Introduction
Caffeine
Overview
Mechanism of action
Effects on performance
WADA status
Summary
Caffeine | |||
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WADA status: now being monitored (stimulants - in competition only), banned from 1962 to 1972 and again from 1984 to 2003 at urinary caffeine concentrations >12 μg/ml | |||
Acute effect | Effect on performance | Caffeine dose | Reference |
Greater reliance on fat metabolism; increased FFAs; lower respiratory exchange ratio (RER) | Increased time trial performance | 6 mg/kg body mass | Mc Naughton et al. [34] |
Counteract central fatigue, directed effect on the CNS | 3% PMAX increase, increase in voluntary activation, maintenance of MVC | 6 mg/kg body mass | Del Coso et al. [35] |
No clear mechanism; effect on CNS (greater motor unit recruitment and altered neurotransmitter function) or direct effect on skeletal muscle | Enhanced time trial performance | 6 mg/kg caffeine 1 h pre-exercise and ~1.5 mg/kg after 2 h of exercise | Cox et al. [33] |
No mechanism proposed | No significant effects observed on performance | 1.5 or 3 mg/kg body mass of caffeine 1 h before cycling | Desbrow et al. [65] |
Direct effect on skeletal muscle; interaction with ryanodine receptor; potentiated calcium release from the SR | Increase in contraction force at low frequency stimulation (20 Hz) | 6 mg/kg 100 min before stimulation | Tarnopolsky et al. [23] |
Blunted pain response | Significantly higher reps during leg press set 3 with caffeine, same RPE | 6 mg/kg 1 h prior to 10-RM bench and leg press | Green et al. [66] |
Glycogen-sparing effect & increased utilization of intramuscular TGs and plasma FFAs with caffeine | Increased cycling time trial performance with caffeine | 9 mg/kg body mass 1 h before exercise | Spriet et al. [13] |
Nicotine
Overview
Mechanism of action
Effect on performance
Nicotine | |||
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WADA status: in order to detect potential patterns of abuse, nicotine has been placed on WADA’s 2012 monitoring program | |||
Acute effect | Effect on performance | Nicotine dose | Reference |
Likely delayed development of (central) fatigue by nicotine receptor activation and/or dopaminergic pathways; no evidence of altered substrate metabolism or cardiorespiratory effects | 17% improvement in time to exhaustion | 7 mg nicotine patch per 24 hours | Mundel et al. [93] |
No mechanism proposed | No effect on anaerobic performance (Wingate test) | nicotine gum | Meier [94] |
Unclear | Improvement in the degree in a real-life motor task, i.e. handwriting (more pronounced in smokers than non-smokers) | 2 and (4 mg) nicotine gum | Tucha et al. [95] |
No mechanism proposed | No effect on cognitive functioning | 2 and 4 mg nicotine gum | Heishman et al. [96] |
No mechanism proposed | No effect on speed and accuracy of motor activity among non-smokers (but improvements in smokers) | 2 and 4 mg nicotine gum | Hindmarch et al. [97] |
Likely by the action of nicotine on cholinergic pathways | Positive effects on fine motor abilities like finger tapping | 2 mg intranasal | West et al. [98] |
WADA status
Detection
Summary
Ethanol (alcohol)
Overview
Mechanism of action
Effects on performance
WADA status
Detection
Summary
Alcohol | ||||
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WADA status: alcohol is prohibited by WADA in competition only. The doping violation threshold is 0.10 g/L. As of 2013, alcohol is banned in the following sports: aeronautics (FAI), archery (FITA), automobile (FIA), karate (WKF), motorcycling (FIM) and powerboating (UIM) | ||||
Acute effect | Chronic effect | Effect on performance | EtOH Dose | Reference |
Reduced left ventricular contractility | Increased left ventricular dimensions and worsened left ventricular dysfunction | Negative effects on cardiac output | 1.15 g/kg body weight | Delgado et al. [149] |
No mechanism proposed; decreased performance possibly due to reduced myocardial contractility and reduced lung ventilation | Increased 800 m-1500 m run times | 0.05 – 0.1 mg/mL blood alcohol concentration | McNaughton et al. [140] | |
Hypoglycemia at 60-minute time-point | Reduced 60-min, treadmill time-trial performance | 25 ml in 150 ml grapefruit juice | Kendrick et al. [141] | |
No mechanism proposed. | Reductions in sustained power output during cycling times trials. | 0.5 ml/kg FFM | Lecoulre et al. [142] |
Tetrahydrocannabinol
Overview
Mechanism of action
Effects on performance
WADA status
Detection
Summary
TETRAHYDROCANNABINOL | |||
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WADA status: the International Olympic Committee included cannabis in the banned substance list beginning in 1989 and since 2004 the World Anti-Doping Agency has prohibited its use for all sports competition [[163]] | |||
Acute effect | Effect on performance | THC dose | Reference |
Resting heart rate and both systolic/diastolic blood pressure were significantly elevated at rest | Physical work capacity at a heart rate of 170 decreased by 25% compared to placebo | 18.2 mg of Δ9-THC | Steadward and Singh [154] |
Induced tachycardia at rest | VE, VO2 and VCO2 were increased above control at ≥50% max effort; Small, but significant reduction in maximal exercise duration; tachycardia up to 80% of maximum effort and during recovery | 7 mg/kg marijuana (containing 1.7% Δ9-THC) | Renaud and Cormier [155] |
Increased heart rate and the rate-pressure product at rest | No effect on blood pressure, ventilation or oxygen uptake during submaximal exercise (15 min at 50% of VO2max); increased heart rate and the rate-pressure product during recovery | Smoking 7.5 mg of Δ9-THC | Avakian et al. [156] |