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Inward Spread of Activation in Twitch Skeletal Muscle Fibers

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Abstract

The sections in this article are:

1 Inward Spread of the Excitatory Process
1.1 Development of the Problem
1.2 Role of the Action Potential
1.3 New Facts and Theories
1.4 Morphological Evidence
1.5 Hypothesis
1.6 Morphological Corroboration
2 Mechanism of Inward Spread of Activation
2.1 Some Physiological Properties of the T‐Tubule System
2.2 Some Electrophysiological Properties of the T‐Tubule System
2.3 Mechanism of Inward Spread of the Excitatory Process
Figure 1. Figure 1.

Electrical (A, C) and mechanical (B, D) responses of a single muscle fiber recorded with an internal electrode and a transducer in hypertonic solution (left) and in normal Ringer's fluid (right). Temperature, 20°C; fiber diameter, 140 jam. [From Hodgkin and Horowicz .]

Figure 2. Figure 2.

Top: experimental setup showing micropipette with tip opening 17 μm in diameter and filled with Ringer's solution resting on the muscle. Bottom: relationship between stimulus strength (in arbitrary units) and electric response. Relation between parameters is discontinuous and response rises in a series of steps. [From Adrian .]

Figure 3. Figure 3.

Calculated relation (Eq. ) between y/y and kt/a2, with kt/a2 given on logarithmic scale. Curves i, ii, and Hi are for points on axis and points 0.5 a and 0.707 a distant from the axis, respectively. [From Hill .]

Figure 4. Figure 4.

Part of muscle fiber photographed a few seconds after intracellular application of Ca at place indicated by arrow. Fiber was stretched to ∼120% of its resting length. I bands are clear; edge of fiber is out of focus. [From Niedergerke .]

Figure 5. Figure 5.

Changes in membrane potential of turtle retractor penis along length of K‐depolarized (nonpropagating) muscle during application of DC field. Stimulus, longitudinal DC of different strengths. 20°C, [K]o = 24 mM. Cathodal half always depolarized, whereas anodal half always polarized during stimulation, leaving membrane potential unchanged in center portion. Extent of change in membrane potential is a function of field strength. [From Sakai and Csapo .]

Figure 6. Figure 6.

Isotonic shortening of isolated single muscle fiber from frog semitendinosus. A: photographs of reversible isotonic AC contractures in a nonpropagating fiber. I: photographs of whole length of fiber marked with graphite particles. R, resting fiber; C, longitudinal AC field at 5 V/cm (100 cycles/s). II: enlargements of end portions of fiber with all frames aligned with one mark placed at distance of ∼5 mm from the ends. Upper row of each set shows resting fiber; those below show effect of AC field, with numbers indicating each field strength. Black lines, displacement of the graphite granules. B: extent and degree of shortening along fiber during longitudinal AC stimulation (100 cycles/s); field strength (V/cm, rms) indicated by numbers on curves. Ordinate, relative shortening of each length element; abscissa, distance along length of fiber, with the midregion strongly compressed. Inset, distribution of shortening along whole fiber (solid line); dotted line, example of results (V/cm, 60 cycles/s) from Csapo and Suzuki (ref. ; Fig. ). [From Sten‐Knudsen .]

Figure 7. Figure 7.

Relation between peak tension and K concentration or membrane potential (○ and +, only tension was measured; +, tension; ×, tension and membrane potential were measured). Numbers on lower scale are internal potentials measured at same time as tension. Scale for K concentration is logarithmic and for potential is approximately linear; difference in scale corresponds to 45 mV for a 10‐fold change. Choline Ringer's solution was used, with K replacing choline. Temperature, 18 °C. [From Hodgkin and Horowicz .]

Figure 8. Figure 8.

Distribution of potential on surface of muscle fiber when pulse is applied to pipette, as determined in model experiments. Walls of pipette (P) and gap between tip of pipette and surface of fiber (F) are drawn to scale. [From Huxley and Taylor .]

Figure 9. Figure 9.

Frames 1–4: edge of isolated frog muscle fiber with pipette in contact. Polarized light was compensated so that A bands appear dark. Pipette was applied in 1 and 2 to an A band and in 3 and 4 to an I band. Left picture is taken just before and right picture during a negative pulse applied to the pipette; a contraction is produced only if pipette is opposite an I band (frame 4). Frames 5–8: successive frames from a cinefilm (16 frames/s) showing shortening induced by local depolarization of frog fiber. Polarized light was compensated so that A bands appear dark. Onset of a negative pulse applied to pipette occurs between frames 5 and 6. [From Huxley and Taylor .]

