Muscle function during repetitive moderate-intensity muscle contractions in myoadenylate deaminase-deficient Dutch subjects

2002 ◽  
Vol 102 (5) ◽  
pp. 531 ◽  
Author(s):  
C. J. de RUITER ◽  
A. M. MAY ◽  
B. G. M. van ENGELEN ◽  
R. A. WEVERS ◽  
G. C. STEENBERGEN-SPANJERS ◽  
...  
Keyword(s):  
Muscle Function ◽  
Muscle Contractions ◽  
Moderate Intensity ◽  
Myoadenylate Deaminase

Muscle function during repetitive moderate-intensity muscle contractions in myoadenylate deaminase-deficient Dutch subjects

2002 ◽  
Vol 102 (5) ◽  
pp. 531-539 ◽  
Author(s):  
C.J. DE RUITER ◽  
A.M. MAY ◽  
B.G.M. VAN ENGELEN ◽  
R.A. WEVERS ◽  
G.C. STEENBERGEN-SPANJERS ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Exercise Test ◽  
Muscle Contractions ◽  
Moderate Intensity ◽  
Control Subjects ◽  
Generating Capacity ◽  
Myoadenylate Deaminase ◽  
Baseline Values ◽  
Isometric Muscle ◽  
Femoris Muscle

We investigated whether the capacity for repetitive submaximal muscle contraction was reduced in a group of subjects (n = 8) with a primary deficiency of myoadenylate deaminase (MAD). Quadriceps femoris muscle fatigue was evaluated using voluntary and electrically stimulated contractions during 20min of repetitive voluntary isometric contractions at 40% of maximal force-generating capacity (MFGC). After 5min of exercise, MFGC had declined significantly to 70.6±4.1% (mean±S.E.M.) and 87.2±1.6% of baseline values in MAD-deficient and sedentary control subjects (n = 8) respectively (P = 0.002 between groups). After 5min of exercise, the half-relaxation time had increased significantly to 113.4±6.1% of basline in MAD-deficient muscle, but had decreased significantly to 94.1±1.3% in control subjects (P = 0.003 between groups). All control subjects completed the 20-min exercise test. Five of the MAD-deficient subjects had to stop exercising due to early muscle fatigue; however, three of the MAD-deficient subjects were able to complete the 20-min exercise test. In conclusion, although the capacity for repetitive submaximal isometric muscle contractions for the group of MAD-deficient subjects was significantly decreased, it remains uncertain whether MAD deficiency is the sole cause of pronounced muscle fatigue.

Muscle function during fatigue in myoadenylate deaminase-deficient Dutch subjects

2000 ◽  
Vol 98 (5) ◽  
pp. 579-585 ◽  
Author(s):  
C. J. DE RUITER ◽  
B. G. M. VAN ENGELEN ◽  
R. A. WEVERS ◽  
A. DE HAAN
Keyword(s):  
Muscle Function ◽  
Adductor Pollicis ◽  
Moderate Intensity ◽  
Force Output ◽  
Short Term ◽  
Shortening Velocity ◽  
Vigorous Exercise ◽  
Adductor Pollicis Muscle ◽  
Left Hand ◽  
Myoadenylate Deaminase

Myoadenylate deaminase (MAD) is an enzyme active in skeletal muscle, probably during exercise of moderate intensity but certainly during vigorous exercise, when the deamination of AMP leads to increased levels of IMP and ammonia. There is controversy about the clinical significance of MAD deficiency. The main objective of the present study was to investigate the extent to which genetically confirmed MAD deficiency affects muscle function under conditions of maximal short-term electrically induced activation. The left hand was immobilized and adductor pollicis muscle function was investigated. To exclude the influence of central factors, such as the patient's motivation, the ulnar nerve was maximally electrically activated and force output was measured at the thumb. Sixty rapid shortening contractions resulted in a decrease of maximal power to 34.2±5.4% and 33.3±6.3% (means±S.D.) of the values for unfatigued muscle in the control and MAD-deficient subjects respectively (P > 0.05; n = 7). Maximal isometric forces and shortening velocities did not differ between groups in unfatigued, fatigued or recovered muscle. None of the subjects experienced exercise-related muscle aches or cramps. In conclusion, MAD deficiency does not appear to affect adductor pollicis muscle force, shortening velocity and relaxation, either during or after maximal short-term activation.

