Energetics and power output of isolated fish fast muscle fibres performing oscillatory work

1991 ◽  
Vol 158 (1) ◽  
pp. 261-273 ◽  
Author(s):  
T. W. Moon ◽  
J. D. Altringham ◽  
I. A. Johnston
Keyword(s):  
High Performance ◽  
Energy Charge ◽  
Fibre Length ◽  
Creatine Phosphate ◽  
High Energy ◽  
Rapid Decline ◽  
Muscle Fibres ◽  
Tight Coupling ◽  
Work Cycle

Fast myotomal muscle fibres were isolated from the cod (Gadus morhua L.) and the energy cost of contraction was measured under conditions simulating swimming. Fibre bundles were subjected to sinusoidal cycles of shortening and lengthening about their in situ fibre length, and stimulated at selected phases in each cycle. The preparations were poisoned with iodoacetic acid and bubbled with nitrogen to block the synthesis of ATP. After an initial rapid decline over the first 10 cycles, force and net work remained steady in some cases for up to 64 oscillatory length cycles, but more commonly declined slowly after about 30 cycles. The total mechanical work performed increased largely in proportion to the number of work cycles. At the end of each experiment fibres were frozen in isopentane cooled in liquid nitrogen and metabolite concentrations determined by high performance liquid chromatography (HPLC) and enzymatic analysis. Concentrations of adenylates did not differ significantly from control values, although a significant increase in IMP concentrations at 64 cycles accounted for the maintenance of relatively high energy charge values. Creatine (C) concentrations increased and creatine phosphate (CP) concentrations decreased, implying a tight coupling of the ATP/ADP reaction to the CP/C reaction. Muscle economy was calculated as the positive work performed during a work cycle divided by the total chemical energy expended. These values (approx. 7 mJ mumol-1) were found to be independent of the number of work cycles performed, although a trend to increase was observed. Muscle efficiency values, calculated assuming a Gibb's force free energy change for CP splitting in vivo of 55 kJ mol-1, were in the range 12–23%.

scholarly journals A MICROCALORIMETRIC STUDY OF TURTLE CORTICAL SLICES: INSIGHTS INTO BRAIN METABOLIC DEPRESSION

1994 ◽  
Vol 191 (1) ◽  
pp. 141-153 ◽  
Author(s):  
C Doll ◽  
P Hochachka ◽  
S Hand
Keyword(s):  
Cortical Neurons ◽  
Heat Dissipation ◽  
Energy Charge ◽  
Utilization Rate ◽  
Rapid Decline ◽  
Metabolic Depression ◽  
Slice Preparation ◽  
Cortical Slices

In previous papers, we have examined turtle cortical neurons in vitro for mechanisms of anoxic metabolic depression ('channel arrest' and changes in electrical parameters). Negative results prompted the current study with the aim of examining more closely the energy profile and metabolism of turtle cortical slices. Calorimetry is used to measure heat dissipation during normoxia and nitrogen perfusion (120 min) and the results are converted into an ATP utilization rate. These indicate that the control rate of ATP utilization (1.72 µmol ATP g-1 min-1) agrees closely with in vivo whole-brain metabolic measurements. Both nitrogen perfusion and pharmacologically induced anoxic (cyanide+N2) groups depressed heat dissipation considerably compared with the control value (nitrogen 37 %; pharmacological anoxia 49 %). The resulting ATP utilization estimates indicate metabolic depressions of 30 % (nitrogen) and 42 % (pharmacological anoxia). The slice preparation did not exhibit a change in any measured adenylate parameter for up to 120 min of anoxia or pharmacological anoxia. Significant changes did occur in [ADP], ATP/ADP ratio and energy charge after 240 min of exposure to anoxic conditions. These results support the idea that the turtle cortical slice preparation has a profound resistance to anoxia, with both nitrogen perfusion and pharmacological anoxia causing a rapid decline in heat dissipation and metabolism.

