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Biomedical subjects

C Juel

Publications and source records attributed to C Juel.

51 records · Page 3Linked to original sources

Anaerobic energy production and O2 deficit-debt relationship during exhaustive exercise in humans.

1. Eight subjects performed one-legged, dynamic, knee-extensor exercise, first at 10 W followed by 10 min rest, then at an intense, exhaustive exercise load (65 W) lasting 3.2 min. After 60 min recovery, exercise was performed for 8-10 min each at 20, 30, 40 and 50 W. Measurements of pulmonary oxygen uptake, heart rate, blood pressure, leg blood flow, and femoral arterial-venous differences of oxygen content and lactate were performed as well as determination of ATP, creatine phosphate (CP) inosine monophosphate (IMP) and lactate concentrations on biopsy material from the quadriceps muscle before and immediately after the intense exercise, and at 3, 10 and 60 min into recovery. 2. Individual linear relations (r = 0.95-1.00) between the power outputs for submaximal exercise and oxygen uptakes (leg and pulmonary) were used to estimate the energy demand during intense exercise. Pulmonary and leg oxygen deficits determined as the difference between energy demand and oxygen uptake were 0.46 and 0.48 l (kg active muscle)-1, respectively. Limb and pulmonary oxygen debts (oxygen uptake during 60 min of recovery - pre-exercise oxygen uptake) were 0.55 and 1.65 l (kg active muscle)-1, respectively. 3. During the intense exercise, muscle [ATP] decreased by 30% and [CP] by 60% from resting concentrations of 6.2 and 22.4 mmol (kg wet wt)-1, respectively, and [IMP] increased to 1.1 mmol (kg wet wt)-1. Muscle [lactate] increased from 2 to 28.1 mmol (kg wet wt)-1, and the concomitant net lactate release was 14.8 mmol (kg wet wt)-1 or about 1/3 of the total net lactate production. During recovery 70% of the accumulated lactate was released to the blood, and the nucleotides and CP returned to about 40 and 85% of pre-exercise values at 3 and 10 min of recovery, respectively. 4. Total reduction in ATP and CP (and elevation of IMP) during the intense exercise amounted to 16.4 mmol ATP (kg wet wt)-1, which together with the lactate production accounted for 83.1 mmol ATP (kg wet wt)-1. In addition 6-8 mmol ATP (kg wet wt)-1 are made available related to accumulation of glycolytic intermediates including pyruvate (and alanine). Estimated leg oxygen deficit corresponded to an ATP production of 94.7 mmol ATP kg-1; this value included 3.1 mmol kg-1 related to unloading of HbO2 and MbO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Ammonia metabolism during intense dynamic exercise and recovery in humans.

This study examined the dynamics for ammonia (NH3) metabolism in human skeletal muscle during and after intense one-legged exercise. Subjects (n = 8) performed dynamic leg extensor exercise to exhaustion (3.2 min). Muscle NH3 release increased rapidly to a maximum of 314 +/- 42 mumol/min and declined immediately on cessation of exercise. Recovery was complete in approximately 20 min. Arterial [NH3] increased less rapidly and reached its maximum 2-3 min into recovery. These data demonstrate that NH3 clearance is more sensitive to the cessation of exercise than is NH3 release from skeletal muscle. Muscle [NH3] increased three to fourfold during exercise and represented 74 +/- 8% of the total net NH3 formation. Thus the change in muscle [NH3] alone underestimates the NH3 production. There was no evidence that the muscle-to-venous blood NH3 ratio shifts in accordance with the H+ data. Thus other factors must contribute to the NH3 release from active muscle. The total net NH3 formed corresponded with the intramuscular inosine 5'-monophosphate accumulation, suggesting that the NH3 was derived from AMP deamination. Changes in the known modulators of AMP deaminase (ATP, ADP, H+) were moderate, so the mechanisms initiating the deamination remain obscure.

Adenine Nucleotides↗

Limb skeletal muscle adaptation in athletes after training at altitude.

Morphological and biochemical characteristics of biopsies obtained from gastrocnemius (GAS) and triceps brachii muscle (TRI), as well as maximal O2 uptake (VO2 max) and O2 deficit, were determined in 10 well-trained cross-country skiers before and after a 2-wk stay (2,100 m above sea level) and training (2,700 m above sea level) at altitude. On return to sea level, VO2 max was the same as the prealtitude value, whereas an increase in O2 deficit (29%) and in short-term running performance (17%) was observed (P less than 0.05). GAS showed maintained capillary supply but a 10% decrease in mitochondrial enzyme activities (P less than 0.05), whereas an increase in capillary supply (P less than 0.05) but unchanged mitochondrial enzyme activities were observed in TRI. Buffer capacity was increased by 6% in both GAS and TRI (P less than 0.05). A positive correlation was found between the relative increase in buffer capacity of GAS and short-term running time (P less than 0.05). Thus the present study indicates no effect of 2 wk of altitude training on VO2 max but provides evidence to suggest an improvement in short-term exercise performance, which may be the result of an increase in muscle buffer capacity.

