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Biomedical subjects

G J Heigenhauser

Publications and source records attributed to G J Heigenhauser.

At least 55 records · Page 3Linked to original sources
PubMed1997

Enhanced pulmonary and active skeletal muscle gas exchange during intense exercise after sprint training in men.

1. This study investigated the effects of 7 weeks of sprint training on gas exchange across the lungs and active skeletal muscle during and following maximal cycling exercise in eight healthy males. 2. Pulmonary oxygen uptake (VO2) and carbon dioxide output (VCO2) were measured before and after training during incremental exercise (n = 8) and during and in recovery from a maximal 30 s sprint exercise bout by breath-by-breath analysis (n = 6). To determine gas exchange by the exercising leg muscles, brachial arterial and femoral venous blood O2 and CO2 contents and lactate concentration were measured at rest, during the final 10 s of exercise and during 10 min of recovery. 3. Training increased (P < 0.05) the maximal incremental exercise values of ventilation (VE, by 15.7 +/- 7.1%), VCO2 (by 9.3 +/- 2.1%) and VO2 (by 15.0 +/- 4.2%). Sprint exercise peak power (3.9 +/- 1.0% increase) and cumulative 30 s work (11.7 +/- 2.8% increase) were increased and fatigue index was reduced (by -9.2 +/- 1.5%) after training (P < 0.05). The highest VE, VCO2 and VO2 values attained during sprint exercise were not significantly changed after training, but a significant (P < 0.05) training effect indicated increased VE (by 19.2 +/- 7.9%), VCO2 (by 9.3 +/- 2.1%) and VO2 (by 12.7 +/- 6.5%), primarily reflecting elevated post-exercise values after training. 4. Arterial O2 and CO2 contents were lower after training, by respective mean differences of 3.4 and 21.9 ml l-1 (P < 0.05), whereas the arteriovenous O2 and CO2 content differences and the respiratory exchange ratio across the leg were unchanged by training. 5. Arterial whole blood lactate concentration and the net lactate release by exercising muscle were unchanged by training. 6. The greater peak pulmonary VO2 and VCO2 with sprint exercise, the increased maximal incremental values, unchanged arterial blood lactate concentration and greater sprint performance all point strongly towards enhanced gas exchange across the lungs and in active muscles after sprint training. Enhanced aerobic metabolism after sprint training may contribute to reduced fatigability during maximal exercise, whilst greater pulmonary CO2 output may improve acid-base control after training.

Adult↗
PubMed1997

Effect of progressive incremental exercise and beta-adrenergic blockade on erythrocyte ion concentrations.

Ion concentrations in whole blood, plasma, and erythrocytes from arterialized venous blood were examined in eight healthy males performing incremental exercise tests to fatigue on an electrically braked cycle ergometer. Exercise was performed during control and low dose (LD) and high dose (HD) of propranolol (beta-blockade). The LD and HD resulted in a significant decrease in peak heart rate compared with control, while peak oxygen uptake during HD was significantly less than either control or LD. Plasma potassium concentration ([K+]) increased significantly during exercise for control, LD, and HD, while LD and HD plasma [K+] were both significantly greater than control. Erythrocyte [K+] increased significantly for control to 119.2 +/- 1.3 mmol/L, for LD to 116.9 +/- 2.0 mmol/L, and for HD to 117.7 +/- 1.2 mmol/L. Plasma lactate concentration ([Lac-]) increased significantly during exercise for control, LD, and HD. Erythrocyte [Lac-] increased significantly for control to 6.4 +/- 0.8 mmol/L, for LD to 6.4 +/- 0.6 mmol/L, and for HD to 5.0 +/- 0.5 mmol/L, with HD [Lac-] less than either control or LD. beta-Blockade did not significantly alter the percent change in mean corpuscular volume (% delta MCV) during exercise. The results indicate that incremental exercise produces an increase in erythrocyte [Lac-] and [K+]. Although beta-blockade increased plasma [K+] at peak exercise, there was no alteration in erythrocyte [K+] response. The treatment did not impair the ability of the erythrocyte to maintain MCV.

