Biomedical subjects

F Lou

Publications and source records attributed to F Lou.

40 records · Page 3Linked to original sources

PubMed1993

Depression of tetanic force induced by loaded shortening of frog muscle fibres.

1. Single fibres isolated from the anterior tibialis muscle of Rana temporaria were allowed to shorten against a high load during a 2.5-4.0 s fused tetanus (1-3 degrees C) and the maximum force produced at the short length was compared with that recorded during a fixed-end tetanus at the same overall fibre length. Changes in length of marked, consecutive segments (ca 0.5 mm in length) along the fibre were measured throughout the tetanus using a photoelectric recording system. 2. Loaded shortening (load ca 3/4 of maximum tetanic force) starting from approximately 2.55 microns sarcomere length and ending near slack fibre length depressed the tetanic force by 13 +/- 2% (mean +/- S.E.M., n = 10) and caused a marked redistribution of sarcomere length along the fibre. Unloaded shortening over the same range caused no force deficit and did not lead to increased dispersion of sarcomere length. 3. Loaded shortening below slack length produced less force depression and less non-uniformity of sarcomere length than did a corresponding intervention above slack length. 4. The force deficit after loaded shortening, both above and below slack fibre length, was positively correlated (P < 0.005) to the coefficient of variation of the sarcomere length along the fibre. 5. The decrease in active force after loaded shortening, and its relation to increased dispersion of sarcomere length along the fibre, could be simulated closely by a computer model in which the muscle fibre was assumed to consist of eleven discrete segments acting in series with a passive elastic element. 6. Experiments were performed in which the length of an individual segment of the intact muscle fibre was strictly controlled throughout a tetanus. Loaded shortening of such a 'length-clamped' segment caused no force depression during the subsequent isometric phase either above or below slack fibre length. 7. The results suggest strongly that force depression after loaded shortening of a single muscle fibre is attributable to non-uniform sarcomere behaviour along the fibre. The experimental evidence supports the view that: (i) the myosin cross-bridges act as independent force generators; and (ii) their steady-state performance during a tetanus is unaffected by the preceding contractile activity.

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PubMed1992

Myofibrillar fatigue versus failure of activation during repetitive stimulation of frog muscle fibres.

1. Single fibres isolated from the anterior tibialis muscle of Rana temporaria (temperature, 2-5 degrees C; sarcomere length, 2.10 microns) were fatigued using two separate protocols that led to different degrees of depression of tetanic force. Under control conditions the fibre was stimulated to produce a 1 s fused isometric tetanus at 300 s intervals. A moderate degree of fatigue (tetanic force reduced to 70-80% of the control value) was produced by decreasing the intervals between tetani to 15 s ('fatiguing protocol 1'). A more pronounced depression of tetanic force (to 40-50% of the control value) was produced by evoking a single twitch at 1-2 s intervals ('fatiguing protocol 2'). 2. Fatiguing protocol 1 reduced the contracture response to submaximal and supramaximal concentrations of caffeine (3-15 mM) in proportion to the decrease in tetanic force. These results support the view that fatiguing stimulation according to protocol 1 leads to a true 'myofibrillar fatigue' with no failure of activation of the muscle fibre. 3. Fatiguing protocol 2 reduced the amplitudes of isometric twitch and tetanus to below 10 and 50% of the control values, respectively. By contrast, the maximal contracture response to caffeine (15 mM) was depressed by merely 2-3% of its prefatigue value. 4. Force and instantaneous fibre stiffness were recorded simultaneously during twitch and tetanus as fatigue was induced by protocol 2. During the initial part of fatigue (tetanic force reduced by 25% of control) stiffness was reduced by merely 9% in accordance with previous measurements during fatigue induced by protocol 1. However, with further depression of twitch and tetanus by protocol 2 there was a marked reduction of fibre stiffness. These results, together with the findings reported under point 3, strongly suggest that at an advanced state of fatigue induced by protocol 2 the decrease in active force is largely due to failure of activation of the contractile system. 5. Muscle fibres were quickly frozen for electron microscopical examination after shortening below slack length (to approximately 1.6 microns sarcomere spacing) during tetanic stimulation. In non-fatigued fibres, and in fibres fatigued according to protocol 1, the myofibrils exhibited a straight appearance throughout the preparation suggesting that the entire volume of the fibre was properly activated. In fibres fatigued by protocol 2, on the other hand, only the most peripheral layers of myofibrils remained straight after shortening, whereas the centre of the fibre showed marked waviness indicating failure of the inward spread of activation in this case.

Animals↗

PubMed1992

[Protection on experimental sinus node dysfunction in rabbits with ginsenosides].

This experiment was carried out to evaluate the effect of ginsenosides from stems and leaves (GSL) on the sinus node dysfunction (SND) by observing the changes of the electrophysiological parameters of sinus node in limited period. Anesthetized rabbits were randomly divided into 3 groups. In the acute experiment, GSL, 50 mg/kg, iv, was given to the GSL group (G), n = 12. Normal saline (NS), the same volume, to the control group (C), n = 12. After GSL was administered 30-50 mg/kg.d for 14 days, iv, another data were obtained from chronic experimental group (CE), n = 15. The results show that the parameters, spontaneous cycle length (SCL), maximal sinus node recovery time (SNRTmax), corrected sinus node recovery time (CSNRT) were shorter in G group and CE group than C group respectively (P less than 0.05, P less than 0.01). It was suggested that GSL exerted protective effects on the experimental sinus node dysfunction.

Animals↗

PubMed1990

Changes in force and stiffness induced by fatigue and intracellular acidification in frog muscle fibres.

1. Changes in force and stiffness were recorded simultaneously during 1 s isometric (fixed ends) tetani of single fibres isolated from the anterior tibialis muscle of Rana temporaria (temperature 1-3 degrees C; sarcomere length, 2.10 micron). Stiffness was measured as the change in force that occurred in response to a 4 kHz sinusoidal length oscillation of the fibre. Some experiments were performed in which stiffness was determined from a fast (0.2 ms) length step that was applied to a 'tendon-free' segment of the muscle fibre during the tetanus plateau. 2. A moderate degree of fatigue was produced by decreasing the time between tetani from 300 s (control) to 15 s. By this treatment the maximum tetanic force (Ftet) was reversibly reduced to 70-75% of the control value. Maximum tetanic stiffness (Stet) was related to Ftet according to the following regression (both variables expressed as percentage of their control values): Stet = 0.369 Ftet + 62.91 (correlation coefficient, 0.95; P less than 0.001). A 25% decrease in isometric force during fatigue was thus associated with merely 9% reduction of fibre stiffness. 3. Whereas the rate of rise of force during tetanus was markedly reduced by fatiguing stimulation, the rate of rise of stiffness was only slightly affected. 4. Intracellular acidification (produced by raised extracellular CO2 concentration) largely reproduced the contractile changes observed during fatigue. However, for a given decrease in tetanic force there was a smaller reduction in fibre stiffness during acidosis than during fatigue. 5. Caffeine (0.5 mM) added to the fibre after development of fatigue and intracellular acidosis greatly potentiated the isometric twitch but did not affect maximum tetanic force. This finding provides evidence that the contractile system was fully activated during the tetanus plateau both in the fatigued state and during acidosis. 6. The results suggest that the decrease in contractile strength after frequent tetanization (intervals between tetani, 15 s) is attributable to altered kinetics of cross-bridge function leading to reduced number of active cross-bridges and, most significantly, to reduced force output of the individual bridge. The possible role of increased intracellular H+ concentration in the development of muscle fatigue is discussed.

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