Adaptation, Physiological↗

Lactate transport in isolated mouse muscles studied with a tracer technique--kinetics, stereospecificity, pH dependency and maximal capacity.

Lactate transport across the sarcolemma of isolated mouse muscles was studied with a 14C tracer technique. The cellular tracer uptake could be inhibited by unlabelled L-lactate (and pyruvate) and to a lesser extent by D-lactase. The stereospecific fraction had a Km of 3.5 mM, and made up 50% of the total transport. The tracer uptake was unaffected by 0.05 mM DIDS and 0.2 mM amiloride, but was inhibited by cinnamate (Ki = 8 mM) and PCMBS (Ki = 0.8 mM). With high concentrations of the latter inhibitor compounds or with high concentrations of unlabelled L-lactate, the tracer uptake was inhibited 80%, which indicates that the main part of the transport involves facilitated diffusion. The remaining fraction (20%) was non-saturable, reduced at high pH, and could not be inhibited; it is probably mediated by diffusion of undissociated lactic acid. Lactate transport was pH-dependent, which is consistent with a lactate-H+ symport. The maximal transport capacity, as calculated from the pH changes measured with pH-sensitive micro-electrodes while the lactate gradient was 30 mM, was 11.8 mmol kg-1 min-1 (pH 6.2).

4-Chloromercuribenzenesulfonate↗

Muscle action potential propagation velocity changes during activity.

Fatigue from high frequency stimulation is associated with EMG signal changes, which are primarily due to a slowing of the sarcolemma conduction velocity. In the present study, in which isolated mouse soleus and extensor digitorum longus muscles have been studied, it is shown that the action potential propagation velocity is (1) decreased by an increased extracellular potassium concentration, (2) independent of extracellular pH, (3) decreased by low intracellular pH, and (4) nearly independent of moderate changes in the sodium gradient. The EDL muscle is more affected than the soleus muscle. The ion effects on propagation velocity are seen within the physiological ranges. The propagation velocity was decreased after 2 min of electrical stimulation and recovered with a time course similar to the pH recovery. The effects of extracellular potassium and internal pH are due to independent mechanisms.

Action Potentials↗

Muscle blood flow during isometric activity and its relation to muscle fatigue.

The effect of isometric exercise on blood flow, blood pressure, intramuscular pressure as well as lactate and potassium efflux from exercising muscle was examined. The contractions performed were continuous or intermittent (5 s on, 5 s off) and varied between 5% and 50% maximal voluntary contraction (MVC). A knee-extensor and a hand-grip protocol were used. Evidence is presented that blood flow through the muscle is sufficient during low-level sustained contractions (less than 10% MVC). Despite this muscle fatigue occurs during prolonged contractions. One mechanism for this fatigue may be the disturbance of the potassium homeostasis. Such changes may also play a role in the development of fatigue during intermittent isometric contractions and even more so in the recovery from such exercise. In addition the role of impaired transport of substances within the muscle, due to long-lasting daily oedema formation, is discussed in relation to fatigue in highly repetitive, monotonous jobs.

Adult↗

Intracellular pH recovery and lactate efflux in mouse soleus muscles stimulated in vitro: the involvement of sodium/proton exchange and a lactate carrier.

The intracellular pH recovery after stimulation of mouse soleus muscles in vitro was studied by means of intracellular pH-sensitive microelectrodes. The lactate efflux and the total lactate content were measured by means of an enzymic method. During electrical stimulation for 2 min in a CO2/HCO3- -buffered Ringer's solution, pHi decreased by 0.5 units. The rate of pHi-recovery was independent of external bicarbonate, but dependent on the buffer concentration. The rate of intracellular pH recovery was reduced by the lactate transport inhibitors PCMBS and cinnamate, whereas the inhibitors of inorganic anion-exchange SITS and DIDS had no effect. The Na+/H+ exchange inhibitor amiloride reduced the rate of pHi recovery. The pHi recovery was faster than the lactate efflux, which could be accounted for by an Na+/H+ exchange. A number of inhibitor compounds were used in order to discriminate between the three possible lactate efflux pathways: the monocarboxylate carrier mechanism, the inorganic anion exchange, and the molecular (non-ionic) diffusion of lactic acid. The lactate efflux was partly inhibited by cinnamate, PCMBS and phloretin, but was unaffected by DIDS and tetrathionate. These experiments demonstrate the existence of a lactate carrier in mammalian skeletal muscles. The lactate carrier is responsible for more than half of the lactate efflux after muscle activity. Both the pHi recovery studies and the lactate efflux measurements showed that, under the given conditions, the inorganic anion-exchange mechanism is not essentially involved in the recovery processes after muscle activity.

