The effects of creatine supplementation on thermoregulation and isokinetic muscular performance following acute (3-day) supplementation.

AIM: The purpose of this investigation was to determine the effects of 3 d of creatine supplementation on thermoregulation and isokinetic muscular performance. METHODS: Fourteen males performed two exercise bouts following 3 d of creatine supplementation and placebo. Subjects exercised for 60 min at 60-65% of VO2max in the heat followed by isokinetic muscular performance at 60, 180, and 300°·s(-1). Dependent variables for pre- and postexercise included nude body weight, urine specific gravity, and serum creatinine levels. Total body water, extracellular water and intracellular water were measured pre-exercise. Core temperature was assessed every 5 min during exercise. Peak torque and Fatigue Index were used to assess isokinetic muscular performance. RESULTS: Core temperature increased during the run for both conditions. Total body water and extracellular water were significantly greater (P<0.05) following creatine supplementation. No significant difference (P>0.05) was found between conditions for intracellular water, nude body weight, urine specific gravity, and serum creatinine. Pre-exercise scores for urine specific gravity and serum creatinine were significantly less (P<0.05) versus post-exercise. No significant differences (P>0.05) were found in peak torque values or Fatigue Index between conditions for each velocity. A significant (P<0.05) overall velocity effect was found for both flexion and extension. As velocity increased, mean peak torque values decreased. CONCLUSION: Three d of creatine supplementation does not affect thermoregulation during submaximal exercise in the heat and is not enough to elicit an ergogenic effect for isokinetic muscle performance following endurance activity.

Cyclooxygenase-2 inhibition by rofecoxib reverses naturally occurring fever in humans.

Cyclooxygenase (COX) exists as constitutive (COX-1) and inducible (COX-2) isoforms. Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and diclofenac inhibit both COX-1 and COX-2. The role of COX-2 in the genesis of fever in monkeys and humans was examined with use of the specific COX-2 inhibitor rofecoxib. Rofecoxib was administered to monkeys made febrile by 6 microg/kg intravenous lipopolysaccharide. Induced pyrexia was followed by oral rofecoxib (1 or 3 mg/kg), diclofenac (3 mg/kg), or vehicle. Rofecoxib and diclofenac rapidly reversed the elevated temperature (P < .05 versus vehicle for 3 mg/kg rofecoxib and diclofenac at 70 to 90 minutes after dosing). A single-dose, parallel-group, double-blind randomized trial was conducted in 94 patients with fever caused by a viral-type illness. Mean baseline temperature was similar for all groups (-38.5 degrees C). Patients received oral doses of 12.5 mg rofecoxib, 25 mg rofecoxib, 400 mg ibuprofen, or placebo and the mean +/- SE change in oral temperature at 4 hours after dosing was -0.97 degrees C +/- 0.11 degrees C, -1.19 degrees C +/- 0.09 degrees C, -1.20 degrees C +/- 0.11 degrees C, and 0.01 C +/- 0.17 C, respectively (P < .001 for active treatments versus placebo). Specific inhibition of COX-2 by rofecoxib results in antipyretic activity in monkeys and humans comparable to dual COX-1/COX-2 inhibitors such as diclofenac or ibuprofen. The data support the hypothesis that it is the COX-2 isoform that is primarily involved in the genesis of fever in humans.

Symptomatology and anatomic patterns of peripheral vascular disease: differing impact of smoking and diabetes.

We retrospectively examined the impact of smoking and diabetes on the clinical presentation and arteriographic pattern of occlusion in 227 patients evaluated for symptomatic infrainguinal arterial disease. The age at which significant symptomatology developed did not differ for diabetics and nondiabetics. Diabetics had significantly more occlusion in the large arteries of the calf, however, particularly in the peroneal and posterior tibial arteries. Despite this, the extent of occlusive disease in the pedal arch was not influenced by diabetes. Diabetics also tended to present more frequently with gangrene or ulcer (greater than 70%) when compared to nondiabetic smokers (41%, p less than .01). Smokers presented with symptomatic disease earlier than nonsmokers (p less than .0005). Intermittent claudication was strongly associated with smoking; among 33 patients with claudication, 32 were smokers. In contrast to the effect of diabetes, smokers appeared to have less extensive occlusive disease in the large arteries of the calf than nonsmokers. Nondiabetic nonsmokers constituted less than 10% of our study population and presented at a significantly older age. Nevertheless, despite the absence of either risk factor, this group also tended to present with gangrene or ulcer relatively frequently (71%). Although diabetes and smoking are both risk factors for atherosclerotic disease, we conclude that their impact on the angiographic pattern of occlusion and clinical presentation differs substantially.

The relative value of carotid noninvasive testing as determined by receiver operator characteristic curves.

To determine the relative value of carotid phonoangiography (CPA), oculoplethysmography-Kartchner (OPG-K), and Doppler ultrasonic arteriography (UA), 90 vessels undergoing carotid endarterectomy were prospectively examined. By analyzing the data on receiver operator characteristic curves, the dynamic relationship between sensitivity and specificity for each of the three noninvasive tests was assessed. Disease was defined by either the percentage of angiographic stenosis or the mean pressure gradient across the carotid (deltaP). All three tests were shown to be relatively insensitive, but quite specific, if disease was defined by 50% and 60% angiographic stenosis or deltaP of greater than 10 and 20 mm Hg. By employing a more rigid definition of disease, 70% stenosis or deltaP of greater than 30 mm Hg, sensitivity was increased for all examinations and was highest in OPG-K and UA for a given specificity. The sensitivity for UA was enhanced to 80% with a comparable specificity, if those 23 UA exams with plaque were treated as positive studies. The combination of CPA, OPG-K, and UA was superior to any one of these tests alone, but the best value balancing maximum sensitivity and specificity still was associated with a 23% false negative rate. This study would suggest that these three tests should be limited to screening patients at risk for carotid stenosis and not for symptomatic patients. To achieve the best balance between sensitivity and specificity, lax threshold criteria for calling the test positive should be employed, and the tests should be used in combination.