Muscle function during fatigue in myoadenylate deaminase-deficient Dutch subjects

Ruiter, C.J. de; Engelen, B.G.M. van; Wevers, Ron A.; Haan, A. de

doi:10.1042/cs19990205

Cited by 10 publications

(8 citation statements)

References 28 publications

(59 reference statements)

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“…If necessary, the timing of the superimposed octet, which was set at an individually adjusted time (usually 1.5-3 s after torque onset) before each attempt, was adjusted. From the attempt with the highest value of VA, the MTC of the knee extensors was calculated using the equation MTC ϭ (maximal voluntary torque) ⅐ VA Ϫ1 ⅐ (100%) Ϫ1 (12). MTC is an estimate of the maximal isometric torque under conditions of maximal muscle activation.…”

Section: Subjectsmentioning

confidence: 99%

Initial phase of maximal voluntary and electrically stimulated knee extension torque development at different knee angles

Ruiter

Kooistra²,

Paalman³

et al. 2004

Journal of Applied Physiology

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We investigated the capacity for torque development and muscle activation at the onset of fast voluntary isometric knee extensions at 30, 60, and 90 degrees knee angle. Experiments were performed in subjects (n = 7) who had high levels (>90%) of activation at the plateau of maximal voluntary contractions. During maximal electrical nerve stimulation (8 pulses at 300 Hz), the maximal rate of torque development (MRTD) and torque time integral over the first 40 ms (TTI40) changed in proportion with torque at the different knee angles (highest values at 60 degrees ). At each knee angle, voluntary MRTD and stimulated MRTD were similar (P < 0.05), but time to voluntary MRTD was significantly longer. Voluntary TTI40 was independent (P > 0.05) of knee angle and on average (all subjects and angles) only 40% of stimulated TTI40. However, among subjects, the averaged (across knee angles) values ranged from 10.3 +/- 3.1 to 83.3 +/- 3.2% and were positively related (r2 = 0.75, P < 0.05) to the knee-extensor surface EMG at the start of torque development. It was concluded that, although all subjects had high levels of voluntary activation at the plateau of maximal voluntary contraction, among subjects and independent of knee angle, the capacity for fast muscle activation varied substantially. Moreover, in all subjects, torque developed considerably faster during maximal electrical stimulation than during maximal voluntary effort. At different knee angles, stimulated MRTD and TTI40 changed in proportion with stimulated torque, but voluntary MRTD and TTI40 changed less than maximal voluntary torque.

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Section: Subjectsmentioning

confidence: 99%

Initial phase of maximal voluntary and electrically stimulated knee extension torque development at different knee angles

Ruiter

Kooistra²,

Paalman³

et al. 2004

Journal of Applied Physiology

Self Cite

187

295

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show abstract

“…Thus, whether AMPD deficiency alters exercise performance is still unresolved. Previous studies have examined this issue with conflicting results: some reporting diminished performance (5,26,28), and others normal performance (6,25,29,33) in AMPD-deficient subjects. There are several factors that may have contributed to variable outcomes across studies, such as a relatively small sample size, the type of exercise employed, and the presence of other neuromuscular complications in deficient subjects.…”

mentioning

confidence: 99%

AMP deaminase deficiency is associated with lower sprint cycling performance in healthy subjects

Fischer

Esbjörnsson²,

Sabina³

et al. 2007

Journal of Applied Physiology

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AMP deaminase (AMPD) deficiency is an inherited disorder of skeletal muscle found in approximately 2% of the Caucasian population. Although most AMPD-deficient individuals are asymptomatic, a small subset has exercise-related cramping and pain without any other identifiable neuromuscular complications. This heterogeneity has raised doubts about the physiological significance of AMPD in skeletal muscle, despite evidence for disrupted adenine nucleotide catabolism during exercise in deficient individuals. Previous studies have evaluated the effect of AMPD deficiency on exercise performance with mixed results. This study was designed to circumvent the perceived limitations in previous reports by measuring exercise performance during a 30-s Wingate test in 139 healthy, physically active subjects of both sexes, with different AMPD1 genotypes, including 12 AMPD-deficient subjects. Three of the deficient subjects were compound heterozygotes characterized by the common c.34C>T mutation in one allele and a newly discovered AMPD1 mutation, c.404delT, in the other. While there was no significant difference in peak power across AMPD1 genotypes, statistical analysis revealed a faster power decrease in the AMPD-deficient group and a difference in mean power across the genotypes (P = 0.0035). This divergence was most striking at 15 s of the 30-s cycling. Assessed by the fatigue index, the decrease in power output at 15 s of exercise was significantly greater in the deficient group compared with the other genotypes (P = 0.0006). The approximate 10% lower mean power in healthy AMPD-deficient subjects during a 30-s Wingate cycling test reveals a functional role for the AMPD1 enzyme in sprint exercise.

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“…Therefore, Ruiter et al concluded that changes in contractile properties of the human adductor pollicis muscle in response to 60 electrically induced shortening contractions were similar for AMPD deficient individuals and the control group. In other words, the absence of AMPD appeared to have no functional consequences despite the decrease in PP [16].…”

Section: Introductionmentioning

confidence: 91%

“…A number of studies have examined different performance parameters or markers of muscle metabolism in relation to the expression of AMPD1 with varied findings [14][15][16][17][18]. Fischer et al examined metabolic differences across AMPD1 genotypes and the influence on muscle power [9].…”

Section: Introductionmentioning

confidence: 99%

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Genetic Predictors of Adenosine Monophosphate Deaminase Deficiency

Hayes¹,

Houston

Baker³

2013

J Sports Med Doping Stud 2013

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In the majority of the population, during high intensity exercise, Adenosine Monohosphate Deaminase (AMPD) Converts Adenosine Monophosphate (AMP) to Inosine Monophosphate (IMP), with the liberation of ammonia in the process. The AMPD reaction displaces the adenylate kinase equilibrium in the direction of ATP formation during exercise, providing additional energy and preventing a large increase in ADP. AMPD deficiency has been proposed to result in faster fatigue development and earlier inhibition of muscle contractions. This review considers a number of genetic mutations that lead to skeletal muscle AMPD deficiency, their pathology and likely symptoms of the disorder.

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Muscle function during fatigue in myoadenylate deaminase-deficient Dutch subjects

Cited by 10 publications

References 28 publications

Initial phase of maximal voluntary and electrically stimulated knee extension torque development at different knee angles

Initial phase of maximal voluntary and electrically stimulated knee extension torque development at different knee angles

AMP deaminase deficiency is associated with lower sprint cycling performance in healthy subjects

Genetic Predictors of Adenosine Monophosphate Deaminase Deficiency

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