Figure 10. Figure 10.

Longitudinal section of a lizard leg muscle fiber. Note pairs of double membranes (arrows M) or tubules lying in sarcoplasm immediately adjacent to this grazed myofibril associated roughly with edges of A bands. In a favorable spot in which Z bands of 2 adjacent myofibrils are in register, some dense material can be seen in sarcoplasm between Z bands (arrows Z). × 33,000. Inset, × 69,000. [From Robertson .]

Figure 11. Figure 11.

Frog muscle SR. Triads consisting of I‐band vesicles (E.R.2) and intermediary vesicles (I.V.) at level of each Z line [Porter and Palade's nomenclature ]. Middle element of each triad appears to be a continuous structure rather than a row of small vesicles. Fixed in buffered 1% OsO4; no further staining. Scale bar, 0.5 μm. [From Huxley .]

Figure 12. Figure 12.

Longitudinal section showing extensive face view of SR. Near top, transverse tubule (tt) can be followed for almost 2 μm as a continuous structure. Discontinuity in terminal cisterna (ci) is indicated. It, Longitudinal tubules; fc, fenestrated collar, × 44,000. [From Peachey .]

Figure 13. Figure 13.

Triad from muscle soaked in Ringer's solution containing 15% ferritin. Ferritin particles fill central element of triad. × 85,000. [From Page .]

Figure 14. Figure 14.

Electron micrograph of longitudinal section of muscle fiber from semitendinosus muscle of a frog (Rana temporaria). Triad is formed by 2 terminal cisternae (TC) of SR adjacent to a transverse tubule (T). Constricted mouth of this transverse tubule suggests a possible source of access resistance. [From Peachey and Adrian .]

Figure 15. Figure 15.

Effect of changing [K]o and [Cl]o on membrane potential. I: repolarization in 2.5 mM K, 120 mM Cl (or 214 mM Cl) after depolarization with elevated K. Potassium concentration in mM shown on records; temperature, 18°–21°C. Corresponding fiber diameters were: A and B, 74.5 μm; C and D, 138 μm; E, 119 μm; F, 132 μm; G, 83 μm; H and I, 62 μm. B and D were shifted downward 3 and 6 mV, respectively, to superimpose end of records. In F the fiber was in high K for 1.7 min, in G for 11 min, and in H for 3 min. E and F were recorded with a microelectrode filled with 3 M KCl in the external circuit; the others were recorded with an agar‐Ringer electrode externally. H and I were rescaled; the others are tracings. Fiber did not contract in any case except I, where it developed maximum tension for 1.5 s and then relaxed with a time constant of ∼1 s. II: comparison of effect of changing [K]o at constant [Cl]o (record A) with effect of changing [Cl]o at constant [K]o (record B, 2.5 mM K). Chloride was replaced with SO4 and K with Na. Lower line, internal potential; upper line, transducer output. Fiber diameter, 134 μm; temperature, 22°C. [From Hodgkin and Horowicz .]

Figure 16. Figure 16.

Resistance (R) and capacitance (C) circuits. Top left, a series RC circuit with a battery (V), a switch (S), a resistor (R), and a capacitor (C). V and Vg, terminals from which measurements can be made. Direction of current flowing (i) when switch is closed is indicated. A: current V/R (middle trace) and voltage VC (bottom trace) transient changes measured across the capacitor when a square voltage pulse (V on top trace) is applied by turning on and off S. q, Charge built up on capacitor; o, time at which S is closed; t, time. B: sinusoidal voltage is applied instead of a square voltage pulse as in A. Abscissas represent angle (=180°) between voltage recorded across resistance (VR, top trace) or capacitor (Vc, bottom trace) and current (i). C: vectorial components of impedance (Z) resulting from resistance (R) and reactance (Xc) separated by a phase angle ϕ. D and E: 2 parallel RC circuits. D is a simple 2‐branch parallel circuit with R and C. in parallel, whereas E is a 3‐branch circuit with R and C. in parallel to each other and to the 3rd, a branch where R and C. are in series with each other.

Figure 17. Figure 17.

