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- Title
ATP-Sensitive K[sup+] Channel Knockout Compromises theMetabolic Benefit of Exercise Training, Resulting inCardiac Deficits.
- Authors
Kane, Garvan C.; Behfar, Atta; Yamada, Satsuki; Perez-Terzic, Carmen; O'Cochlain, Fearghas; Reyes, Santiago; Dzeja, Petras P.; Miki, Takashi; Seino, Susumu; Terzic, Andre
- Abstract
Exercise training elicits a metabolic and cardiovascular response that underlies fitness. The molecular mechanisms that orchestrate this adaptive response and secure the wide-ranging gains of a regimented exercise program are poorly understood. Formed through association of the Kir6.2 pore and the sulfonylurea receptor, the stress-responsive ATP-sensitive K[sup+] channels (K[subATP] channels), with their metabolic-sensing capability and broad tissue expression, are potential candidates for integrating the systemic adaptive response to repetitive exercise. Here, the responses of mice lacking functional Kir6.2-containing K[subATP] channels (Kir6.2-KO) were compared with wild-type controls following a 28-day endurance swimming protocol. While chronic aquatic training resulted in lighter, leaner, and fitter wild-type animals, the Kir6.2-KO manifested less augmentation in exercise capacity and lacked metabolic improvement in body fat composition and glycemic handling with myocellular defects. Moreover, the repetitive stress of swimming unmasked a survival disadvantage in the Kir6.2-KO, associated with pathologic calcium-dependent structural damage in the heart and impaired cardiac performance. Thus, Kir6.2-containing KATP channel activity is required for attainment of the physiologic benefits of exercise training without injury. Diabetes 53 (Suppl. 3): S169-S175, 2004
- Subjects
EXERCISE physiology; ADENOSINE triphosphate; POTASSIUM channels; AQUATIC exercises; FAT; METABOLISM; HEART injuries
- Publication
Diabetes, 2004, Vol 53, pS169
- ISSN
0012-1797
- Publication type
Article
- DOI
10.2337/diabetes.53.suppl_3.S169