Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats.
Data regarding the effectiveness of chronic exercise training in improving survival in patients with congestive heart failure (CHF) are inconclusive. Therefore, we conducted a study to determine the effect of exercise training on survival in a well-defined animal model of heart failure (HF), using the lean male spontaneously hypertensive HF (SHHF) rat. In this model, animals typically present with decompensated, dilated HF between approximately 18 and 23 mo of age. SHHF rats were assigned to sedentary or exercise-trained groups at 9 and 16 mo of age. Exercise training consisted of 6 mo of low-intensity treadmill running. Exercise training delayed the onset of overt HF and improved survival (P < 0.01), independent of any effects on the hypertensive status of the rats. Training delayed the myosin heavy chain (MyHC) isoform shift from alpha- to beta-MyHC that was seen in sedentary animals that developed HF. Exercise was associated with a concurrent increase in cardiomyocyte length (approximately 6%), width, and area and prevented the increase in the length-to-width ratio seen in sedentary animals in HF. The increases in proteinuria, plasma atrial natriuretic peptide, and serum leptin levels observed in rats with HF were suppressed by low-intensity exercise training. No significant alterations in sarco(endo)plasmic reticulum Ca2+ ATPase, phospholamban, or Na+/Ca2+ exchanger protein expression were found in response to training. Our results indicate that 6 mo of low-intensity exercise training delays the onset of decompensated HF and improves survival in the male SHHF rat. Similarly, exercise intervention prevented or suppressed alterations in several key variables that normally occur with the development of overt CHF. These data support the idea that exercise may be a useful and inexpensive intervention in the treatment of HF.
Emter
Craig A
CA
Dept. of Integrative Physiology, Univ. of Colorado at Boulder, Boulder, CO 80309-0354, USA.
McCune
Sylvia A
SA
Sparagna
Genevieve C
GC
Radin
M Judith
MJ
Moore
Russell L
RL
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism; D002469:Cell Separation; D048429:Cell Size; D002950:Citrate (si)-Synthase / Q000378:metabolism; D006333:Heart Failure / Q000473:pathology / Q000517:prevention & control*; D007536:Isomerism; D020738:Leptin / Q000097:blood; D008297:Male; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000473:pathology; D018995:Myosin Heavy Chains / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011507:Proteinuria / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D016019:Survival Analysis
D020738:Leptin; D009320:Atrial Natriuretic Factor; D002950:Citrate (si)-Synthase; D018995:Myosin Heavy Chains; D002118:Calcium