Amiloride↗

The effect of beta 2-adrenoceptor activation on ion-shifts and fatigue in mouse soleus muscles stimulated in vitro.

The resting membrane potential (RMP), the intracellular free Na+ concentration ([Na+]i) and the intracellular free K+ concentration ([K+]i), were measured with double-barrelled ion-selective microelectrodes in mouse soleus muscles in vitro. In addition, the Na+ contents and K+ contents have been measured with the flame photometric technique. At rest the beta 2-selective adrenoceptor agonist terbutaline (10(-5) M) increased the membrane potential and [K+]i, and decreased [Na+]i when compared with control muscles. During a 5 min stimulation period the muscles, which were incubated with the beta 2-adrenoceptor agonist, showed a smaller depolarization, a smaller decrease in [K+]i and a smaller increase in [Na+]i than stimulated control muscles. This difference was probably associated with an increased rate of Na-K-pumping in the beta 2-adrenoceptor stimulated muscles. The beta 2-agonist treated muscles were more resistant to fatigue than control muscles. This effect was significant with 10(-6) M terbutaline (25 degrees C). A depolarization obtained by increasing [K+]o was shown to reduce the maximal tension. It is postulated, that the K+ shifts, which are responsible for the depolarization during muscle activity, are one of the mechanisms underlying muscle fatigue.

Adrenergic beta-Agonists↗

Potassium and sodium shifts during in vitro isometric muscle contraction, and the time course of the ion-gradient recovery.

Intracellular potassium ([K+]i), interstitial potassium ([K+]inter), intracellular sodium ([Na+]i), and resting membrane potential (RMP) were measured before and after repetitive stimulation of mouse soleus and EDL (extensor digitorum longus) muscles. At rest, RMP was -69.8 mV for soleus and -74.9 mV for EDL (37 degrees C). [K+]i was 168 mM and 182 mM, respectively. In soleus, free [Na+]i was 12.7 mM. After repetitive stimulation (960 stimuli) RMP had decreased by 11.9 mV for soleus and by 18.2 mV for EDL. [K+]i was reduced by 32 mM and 48 mM, respectively, whereas [K+]inter was doubled. In soleus [Na+]i had increased by 10.6 mM, demonstrating that the [K+]i-decrease is three times higher than the [Na+]i-increase. It is concluded that this difference reflects different activity induced movements of Na and K, and that the difference is not due to the Na/K pumping ratio. The possible involvement of the potassium loss in muscle fatigue is discussed. After stimulation RMP recovered with a time constant of 0.9 min for soleus and 1.5 min for EDL. Within the first minutes after stimulation the intracellular potassium concentration increased by 20.4 mM/min for soleus and 21.7 mM/min for EDL. Free [Na+]i decreased with less than 10 mM/min. The mechanisms underlying the different rate of changes are discussed.

Animals↗

Pre- and postsynaptic effects of dopamine antagonists on dopaminergic synaptic transmission in Helix pomatia.

The rate of transmitter mobilization in identified dopaminergic synapses was decreased by the dopamine antagonists pimozide, chlorpromazine, haloperidol, cis-flupenthixol, curare, clozapine and high concentrations of ergometrine. The depolarizing postsynaptic potential was inhibited by pimozide, chlorpromazine, haloperidol, cis-flupenthixol, curare, clozapine, (+)-butaclamol and high concentrations of ergometrine. The hyperpolarizing synaptic potential was inhibited by naloxone, methysergide, (+)-butaclamol, haloperidol, 6-hydroxydopamine and low concentrations of ergometrine, while pimozide, cis-flupenthixol, trans-flupenthixol, curare, clozapine, promethazine, chlorpromazine and (-)-butaclamol had no clear effect. The presynaptic receptors involved in modulation of the mobilization rate showed similarities with the dopamine receptors mediating depolarizations. The dopamine antagonists changed dynamics of synaptic transmission.

Animals↗

Enkephalin increases the efficacy of dopaminergic transmission in Helix pomatia.

A dopaminergic synaptic connection in Helix pomatia was studied. Transmitter mobilization was measured during incubation with met-enkephalin. Enkephalin decreased the time constant for transmitter mobilization. The effect was blocked by naloxone. It is postulated that the presynaptic cell possesses opiate receptors and that these receptors mediate the enkephalin-induced increase in efficacy of dopaminergic transmission.

Animals↗