Impedance‐locus plots. A: theoretical impedance locus. Dot‐dashed line, impedance locus for model of inside‐outside admittance shown at upper left (I), fitted to limiting value of R obtained at low frequencies. Solid line, locus for more complicated model with 2 time constants of inside‐outside admittance shown at upper right (II), with additional parameters Re/Rm and Ce/Cm adjusted to give best fit of observations. B: impedance‐locus plots obtained with intracellular microelectrodes from frog sartorius muscle fiber. Current‐applying and voltage‐recording electrodes were placed close together distant from the fiber ends. Filled circles, after correction for stray capacitances around microelectrodes. Measurements made at frequencies (6/decade) from 1 cycle/s to 10 kilocycles/s; frequencies (cycles/s) are labeled on a few points. Theoretical impedance locus for model with 2 time constants is superimposed (solid line).

Adapted from Falk and Fatt
Figure 18. Figure 18.

Delay of activation between superficial and central myofibrils. A: wavy myofibrils before stimulation; dots have been drawn over a myofibril on edge and near center. Arrows t and b indicate top and bottom of waves, respectively, in A‐C. B and C: wavy myofibrils, with dots drawn in exactly the same positions as in A. In B, edge myofibril has started to contract, whereas myofibril near center has same height as before. In C, height of central myofibril has decreased compared with dots, showing it has begun to flatten. Time interval between B and C, 2.5 ms; calibration bar, 100 μm. [From Gonzalez‐Serratos .]

Figure 19. Figure 19.

Velocity of inward spread of activation and effect of temperature. A: time course of straightening of myofibrils of same fiber but at different temperatures, ○, Myofibrils near surface; ×, myofibrils near center. B: relationship between velocity of inward spread of activation and temperature. Velocity is on logarithmic scale. Each symbol indicates a different experiment. [From Gonzalez‐Serratos .]

Figure 20. Figure 20.

Tubular space constant. A: steady‐state potential across wall of tubule system [Eq. of Adrian et al. ] when potential difference across surface membrane of fiber is altered from −90 to −55 mV (uα = 35 mV; see Eq. ). Potential distribution is shown for 2 tubule length constants (λT, 120 and 60 μm). Diameter of fiber is 100 μm. B: calculated values of λT [based on experimental results applied to Eq. of Adrian et al. ] plotted against fiber radius. Open circles, fibers in Ringer's solution; filled circles, fibers in hypotonic Ringer's solution; open triangles, fibers in tetraethylammonium Ringer's solution; open squares, fibers in sucrose Ringer's solution. [From Adrian et al. .]

Figure 21. Figure 21.

Sample photomicrographs from a cinerecording selected at different times during isotonic contracture in 60 mM K. Sample pictures selected at following times after contracture started: A, 0.43 s; C, 0.65 s; E, 0.78 s; B, 2.2 s; D, 2.3 s; and F, 3.7 s. Contracture reached plateau between D and F. Elongation due to relaxation started in F. Shortening of fiber can be followed as a movement to right of any piece of connective tissue. During tetanic stimulation with 50 shocks/s fiber shortened same amount but myofibrils remained straight without forming waves. Calibration bar, 100 μm; temperature, 5°C. [From Gonzalez‐Serratos .]

Figure 22. Figure 22.

Relationship between Vc and fiber radius a. Crosses, experimental results. Continuous line, regression line of Vc against a. Circles correspond to Vc = VsJo(aT) when Vs = Vsm at a = 0, which is 46.2 mV and λT = 26μm. Values of a chosen were similar to ones found experimentally.

Figure 23. Figure 23.

Frames from cinefilm of relaxed muscle fiber (A) and of maximum contraction elicited by train of 3‐ms depolarizing pulses (B and C). A: holding potential, −90 mV; sarcomere length, 3.57 μm. Arrow indicates site of insertion of current‐passing electrode. Voltage‐recording electrode can be seen on opposite side of fiber. B: 43‐mV depolarizing pulses; axial sarcomeres have shortened to 3.34 μm. C: 44‐mV depolarizing pulses; axial sarcomere length, 3.12 μm; superficial sarcomere length, 3.40 μm. Small localized contraction can be seen in region of current electrode in B and C. Bathing solution, 54 mM sodium Ringer's. Grid spacing, 10 μm. White lines in each frame mark every 9th sarcomere. Sarcomere length determined as mean of 20 sarcomeres. [From Costantin .]

Figure 24. Figure 24.

