Acute caffeine administration decreased NOS and Bcl2 expression in rat skeletal muscles.

Caffeine (Caf) is largely used to delay fatigue, improving physical activity. However, its role remains elusive, and there are no hemodynamic or immunohistochemical data regarding its effects on skeletal muscle. We studied the hemodynamic and NOS expression of Bax/Bcl2 in skeletal muscle after single Caf administration. Thirty-two male rats were divided into six groups: the first was iv-injected with Caf (16mg/kg), the second with Caf+L-NAME, the third with Caf+L-arg, the fourth with Caf+L-NAME+L-arg, fifth with saline. Mean arterial blood pressure (MAP) was monitored for 30', then the animals were killed. The sixth group was injected with Caf and killed after 2h. The quadriceps were isolated and processed by immunohistochemistry. We found that Caf increased MAP temporarily, while Caf+L-NAME increased it for a longer period. In untreated muscle, all NOS isoforms was expressed with different intensity and localisation, and Bcl2 was strongly expressed among the myofibrils. In Caf and Caf+L-NAME treated animals, NOS expression was lost; Bcl2 expression decreased among myofibrils but increased inside the subsarcolemma. The L-arg administration reversed these Caf and L-NAME effects. Two hours after Caf, NOS expression increased. We concluded that improved physical performance could be related to Caf's ability to interfere with the endogenous muscular synthesis of NO.