EMG�Force Relationship during Voluntary Static Contractions (M. Biceps)

Author(s):  
G. Rau ◽  
J. Vredenbregt
2002 ◽  
Vol 282 (3) ◽  
pp. H1055-H1062 ◽  
Author(s):  
David P. Dobesh ◽  
John P. Konhilas ◽  
Pieter P. de Tombe

This study was undertaken to determine the impact of sarcomere length (SL) on the level of cooperative activation of the cardiac myofilament at physiological [Mg2+]. Active force development was measured in skinned rat cardiac trabeculae as a function of free [Ca2+] at five SLs (1.85–2.25 μm; 1 mM free [Mg2+]; 15°C). Only muscle preparations with minimal force rundown during the entire protocol were included in the analysis (average 7.2 ± 1.7%). Median SL was measured by on-line computer video micrometry and controlled within 0.01 μm. Care was taken to ensure a sufficient number of data points in the steep portion of the [Ca2+]-force relationship at every SL to allow for accurate fit of the data to a modified Hill equation. Multiple linear regression analysis of the fit parameters revealed that both maximum, Ca2+-saturated force and Ca2+sensitivity were a significant function of SL ( P < 0.001), whereas the level of cooperativity did not depend on SL ( P = 0.2). Further analysis of the [Ca2+]-force relationships revealed a marked asymmetry that, also, was not affected by SL ( P = 0.2–0.6). Finally, we found that the level of cooperativity in isolated skinned myocardium was comparable to that reported for intact, nonskinned myocardium. Our results suggest that an increase in SL induces an increase in the Ca2+ responsiveness of the cardiac sarcomere without affecting the level of cooperativity.


1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.


1981 ◽  
Vol 51 (4) ◽  
pp. 929-933 ◽  
Author(s):  
D. Richardson

Six male subjects within the age range of 20–35 yr consented to perform static calf muscle contractions at 7.5, 15, and 30% of their maximum voluntary contractile strength (MVC) for a period of 2 min each. Isometric contractions were performed in a sitting position by pressing the knee against a solid support plate via plantar flexion. Calf muscle blood flow (BF) was measured periodically before, during, and after each contraction by a Whitney gauge. Average resting BF was 3.9 ml . min-1 . 100 ml-1 of calf volume. During the 7.5, 15, and 30% MVC contractions, BF increased to steady-state levels of 7.2, 7.9, and 5.3 ml . min-1 . 100 ml-1, respectively. The values for 7.5 and 15% MVC were significantly higher than resting BF (P less than or equal to 0.05). The postcontraction hyperemia, measured as the area under the postcontraction BF curve, averaged 4.4, 10.1, and 23.2 ml/100 ml, respectively, for the 7.5, 15, and 30% MVC efforts. Comparison of these values with corresponding hyperemic volumes during contraction showed that the portions of the total BF response that occurred in the postcontraction periods were 41, 57, and 88%, respectively, for the 7.5, 15, and 30% efforts. These results demonstrate that during static calf muscle contractions BF increases by only a modest amount, and at even small forces of contraction a sizable portion of the total flow response occurs in the postcontraction period.


2000 ◽  
Vol 32 (2) ◽  
pp. 459 ◽  
Author(s):  
BJ??RN A. ALKNER ◽  
PER A. TESCH ◽  
HANS E. BERG

1993 ◽  
Vol 61 ◽  
pp. 225
Author(s):  
Yasushi Miyagi ◽  
Sei Kobayashi ◽  
Junji Nishimura ◽  
Masashi Fukui ◽  
Hideo Kanaide

2000 ◽  
Vol 279 (5) ◽  
pp. H2414-H2423 ◽  
Author(s):  
Christian C. Evans ◽  
James R. Pena ◽  
Ronald M. Phillips ◽  
Mariappan Muthuchamy ◽  
David F. Wieczorek ◽  
...  

We used transgenic (TG) mice overexpressing mutant α-tropomyosin [α-Tm(Asp175Asn)], linked to familial hypertrophic cardiomyopathy (FHC), to test the hypothesis that this mutation impairs cardiac function by altering the sensitivity of myofilaments to Ca2+. Left ventricular (LV) pressure was measured in anesthetized nontransgenic (NTG) and TG mice. In control conditions, LV relaxation was 6,970 ± 297 mmHg/s in NTG and 5,624 ± 392 mmHg/s in TG mice ( P < 0.05). During β-adrenergic stimulation, the rate of relaxation increased to 8,411 ± 323 mmHg/s in NTG and to 6,080 ± 413 mmHg/s in TG mice ( P < 0.05). We measured the pCa-force relationship (pCa = −log [Ca2+]) in skinned fiber bundles from LV papillary muscles of NTG and TG hearts. In control conditions, the Ca2+ concentration producing 50% maximal force (pCa50) was 5.77 ± 0.02 in NTG and 5.84 ± 0.01 in TG myofilament bundles ( P < 0.05). After protein kinase A-dependent phosphorylation, the pCa50 was 5.71 ± 0.01 in NTG and 5.77 ± 0.02 in TG myofilament bundles ( P < 0.05). Our results indicate that mutant α-Tm(Asp175Asn) increases myofilament Ca2+-sensitivity, which results in decreased relaxation rate and blunted response to β-adrenergic stimulation.


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