To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO 2 peak, and 12 subjects rested for 45 min in a nonexercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO 2 peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO 2 peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO 2 peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 ± 314 vs R5-30 = 7150 ± 326, R35-60 = 6794 ± 349, and R65-90 = 6628 ± 311, P<0.05), while exercise at 50% of VO 2 peak caused no change, and exercise at 80% of VO 2 peak produced a significant increase at R5-30 (7468 ± 267 vs 9818 ± 366, P<0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO 2 peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO 2 peak, exercise at 30% of VO 2 peak decreased post-exercise HR and RP. Correspondence

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The objective of this study was to determine intraocular pressure (IOP) and cardiac changes in normocapnic dogs maintained under controlled ventilation and anesthetized using sevoflurane or desflurane. Sixteen healthy adult mixed-breed dogs, seven males and nine females, weighing 10-15 kg were used. The dogs were randomly assigned to one of two groups composed of eight animals anesthetized with sevoflurane (SEVO) or desflurane (DESF). In both groups, anesthesia was induced with propofol (10 mg/kg), and neuromuscular blockade was achieved with rocuronium (0.6 mg/kg/h i.v.). No premedication was given. Ventilation was adjusted to maintain end-tidal carbon dioxide partial pressure at 35 mmHg. Anesthesia was maintained with 1.5 minimum alveolar concentration (MAC) of sevoflurane or desflurane. In both groups IOP was measured by applanation tonometry (Tono-Pen) before induction of anesthesia. IOP, mean arterial pressure (MAP), heart rate (HR), cardiac index (CI) and central venous pressure (CVP) were also measured 45 min after the beginning of inhalant anesthesia and then every 20 min for 60 min. A one-way repeated measures anova was used to compare data within the same group and Student's t-test was used to assess differences between groups. P < 0.05 was considered statistically significant. Measurements showed normal IOP values in both groups, even though IOP increased significantly from baseline during the use of desflurane. IOP did not differ between groups. CI in the desflurane group was significantly greater than in the sevoflurane group. Sevoflurane and desflurane have no clinically significant effects on IOP, MAP, HR, CI or VCP in the dog.

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Administration of nitrous oxide with desflurane results in maintenance of normal IOP and prevents a decrease in horizontal PD during anesthesia. Therefore, this may be a suitable protocol in dogs undergoing intraocular surgeries that require mydriasis and maintenance of normal IOP.

Purpose -To compare the lower (LL) and upper limits (UL) of exercise intensity prescription based on standard exercise test (60-70% of estimated VO 2 max or 70-85% of HRmax measured) with exercise intensity prescription based on cardiopulmonary exercise test [anaerobic threshold (AT) and respiratory compensation point (RCP)].Methods AT (4mph= 34.4±4.5 vs 19.6±4.6 and 5mph= 28.9±2 vs 18.9±5.4, and LPC= 32.0±4.1 vs 17.2±2.8 and MPC= 31.6±4.9 LA (4mph= 34,4±4,5 vs 19,6±4,6 e 5mph= 28,9±2 vs 18,9±5,4, e BCF= 32,0±4,1 vs 17,2±2,8 e MCF= 31,6±4,9 vs 21,1±5,9±7,8 vs 113,1± 15,6 e 5mph= 130,3±5,2 vs 114,1± 18,9, e BCF= 127,6±7,2 vs 109,3±13,2 e MCF= 131,2± 5,7 vs 117,4± 19,2bpm Embora pareçam existir poucas dúvidas quanto a melhora na qualidade de vida e, sobretudo, na condição de saúde alcançada através de um programa de condicionamento físico, esses benefícios dependem de uma prescrição Métodos -Realizaram teste ergoespirométrico progressivo até a exaustão 47 homens (30±5 anos), divididos em subgrupos, de acordo com a velocidade da esteira durante o teste (4 ou 5mph) e a capacidade física medida [baixa (BCF) e moderada (MCF)]. Resultados -Os L.inf. de prescrição indireta apresentaram valores de VO 2 e FC significantemente maiores que os valores de VO 2 e FC no

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The aim of this study was to test the hypothesis that magnesium supplementation influences the physical performance of volleyball players, as the efficacy of this approach remains questionable. Twenty-five professional male volleyball players were assigned randomly to experimental (350 mg Mg · d(-1), 4 weeks) and control groups (500 mg maltodextrin · d(-1), 4 weeks) maintaining inter-group homogeneity of urinary magnesium. Erythrocyte, plasma and urinary magnesium levels, plasma creatine kinase activity, lactate production, maximal oxygen uptake (VO2 max) and plyometric (squat jump, countermovement jump, countermovement jump with arm swing) and isokinetic (peak torque, potency and total work) performances were evaluated before (T0) and after (T1) supplementation. Levels of erythrocyte and urinary magnesium and creatine kinase activity and VO2 max remained within normal ranges in both groups. Plasma magnesium decreased significantly only within the experimental group. Significant decreases in lactate production and significant increases (of up to 3 cm) in countermovement jump and countermovement jump with arm swing values were detected in the experimental group following magnesium supplementation, but not in the control group at T1. It is concluded that magnesium supplementation improved alactic anaerobic metabolism, even though the players were not magnesium-deficient.