The warm-up phenomenon, described in patients with coronary artery disease, refers to the improved performance following a first exercise test. The aim of this study was to investigate the causes of the warm-up phenomenon. Fifteen patients with coronary artery disease and positive exercise test were enrolled. Patients were off treatment throughout the study. They underwent two consecutive treadmill exercise tests according to the Bruce protocol, with a recovery period of 10 min to re-establish baseline conditions. A third exercise test was then performed 2 h later. Before the onset of ischaemia, the rate-pressure product for a similar degree of workload was similar during the first and second exercise test, while it was lower during the third test (P < 0.05). Time to 1.5 mm ST-segment depression during the second and third exercise test was greater than during the first test (454 +/- 133 and 410 +/- 161 vs 354 +/- 127 s, P < 0.01, respectively). Similarly, the time to anginal pain onset was increased during the second and third exercise tests, compared to the first test (356 +/- 208 and 310 +/- 203 vs 257 +/- 204 s, P < 0.01, respectively). In contrast, rate-pressure product at 1.5 mm ST-segment depression during the second test was higher than that during the first test (232 +/- 47 vs 210 +/- 39 beats.min-1.mmHg.10(2), P < 0.01), while in the third test it was similar to that during the first (209 +/- 43 beats.min-1.mmHg.10(2), P = ns). The warm-up phenomenon observed a few minutes after exercise is characterized by an increase of both time to ischaemia and ischaemic threshold; this adaptation to ischaemia may be due to an improvement of myocardial perfusion or to preconditioning. Conversely, the warm-up phenomenon observed a few hours after repeated exercise is characterized by an increase of time to ischaemia but not of ischaemic threshold and is caused by a slower increase of cardiac workload. Thus, the mechanisms of the warm-up phenomenon may be different, time dependent and related to previous training.

AimsThe increased tolerance to myocardial ischaemia observed during the second of two sequential exercise tests, i.e. the warm-up phenomenon, has been proposed as a clinical model of ischaemic preconditioning. As ATPsensitive K + channels appear to be a mediator of ischaemic preconditioning in both experimental and clinical studies, the aim of this study was to investigate the role of K ATP channels in the warm-up phenomenon. Methods and ResultsTwenty-six patients with coronary artery disease were randomized to receive 10 mg oral glibenclamide, a selective ATP-sensitive K + channel blocker, or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 ml . min 1 ) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusions, both patient groups underwent two consecutive treadmill exercise tests, with a recovery period of 15 min to re-establish baseline conditions. Before exercise tests, blood glucose levels were similar in placebo and glibenclamide groups (96 10 vs 105 22 mg . 100 ml 1 , P=ns). After placebo administration, rate-pressure product at 1·5 mm STsegment depression significantly increased during the second exercise test compared to the first (220 41 vs 186 29 beats . min 1 . mmHg . 10 2 , P<0·01), but it did not change after glibenclamide (191 34 vs 187 42 beats . min 1 . mmHg . 10 2 , P=ns), with a significant drugtest interaction (P=0·0091, at two-way ANOVA).Conclusions Glibenclamide, at a dose previously shown to abolish ischaemic preconditioning during coronary angioplasty, prevents the increase of ischaemic threshold observed during the second of two sequential exercise tests. These findings confirm that ischaemic preconditioning plays a key role in the warm-up phenomenon and that in this setting is, at least partially, mediated by activation of ATP-sensitive K + channels.

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Stuttering is an abnormality in the fluency of speech, which is characterized by interruption of the normal rhythm due to involuntary repetition and prolongation, or arrest, of uttered letters or syllables.The aphasic syndrome and dysarthria can be associated with classic migraine, but, to our knowledge, no study has so far described stuttering as the only neurological symptom accompanying an attack.Key words: stuttering, migraine, aphasia ( Headache 2000;40:170-172) CASE HISTORYA 26-year-old, right-handed woman presented to the emergency room because of frontal and temporal bilateral headache and stuttering.The patient had been well until three hours before when she developed a severe headache and right arm and perioral paresthesia with a progressive disturbance in the fluency of her speech with stuttering.She had never stuttered previously, and there was no family history of developmental stuttering. The patient reported having had insulin-dependent diabetes mellitus since the age of six years and only had one or two episodes of headache per year in the past; these headaches had the same features as the current episode except for the stuttering. There was no history of hypertension; use of tobacco, alcohol, or illicit drugs; auditory symptoms, vertigo, or dysarthria; neck pain; night sweats; or weight loss.Her temperature was 36.5 Њ C. Her pulse was 88 beats per minute, and the respirations were 16 breaths were minute . Her blood pressure was 115/80 mm Hg.The results of the general physical examination were normal. On neurological examination, her muscle strength, sensation of pinprick, vibration, temperature, and joint position were normal; cranial nerve functions were preserved; and the visual fields were intact. Coordination and gait were normal, and Romberg's test was negative. The deep or tendon reflexes were ϩϩ and equal in both arms and legs. Babinski's sign was not present.The fluency evaluation revealed severe stuttering characterized by multiple repetitions or blocks, or both, with 20 or more repetitions per word during both conversational speech and oral reading. No starters or secondary stuttering characteristics, and no specific word fears or avoidance, were exhibited. No deficit in naming, spontaneous speech, comprehension, repetition, reading, and writing was observed.Blood glucose levels and other hematological and chemical values, including the level of angiotensin-converting enzyme, were normal.The results of a CT examination of the brain, performed during the attack, were normal, and EEG findings did not show abnormalities or focal or generalized paroxysmal activity.Ketoprofen was administered with only a slight improvement in the patient's symptoms, but stuttering, headache, and right arm and perioral paresthesia promptly and completely disappeared after subcutaneous administration of sumatriptan, 6 mg.One week later, a repeated CT and MRI of the brain performed after the intravenous injection of contrast material did not show any abnormality. A serological test for syphilis and a test ...

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