Implication of L-type Ca2+ channels in noncholinergic adrenal catecholamine secretion by endothelin-1 in vivo

1995 ◽  
Vol 269 (2) ◽  
pp. R287-R293 ◽  
Author(s):  
N. Yamaguchi
Keyword(s):  
High Performance ◽  
Cholinergic Receptor ◽  
Secondary Response ◽  
Control Group ◽  
Rapid Decline ◽  
Chromatography Method ◽  
Endothelin 1 ◽  
Liquid Chromatography Method ◽  
Ca2 Channels

The aim of the present study was to investigate if either dihydropyridine-sensitive L-type Ca2+ channels or cholinergic receptor-mediated mechanisms are implicated in endothelin-1 (ET)-induced adrenal catecholamine (CA) secretion in anesthetized dogs. ET was locally administered to the left adrenal gland via the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography method. In the control group, local infusion (1 min, 0.5 ml/min) of ET (the fixed total dose of 0.5 microgram given to the gland or approximately 0.0197 microgram/kg of body weight) resulted in a sharp increase in the basal CA output, followed by a rapid decline, and a relatively slow secondary response lasted over a period of 15-30 min. In the second group treated with nifedipine (5 micrograms or approximately 0.207 microgram/kg) similarly administered 10 min before ET infusion, the ET-induced first steep increase in CA output was significantly attenuated by approximately 75% (P < 0.05, n = 6). In dogs similarly receiving either pentolinium (1 mg or approximately 0.041 mg/kg) or atropine (0.5 mg or approximately 0.018 mg/kg), the ET-induced CA response remained unchanged. The results indicate that ET-induced adrenal CA release was largely mediated by the activation of dihydropyridine-sensitive L-type Ca2+ channels. Furthermore, neither nicotinic nor muscarinic receptors were functionally implicated in the CA response to ET. The study suggests the existence of noncholinergic mechanisms involved in the secretory action of ET on the adrenal medulla in the dog in vivo.

scholarly journals Computational modelling of muscle fibre operating ranges in the hindlimb of a small ground bird (Eudromia elegans), with implications for modelling locomotion in extinct species

2021 ◽  
Vol 17 (4) ◽  
pp. e1008843
Author(s):  
Peter J. Bishop ◽  
Krijn B. Michel ◽  
Antoine Falisse ◽  
Andrew R. Cuff ◽  
Vivian R. Allen ◽  
...  
Keyword(s):  
Muscle Function ◽  
Computational Models ◽  
Fibre Length ◽  
Computational Modelling ◽  
Length Change ◽  
Muscle Fibres ◽  
Extinct Species ◽  
Length Changes ◽  
Experimental Findings

The arrangement and physiology of muscle fibres can strongly influence musculoskeletal function and whole-organismal performance. However, experimental investigation of muscle function during in vivo activity is typically limited to relatively few muscles in a given system. Computational models and simulations of the musculoskeletal system can partly overcome these limitations, by exploring the dynamics of muscles, tendons and other tissues in a robust and quantitative fashion. Here, a high-fidelity, 26-degree-of-freedom musculoskeletal model was developed of the hindlimb of a small ground bird, the elegant-crested tinamou (Eudromia elegans, ~550 g), including all the major muscles of the limb (36 actuators per leg). The model was integrated with biplanar fluoroscopy (XROMM) and forceplate data for walking and running, where dynamic optimization was used to estimate muscle excitations and fibre length changes throughout both gaits. Following this, a series of static simulations over the total range of physiological limb postures were performed, to circumscribe the bounds of possible variation in fibre length. During gait, fibre lengths for all muscles remained between 0.5 to 1.21 times optimal fibre length, but operated mostly on the ascending limb and plateau of the active force-length curve, a result that parallels previous experimental findings for birds, humans and other species. However, the ranges of fibre length varied considerably among individual muscles, especially when considered across the total possible range of joint excursion. Net length change of muscle–tendon units was mostly less than optimal fibre length, sometimes markedly so, suggesting that approaches that use muscle–tendon length change to estimate optimal fibre length in extinct species are likely underestimating this important parameter for many muscles. The results of this study clarify and broaden understanding of muscle function in extant animals, and can help refine approaches used to study extinct species.