Adrenergic beta-Antagonists↗
PubMed1997

Lactate transport by rainbow trout white muscle: kinetic characteristics and sensitivity to inhibitors.

This study used an isolated-perfused tail-trunk preparation of rainbow trout to examine the uptake and release of lactate (Lac) and metabolic protons (delta H+M) in resting and exercised fish white muscle. In exercised muscle, L(+)-Lac efflux was inhibited (approximately 40%) by 5 mM alpha-cyano-4-hydroxycinnamate (CIN), but not by 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) or 0.1 mM amiloride. These results suggest that Lac release occurs through a Lac(-)-H- symport and the free diffusion of lactic acid (HLac) or Lac-, but not via the Lac-/HCO3(-)-Cl- antiporter. Lac efflux was accompanied by delta H+m influx in all treatments, and increased delta H+m influx occurred after SITS treatment. In resting muscle, Lac uptake rates were greater than Lac efflux rates in the postexercise preparation. L-Lac influx exhibited partial saturation kinetics, whereas D(-)-Lac influx was linearly related to its extracellular concentration (0-32 mM). At 16 mM extracellular L-Lac, with a negligible transmembrane L-HLac gradient and an outwardly directed not driving force on L-Lac-, CIN, and SITS reduced net L-Lac uptake by 75 and 45%, respectively. At 16 mM extracellular concentration, D-Lac influx was 64% of the net L-Lac influx. These results suggest that in trout muscle at 16 mM extracellular L-Lac, the Lac -H+ symport accounts for 30-36%, the Lac-/HCO3(-)-Cl- antiport for 39-45%, and diffusion for 19-25% of uptake, although the latter is probably overestimated and the former underestimated for methodological reasons. Net L-Lac efflux was not affected by extracellular D-Lac concentration and/or D-Lac influx, implying the existence of a concurrent L-Lac efflux during L-Lac influx. The D-Lac influx kinetics data indicated that the Lac-/HCO3 antiport was not saturable in the extracellular D-Lac concentration range of 0-32 mM. This study clearly demonstrates the involvement of carrier-mediated transport in transmembrane Lac movement in fish muscle and supports the "active lactate retention" mechanism proposed by Turner and Wood (J. Exp. Biol. 105: 895-401, 1983).

Animals↗
PubMed1997

Distribution of lactate and other ions in inactive skeletal muscle: influence of hyperkalemic lactacidosis.

The purpose of this study was to quantify changes in intracellular ion and acid-base status resulting from the net flux of ions between perfusate and noncontracting muscle of differing fibre type in response to a perfusate that simulated the ionic conditions seen during intense exercise. Isolated rat hind limbs were perfused for 80 min with a bovine erythrocyte perfusate. Two series of experiments were performed: a normal perfusate (NP, n = 8) or a lactacidotic perfusate (LP, n = 8) that simulated arterial plasma and blood composition during intense exercise ([Lac-] = 11.0 mequiv. L-1, [K+] = 7.5 mequiv. L-1, and nonvolatile acid concentration = 71 nequiv.L-1). Net ion fluxes were determined by the arteriovenous difference across the hind limb and perfusate flow. Muscle ion concentrations were measured in the soleus (SOL), plantaris (PLT), and white gastrocnemius (WG) muscles. In the NP group, small net effluxes of K+ and Lac- from muscle were observed, but there was no net flux of Na+ or CI-. During LP, an initial rapid net influx of Lac- into muscle (151.2 +/- 9.4 mu equiv. min-1. 100 g-1 at 5 min) was followed by a steady-state net influx of 24-37 mu equiv. min-1. 100 g-1 between 20 and 60 min. During LP, net influx of Na+, CI-, and K+ was greater than during NP and average 58.0 +/- 11.2, 30.0 +/- 7.5, and 7.5 +/- 1.9 mu equiv. min-1. 100 g-1, respectively. Following LP, muscle content of Na+ (WG only) and Lac- (WG, PLT, and SOL) was increased to a greater extent than following NP. The increased [Lac-]i contributed to an elevated [H+]i only in the slow oxidative SOL, consistent with the higher concentration of Lac- transporters, lower capacity to bind protons, and better regulation of [Na+]i in slow oxidative muscles. Calculated membrane potential (Em) was unchanged with NP but decreased on average from -76.2 +/- 1.2 to 63.4 +/- 2.2 mV with LP perfusion, with no difference among fibre types. The steady-state distribution of Lac- across the sarcolemma appears to be a function of both metabolic and transport processes; specifically, Lac- distribution was not fully explained by the membrane potential nor by the nonionic distribution of HLac as determined by the transmembrane pH gradient. It is concluded that inactive skeletal muscle modifies the ionic composition of blood perfusing the muscles. However, the altered ionic composition of these muscles may compromise their function as a result of an altered membrane potential in fast and slow muscles and increased [H+]i in slow oxidative muscles.

