Effects of cocaine on glycogen metabolism and endurance during high intensity exercise.

Because cocaine causes a rapid sympathetic response and central euphoria, we tested whether it would improve endurance or alter carbohydrate metabolism during high-intensity activity. Thirty male rats (10 animals/group) were injected intraperitoneally with either saline (S) or one of two doses of cocaine-HCl (12.5 (C-1) or 20.0 (C-2) mg.kg-1 b.w.). Ten minutes later they began gradually running on a rodent treadmill. Within 2 min they were running at 56 m.min-1 until fatigued. The run time to exhaustion (mean +/- SE) for C-2 (569 +/- 97 s) was less than S (859 +/- 71) and C-1 (923 +/- 65) (P < 0.05) and 25% shorter (marginally insignificant) than a pretreatment run (754 +/- 67 s) (P > 0.05). Plasma lactate concentrations at exhaustion were 4.0 +/- 0.5 (S), 7.3 +/- 1.1 (C-1), and 13.9 +/- 2.5 (C-2) mmol (P < 0.05, S vs C-2). Lactate concentrations in white vastus muscle were also elevated by C (4.7 +/- 0.6 (S), 8.1 +/- 1.3 (C-1), and 15.0 +/- 3.7 (C-2) mumol.g-1, (P < 0.05, S vs C-2)], which correlated with the reduction in glycogen content in both C groups (9.9 +/- 2.3 (C-2), 10.3 +/- 1.2 (C-1), vs 33.9 +/- 2.0 (S) mumol.g-1]. These results show that, in spite of its purported stimulatory effect, cocaine treatment (20 mg.kg-1) immediately prior to intense exercise causes accelerated glycogen degradation and lactate accumulation in white vastus muscle during exercise and premature fatigue.