Role of ATP-sensitive K+ channels in ischemic preconditioning of skeletal muscle against infarction

1997 ◽  
Vol 273 (1) ◽  
pp. H44-H51 ◽  
Author(s):  
C. Y. Pang ◽  
P. Neligan ◽  
H. Xu ◽  
W. He ◽  
A. Zhong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Energy Charge ◽  
Katp Channels ◽  
High Energy ◽  
Intraarterial Infusion ◽  
Muscle Flaps ◽  
Charge Potential

We studied the role and mechanism of ATP-sensitive K+ (KATP) channels in ischemic preconditioning (IPC) of skeletal muscle against infarction in vivo. Surgically denervated, noncontractile latissimus dorsi muscle flaps in pentobarbitone-anesthetized pigs were assigned to nine groups: control; IPC (3 cycles of 10-min ischemia/reperfusion); preischemic lemakalim (LMK, 0.18 mg/muscle); postischemic LMK; sodium 5-hydroxydecanoate (5-HD, 27 mg/muscle) before IPC; glibenclamide (Glib 0.3 mg/kg iv) before IPC; 5-HD before preischemic LMK; 5-HD before ischemia; and Glib before ischemia. Except for Glib, all drugs were delivered to each muscle by 10-min local intraarterial infusion to avoid systemic effects. All muscle flaps underwent 4 h of global ischemia. Infarction was assessed at 48 h of reperfusion. In a separate study, muscle biopsies were taken before, during, and after ischemia for assay of high-energy phosphate and lactate contents and myeloperoxidase (MPO) activity. It was observed that muscle infarction in the IPC (24 +/- 2%) and preischemic LMK (21 +/- 2%) groups were smaller (P < 0.05) than that in the control (42 +/- 2%). The anti-infarction effect of IPC and LMK was blocked by 5-HD or Glib. IPC and preischemic LMK caused a higher (P < 0.05) muscle content of ATP and energy charge potential, a lower (P < 0.05) muscle content of lactate during ischemia, and a lower (P < 0.05) muscle MPO activity throughout 16 h of reperfusion compared with the control. These observations indicated for the first time that KATP channels are also involved in the anti-infarction effect of IPC in noncontractile skeletal muscle in vivo. Presently, the cause and importance of energy-sparing and neutrophil-inhibitory effects of IPC and LMK are not known.

Direct observation of the phosphate acceptor and phosphagen pool sizes in vivo

1990 ◽  
Vol 258 (5) ◽  
pp. R1132-R1139 ◽  
Author(s):  
A. Van Waarde ◽  
G. van den Thillart ◽  
M. Verhagen ◽  
C. Erkelens ◽  
A. Addink ◽  
...  
Keyword(s):  
High Performance ◽  
31P Nmr ◽  
Direct Analysis ◽  
Muscular Contraction ◽  
High Energy ◽  
Reversed Phase ◽  
High Energy Phosphate ◽  
End Products ◽  
Pool Sizes

Earthworms were subjected to environmental anoxia (200 min) and electrical stimulation (5 min, 6 V, 50 Hz). The levels of high-energy phosphate compounds and the intracellular pH were monitored during anoxia, muscular contraction, and recovery by in vivo phosphorus-31 nuclear magnetic resonance (31P-NMR). Several key metabolites were determined by enzymatic analysis and reversed-phase high-performance liquid chromatography of perchlorate extracts. Because lombricine, the phosphagen phosphate acceptor of earthworms, is a phosphodiester, 31P-NMR permitted direct analysis of the extent of phosphorylation of the lombricine pool in vivo. Total lombricine, lombricine phosphate, ATP, and H+ were measured by NMR, and free ADP was calculated from the lombricine kinase equilibrium constant. The ADP concentration was not significantly changed by anoxia, but it rose threefold after stimulation. L-Lactate accumulated on stimulation, whereas multiple end products (L-lactate, alanine, succinate, and glutamine) were formed during environmental anaerobiosis.

scholarly journals Effect of Dihydroergocristine on Energy Metabolism Studied in the Isolated Perfused Rat Brain Affected by Ischemia and in Neuroblastoma Cells Deprived of Oxygen and Glucose

