Comparative effects of zopiclone and loprazolam on psychomotor and physical performance in active individuals.

OBJECTIVE: Sedative hypnotics are used by athletes to alleviate precompetition anxiety and insomnia. The effects of these agents on exercise tolerance have not been extensively researched. DESIGN: To determine the effects of sedative hypnotics on psychomotor and physical performance, a double-blind, placebo- (P) controlled, cross-over designed trial investigated the effects of zopiclone (Z) and loprazolam (L) on performance in 12 athletes. INTERVENTION: Subjects ingested either P, Z (7.5 mg), or L (2 mg) on three different occasions separated by a 1-week washout period. Eye-hand coordination tests, a 30-m sprint test, an agility test, and a graded treadmill run to exhaustion for determination of VO2max were performed 10 hours after drug administration. RESULTS: Subjects reported a significantly greater hangover effect following ingestion of L (8/11 subjects) compared with ingestion of Z (3/11 subjects; p < 0.01). A greater number of subjects felt alert after ingestion of P (9/11 subjects) and Z (9/11 subjects) compared with L (4/11 subjects; p < 0.01). The results of the eye-hand coordination tests, the 30-m sprint, the T-test, the VO2max, and the time to exhaustion during the treadmill run were not significantly altered following the ingestion of P, Z, and L. There was a significant difference between the delta values for Z and L for the number of missed responses in the eye-hand coordination tests (p < 0.02). Therefore, following the ingestion of L, subjects experienced a significant hangover effect and altered reaction time, whereas the ingestion of Z did not significantly impair either psychomotor or physical performance in the administered tests. CLINICAL RELEVANCE: Investigate the extent of the effects of sedative hypnotics on exercise performances, enabling team physicians to prescribe such drugs to the athlete more effectively.

Pseudoephedrine is without ergogenic effects during prolonged exercise.

This study was designed to measure whether a single dose of 120 mg pseudoephedrine ingested 120 min before exercise influences performance during 1 h of high-intensity exercise. The effects of exercise on urinary excretion of the drug were also studied. Ten healthy male cyclists were tested on two occasions, separated by at least 7 days, by using a randomly assigned, double-blind, placebo-controlled, crossover design. Exercise performance was tested during a 40-km trial on a laboratory cycle ergometer, and skeletal muscle function was measured during isometric contractions. On a third occasion, subjects ingested 120 mg pseudoephedrine but did not exercise [control (C)]. Pseudoephedrine did not influence either time trial performance [drug (D) vs. placebo: 58.1 +/- 1.4 (SE) vs. 58.7 +/- 1.5 min] or isometric muscle function. Urinary pseudoephedrine concentrations were significantly increased 1 h after exercise (D vs. C: 114.3 +/- 27.2 vs. 35.4 +/- 13.1 micrograms/ml; P < 0.05). Peak plasma pseudoephedrine concentrations (P < 0.05) but not time taken to reach peak plasma concentrations or the area under the plasma pseudoephedrine concentration vs. time curve was significantly increased in the total group with exercise (D vs. C). In three subjects, plasma pseudoephedrine concentrations were not influenced by exercise. Only these subjects showed increased urinary pseudoephedrine excretion during exercise. We conclude that a single therapeutic dose of pseudoephedrine did not have a measurable ergogenic effect during high-intensity exercise of 1-h duration, but plasma drug concentrations and urinary excretion were altered by exercise. These findings have practical relevance to doping control regulations in international sporting competitions.

Chronic beta-blockade does not influence muscle power output during high-intensity exercise of short-duration.

Patients receiving beta-receptor antagonists for the treatment of hypertension frequently complain of impaired exercise tolerance. To determine whether these medications impair skeletal muscle contractile function, we measured isokinetic muscle function in ten healthy male cyclists receiving nebivolol (N), atenolol (A), propranolol (P) and the calcium channel antagonist diltiazem (D). The subjects performed standardized tests of muscle power on an isokinetic cycle ergometer following subacute ingestion of N, A, P, D and placebo (PL) in a double blind crossover trial. Subjects exercised maximally for 10 s at 90, 110, 120, 130 and 150 rpm with 2-min rest between sessions. Thereafter, they performed a 30-s fatigue test at 120 rpm. Resting heart rate was decreased 13.4%, 21.9% and 14.6% by N, A and P, respectively (P < 0.05 vs PL). Resting systolic blood pressure was decreased 6.7% by A only (P < 0.05 vs PL). Peak power, average power and work done was not different among treatment groups at any crank velocity, nor was there any difference in total work done or rate of work decline in the 30-s test. We concluded from our study that peak isokinetic muscle power during maximal exercise of short duration is not affected by beta-blockade or the calcium antagonist diltiazem. Fatigue during beta-receptor antagonism would not appear therefore to be due to changes in the ability of skeletal muscle to produce peak power output during exercise of short duration.

The effects of antihypertensive medications on the physiological response to maximal exercise testing.

This study compared the effects of clinically prescribed doses of cilazapril, nifedipine, and atenolol on maximal exercise performance in physically active subjects. In a double-blind crossover trial, 10 healthy male volunteers performed progressive aerobic exercise to exhaustion for determination of maximal oxygen consumption (VO2 max), after single dose ingestion of cilazapril, nifedipine, atenolol, and placebo. Measurements were made at exhaustion and at a single submaximal workload (250 W). Exercise time to exhaustion and peak workload were decreased by all agents (p less than 0.05 vs. placebo), but VO2 max was decreased by atenolol only (p less than 0.05 vs. placebo). Although both atenolol and cilazapril decreased the maximum systolic blood pressure, the peak heart rate was decreased only by atenolol (p less than 0.001 vs. placebo). Whereas submaximal oxygen consumption, minute ventilation, and blood lactate concentrations were not different between groups, ratings of perceived exertion were increased during submaximal exercise by atenolol and cilazapril (p less than 0.05 vs. placebo). Cilazapril, nifedipine, and atenolol all impaired exercise performance and increased ratings of perceived exertion during submaximal exercise without altering rates of oxygen consumption or blood lactate accumulation. Maximal exercise performance was impaired to a greater extent by atenolol than by nifedipine or cilazapril. This study suggests that either angiotensin-converting enzyme inhibitors or calcium-channel antagonists might be preferable for the management of hypertension in athletic patients as they have a lesser effect on exercise performance, at least in healthy individuals.