Force-velocity and force-power properties of single muscle fibers from elite master runners and sedentary men

1996 ◽  
Vol 271 (2) ◽  
pp. C676-C683 ◽  
Author(s):  
J. J. Widrick ◽  
S. W. Trappe ◽  
D. L. Costill ◽  
R. H. Fitts
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Power Output ◽  
Peak Power ◽  
Isometric Force ◽  
Peak Force ◽  
Peak Power Output ◽  
Type I ◽  
Shortening Velocity ◽  
Force Velocity

Gastrocnemius muscle fiber bundles were obtained by needle biopsy from five middle-aged sedentary men (SED group) and six age-matched endurance-trained master runners (RUN group). A single chemically permeabilized fiber segment was mounted between a force transducer and a position motor, subjected to a series of isotonic contractions at maximal Ca2+ activation (15 degrees C), and subsequently run on a 5% polyacrylamide gel to determine myosin heavy chain composition. The Hill equation was fit to the data obtained for each individual fiber (r2 > or = 0.98). For the SED group, fiber force-velocity parameters varied (P < 0.05) with fiber myosin heavy chain expression as follows: peak force, no differences: peak tension (force/fiber cross-sectional area), type IIx > type IIa > type I; maximal shortening velocity (Vmax, defined as y-intercept of force-velocity relationship), type IIx = type IIa > type I; a/Pzero (where a is a constant with dimensions of force and Pzero is peak isometric force), type IIx > type IIa > type I. Consequently, type IIx fibers produced twice as much peak power as type IIa fibers, whereas type IIa fibers produced about five times more peak power than type I fibers. RUN type I and IIa fibers were smaller in diameter and produced less peak force than SED type I and IIa fibers. The absolute peak power output of RUN type I and IIa fibers was 13 and 27% less, respectively, than peak power of similarly typed SED fibers. However, type I and IIa Vmax and a/Pzero were not different between the SED and RUN groups, and RUN type I and IIa power deficits disappeared after power was normalized for differences in fiber diameter. Thus the reduced absolute peak power output of the type I and IIa fibers from the master runners was a result of the smaller diameter of these fibers and a corresponding reduction in their peak isometric force production. This impairment in absolute peak power production at the single fiber level may be in part responsible for the reduced in vivo power output previously observed for endurance-trained athletes.

scholarly journals Effect of intermittent weight bearing on soleus fiber force-velocity-power and force-pCa relationships

1997 ◽  
Vol 82 (6) ◽  
pp. 1905-1910 ◽  
Author(s):  
J. J. Bangart ◽  
J. J. Widrick ◽  
R. H. Fitts
Keyword(s):  
Power Output ◽  
Peak Power ◽  
Weight Bearing ◽  
Peak Power Output ◽  
Type I ◽  
Shortening Velocity ◽  
Functional Changes ◽  
Maximal Activation ◽  
Force Velocity ◽  
Type I Fibers

Bangart, J. J., J. J. Widrick, and R. H. Fitts. Effect of intermittent weight bearing on soleus fiber force-velocity-power and force-pCa relationships. J. Appl. Physiol. 82(6): 1905–1910, 1997.—Rat permeabilized type I soleus fibers displayed a 33% reduction in peak power output and a 36% increase in the free Ca2+ concentration required for one-half maximal activation after 14 days of hindlimb non-weight bearing (NWB). We examined the effectiveness of intermittent weight bearing (IWB; consisting of four 10-min periods of weight bearing/day) as a countermeasure to these functional changes. At peak power output, type I fibers from NWB animals produced 54% less force and shortened at a 56% greater velocity than did type I fibers from control weight-bearing animals while type I fibers from the IWB rats produced 26% more absolute force than did fibers from the NWB group and shortened at a velocity that was only 80% of the NWB group mean. As a result, no difference was observed in the average peak power of fibers from the IWB and NWB animals. Hill plot analysis of force-pCa relationships indicated that fibers from the IWB group required similar levels of free Ca2+ to reach half-maximal activation in comparison to fibers from the weight-bearing group. However, at forces <50% of peak force, the force-pCa curve for fibers from the IWB animals clearly fell between the relationships observed for the other two groups. In summary, IWB treatments 1) attenuated the NWB-induced reduction in fiber Ca2+sensitivity but 2) failed to prevent the decline in peak power that occurs during NWB because of opposing effects on fiber force (an increase vs. NWB) and shortening velocity (a decrease vs. NWB).