Acidosis, Lactic↗
PubMed1996

Cardiorespiratory status after treatment for acute lymphoblastic leukemia.

The use of certain chemotherapeutic agents is associated with dose-related cardiotoxicity and, potentially, with restrictive lung disease. Therefore, we assessed the cardiopulmonary status and exercise capacity of 19 patients (pts; 9M:10F) 1.1 to 7.1 years (mean 4.6 +/- 1.5 years) after successful treatment of acute lymphoblastic leukemia (ALL) with Dana Farber Cancer Institute protocols. As body mass and nutritional status may influence exercise capacity, we also evaluated their anthropometric status and the plasma levels of rapid turnover proteins. Seven pts designated as "standard risk for relapse" (SR) had received low cumulative doses of doxorubicin (50 +/- 21 mg/m2), while twelve pts at "high or very high risk for relapse" (HR/VHR) had received higher doses (349 +/- 16 mg/m2). The evaluations included a questionnaire, anthropometric assessments, echocardiography, pulmonary function studies, exercise testing, and nutritional assays. Patients' data were compared with published normative data or with control values from our laboratories. In addition, we compared SR pt data with HR/VHR pt data. No pt had overt symptoms or signs of cardiorespiratory compromise. The pts had a higher percent of body fat than age-matched healthy controls (29.7 +/- 7.9% vs. 20 +/- 6%; P < 0.001). On echocardiography, cardiac systolic function was within normal limits in all. However, HR/VHR pts had lower left ventricular (LV) shortening fractions than SR pts (P < 0.05). LV filling velocity, indicative of diastolic function (the E/A ratio), was normal in most pts. Pulmonary function studies were normal. Exercise capacity was below predicted in most cases but heart rates at peak exercise and leg muscle function were within normal limits, suggesting a deconditioned state. Plasma levels of rapid turnover proteins were also normal. Despite lack of overt morbidity in our pt population, subtle abnormalities persist in cardiac function while pulmonary function is normal. Longitudinal studies will identify if further abnormalities or overt morbidity develop. In later years, continuing obesity and a sedentary state may contribute to clinically relevant heart disease.

Anthropometry↗
PubMed1996

Plasma metabolites, volume and electrolytes following 30-s high-intensity exercise in boys and men.

