title: The dysfunction of ammonia in heart failure increases with an increase in the intensity of resistance exercise, even with the use of appropriate drug therapy.
abstract: BACKGROUND
  Hyperammonemia during rest periods is a dysfunction in heart failure (HF). The low formation of ammonia during exercise reflects an inefficiency of purine metabolism. Hyperkalemia in response to physical exercise is common in HF and may contribute to a contractile inefficiency in type II fibers, leading to early fatigue. We tested the hypothesis that during resistance exercise of high intensity and low volume, this disorder of ammonia metabolism would be more intense, due to the hyperkalemia present in HF.
  
  
  METHODS
  Alternating resistance exercise (RE) of low intensity and high volume, and high intensity and low volume, were applied to 18 patients with an interval of 7 days between them (functional class II-III New York Heart Association, FE = 33.5 ± 4%) and compared with 22 healthy controls matched for age and gender. Ammonia, potassium and lactate levels were assessed before and immediately after the RE.
  
  
  RESULTS
  Significant differences: Deltas (control vs. HF) in 40% RE: lactate (mg/dl) 26.3 ± 10 vs. 37.7 ± 7; p < 0,001, ammonia (ug/dl) 92.5 ± 18 vs. 48.9 ± 9; p < 0.001. Deltas (control vs. HF) in 80%RE: lactate(mg/dl) 45.0 ± 12 vs. 54.1 ± 11; p < 0.05, ammonia(ug/dl) 133.5 ± 22 vs. 32.2 ± 7; p < 0.001, potassium (mEq/L) 1.6 ± 0.4 vs. 2.0 ± 0.8; p < 0.05. A negative correlation was found between the deltas of ammonia and potassium (r = -0.74, p < 0.001) in the HF group.
  
  
  CONCLUSIONS
  We conclude that in HF, there is an inefficiency of purine metabolism that increases with increasing exercise intensity, but not with an increase of total volume. These findings suggest that hyperkalemia may play an important role in the disorders of purine metabolism.
authors.affiliation: Division of Cardiology, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.
authors.forename: Wladimir M
authors.initials: WM
authors.lastname: Medeiros
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Carvalho
authors.forename: Paulo
authors.initials: P
authors.lastname: Peres
authors.forename: Fabio A
authors.initials: FA
authors.lastname: De Luca
authors.forename: Carlos
authors.initials: C
authors.lastname: Gun
mesh_terms: D000328:Adult; D000641:Ammonia / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D001938:Brazil; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D018592:Cross-Over Studies; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D022124:Hyperammonemia / Q000097:blood / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D006947:Hyperkalemia / Q000097:blood / Q000209:etiology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000503:physiopathology; D011188:Potassium / Q000097:blood; D011687:Purines / Q000378:metabolism; D055070:Resistance Training; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D002317:Cardiovascular Agents; D011687:Purines; D019344:Lactic Acid; D000641:Ammonia; D011188:Potassium