Sample pictures from a cinerecording (100 frames/s) of isotonic contraction of isolated muscle fiber during tetanic stimulation (70 shocks/s). In A and B the fiber was in normal Ringer's solution; in C and D it was in 62.5 mM [Na+]. Times at which pictures were taken after beginning of tetanus were as follows: A, 246 ms; B, 965 ms; C, 211 ms; and D, 945 ms. Calibration bar, 100 μm. Water‐immersion objective, × 40; numerical aperture, 0.75. [From Bezanilla et al. .]



Figure 1.

Electrical (A, C) and mechanical (B, D) responses of a single muscle fiber recorded with an internal electrode and a transducer in hypertonic solution (left) and in normal Ringer's fluid (right). Temperature, 20°C; fiber diameter, 140 jam. [From Hodgkin and Horowicz .]



Figure 2.

Top: experimental setup showing micropipette with tip opening 17 μm in diameter and filled with Ringer's solution resting on the muscle. Bottom: relationship between stimulus strength (in arbitrary units) and electric response. Relation between parameters is discontinuous and response rises in a series of steps. [From Adrian .]



Figure 3.

Calculated relation (Eq. ) between y/y and kt/a2, with kt/a2 given on logarithmic scale. Curves i, ii, and Hi are for points on axis and points 0.5 a and 0.707 a distant from the axis, respectively. [From Hill .]



Figure 4.

Part of muscle fiber photographed a few seconds after intracellular application of Ca at place indicated by arrow. Fiber was stretched to ∼120% of its resting length. I bands are clear; edge of fiber is out of focus. [From Niedergerke .]



Figure 5.

Changes in membrane potential of turtle retractor penis along length of K‐depolarized (nonpropagating) muscle during application of DC field. Stimulus, longitudinal DC of different strengths. 20°C, [K]o = 24 mM. Cathodal half always depolarized, whereas anodal half always polarized during stimulation, leaving membrane potential unchanged in center portion. Extent of change in membrane potential is a function of field strength. [From Sakai and Csapo .]



Figure 6.

Isotonic shortening of isolated single muscle fiber from frog semitendinosus. A: photographs of reversible isotonic AC contractures in a nonpropagating fiber. I: photographs of whole length of fiber marked with graphite particles. R, resting fiber; C, longitudinal AC field at 5 V/cm (100 cycles/s). II: enlargements of end portions of fiber with all frames aligned with one mark placed at distance of ∼5 mm from the ends. Upper row of each set shows resting fiber; those below show effect of AC field, with numbers indicating each field strength. Black lines, displacement of the graphite granules. B: extent and degree of shortening along fiber during longitudinal AC stimulation (100 cycles/s); field strength (V/cm, rms) indicated by numbers on curves. Ordinate, relative shortening of each length element; abscissa, distance along length of fiber, with the midregion strongly compressed. Inset, distribution of shortening along whole fiber (solid line); dotted line, example of results (V/cm, 60 cycles/s) from Csapo and Suzuki (ref. ; Fig. ). [From Sten‐Knudsen .]



Figure 7.

Relation between peak tension and K concentration or membrane potential (○ and +, only tension was measured; +, tension; ×, tension and membrane potential were measured). Numbers on lower scale are internal potentials measured at same time as tension. Scale for K concentration is logarithmic and for potential is approximately linear; difference in scale corresponds to 45 mV for a 10‐fold change. Choline Ringer's solution was used, with K replacing choline. Temperature, 18 °C. [From Hodgkin and Horowicz .]



Figure 8.

Distribution of potential on surface of muscle fiber when pulse is applied to pipette, as determined in model experiments. Walls of pipette (P) and gap between tip of pipette and surface of fiber (F) are drawn to scale. [From Huxley and Taylor .]



Figure 9.

Frames 1–4: edge of isolated frog muscle fiber with pipette in contact. Polarized light was compensated so that A bands appear dark. Pipette was applied in 1 and 2 to an A band and in 3 and 4 to an I band. Left picture is taken just before and right picture during a negative pulse applied to the pipette; a contraction is produced only if pipette is opposite an I band (frame 4). Frames 5–8: successive frames from a cinefilm (16 frames/s) showing shortening induced by local depolarization of frog fiber. Polarized light was compensated so that A bands appear dark. Onset of a negative pulse applied to pipette occurs between frames 5 and 6. [From Huxley and Taylor .]



Figure 10.

Longitudinal section of a lizard leg muscle fiber. Note pairs of double membranes (arrows M) or tubules lying in sarcoplasm immediately adjacent to this grazed myofibril associated roughly with edges of A bands. In a favorable spot in which Z bands of 2 adjacent myofibrils are in register, some dense material can be seen in sarcoplasm between Z bands (arrows Z). × 33,000. Inset, × 69,000. [From Robertson .]