It has been shown that boys recover faster than men following brief, high-intensity exercise. Better to understand this difference, plasma metabolite concentration, volume, electrolyte concentration [electrolyte], and hydrogen ion concentration [H+] changes were compared in five prepubescent boys [mean age 9.6 (SD 0.9) years] and 5 men [mean age 24.9 (SD 4.3) years] following 30-s, all-out cycling. Blood was collected prior to, at the end, and at the 1st, 3rd and 10th min following exercise. At the 10th min of recovery, the men's lactate concentration was 14.2 (SD 1.8) mmol.l-1 and [H+] was 66.1 (SD 5.9) nmol.l-1, compared with 5.7 (SD 0.7) mmol.l-1 and 47.5 (SD 1.2) nmol.l-1 respectively, in the boys (P < 0.01 for both). The glycerol concentration was higher in the boys at the end of exercise and until the 3rd min of recovery. Plasma volume (PV) decreased more in the men [16.9 (SD 3.0)%] than in the boys [9.4 (SD 2.8)%]. In both groups, [electrolyte] increased after exercise, tending to be higher in the men. Recovery of plasma [electrolyte] and PV started earlier in the boys (1st min) than in the men (3rd min). These findings would support the notion of a lesser reliance on glycolytic energy pathways in children and may explain the faster recovery of muscle power in boys compared to men.

Adult↗
PubMed1996

Epinephrine infusion does not enhance net muscle glycogenolysis during prolonged aerobic exercise.

The role of physiological elevations of plasma epinephrine concentration on muscle glycogenolysis during prolonged exercise was investigated. Eight healthy volunteers cycled for 90 min at 65%. VO2max on two occasions; one with an infusion of epinephrine (EPI) and once without (control). Biopsy samples were taken from the vastus lateralis muscle both prior to and following exercise for the analysis of muscle glycogen. EPI infusion significantly elevated venous plasma EPI approximately 2.5-fold over control values throughout exercise (90 min: 5.78 +/- 0.95 vs. 2.35 +/- 0.49 nM). EPI infusion did not significantly alter net glycogenolysis as compared to control (310.0 +/- 30.8 vs. 229.5 +/- 41.1 mmol glucosyl units/kg dry mass). Venous concentrations of plasma FFA and whole blood glycerol were unaffected by EPI infusion. Whole blood glucose was significantly elevated during EPI infusion at 10, 30, 60 and 90 min of exercise compared to control values. Whole blood lactate was elevated to a greater extent during EPI infusion as compared to control at 10, 30, and 60 min of exercise. In conclusion, EPI infusion had no effect on muscle glycogenolysis and appeared to have little effect on adipose tissue lipolysis. The explanation for the elevation of blood lactate is unknown while the elevation in blood glucose suggests that EPI infusion potentiated liver glycogenolysis.

Adipose Tissue↗
PubMed1996

Progressive effect of endurance training on metabolic adaptations in working skeletal muscle.

We investigated the hypothesis that a program of prolonged endurance training, previously shown to decrease metabolic perturbations to acute exercise within 5 days of training, would result in greater metabolic adaptations after a longer training duration. Seven healthy male volunteers [O2 consumption = 3.52 +/- 0.20 (SE) l/min] engaged in a training program consisting of 2 h of cycle exercise at 59% of pretraining peak O2 consumption (VO2peak) 5-6 times/wk. Responses to a 90-min submaximal exercise challenge were assessed pretraining (PRE) and after 5 and 31 days of training. On the basis of biopsies obtained from the vastus lateralis muscle, it was found that, after 5 days of training, muscle lactate concentration, phosphocreatine (PCr) hydrolysis, and glycogen depletion were reduced vs. PRE (all P < 0.01). Further training (26 days) showed that, at 31 days, the reduction in PCr and the accumulation of muscle lactate was even less than at 5 days (P < 0.01). Muscle oxidative potential, estimated from the maximal activity of succinate dehydrogenase, was increased only after 31 days of training (+41%; P < 0.01). In addition, VO2peak was only increased (10%) by 31 days (P < 0.05). The results show that a period of short-term training results in many characteristic training adaptations but that these adaptations occurred before increases in mitochondrial potential. However, a further period of training resulted in further adaptations in muscle metabolism and muscle phosphorylation potential, which were linked to the increase in muscle mitochondrial capacity.

Adaptation, Physiological↗
PubMed1996

Regulation of muscle glycogen phosphorylase activity following short-term endurance training.