Muscle function during fatigue in myoadenylate deaminase-deficient Dutch subjects

2000 ◽  
Vol 98 (5) ◽  
pp. 579 ◽  
Author(s):  
C.J. DE RUITER ◽  
B.G.M. VAN ENGELEN ◽  
R.A. WEVERS ◽  
A. DE HAAN
Keyword(s):  
Muscle Function ◽  
Myoadenylate Deaminase

scholarly journals PDH activation during in vitro muscle contractions in PDH kinase 2 knockout mice: effect of PDH kinase 1 compensation

2011 ◽  
Vol 300 (6) ◽  
pp. R1487-R1493 ◽  
Author(s):  
Emily C. Dunford ◽  
Eric A. Herbst ◽  
Nam Ho Jeoung ◽  
William Gittings ◽  
J. Greig Inglis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Hypoxia Inducible Factor ◽  
Physiological Role ◽  
Muscle Contractions ◽  
Carbohydrate Oxidation ◽  
Moderate Intensity ◽  
Initial Force ◽  
40 Hz

Pyruvate dehydrogenase (PDH) plays an important role in regulating carbohydrate oxidation in skeletal muscle. PDH is deactivated by a set of PDH kinases (PDK1, PDK2, PDK3, PDK4), with PDK2 and PDK4 being the most predominant isoforms in skeletal muscle. Although PDK2 is the most abundant isoform, few studies have examined its physiological role. The role of PDK2 on PDH activation (PDHa) at rest and during muscle stimulation at 10 and 40 Hz (eliciting low- and moderate-intensity muscle contractions, respectively) in isolated extensor digitorum longus muscles was studied in PDK2 knockout (PDK2KO) and wild-type (WT) mice ( n = 5 per group). PDHa activity was unexpectedly 35 and 77% lower in PDK2KO than WT muscle ( P = 0.043), while total PDK activity was nearly fourfold lower in PDK2KO muscle ( P = 0.006). During 40-Hz contractions, initial force was lower in PDK2KO than WT muscle ( P < 0.001) but fatigued similarly to ∼75% of initial force by 3 min. There were no differences in initial force or rate of fatigue during 10-Hz contractions. PDK1 compensated for the lack of PDK2 and was 1.8-fold higher in PDK2KO than WT muscle ( P = 0.019). This likely contributed to ensuring that resting PDHa activity was similar between the groups and accounts for the lower PDH activation during muscle contraction, as PDK1 is a very potent inhibitor of the PDH complex. Increased PDK1 expression appears to be regulated by hypoxia inducible factor-1α, which was 3.5-fold higher in PDK2KO muscle. It is clear that PDK2 activity is essential, even at rest, in regulation of carbohydrate oxidation and production of reducing equivalents for the electron transport chain. In addition, these results underscore the importance of the overall kinetics of the PDK isoform population, rather than total PDK activity, in determining transformation of the PDH complex and PDHa activity during muscle contraction.

A Comparison of a Moderate with Moderate-high Intensity Oral Anticoagulant Treatment in Patients with Mechanical Heart Valve Prostheses

1997 ◽  
Vol 77 (05) ◽  
pp. 0839-0844 ◽  
Author(s):  
Vittorio Pengo ◽  
Fabio Barbero ◽  
Alberto Banzato ◽  
Elisabetta Garelli ◽  
Franco Noventa ◽  
...  
Keyword(s):  
Heart Valve ◽  
High Intensity ◽  
Oral Anticoagulant ◽  
Oral Anticoagulants ◽  
Mechanical Heart Valve ◽  
Moderate Intensity ◽  
Minor Bleeding ◽  
Anticoagulant Treatment ◽  
Oral Anticoagulant Treatment ◽  
Valve Prostheses

SummaryBackground. The long-term administration of oral anticoagulants to patients with mechanical heart valve prostheses is generally accepted. However, the appropriate intensity of oral anticoagulant treatment in these patients is still controversial.Methods and Results. From March 1991 to March 1994, patients referred to the Padova Thrombosis Center who had undergone mechanical heart valve substitution at least 6 months earlier were randomly assigned to receive oral anticoagulants at moderate intensity (target INR = 3) or moderate-high intensity (target INR = 4). Principal end points were major bleeding, thromboembolism and vascular death. Minor bleeding was a secondary end-point.A total of 104 patients were assigned to the target 3 group and 101 to the target 4 group; they were followed for from 1.5 years to up 4.5 years (mean, 3 years). Principal end-points occurred in 13 patients in the target 3 group (4 per 100 patient-years) and in 20 patients in the target 4 group (6.9 per 100 patient-years). Major hemorrhagic events occurred in 15 patients, 4 in the target 3 group (1.2 per 100 patient-years) and 11 in the target 4 group (3.8 per 100 patient-years) (p = 0.019). The 12 recorded episodes of thromboembolism, 4 of which consisted of a visual deficit, were all transient ischemic attacks, 6 in the target 3 group (1.8 per 100 patient-years) and 6 in the target 4 group (2.1 per 100 patient- years). There were 3 vascular deaths in each group (0.9 and 1 per 100 patient-years for target 3 and target 4 groups, respectively). Minor bleeding episodes occurred 85 times (26 per 100 patient-years) in the target 3 group and 123 times (43 per 100 patient-years) in the target 4 group (p = 0.001).Conclusions. Mechanical heart valve patients on anticoagulant treatment who had been operated on at least 6 months earlier experienced fewer bleeding complications when maintained on a moderate intensity regimen (target INR = 3) than those on a moderate-high intensity regimen (target INR = 4). The number of thromboembolic events and vascular deaths did not differ between the two groups.

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