1984 ◽  
Vol 4 (4) ◽  
pp. 610-614 ◽  
Author(s):  
A. Rachman ◽  
L. Kellmann ◽  
J. Krieglstein
Keyword(s):  
Energy Metabolism ◽  
Rat Brain ◽  
Energy State ◽  
Cell Metabolism ◽  
Neuroblastoma Cells ◽  
Creatine Phosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Isolated Perfused Rat Brain

The effect of dihydroergocristine on energy metabolism was studied in the isolated perfused rat brain affected by ischemia and in cultivated C-1300 neuroblastoma cells deprived of oxygen and glucose. Creatine phosphate, ATP, ADP, AMP, glucose, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, pyruvate, and lactate were measured enzymatically. After a perfusion period of 30 min, the cortex of the isolated perfused rat brain exhibited an energy state not different from that in vivo. Dihydroergocristine added to the perfusion medium (5 μmol/L) did not influence these substrate levels under normal perfusion conditions. However, this drug was able to retard the breakdown of high-energy phosphates during ischemia and to accelerate the restoration of the energy state during the postischemic reperfusion period. The perfusion rate was not changed by the drug, and therefore it was assumed that dihydroergocristine could act directly on cell metabolism. This view was supported by the results obtained from experiments using cultivated N-2a neuroblastoma cells. These cells were incubated in a buffered salt solution deprived of glucose and oxygen for 15 min. Under these conditions, dihydroergocristine (2 μmol/L) added to the incubation medium caused changes in the concentrations of the high-energy phosphates similar to those in the isolated brain preparation: It increased the ATP concentration and decreased the ADP concentration significantly.

Oxygen delivery does not limit cardiac performance during high work states

1999 ◽  
Vol 277 (1) ◽  
pp. H50-H57 ◽  
Author(s):  
Jianyi Zhang ◽  
Yo Murakami ◽  
Yi Zhang ◽  
Yong K Cho ◽  
Yun Ye ◽  
...  
Keyword(s):  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Creatine Phosphate ◽  
High Energy ◽  
Artery Occlusion ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Myocardial Oxygenation ◽  
High Work

This study tested the hypothesis that the loss of myocardial high-energy phosphates (HEP), which occurs during high cardiac work states [J. Zhang, D. J. Duncker, Y. Xu, Y. Zhang, G. Path, H. Merkle, K. Hendrich, A. H. L. From, R. Bache, and K. Uğurbil. Am. J. Physiol. 268: ( Heart Circ. Physiol. 37): H1891–H1905, 1995], is not the result of insufficient intracellular O2 availability. To evaluate the state of myocardial oxygenation, the proximal histidine signal of deoxymyoglobin (Mb-δ) was determined with1H nuclear magnetic resonance spectroscopy (MRS), whereas HEP were examined with31P MRS. Normal dogs ( n = 11) were studied under basal conditions and during combined infusion of dobutamine and dopamine (20 μg ⋅ kg−1 ⋅ min−1iv each), which increased rate-pressure products to >50,000 mmHg ⋅ beats ⋅ min−1. Creatine phosphate (CP) was expressed as CP/ATP, and myocardial myoglobin desaturation was normalized to the Mb-δ resonance present during total coronary artery occlusion. This Mb-δ resonance appeared at 71 parts per million downfield from the water resonance. CP/ATP decreased from 2.22 ± 0.12 during the basal state to 1.83 ± 0.09 during the high work state ( P < 0.01), whereas ΔPi/CP increased from 0 to 0.21 ± 0.04 ( P < 0.01). Despite these HEP changes, Mb-δ remained undetectable. In contrast, when a coronary stenosis was applied to produce a similar decrease in CP/ATP, Mb-δ reached 0.38 ± 0.10 of the value present during total coronary occlusion. These data demonstrate that Mb-δ is readily detected in vivo during limitation of coronary blood flow sufficient to cause a decrease of myocardial CP/ATP. However, similar HEP changes that occur at high work states in the absence of coronary occlusion are not associated with a detectable Mb-δ resonance. The findings support the hypothesis that the myocardial HEP changes observed at high work states are not due to inadequate O2 availability to the mitochondria and emphasize the limitations of interpreting HEP alterations in the absence of knowing the level of myocyte oxygenation.