The purpose of this study was to examine the regulation (hormonal, substrate, and allosteric) of muscle glycogen phosphorylase (Phos) activity and glycogenolysis after short-term endurance training. Eight untrained males completed 6 days of cycle exercise (2 h/day) at 65% of maximal O2 uptake (Vo2max). Before and after training subjects cycled for 15 min at 80% of Vo2max, and muscle biopsies and blood samples were obtained at 0 and 30 s, 7.5 and 15 min, and 0, 5, 10, and 15 min of exercise. Vo2max was unchanged with training but citrate synthase (CS) activity increased by 20%. Muscle glycogenolysis was reduced by 42% during the 15-min exercise challenge following training (198.8 +/- 36.9 vs. 115.4 +/- 25.1 mmol/kg dry muscle), and plasma epinephrine was blunted at 15 min of exercise. The Phos a mole fraction was unaffected by training. Muscle phosphocreatine utilization and free Pi and AMP accumulations were reduced with training at 7.5 and 15 min of exercise. It is concluded that posttransformational control of Phos, exerted by reductions in substrate (free Pi) and allosteric modulator (free AMP) contents, is responsible for a blunted muscle glycogenolysis after 6 days of endurance training. The increase in CS activity suggests that the reduction of muscle glycogenolysis was due in part to an enhanced mitochondrial potential.

Adult↗
PubMed1996

Human skeletal muscle malonyl-CoA at rest and during prolonged submaximal exercise.

Previous literature has indicated that contraction-induced decreases in malonyl-CoA are instrumental in the regulation of fatty acid oxidation during prolonged submaximal exercise. This study was designed to measure malonyl-CoA in human vastus lateralis muscle at rest and during submaximal exercise. Eight males and one female cycled for 70 min (10 min at 40% and 60 min at 65% maximal O2 uptake). Needle biopsies were obtained at rest and at 10 min, 20 min, and 70 min of exercise. Malonyl-CoA content in preexercise biopsy samples determined by high-performance liquid chromatography (HPLC) was 1.53 +/- 0.18 micromol/kg dry mass (dm). Malonyl-CoA content did not change significantly during exercise (1.39 +/- 0.21 at 10 min, 1.46 +/- 0.14 at 20 min, and 1.22 +/- 0.15 micromol/kg dm at 70 min). In contrast, malonyl-CoA content determined by HPLC in perfused rat red gastrocnemius muscle decreased significantly during 20 min of stimulation at 0.7 Hz [3.44 +/- 0.54 to 1.64 +/- 0.23 nmol/g dm, (n=9)]. We conclude that human skeletal muscle malonyl-CoA content 1) is less than reported in rat skeletal muscle at rest, 2) does not decrease with prolonged submaximal exercise, and 3) is not predictive of increased fatty acid oxidation during exercise.

Adult↗
PubMed1996

Ammonia movement and distribution after exercise across white muscle cell membranes in rainbow trout.

Manipulations of pH and electrical gradients in a perfused preparation were used to analyze the factors controlling ammonia distribution and flux in trout white muscle after exercise. Trout were exercised to exhaustion, and then an isolated-perfused white muscle preparation with discrete arterial inflow and venous outflow was made from the posterior portion of the tail. The tail-trunks were perfused with low (7.4)-, medium (7.9)-, and high (8.4)-pH saline, achieved by varying HCO3- concentration ([HCO3-]) at constant Pco2. Intracellular and extracellular pH, ammonia, CO2, K+, Na+, and Cl- were measured. Muscle intracellular pH was not affected by changes in extracellular pH. Increasing extracellular pH caused a decrease in the transmembrane NH3 partial pressure (PNH3) gradient and a decrease in ammonia efflux. When extracellular K+ concentration was increased from 3.5 to 15 mM in the medium-pH group, a depolarization of the muscle cell membrane potential from -92 to -60 mV and a 0.1-unit depression in intracellular pH occurred. Ammonia efflux increased despite a marked reduction in the PNH3 gradient. Amiloride (10(-4) M) had no effect, indicating that Na+/H(+)-NH4+ exchange does not participate in ammonia transport in this system. A comparison of observed intracellular-to-extracellular ammonia distribution ratios with those modeled according to either pH or Nernst potential distributions supports a model in which ammonia distribution across white muscle cell membranes is affected by both pH and electrical gradients, indicating that the membranes are permeable to both NH3 and NH4+. Membrane potential, acting to retain high levels of NH4+ in the intracellular compartment, appears to have the dominant influence during the postexercise period. However, at rest, the pH gradient may be more important, resulting in much lower intracellular ammonia levels and distribution ratios. We speculate that the muscle cell membrane NH3-to-NH4+ permeability ratio in trout may change between the rest and postexercise condition.