scholarly journals Force-velocity-power and force-pCa relationships of human soleus fibers after 17 days of bed rest

1998 ◽  
Vol 85 (5) ◽  
pp. 1949-1956 ◽  
Author(s):  
J. J. Widrick ◽  
K. M. Norenberg ◽  
J. G. Romatowski ◽  
C. A. Blaser ◽  
M. Karhanek ◽  
...  
Keyword(s):  
Peak Power ◽  
Weight Bearing ◽  
Bed Rest ◽  
Force Transducer ◽  
Hindlimb Suspension ◽  
Peak Power Output ◽  
Type I ◽  
Shortening Velocity ◽  
Adult Men ◽  
Force Velocity

Soleus muscle fibers from the rat display a reduction in peak power and Ca2+ sensitivity after hindlimb suspension. To examine human responses to non-weight bearing, we obtained soleus biopsies from eight adult men before and immediately after 17 days of bed rest (BR). Single chemically skinned fibers were mounted between a force transducer and a servo-controlled position motor and activated with maximal (isotonic properties) and/or submaximal (Ca2+ sensitivity) levels of free Ca2+. Gel electrophoresis indicated that all pre- and post-BR fibers expressed type I myosin heavy chain. Post-BR fibers obtained from one subject displayed increases in peak power and Ca2+ sensitivity. In contrast, post-BR fibers obtained from the seven remaining subjects showed an average 11% reduction in peak power ( P < 0.05), with each individual displaying a 7–27% reduction in this variable. Post-BR fibers from these subjects were smaller in diameter and produced 21% less force at the shortening velocity associated with peak power. However, the shortening velocity at peak power output was elevated 13% in the post-BR fibers, which partially compensated for their lower force. Post-BR fibers from these same seven subjects also displayed a reduced sensitivity to free Ca2+( P < 0.05). These results indicate that the reduced functional capacity of human lower limb extensor muscles after BR may be in part caused by alterations in the cross-bridge mechanisms of contraction.

scholarly journals Altered single cell force-velocity and power properties in exercise-trained rat myocardium

2003 ◽  
Vol 94 (5) ◽  
pp. 1941-1948 ◽  
Author(s):  
Gary M. Diffee ◽  
Eunhee Chung
Keyword(s):  
Exercise Training ◽  
Power Output ◽  
Peak Power ◽  
Muscle Length ◽  
Work Capacity ◽  
Peak Power Output ◽  
Sprague Dawley ◽  
Shortening Velocity ◽  
External Work ◽  
Force Velocity

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. The ability of the myocardium to perform external work is a critical aspect of ventricular function, but previous studies of myocardial adaptation to exercise training have been limited to measurements of isometric tension or unloaded shortening velocity, conditions in which work output is zero. We measured force-velocity properties in single permeabilized myocyte preparations to determine the effect of exercise training on loaded shortening and power output. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from T and C hearts, chemically skinned, and attached to a force transducer. Shortening velocity was determined during loaded contractions at 15°C by using a force-clamp technique. Power output was calculated by multiplying force times velocity values. We found that unloaded shortening velocity was not significantly different in T vs. C myocytes (T = 1.43 muscle lengths/s, n = 46 myocytes; C = 1.12 muscle lengths/s, n = 43 myocytes). Training increased the velocity of loaded shortening and increased peak power output (peak power = 0.16 P/Po × muscle length/s for T myocytes; peak power = 0.10 P/Po× muscle length/s for C myocytes, where P/Po is relative tension). We found no effect of training on myosin heavy chain isoform content. These results suggest that training alters power output properties of single cardiac myocytes and that this adaptation may improve the work capacity of the myocardium.

