Effects of varied fatigue protocols on sarcoplasmic reticulum calcium uptake and release rates

The purpose of this investigation was to examine changes in sarcoplasmic reticulum (SR) function in muscles subjected to different patterns of muscle activity. Frog sartorius muscles were stimulated with tetanic trains (100 ms, 100 Hz) delivered at rates of 2.0, 0.5, and 0.2 trains/s. In one set of experiments, stimulation was continued until force had declined to ∼17% of initial (constant fatigue), whereas in the other set, stimulation was continued for 1 min (constant duration). In the constant-fatigue experiments, Ca2+ uptake (1 mM MgATP) and release rates (25 μM AgNO3, 5 mM 4-chloro- m-cresol) were depressed by similar extents following each protocol. This occurred despite 1, 4, and 17 min of stimulation, respectively, used to induce fatigue. In the constant-duration experiments, larger reductions in SR function occurred following the highest frequency stimulation protocol. These data suggest that when muscles are fatigued to similar extents, depressions in SR function are independent of the activity protocol. On the other hand, when a constant duration of activity is imposed, changes in SR function are closely linked to the extent of force reduction.

Resting membrane potentials: a student test of alternate hypotheses.

The frog sartorius muscle is a model tissue for demonstrating to physiology students the principles underlying both membrane phenomena and hypothesis testing. Myocytes can be impaled with conventional glass microelectrodes to measure membrane voltage (Vm). Further, Vm is observed as extracellular K+ is altered and a K+ channel blocker is added. After the experiment, students examine the underlying assumptions of the Nernst equilibrium and the Goldman-Hodgkin-Katz equation. They ultimately determine which of the two algorithms best predicts the measured Vm. In addition, students learn micromanipulation and impalement techniques. This experiment facilitates the student's understanding of membrane permeability, ionic gradients, and membrane voltage.

Na+ and K+ effect on contractility of frog sartorius muscle: implication for the mechanism of fatigue

Although a decrease in extracellular Na+ and an increase in K+ concentration are believed to contribute to the decrease in force during fatigue, the force of unfatigued muscle decreases only with quite large changes in Na+ and K+ concentration. The objective of this study was to determine whether concomitant and smaller changes in Na+ and K+ concentration have greater effects on muscle contractility than individual changes. At 3 mM K+, a large decrease in Na+ from 120 to 60 mM had no effect on the twitch force, while the tetanic force decreased by 31.2%. At 120 mM Na+, an increase in K+ from 3 to 9 mM potentiated the twitch force by 41.1%, had no effect on the tetanic force at 7 mM, and decreased the tetanic force by 40.4% at 9 mM; both the twitch force and tetanic force were completely abolished at 11 mM K+. The potentiation of the twitch force between 3 and 9 mM K+ was less at 60, 80, and 100 mM than at 120 mM Na+. A reduction in Na+ concentration also reduced the K+ concentration at which the twitch force and tetanic force decreased and were completely abolished. It is shown that the combined effects of Na+ and K+ on the twitch and tetanic contractions were greater than the sum of their individual effects. Furthermore, it is proposed that neither Na+ nor K+ alone can be considered as an important factor in the decrease in force during fatigue, whereas together they are important for the tetanic contraction, but not for the twitch contraction.

Evidence for sensing and integration of biological signals by the capillary network

The aim of this study was to explore the phenomenon first described by Dietrich (Microvasc. Res. 38: 125-135, 1989) in which a local application of norepinephrine (NE) on a capillary can temporarily reduce flow via constriction of the feeding arteriole. Our objectives were to show that this phenomenon of remote response is not limited to vasoconstriction, can be elicited by materials other than NE, shows stimulus-strength dependency, and can be integrated within the capillary network. We used an intravital micropharmacological approach to iontophoretically apply (in mM concentrations in the pipette) NE, acetylcholine (ACh), 5'-N-ethylcarboxamidoadenosine (NECA, adenosine analogue), K+, and H+ on capillaries of the frog sartorius muscle in situ. Responses were measured in terms of changes in velocity of red blood cells (VRBC) in capillaries or in terms of changes in arteriolar diameter. ACh (3 mM) caused significant increases in diameter (from 34 to 37 microns) and in VRBC (from 250 to 340 microns/s, i.e., 36%). NE (3 mM) reduced VRBC by 16%. The magnitude of ACh and NE velocity responses increased with increasing pipette concentration and with increasing iontophoretic current. The ACh response was blocked by a local pretreatment with atropine. NECA, K+, and H+ caused 20-40% increases in VRBC. Dual application of NE on two capillaries fed by the same arteriole resulted in a greater VRBC reduction than for single NE application. Dual application of NE and ACh significantly attenuated the ACh response.(ABSTRACT TRUNCATED AT 250 WORDS)