ACE Inhibition and Physical Exercise

Predel, Hans‐Georg; Rohden, C.; Heine, Oliver; Prinz, U; Rost, R.

doi:10.1097/00005344-199423001-00006

Cited by 16 publications

(1 citation statement)

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“…Indeed, losartan (an angiotensin II type 1 receptor blocker) and Enalapril (an ACE inhibitor) can increase peak VO 2max by approximately 16% in heart failure patients and are synergistic when combined [44]. There appears to be no similar response to ACE inhibition or AT 1 receptor blockade in health [45]. There appears to be no similar response to ACE inhibition or AT 1 receptor blockade in health [45].…”

Section: Discussionmentioning

confidence: 99%

The Role of Insertion Allele of Angiotensin Converting Enzyme Gene in Higher Endurance Efficiency and Some Aspects of Pathophysiological and Drug Effects

Dekany

Harbula²,

Berkes³

et al. 2006

CMC

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The ACE I allele is a genetic marker for higher endurance efficiency in acute physical activity and higher adaptation of the cardiovascular system. The measurement of acute physical status needs to be completed with examination of genotype, which is related to the athletic excellence also, because the D allele could be associated with good performance by endurance athletes in future world championships. Further studies are needed to assess the view that the ACE D allele has a significant role in athletic efficiency.

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Section: Discussionmentioning

confidence: 99%

The Role of Insertion Allele of Angiotensin Converting Enzyme Gene in Higher Endurance Efficiency and Some Aspects of Pathophysiological and Drug Effects

Dekany

Harbula²,

Berkes³

et al. 2006

CMC

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Phenotype modulators in myophosphorylase deficiency

Martinuzzi¹,

Sartori²,

Fanin

et al. 2003

Annals of Neurology

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Myophosphorylase deficiency is characterized by exercise intolerance, muscle cramps, and recurrent myoglobinuria. Some patients are severely affected, whereas others are minimally affected or asymptomatic. The molecular basis of the disease has been elucidated but does not provide an explanation for the clinical variability. In a large cohort of patients with myophosphorylase deficiency, we tested the hypothesis that polymorphic variants in either myoadenylate deaminase (MADA) or angiotensin-converting enzyme (ACE) could act as modulators of phenotype expression. Forty-seven patients were evaluated. Clinical severity was assessed according to a severity scale of four grades. MADA activity was studied by histochemical and biochemical analysis of muscle, and the Q12X mutation in the adenine monophosphate deaminase 1 gene (AMPD1) and the insertion/deletion polymorphism in the ACE gene were assessed genetically. A complete MADA defect together with the Q12X mutation was detected in one severely affected patient. Eleven patients were heterozygous for the Q12X mutation. There was no association between clinical grading and MADA status. In contrast, we found a highly significant (p < 0.01) association between ACE genotype and clinical severity, with strong correlation between severe phenotype and number of D alleles. We show that ACE insertion/deletion polymorphism may play a significant role as phenotype modulator in McArdle's disease.

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Randomized, placebo‐controlled, double‐blind pilot trial of ramipril in McArdle's disease

Martinuzzi¹,

Liava²,

Trevisi³

et al. 2007

Muscle and Nerve

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McArdle's disease causes limitation in exercise capacity as well as disability, the severity of which has been associated with the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) haplotype-patients with the genotype associated with higher ACE activity show the most severe phenotype. Modulation of ACE activity through the use of inhibitors may thus positively affect disease expression. In a double-blind, randomized, placebo-controlled trial, we assessed the efficacy of an ACE inhibitor (2.5 mg ramipril) in 8 patients with McArdle's disease. End-points were changes in parameters of exercise physiology (cycloergometer and muscle 31P-magnetic resonance spectroscopy), quality of life (QoL) according to the Short Form 36 (SF-36), and disability according to the World Health Organization-Disability Assessment Scale II (WHO-DAS II). Patients had lower QoL and higher disability than controls. Measures of exercise physiology were not changed by ramipril in the whole group, but treatment induced higher peak VO2 (P = 0.017) in ACE D/D patients, yet not in I/D patients. Treatment significantly improved disability (P < 0.05). McArdle's disease is a disabling condition affecting patients' QoL. Treatment with ramipril improves disability and modifies exercise physiology only in D/D patients, raising the possibility of a differential haplotype-linked sensitivity to the treatment.

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ACE Inhibition and Physical Exercise

Cited by 16 publications

References 0 publications

The Role of Insertion Allele of Angiotensin Converting Enzyme Gene in Higher Endurance Efficiency and Some Aspects of Pathophysiological and Drug Effects

The Role of Insertion Allele of Angiotensin Converting Enzyme Gene in Higher Endurance Efficiency and Some Aspects of Pathophysiological and Drug Effects

Phenotype modulators in myophosphorylase deficiency

Randomized, placebo‐controlled, double‐blind pilot trial of ramipril in McArdle's disease

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