Metabolic, hemodynamic and structural adjustments to low intensity exercise training in a metabolic syndrome model

Imagem de Miniatura
Arquivos
art_MACHI_Metabolic_hemodynamic_and_structural_adjustments_to_low_intensity_2013.PDF (1.75 MB)
Citações na Scopus
22
Tipo de produção
article
Data de publicação
2013
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOMED CENTRAL LTD
Autores
MORVAN, Eduardo
LIMA, Nathalia Edviges Alves
ANGELIS, Katia De
WICHI, Rogerio Brandao
RODRIGUES, Bruno
MAIFRINO, Laura Beatriz Mesiano
Citação
CARDIOVASCULAR DIABETOLOGY, v.12, article ID 89, 10p, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: The increase in fructose consumption is paralleled by a higher incidence of metabolic syndrome, and consequently, cardiovascular disease mortality. We examined the effects of 8 weeks of low intensity exercise training (LET) on metabolic, hemodynamic, ventricular and vascular morphological changes induced by fructose drinking in male rats. Methods: Male Wistar rats were divided into (n = 8 each) control (C), sedentary fructose (F) and ET fructose (FT) groups. Fructose-drinking rats received D-fructose (100 g/l). FT rats were assigned to a treadmill training protocol at low intensity (30% of maximal running speed) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, white adipose tissue (WAT) and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BS) was evaluated by the tachycardic and bradycardic responses. Right atria, left ventricle (LV) and ascending aorta were prepared to morphoquantitative analysis. Results: LET reduced WAT (-37.7%), triglyceride levels (-33%), systolic AP (-6%), heart weight/body weight (-20.5%), LV (-36%) and aortic (-76%) collagen fibers, aortic intima-media thickness and circumferential wall tension in FT when compared to F rats. Additionally, FT group presented improve of BS, numerical density of atrial natriuretic peptide granules (+42%) and LV capillaries (+25%), as well as the number of elastic lamellae in aorta compared with F group. Conclusions: Our data suggest that LET, a widely recommended practice, seems to be particularly effective for preventing metabolic, hemodynamic and morphological disorders triggered by MS.
Palavras-chave
Fructose, Exercise training, Triglycerides, Baroreflex sensitivity, Cardiovascular remodeling, Aorta remodeling
URI
https://observatorio.fm.usp.br/handle/OPI/2386
Referências
  1. Alberti KGMM, 2006, DIABETIC MED, V23, P469, DOI 10.1111/j.1464-5491.2006.01858.x
  2. Basciano H., 2005, NUTR METAB, V2, P5, DOI 10.1186/1743-7075-2-5
  3. Bray GA, 2004, AM J CLIN NUTR, V79, P537
  4. Brito JO, 2008, BRAZ J MED BIOL RES, V41, P804, DOI 10.1590/S0100-879X2008005000030
  5. Cambri LT, 2011, LIPIDS HLTH DIS, V21, P164
  6. Carallo C, 1999, HYPERTENSION, V34, P217
  7. Carroll S, 2004, SPORTS MED, V34, P371, DOI 10.2165/00007256-200434060-00004
  8. DAI S, 1994, CAN J PHYSIOL PHARM, V72, P771
  9. Dandona Paresh, 2004, Metab Syndr Relat Disord, V2, P2, DOI 10.1089/met.2004.2.2
  10. de Lemos Edite Teixeira, 2007, Med Sci Monit, V13, pBR168
  11. de Lemos ET, 2009, NUTRITION, V25, P330, DOI 10.1016/j.nut.2008.08.014
  12. Farah V, 2007, AM J PHYSIOL-HEART C, V293, pH1083, DOI 10.1152/ajpheart.00106.2006
  13. Ferder L, 2010, CURR HYPERTENS REP, V12, P105, DOI 10.1007/s11906-010-0097-3
  14. Franklin BA, 2011, CIRCULATION, V123, P2274, DOI 10.1161/CIRCULATIONAHA.110.981613
  15. Giani JF, 2010, AM J PHYSIOL-HEART C, V298, pH1003, DOI 10.1152/ajpheart.00803.2009
  16. GUNDERSEN HJG, 1981, J MICROSC-OXFORD, V121, P65
  17. Hanson RL, 2002, DIABETES, V51, P3120, DOI 10.2337/diabetes.51.10.3120
  18. Harthmann AD, 2007, AUTON NEUROSCI-BASIC, V133, P115, DOI 10.1016/j.autneu.2006.10.004
  19. Heeren MV, 2009, MATURITAS, V62, P200, DOI 10.1016/j.maturitas.2008.12.011
  20. Hunt BE, 2001, CIRCULATION, V103, P2424
  21. HWANG IS, 1987, HYPERTENSION, V10, P512
  22. Ignarro LJ, 2007, CARDIOVASC RES, V73, P326, DOI 10.1016/j.cardiores.2006.06.030
  23. Kamide K, 2002, AM J HYPERTENS, V15, P66, DOI 10.1016/S0895-7061(01)02232-4
  24. Kaushal P, 2002, J AM COLL CARDIOL, V39, P1524, DOI 10.1016/S0735-1097(02)01787-4
  25. Lakka HM, 2002, JAMA-J AM MED ASSOC, V288, P2709, DOI 10.1001/jama.288.21.2709
  26. Lehnen AM, 2013, J DIABETES RES, DOI 10.1155/2013/761314
  27. Machi JF, 2013, EUR J APPL PHYSIOL, V113, P41, DOI 10.1007/s00421-012-2411-z
  28. MALLIANI A, 1991, CIRCULATION, V84, P482
  29. MARTNCORDERO L, 2011, CARDIOVASC DIABETOL, V20, P42
  30. Moraes-Silva IC, 2010, CLIN EXP PHARMACOL P, V37, pe114, DOI 10.1111/j.1440-1681.2009.05333.x
  31. Mostarda C, 2010, CLIN EXP PHARMACOL P, V37, P447, DOI 10.1111/j.1440-1681.2009.05327.x
  32. Mostarda C, 2012, CLINICS, V67, P815, DOI 10.6061/clinics/2012(07)18
  33. Nishikimi T, 1996, HYPERTENSION, V28, P22
  34. Potteiger JA, 2012, EUR J APPL PHYSIOL, V112, P2035, DOI 10.1007/s00421-011-2174-y
  35. REAVEN GM, 1988, HYPERTENSION, V12, P129
  36. Rodrigues B, 2007, CARDIOVASC DIABETOL, V13, P6
  37. Rubattu S, 2007, J HYPERTENS, V25, P833, DOI 10.1097/HJH.0b013e32803cae3c
  38. Sanches IC, 2012, MENOPAUSE, V19, P562, DOI 10.1097/gme.0b013e3182358c9c
  39. Silva Renata Juliana da, 2011, Clinics (Sao Paulo), V66, P1793
  40. Tappy L, 2010, NUTRITION, V26, P1044, DOI 10.1016/j.nut.2010.02.014
  41. Teixeira-Lemos E, 2011, CARDIOVASC DIABETOL, V10, DOI 10.1186/1475-2840-10-12
  42. Tjonna AE, 2008, CIRCULATION, V118, P346, DOI 10.1161/CIRCULATIONAHA.108.772822
  43. Xu XH, 2011, CURR BIOL, V21, P114, DOI 10.1016/j.cub.2010.12.006
  44. Xu XZ, 2010, DIABETES, V59, P997, DOI 10.2337/db09-1241

Coleções
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/59
Artigos e Materiais de Revistas Científicas - ODS/03
Artigos e Materiais de Revistas Científicas - ODS/06