β-Myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions

2006 ◽  
Vol 290 (2) ◽  
pp. H869-H877 ◽  
Author(s):  
Aaron C. Hinken ◽  
Kerry S. McDonald
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Power Output ◽  
Cardiac Myocyte ◽  
Isometric Force ◽  
Force Transducer ◽  
Sprague Dawley ◽  
Shortening Velocity ◽  
Absolute Power ◽  
Artery Disease

During ischemia intracellular concentrations of Pi and H+ increase. Also, changes in myosin heavy chain (MHC) isoform toward β-MHC have been reported after ischemia and infarction associated with coronary artery disease. The purpose of this study was to investigate the effects of myoplasmic changes of Pi and H+ on the loaded shortening velocity and power output of cardiac myocytes expressing either α- or β-MHC. Skinned cardiac myocyte preparations were obtained from adult male Sprague-Dawley rats (control or treated with 5- n-propyl-2-thiouracil to induce β-MHC) and mounted between a force transducer and servomotor system. Myocyte preparations were subjected to a series of isotonic force clamps to determine shortening velocity and power output during Ca2+ activations in each of the following solutions: 1) pCa 4.5 and pH 7.0; 2) pCa 4.5, pH 7.0, and 5 mM Pi; 3) pCa 4.5 and pH 6.6; and 4) pCa 4.5, pH 6.6, and 5 mM Pi. Added Pi and lowered pH each caused isometric force to decline to the same extent in α-MHC and β-MHC myocytes; however, β-MHC myocytes were more resistant to changes in absolute power output. For example, peak absolute power output fell 53% in α-MHC myocytes, whereas power fell only 38% in β-MHC myocytes in response to elevated Pi and lowered pH (i.e., solution 4). The reduced effect on power output was the result of a greater increase in loaded shortening velocity induced by Pi in β-MHC myocytes and an increase in loaded shortening velocity at pH 6.6 that occurred only in β-MHC myocytes. We conclude that the functional response to elevated Pi and lowered pH during ischemia is MHC isoform-dependent with β-MHC myocytes being more resistant to declines in power output.

The energetics of the jump of the locust Schistocerca gregaria

1975 ◽  
Vol 63 (1) ◽  
pp. 53-83 ◽  
Author(s):  
H. C. Bennet-Clark
Keyword(s):  
Safety Factor ◽  
Power Output ◽  
Peak Power ◽  
Schistocerca Gregaria ◽  
Isometric Force ◽  
Maximum Velocity ◽  
Peak Power Output ◽  
Stored Energy ◽  
Distance Curve ◽  
Velocity Of Shortening

The anatomy of the metathoracic leg is redescribed with particular reference to storage of energy in cuticular elements and the way in which the stored energy is used in jumping. The jump of adult male locusts requires an energy of 9 mJ and that of the female requires 11 mJ. The semilunar processes of each metafemur store 4 mJ at a stress of 15 N, and the extensor tibiae apodeme stores a further 3 mJ at the same stress. The total stored energy in both metathoracic legs is 14 mJ. The extensor tibiae muscle produces a maximum isometric force of over 15 N at 30 degrees C and, when loaded with the extensor apodeme and semilunar processes, attains this force in 0.3 sec with a strain of 0.8 mm. The peak power output is 36 mW or 0.45 W.g-1. The peak isometric force is attained when the tibia is fully flexed and the force falls as the tibia extends. The extensor tibiae muscle A band is 5.5 mum long and the peak force is over 0.75 N.m-2. The peak velocity of shortening is 7 mm.sec-1 or about 1.75 lengths/sec at 30 degrees C. The tensile strength of the extensor apodeme is 0.6 kN.mm-2 and Young's modulus is 19 kN.mm-2. The safety factor does not exceed 1.2 and the safety factor of the semilunar processes and tibial cuticle is little higher. The jump impulse lasts 25–30 msec. A velocity of 3.2 m.sec-1 is reached after a peak acceleration of 180 m.sec-2. The peak power output is 0.75 W at close to maximum velocity. Energy losses in rotating the femur and tibia are small and it is shown that the leg is able to extend at 7 times the normal rate with losses of about 20%. Most of the stored energy is converted to kinetic energy as the animal jumps. A model is based on the relaxation of a spring that has the properties of the elastic elements of the locust leg into a lever with the same kinematics as the locust leg produces a force-distance curve similar to that measured for locust jumps. The major part of the jump energy is stored before the jump.