Energy expended during oxygen deficit period of submaximal exercise in man

1980 ◽  
Vol 48 (5) ◽  
pp. 770-775 ◽  
Author(s):  
P. Pahud ◽  
E. Ravussin ◽  
E. Jequier
Keyword(s):  
Steady State ◽  
Coupling Efficiency ◽  
Creatine Phosphate ◽  
High Energy ◽  
Oxygen Deficit ◽  
Physical Work ◽  
Direct Calorimetry ◽  
External Work ◽  
Exercise Efficiency

Aerobic (MR) and anaerobic (Man) metabolism was determined during the transition from mild (50 W external work) to heavier exercise (50% VO2max) in six subjects. The overall exercise efficiency was calculated during the oxygen deficit period and during steady-state exercise. MR was obtained by indirect calorimetry and Man by solving the heat balance equation: MR + Man - S = (R + C + E) + W, where radiative, convective, and evaporative heat losses (R + C + E) were measured by direct calorimetry, work output (W) by ergometry, and heat storage (S) by thermometry. (MR + Man) during the oxygen deficit period was found to be lower than MR during steady state. In the 1st min of exercise, mean mixed work efficiency (aerobic + anaerobic) was 33%, which was greater than aerobic efficiency (26.6%) during steady state. The mean anaerobic efficiency efficiency was 41%. This difference reflects the fact that the energy released by splitting of preformed high-energy bonds (i.e., creatine phosphate) is less than the energy released when high-energy bonds expended during mechanical work are continuously regenerated through oxidative phosphorylation. The reported measurements of overall energy metabolism in man provide means for estimating in vivo the coupling efficiency of physical work (i.e., 41%) as well as the efficiency with which energy released by substrate oxidations is recovered in the form of high-energy bonds (i.e., phosphorylation efficiency = 64%).

Hyperperfusion and cardioplegia effects on myocardial high-energy phosphate distribution and energy expenditure

1994 ◽  
Vol 267 (3) ◽  
pp. H894-H904 ◽  
Author(s):  
J. Zhang ◽  
L. Shorr ◽  
M. Yoshiyama ◽  
H. Merkle ◽  
M. Garwood ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Oxidative Phosphorylation ◽  
Contractile Function ◽  
Creatine Phosphate ◽  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphate ◽  
Myocardial Layers ◽  
Compound Distribution

This study examines the hypothesis that high-energy phosphate (HEP) compound levels in unstimulated in vivo myocardium are defined by 1) the level of perfusion and 2) non-perfusion-dependent metabolic characteristics. This hypothesis was tested by determining 1) the effects of pharmacological hyperperfusion of functioning myocardium on transmural HEP compound distribution, contractile function, and myocardial oxygen consumption rate (MVO2) as well as 2) the effect of KCl cardioplegia on transmural myocardial HEP compound distribution. Creatine phosphate (CP) and ATP were measured across the anterior left ventricular wall using spatially localized 31P-nuclear magnetic resonance (NMR). At baseline, the CP-to-ATP (CP/ATP) ratio was significantly lower in the subendocardium than in the subepicardium. This transmural HEP gradient was abolished by hyperperfusion without significant effects on contractile function or MVO2. Similarly, KCl arrest significantly increased CP and CP/ATP in all myocardial layers, and the transmural gradient of CP/ATP was abolished again. These studies indicate that in present experimental model 1) myocardial performance is not constrained by inadequate perfusion in any myocardial layer although modest oxygen limitation affects the kinetics of oxidative phosphorylation in the inner myocardial layers and 2) in all myocardial layers, submaximal activation of intermediary metabolism and oxidative phosphorylation reactions results in lower steady-state CP and higher ADP levels relative to their respective values when energy expenditure is markedly reduced by KCl arrest.

Sign in / Sign up

Export Citation Format

Share Document