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Influences of Lifelong Exercise and Mild (8%) Caloric Restriction on IGF‐1 and Heat Shock Proteins in the Plantaris of the Aging Fischer‐344 Rat
Author(s) -
Kim JongHee,
Kwak HyoBum,
Leeuwenburgh Christiaan,
Lawler John M
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1311-a
A major characteristic of aging skeletal muscle is reduction of muscle mass called sarcopenia caused by reductions in fiber number and cross‐sectional area. Increased oxidative stress and impaired stress‐response may contribute to sarcopenia with aging. Insulin like growth factor‐1 (IGF‐1) and heat shock proteins (HSPs) are important anti‐atrophy agents involved in regulating cell growth, differentiation, and cell survival. Our purpose was to identify the effect of 8%CR and lifelong exercise on IGF‐1 and HSP signaling (HSP90, HSP70, HSF‐1 HSP25, phosphorylated HSP25 [p‐HSP25]) in the Fischer‐344 rat plantaris. We divided male Fischer‐344 rats at 11 weeks into four groups: young fed ad libitum until 6 mo. old (YAL, n=12); fed ad libitum until 24 mo. old (OAL, n=11); 8% caloric restriction to 24 mo of age (OCR, n=12); wheel running 24 mo. with 8% caloric restriction (OExCR, n=12). IGF‐1 protein expression decreased (−57%) in OAL as compared to 6AL. Lifelong exercise but not 8%CR resulted in a significant increase (+51%) in IGF‐1 compared with 24AL. Age, 8%CR, and lifelong exercise had no effect on HSP90, HSP70, and HSF‐1 levels. However, HSP25 (−46%) and p‐HSP25 (−25%) levels were lower in OAL compared to YAL rats, while 8%CR and OExCR resulted in significantly greater for both HSP25 (123%, 50%) and p‐HSP25 (50%, 108%), respectively. Our results indicate that lifelong wheel running exercise combined with mild caloric restriction could confer protection against muscle sarcopenia via IGF‐1 and HSP25 signaling pathways. Supported by a grant from NIH R01 AG17994