Acid-Base Equilibrium↗
PubMed1996

Lactate and metabolic H+ transport and distribution after exercise in rainbow trout white muscle.

An isolated-perfused tail-trunk preparation was employed to study the influence of transmembrane pH gradient and membrane potential on the transport and distribution of L(+)-lactate (Lac), metabolic H+ (delta Hm+), and related parameters in rainbow trout white muscle after exhaustive exercise. One resting [arterial pH (pHa) approximately 7.9] and four postexercise treatments (pHa approximately 7.4, 7.9, 8.4, and, high K+, pHa approximately 7.9, partially depolarized by 15 mM K+) were examined. Variations in HCO3- concentration (2-18 mM) at a constant PCO2 approximately 2 Torr were used to alter pHa. The elevated intracellular Lac (approximately 50 mM) remained unchanged after 60 min of perfusion because of very low rates of lactate efflux and oxidation. H+, HCO3-, and Lac- distributions were all well out of electrochemical equilibrium. Total CO2 efflux was reduced at high extracellular pH (pHe); alterations in the net driving force on HCO3- may have overshadowed the influence of PCO2 gradients in driving total CO2 efflux. Lac efflux and delta Hm+ flux were completely uncoupled. delta Hm+ flux reacted to both acid-base and electrochemical gradients as delta Hm+ efflux dropped and even reversed when pHe decreased, whereas partial depolarization in conjunction with depressed intracellular pH resulted in elevated delta Hm+ efflux. Lac efflux did not respond to changes in pHe. Changes in Lac efflux corresponded more closely to changes in the Lac- concentration gradient than in the lactic acid gradient. This study provides circumstantial evidence for the involvement of electroneutral mechanisms (i.e., Lac(-)-H+ cotransport and/or Lac-/anion exchange) in lactate efflux, but does not eliminate the possibility of an active transport mechanism contributing to the retention of Lac.

Animals↗
PubMed1996

Importance of muscle phosphocreatine during intermittent maximal cycling.

To examine the importance of phosphocreatine (PCr) degradation in maintaining power output during maximal intermittent cycling, seven healthy men completed three bouts of isokinetic cycling (30 s, 100 revolutions/min) with 4 min of rest between bouts. After bout 2, blood flow to one leg was occluded by cuffing the thigh (Cuff) during the rest period to prevent PCr resynthesis while the circulation to the other leg was intact (Cont). The cuff was then removed and bout 3 completed. Muscle biopsies were sampled from the vastus lateralis of both legs just before and immediately after bout 3. Total work produced by the Cuff and Cont legs was similar during bouts 1 (9.3 +/- 0.5 and 9.6 +/- 0.5 kJ, respectively) and 2 (8.1 +/- 0.4 and 8.3 +/- kJ, respectively). Cuffing prevented the resynthesis of PCr because pre-bout 3 contents were 20.7 +/- 8.4 and 63.0 +/- 3.3 mmol/kg dry muscle in the Cuff and Cont legs, respectively. Cuffing also resulted in significantly higher muscle levels of lactate, H+ concentration (287 +/- 26 vs. 217 +/- 15 nM), ADP, AMP, and acetyl-CoA before bout 3 but had no effect on other glycolytic intermediates, ATP, or acetylcarnitine. Total work in bout 3 was significantly reduced by 15% in the Cuff leg (5.8 +/- 0.4 vs. 6.8 +/- 0.6 kJ). PCr degradation during bout 3 was 3.1 and 47.5 mmol/kg dry muscle in the Cuff and Cont legs, respectively, and lactate accumulation was minimal in both legs. Changes in all other metabolites during bout 3 were not different between legs. The results suggest that PCr contributed approximately 15% of the total ATP provision during the third 30-s bout of maximal isokinetic cycling and that most of the ATP was provided during the initial 15 s. Muscle glycogenolysis contributed minimally to ATP provision (approximately 10-15%) during the third 30-s bout, suggesting that aerobic metabolism becomes the dominant source of ATP during this model of repeated sprinting.

