Aging is associated with hepatic growth hormone resistance resulting in a fall in serum insulin-like growth factor-1 (IGF-1) level. However, whether loss of IGF-1 contributes to cardiac aging is unclear. This study was designed to examine the effect of cardiac overexpression of IGF-1 on cardiomyocyte contractile function in young (3 mo) and old (26-28 mo) mice. Cardiomyocyte contractile function was evaluated including peak shortening (PS), time-to-90% PS, time-to-90% relengthening (TR₉₀) and maximal velocity of shortening/relengthening (± dL/dt). Levels of advanced glycation endproduct (AGE), protein carbonyl, sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA2a), phospholamban (PLB) and Na⁺-Ca²⁺ exchanger (NCX) were assessed by Western blot. SERCA activity was measured by ⁴⁵Ca²⁺ uptake. Aging induced a decline in plasma IGF-1 levels. Aged cells exhibited depressed ± dL/dt, prolonged TR90 and a steeper PS decline in response to increasing stimulus frequency compared with young myocytes. IGF-1 transgene alleviated aging-induced loss in plasma IGF-1 and aging-induced mechanical defects with little effect in young mice. The beneficial effect of IGF-1 transgene on aging-associated cardiomyocyte contractile dysfunction was somewhat mimicked by short-term in vitro treatment of recombinant IGF-1 (500 nM). AGE and protein carbonyl levels were higher in aged mice which were not affected by IGF-1. Expression of SERCA2a (but not NCX and PLB) and SERCA activity were reduced with aging, which was ablated by the IGF-1 transgene. Collectively, our data suggest beneficial role of IGF-1 in aging-induced cardiac contractile dysfunction, possibly related to improved Ca²⁺ uptake.