Diaphragm contractile dysfunction in MyoD  gene-inactivated mice

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.

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

AJP Cell Physiology ◽

10.1152/ajpcell.1996.271.2.c676 ◽

1996 ◽

Vol 271 (2) ◽

pp. C676-C683 ◽

Cited By ~ 72

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.

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Coordinated changes in contractility, energetics, and isomyosins after aortic stenosis

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.252.2.h275 ◽

1987 ◽

Vol 252 (2) ◽

pp. H275-H282

Author(s):

Y. Lecarpentier ◽

L. B. Bugaisky ◽

D. Chemla ◽

J. J. Mercadier ◽

K. Schwartz ◽

...

Keyword(s):

Cardiac Hypertrophy ◽

Peak Power ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Ascending Aorta ◽

Peak Power Output ◽

Shortening Velocity ◽

Old Rats ◽

Quantitative Changes

To investigate possible alterations of myocardial performance in young rats, cardiac hypertrophy was induced by stenosis of the ascending aorta (AS) in three groups of 25-day-old rats that were compared with three groups of sham-operated controls (C). The cardiac overload duration was 8-10 days, 1 mo, and 2 mo in groups 1, 2, and 3, respectively. Mechanics and energetics were studied in left ventricular papillary muscles, and determination of the V1 and V3 isomyosin pattern was achieved in the same papillary muscle. The majority of quantitative changes concerning the cardiac growth process, contractility, and isomyosin shifts occurred within 8-10 days of stenosis. At this point, the degree of left ventricular hypertrophy relative to C was 53 +/- 6%, whereas maximum unloaded shortening velocity (Vmax) decreased significantly (2.8 +/- 0.1 in C vs. 1.9 +/- 0.1 Lmax/s in AS), peak power output (Emax) decreased (1.8 +/- 0.3 in C vs. 0.6 +/- 0.1 in AS), and the curvature of Hill's hyperbola increased (1.3 +/- 0.4 in C vs. 2.0 +/- 0.7 in AS); moreover, the percent V1 isomyosin decreased significantly (98 +/- 1 in C vs. 51 +/- 3% in AS) and the percent V3 isomyosin increased significantly (2 +/- 1 in C vs. 26 +/- 2% in AS). Beyond 8-10 days of AS, additional changes in cardiac hypertrophy and in mechanical and biochemical parameters were less marked.(ABSTRACT TRUNCATED AT 250 WORDS)

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Salbutamol enhances isotonic contractile properties of rat diaphragm muscle

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.2.525 ◽

1998 ◽

Vol 85 (2) ◽

pp. 525-529 ◽

Cited By ~ 26

Author(s):

H. F. M. Van Der Heijden ◽

W. Z. Zhan ◽

Y. S. Prakash ◽

P. N. R. Dekhuijzen ◽

G. C. Sieck

Keyword(s):

Power Output ◽

Maximum Power ◽

Contractile Properties ◽

Diaphragm Muscle ◽

Rat Diaphragm ◽

Shortening Velocity ◽

Maximum Power Output ◽

Isometric Twitch ◽

Camp Levels

The effects of the β2-adrenoceptor agonist salbutamol (Slb) on isometric and isotonic contractile properties of the rat diaphragm muscle (Diamus) were examined. A loading dose of 25 μg/kg Slb was administered intracardially before Diamus excision to ensure adequate diffusion. Studies were then performed with 0.05 μM Slb in the in vitro tissue chamber. cAMP levels were determined by radioimmunoassay. Compared with controls (Ctl), cAMP levels were elevated after Slb treatment. In Slb-treated rats, isometric twitch and maximum tetanic force were increased by ∼40 and ∼20%, respectively. Maximum shortening velocity increased by ∼15% after Slb treatment, and maximum power output increased by ∼25%. During repeated isotonic activation, the rate of fatigue was faster in the Slb-treated Diamus, but both Slb-treated and Ctl Diamusfatigued to the same maximum power output. Still, endurance time during repetitive isotonic contractions was ∼10% shorter in the Slb-treated Diamus. These results are consistent with the hypothesis that β-adrenoceptor stimulation by Slb enhances Diamus contractility and that these effects of Slb are likely mediated, at least in part, by elevated cAMP.

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

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.6.1905 ◽

1997 ◽

Vol 82 (6) ◽

pp. 1905-1910 ◽

Cited By ~ 19

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).

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Similar maximal oxygen uptake assessment from a step cycling incremental test and verification tests on the same or different day

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2019-0405 ◽

2020 ◽

Vol 45 (4) ◽

pp. 357-361 ◽

Cited By ~ 2

Author(s):

Leonardo Trevisol Possamai ◽

Fernando de Souza Campos ◽

Paulo Cesar do Nascimento Salvador ◽

Rafael Alves de Aguiar ◽

Luiz Guilherme Antonacci Guglielmo ◽

...

Keyword(s):

Oxygen Uptake ◽

Power Output ◽

Maximal Oxygen Uptake ◽

Peak Power ◽

Individual Variability ◽

Peak Power Output ◽

Time To Exhaustion ◽

Incremental Test ◽

Incremental Protocol

The present study aimed to compare maximal oxygen uptake of a step incremental test with time to exhaustion verification tests (TLIM) performed on the same or different day. Nineteen recreationally trained cyclists (age: 23 ± 2.7 years; maximal oxygen uptake: 48.0 ± 5.8 mL·kg−1·min−1) performed 3 maximal tests as follows: (i) same day: an incremental test with 3-min stages followed by a TLIM at 100% of peak power output of the incremental test (TLIM-SAME) interspaced by 15 min; and (ii) different day: a TLIM at 100% of peak power output of the incremental test (TLIM-DIFF). The maximal oxygen uptake was determined for the 3 tests. The maximal oxygen uptake was not different among the tests (incremental: 3.83 ± 0.41; TLIM-SAME: 3.72 ± 0.42; TLIM-DIFF: 3.75 ± 0.41 L·min−1; P = 0.951). Seven subjects presented a variability greater than ±3% in both verification tests compared with the incremental test. The same-day verification test decreased the exercise tolerance (240 ± 38 vs. 310 ± 36 s) compared with TLIM-DIFF (P < 0.05). In conclusion, the incremental protocol is capable of measuring maximal oxygen uptake because similar values were observed in comparison with verification tests. Although the need for the verification phase is questionable, the additional tests are useful to evaluate individual variability. Novelty Step incremental test is capable of measuring maximal oxygen uptake with similar values during TLIM on the same or different day. Although the necessity of the verification phase is questionable, it can allow the determination of variability in maximal oxygen uptake.

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Determination of the peak power output during maximal brief pedalling bouts

Journal of Sports Sciences ◽

10.1080/02640418508729750 ◽

1985 ◽

Vol 3 (3) ◽

pp. 181-187 ◽

Cited By ~ 25

Author(s):

Yoshio Nakamura ◽

Yoshiteru Mutoh ◽

Mitsumasa Miyashita

Keyword(s):

Power Output ◽

Peak Power ◽

Peak Power Output

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00889.2002 ◽

2003 ◽

Vol 94 (5) ◽

pp. 1941-1948 ◽

Cited By ~ 25

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.

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