Figure 11.

Frog muscle SR. Triads consisting of I‐band vesicles (E.R.2) and intermediary vesicles (I.V.) at level of each Z line [Porter and Palade's nomenclature ]. Middle element of each triad appears to be a continuous structure rather than a row of small vesicles. Fixed in buffered 1% OsO4; no further staining. Scale bar, 0.5 μm. [From Huxley .]



Figure 12.

Longitudinal section showing extensive face view of SR. Near top, transverse tubule (tt) can be followed for almost 2 μm as a continuous structure. Discontinuity in terminal cisterna (ci) is indicated. It, Longitudinal tubules; fc, fenestrated collar, × 44,000. [From Peachey .]



Figure 13.

Triad from muscle soaked in Ringer's solution containing 15% ferritin. Ferritin particles fill central element of triad. × 85,000. [From Page .]



Figure 14.

Electron micrograph of longitudinal section of muscle fiber from semitendinosus muscle of a frog (Rana temporaria). Triad is formed by 2 terminal cisternae (TC) of SR adjacent to a transverse tubule (T). Constricted mouth of this transverse tubule suggests a possible source of access resistance. [From Peachey and Adrian .]



Figure 15.

Effect of changing [K]o and [Cl]o on membrane potential. I: repolarization in 2.5 mM K, 120 mM Cl (or 214 mM Cl) after depolarization with elevated K. Potassium concentration in mM shown on records; temperature, 18°–21°C. Corresponding fiber diameters were: A and B, 74.5 μm; C and D, 138 μm; E, 119 μm; F, 132 μm; G, 83 μm; H and I, 62 μm. B and D were shifted downward 3 and 6 mV, respectively, to superimpose end of records. In F the fiber was in high K for 1.7 min, in G for 11 min, and in H for 3 min. E and F were recorded with a microelectrode filled with 3 M KCl in the external circuit; the others were recorded with an agar‐Ringer electrode externally. H and I were rescaled; the others are tracings. Fiber did not contract in any case except I, where it developed maximum tension for 1.5 s and then relaxed with a time constant of ∼1 s. II: comparison of effect of changing [K]o at constant [Cl]o (record A) with effect of changing [Cl]o at constant [K]o (record B, 2.5 mM K). Chloride was replaced with SO4 and K with Na. Lower line, internal potential; upper line, transducer output. Fiber diameter, 134 μm; temperature, 22°C. [From Hodgkin and Horowicz .]



Figure 16.

Resistance (R) and capacitance (C) circuits. Top left, a series RC circuit with a battery (V), a switch (S), a resistor (R), and a capacitor (C). V and Vg, terminals from which measurements can be made. Direction of current flowing (i) when switch is closed is indicated. A: current V/R (middle trace) and voltage VC (bottom trace) transient changes measured across the capacitor when a square voltage pulse (V on top trace) is applied by turning on and off S. q, Charge built up on capacitor; o, time at which S is closed; t, time. B: sinusoidal voltage is applied instead of a square voltage pulse as in A. Abscissas represent angle (=180°) between voltage recorded across resistance (VR, top trace) or capacitor (Vc, bottom trace) and current (i). C: vectorial components of impedance (Z) resulting from resistance (R) and reactance (Xc) separated by a phase angle ϕ. D and E: 2 parallel RC circuits. D is a simple 2‐branch parallel circuit with R and C. in parallel, whereas E is a 3‐branch circuit with R and C. in parallel to each other and to the 3rd, a branch where R and C. are in series with each other.



Figure 17.

Impedance‐locus plots. A: theoretical impedance locus. Dot‐dashed line, impedance locus for model of inside‐outside admittance shown at upper left (I), fitted to limiting value of R obtained at low frequencies. Solid line, locus for more complicated model with 2 time constants of inside‐outside admittance shown at upper right (II), with additional parameters Re/Rm and Ce/Cm adjusted to give best fit of observations. B: impedance‐locus plots obtained with intracellular microelectrodes from frog sartorius muscle fiber. Current‐applying and voltage‐recording electrodes were placed close together distant from the fiber ends. Filled circles, after correction for stray capacitances around microelectrodes. Measurements made at frequencies (6/decade) from 1 cycle/s to 10 kilocycles/s; frequencies (cycles/s) are labeled on a few points. Theoretical impedance locus for model with 2 time constants is superimposed (solid line).

