Abstract

Cocaine abuse in athletes and the associated morbidity and mortality has piqued interest in its mechanisms of action. Acute cocaine intoxication initially enhances muscle performance, but ultimately leads to premature muscle fatigue and may precipitate renal failure, and death. In rats, cocaine administration accelerates muscle glycogen utilization and fatigue during treadmill exercise. Blood flow to rat hindlimb muscles during exercise is not reduced after cocaine administration (Hagen et al., MSSE 29: S218, 1997), suggesting that cocaine may elevate muscle metabolism. PURPOSE: To determine whether acute cocaine administration increases skeletal muscle metabolism and oxygen uptake, thereby accelerating microvascular PO2 (PO2m) on-kinetics. METHODS: PO2m was measured by phosphorescence quenching in the extensor digitorum longus muscle (EDL) of anesthetized female Sprague-Dawley rats at rest and during the rest-to-contraction transition (1 Hz, 6V). In each rat, PO2m was measured during a control stimulation (STIM 1) and after administration of either cocaine (C, n=13; 5 mg/kg i.v.) or an equivalent volume of saline (S; n=10) (STIM 2). EDL twitch tension was measured during each contraction bout using a muscle tension analyzer. RESULTS: During STIM 1, resting PO2m (R-PO2m), the time delay (TD) between the onset of contractions and the fall in PO2m, the time constant (Tau) and the magnitude and of the fall in PO2m at the onset of contractions (D-PO2m) were the same in the S and C groups. Cocaine administration had no effect on R-PO2m during prior to STIM 2 (S, 23 ± 2; C, 26 ± 1 mmHg). Further, cocaine had no effect on D-PO2m (S, -12 ± 2 vs. C, -15 ± 1 mmHg), TD (S, 6 ± 1; C, 6 ± 1 s) or Tau (S, 8 ± 2; C, 9 ± 2 s). Neither twitch tension (S, 31 ± 7; C, 28 ± 7 N) nor any other indices of muscle contractile function were different during STIM 2. CONCLUSION: The results of this study indicate that acute cocaine administration does not alter resting PO2m, PO2m on-kinetics, or contractile function in the rat EDL muscle. Thus, these data do not support the notion that cocaine enhances muscle metabolism in contracting skeletal muscle.

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