDL2-C (r = .64, P < .05). Partial correlation analysis showed that these correlations either remain or improve after adjusting for age, VO2max, and body fatness. These results indicate that skeletal muscle capillary density and diffusion capacity are related to lipid and apolipoprotein concentrations for both type I and type II fibers.

Adipose Tissue↗
PubMed1999

No effect of antioxidant supplementation in triathletes on maximal oxygen uptake, 31P-NMRS detected muscle energy metabolism and muscle fatigue.

A double-blind placebo-controlled cross-over trial was undertaken to evaluate the effect of antioxidant supplementation on maximal oxygen uptake during bicycling, 31-phosphorus nuclear magnetic response spectroscopy (31P-NMRS) detected muscle energy metabolism during plantar flexion and muscle fatigue evaluated by 1-s electrical stimulation at low (10 Hz) and high (50 Hz) frequency. Seven male triathletes received daily oral antioxidant supplementation in capsule form including 100 mg coenzyme Q10 (CoQ10), 600 mg ascorbic acid and 270 mg alpha-tocopherol or placebo over a 6-week interval. Serum concentration of CoQ10 was significantly higher in the antioxidant phase (1.80+/-1 microg x ml(-1), mean +/- SD) than control (0.9+/-0.21 microg ml(-1)) or placebo phase (0.9+/-0.3 microg x ml(-1)) (P<0.01). Maximal oxygen uptake was 63.8+/-3.0 ml x min(-1) x kg(-1) in the control phase, and did not change significantly in the antioxidant (67.6+/-10.8 ml x min(-1) x kg(-1)) or the placebo phase (61.9+/-4.5 ml x min(-1) x kg(-1)). The combined 31P-NMRS/low frequency fatigue test (plantar flexion of the foot) did not show differences in the gastrocnemius muscle pH (6.77+/-0.14), phosphocreatine reduction at the end of exercise (23+/-14% of rest) and half-time for recovery of phosphocreatine (33+/-12 sec) between the placebo and the antioxidant trial. No difference in muscle fatigue at 10 Hz electrical stimulation was found between the three phases. In conclusion, the results demonstrate no effect of antioxidative vitamin supplementation on maximal oxygen uptake, muscle energy metabolism or muscle fatigue in triathletes.

Adult↗