Adult↗
PubMed1996

Variability of triacylglycerol content in human skeletal muscle biopsy samples.

The variability of the triacylglycerol store in human skeletal muscle (TGm) was examined using the needle biopsy technique. In 13 subjects, three biopsies were sampled from the vastus lateralis muscle of one leg at rest and after 90 min of cycling at 65% of maximal O2 uptake on one or two occasions. Visible fat and blood were removed before the samples were frozen, and remaining blood, connective tissue, and fat were removed from freeze-dried fiber bundles. TGm content was measured in two aliquots of powdered muscle from each biopsy. Within-biopsy variability was low at 6%. Despite precautions, many biopsies from inactive subjects were contaminated with adipose tissue. The TGm between-biopsy coefficient of variation (CV) was 23.5 +/- 14.6% (SD, n = 24) for rest and exercise time points where three noncontaminated biopsies existed. The between-biopsy variability at rest (19.8 +/- 7.9%, n = 10) was not significantly different from that at exercise (26.1 +/- 17.4%, n = 14). The muscle glycogen between-biopsy CV for rest and exercise time points was 10.0 +/- 10.3%. The resting TGm content was 26.3 +/- 4.3 mmol/kg dry muscle, and the net utilization during the 90 min of exercise was less than the between-biopsy variability. It is concluded that the TGm store measured in repeated biopsies of human skeletal muscle is variable, with a CV of 20-26%. Therefore, because of this high variability, only changes greater than approximately 24% of resting TGm content may be considered meaningful.

Adult↗
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

Skeletal muscle pyruvate dehydrogenase activity during maximal exercise in humans.

The regulation of the active form of pyruvate dehydrogenase (PDHa) and related metabolic events were examined in human skeletal muscle during repeated bouts of maximum exercise. Seven subjects completed three consecutive 30-s bouts of maximum isokinetic cycling, separated by 4 min of recovery. Biopsies of the vastus lateralis were taken before and immediately after each bout. PDHa increased from 0.45 +/- 0.15 to 2.96 +/- 0.38, 1.10 +/- 0.11 to 2.91 +/- 0.11, and 1.28 +/- 0.18 to 2.82 +/- 0.32 mmol.min-1.kg wet wt-1 during bouts 1, 2, and 3, respectively. Glycolytic flux was 13-fold greater than PDHa in bouts 1 and 2 and 4-fold greater during bout 3. This discrepancy between the rate of pyruvate production and oxidation resulted in substantial lactate accumulation to 89.5 +/- 11.6 in bout 1, 130.8 +/- 13.8 in bout 2, and 106.6 +/- 10.1 mmol/kg dry wt in bout 3. These events coincided with an increase in the mitochondrial oxidation state, as reflected by a fall in mitochondrial NADH/NAD, indicating that muscle lactate production during exercise was not an O2-dependent process in our subjects. During exercise the primary factor regulating PDHa transformation was probably intracellular Ca2+. In contrast, the primary regulatory factors causing greater PDHa during recovery were lower ATP/ADP and NADH/NAD and increased concentrations of pyruvate and H+. Greater PDHa during recovery facilitated continued oxidation of the lactate load between exercise bouts.

Adenine Nucleotides↗