scholarly journals Force-velocity and power characteristics of rat soleus muscle fibers after hindlimb suspension

1994 ◽  
Vol 77 (4) ◽  
pp. 1609-1616 ◽  
Author(s):  
K. S. McDonald ◽  
C. A. Blaser ◽  
R. H. Fitts
Keyword(s):  
Isometric Force ◽  
Fiber Type ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Hindlimb Suspension ◽  
Type I ◽  
Shortening Velocity ◽  
Power Characteristics ◽  
Sds Page ◽  
Force Velocity

The effects of 1, 2, and 3 wk of hindlimb suspension (HS) on force-velocity and power characteristics of single rat soleus fibers were determined. After 1, 2, or 3 wk of HS, small fiber bundles were isolated, placed in skinning solution, and stored at -20 degrees C until studied. Single fibers were isolated and placed between a motor arm and force transducer, functional properties were studied, and fiber protein content was subsequently analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Additional fibers were isolated from soleus of control and after 1 and 3 wk of HS, and fiber type distribution and myosin light chain stoichiometry were determined from SDS-PAGE analysis. After 1 wk of HS, percent type I fibers declined from 82 to 74%, whereas hybrid fibers increased from 10 to 18%. Percent fast type II fibers increased from 8% in control and 1 wk of HS to 26% by 3 wk of HS. Most fibers showed an increased unloaded maximal shortening velocity (Vo), but myosin heavy chain remained entirely slow type I. The mechanism for increased Vo is unknown. There was a progressive decrease in fiber diameter (14, 30, and 38%) and peak force (38, 56, and 63%) after 1, 2, and 3 wk of HS, respectively. One week of HS resulted in a shift of the force-velocity curve, and between 2 and 3 wk of HS the curve shifted further such that Vo was higher than control at all relative loads < 45% peak isometric force. Peak absolute power output of soleus fibers progressively decreased through 2 wk of HS but showed no further change at 3 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragm contractile dysfunction in MyoD gene-inactivated mice

2002 ◽  
Vol 283 (3) ◽  
pp. R583-R590 ◽  
Author(s):  
Jessica L. Staib ◽  
Steven J. Swoap ◽  
Scott K. Powers
Keyword(s):  
Power Output ◽  
Peak Power ◽  
Contractile Properties ◽  
Peak Power Output ◽  
Force Frequency ◽  
Shortening Velocity ◽  
Frequency Relationship ◽  
Myod Gene

MyoD is one of four myogenic regulatory factors found exclusively in skeletal muscle. In an effort to better understand the role that MyoD plays in determining muscle contractile properties, we examined the effects of MyoD deletion on both diaphragmatic contractile properties and myosin heavy chain (MHC) phenotype. Regions of the costal diaphragm from wild-type and MyoD knockout [ MyoD (−/−)] adult male BALB/c mice ( n = 8/group) were removed, and in vitro diaphragmatic contractile properties were measured. Diaphragmatic contractile measurements revealed that MyoD (−/−) animals exhibited a significant ( P < 0.05) downward shift in the force-frequency relationship, a decrement in maximal specific tension (Po; −33%), a decline in maximal shortening velocity (Vmax; −37%), and concomitant decrease in peak power output (−47%). Determination of MHC isoforms in the diaphragm via gel electrophoresis revealed that MyoD elimination resulted in a fast-to-slow shift ( P < 0.05) in the MHC phenotype toward MHC types IIA and IIX in MyoD (−/−) animals. These data indicate that MyoD deletion results in a decrease in diaphragmatic submaximal force generation and Po, along with decrements in both Vmax and peak power output. Hence, MyoD plays an important role in determining diaphragmatic contractile properties.

