Abstract

Actovegin is a deproteinated calf blood extract that has been used clinically for over 60 years to treat a wide range of conditions. The drug is thought to exert its therapeutic benefits by enhancing oxidative phosphorylation and cell metabolism. It is postulated that Actovegin has insulin-like properties and can increase glucose uptake in the cell. Due to its proposed mechanism of action, Actovegin has also been speculated as an aerobic performance enhancing drug and few studies have been sought out to confirm this speculation. In addition, the effects of this drug on mitochondrial respiration have only been investigated in skeletal muscle and liver tissue through an acute administration protocol.

This thesis explores the effects of Actovegin from a functional and mechanistic perspective. The objectives were to determine if non-acute Actovegin injections every 2nd day for 14 days can increase aerobic exercise capacity and mitochondrial respiration in skeletal muscle and cardiac tissue in trained and sedentary mice versus equivalent groups receiving a placebo. Effects on blood glucose and body mass were also investigated. Using an aerobic exercise capacity test and high-resolution respirometry, the data revealed that Actovegin injections over a two-week period: (1) increased aerobic exercise capacity (2) increased skeletal muscle mitochondrial respiration, (3) did not have a significant effect on cardiac mitochondrial respiration. These results suggest that non-acute Actovegin injections may enhance aerobic exercise performance and reduce the heart’s need to increase contractile capacity in a high-intensity exercise setting.