Adapted from Falk and Fatt


Figure 18.

Delay of activation between superficial and central myofibrils. A: wavy myofibrils before stimulation; dots have been drawn over a myofibril on edge and near center. Arrows t and b indicate top and bottom of waves, respectively, in A‐C. B and C: wavy myofibrils, with dots drawn in exactly the same positions as in A. In B, edge myofibril has started to contract, whereas myofibril near center has same height as before. In C, height of central myofibril has decreased compared with dots, showing it has begun to flatten. Time interval between B and C, 2.5 ms; calibration bar, 100 μm. [From Gonzalez‐Serratos .]



Figure 19.

Velocity of inward spread of activation and effect of temperature. A: time course of straightening of myofibrils of same fiber but at different temperatures, ○, Myofibrils near surface; ×, myofibrils near center. B: relationship between velocity of inward spread of activation and temperature. Velocity is on logarithmic scale. Each symbol indicates a different experiment. [From Gonzalez‐Serratos .]



Figure 20.

Tubular space constant. A: steady‐state potential across wall of tubule system [Eq. of Adrian et al. ] when potential difference across surface membrane of fiber is altered from −90 to −55 mV (uα = 35 mV; see Eq. ). Potential distribution is shown for 2 tubule length constants (λT, 120 and 60 μm). Diameter of fiber is 100 μm. B: calculated values of λT [based on experimental results applied to Eq. of Adrian et al. ] plotted against fiber radius. Open circles, fibers in Ringer's solution; filled circles, fibers in hypotonic Ringer's solution; open triangles, fibers in tetraethylammonium Ringer's solution; open squares, fibers in sucrose Ringer's solution. [From Adrian et al. .]



Figure 21.

Sample photomicrographs from a cinerecording selected at different times during isotonic contracture in 60 mM K. Sample pictures selected at following times after contracture started: A, 0.43 s; C, 0.65 s; E, 0.78 s; B, 2.2 s; D, 2.3 s; and F, 3.7 s. Contracture reached plateau between D and F. Elongation due to relaxation started in F. Shortening of fiber can be followed as a movement to right of any piece of connective tissue. During tetanic stimulation with 50 shocks/s fiber shortened same amount but myofibrils remained straight without forming waves. Calibration bar, 100 μm; temperature, 5°C. [From Gonzalez‐Serratos .]



Figure 22.

Relationship between Vc and fiber radius a. Crosses, experimental results. Continuous line, regression line of Vc against a. Circles correspond to Vc = VsJo(aT) when Vs = Vsm at a = 0, which is 46.2 mV and λT = 26μm. Values of a chosen were similar to ones found experimentally.



Figure 23.

Frames from cinefilm of relaxed muscle fiber (A) and of maximum contraction elicited by train of 3‐ms depolarizing pulses (B and C). A: holding potential, −90 mV; sarcomere length, 3.57 μm. Arrow indicates site of insertion of current‐passing electrode. Voltage‐recording electrode can be seen on opposite side of fiber. B: 43‐mV depolarizing pulses; axial sarcomeres have shortened to 3.34 μm. C: 44‐mV depolarizing pulses; axial sarcomere length, 3.12 μm; superficial sarcomere length, 3.40 μm. Small localized contraction can be seen in region of current electrode in B and C. Bathing solution, 54 mM sodium Ringer's. Grid spacing, 10 μm. White lines in each frame mark every 9th sarcomere. Sarcomere length determined as mean of 20 sarcomeres. [From Costantin .]



Figure 24.

Sample pictures from a cinerecording (100 frames/s) of isotonic contraction of isolated muscle fiber during tetanic stimulation (70 shocks/s). In A and B the fiber was in normal Ringer's solution; in C and D it was in 62.5 mM [Na+]. Times at which pictures were taken after beginning of tetanus were as follows: A, 246 ms; B, 965 ms; C, 211 ms; and D, 945 ms. Calibration bar, 100 μm. Water‐immersion objective, × 40; numerical aperture, 0.75. [From Bezanilla et al. .]

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Hugo Gonzalez‐Serratos. Inward Spread of Activation in Twitch Skeletal Muscle Fibers. Compr Physiol 2011, Supplement 27: Handbook of Physiology, Skeletal Muscle: 325-353. First published in print 1983. doi: 10.1002/cphy.cp100112