scholarly journals Sex-Related Changes in Physical Performance, Well-Being, and Neuromuscular Function of Elite Touch Players During a 4-Day International Tournament

2020 ◽  
Vol 15 (8) ◽  
pp. 1138-1146
Author(s):  
Nick Dobbin ◽  
Cari Thorpe ◽  
Jamie Highton ◽  
Craig Twist
Keyword(s):  
Physical Performance ◽  
Power Output ◽  
Peak Power ◽  
Well Being ◽  
Neuromuscular Function ◽  
Peak Force ◽  
Peak Power Output ◽  
Jump Height ◽  
Countermovement Jump ◽  
Males And Females

Purpose: To examine the within- and between-sexes physical performance, well-being, and neuromuscular function responses across a 4-day international touch rugby (Touch) tournament. Methods: Twenty-one males and 20 females completed measures of well-being (fatigue, soreness, sleep, mood, and stress) and neuromuscular function (countermovement jump height, peak power output, and peak force) during a 4-day tournament with internal, external, and perceptual loads recorded for all matches. Results: Relative and absolute total, low-intensity (females), and high-intensity distance were lower on day 3 (males and females) (effect size [ES] = −0.37 to −0.71) compared with day 1. Mean heart rate was possibly to most likely lower during the tournament (except day 2 males; ES = −0.36 to −0.74), whereas rating of perceived exertion-training load was consistently higher in females (ES = 0.02 to 0.83). The change in mean fatigue, soreness, and overall well-being was unclear to most likely lower (ES = −0.33 to −1.90) across the tournament for both sexes, with greater perceived fatigue and soreness in females on days 3 to 4 (ES = 0.39 to 0.78). Jump height and peak power output were possibly to most likely lower across days 2 to 4 (ES = −0.30 to −0.84), with greater reductions in females (ES = 0.21 to 0.66). Well-being, countermovement jump height, and peak force were associated with changes in external, internal, and perceptual measures of load across the tournament (η2 = −.37 to .39). Conclusions: Elite Touch players experience reductions in well-being, neuromuscular function, and running performance across a 4-day tournament, with notable differences in fatigue and running between males and females, suggesting that sex-specific monitoring and intervention strategies are necessary.

Single fiber analyses of type IIA myosin heavy chain distribution in hyper- and hypothyroid soleus

1993 ◽  
Vol 265 (3) ◽  
pp. C842-C850 ◽  
Author(s):  
V. J. Caiozzo ◽  
S. Swoap ◽  
M. Tao ◽  
D. Menzel ◽  
K. M. Baldwin
Keyword(s):  
Skeletal Muscle ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Relative Proportion ◽  
Relative Number ◽  
Single Fiber ◽  
Type I ◽  
Shortening Velocity ◽  
Type I Fibers ◽  
Laser Cytometer

The objectives of this study were to 1) examine the effect of hypo- and hyperthyroidism (triiodothyronine treatment) on the distribution of type IIA myosin heavy chain (MHC) in the soleus at the single fiber level and 2) correlate changes in the single fiber distribution of type IIA MHC with the maximal shortening velocity of whole skeletal muscle. The presence of the type IIA MHC in single fibers was determined using a monoclonal antibody reactive to the type IIA MHC and quantified with a Meridian ACAS 570 interactive laser cytometer. The findings of this study demonstrate that 1) hyperthyroidism significantly increases the relative number of muscle fibers that express type IIA MHC, 2) not all type I fibers are capable of expressing fast type IIA MHC under hyperthyroid conditions, and 3) there is a high correlation between maximal shortening velocity and the relative number of type IIA fibers. This latter observation suggests that the maximal shortening velocity of whole skeletal muscle may not be solely determined by its fastest fiber(s) but rather by the relative proportion of fibers expressing fast type IIA MHC.

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