The purpose of the present study was to evaluate the effects of aerobic physical training (APT) on heart rate variability (HRV) and cardiorespiratory responses at peak condition and ventilatory anaerobic threshold. Ten young (Y: median = 21 years) and seven middle-aged (MA = 53 years) healthy sedentary men were studied. Dynamic exercise tests were performed on a cycloergometer using a continuous ramp protocol (12 to 20 W/min) until exhaustion. A dynamic 24-h electrocardiogram was analyzed by time (TD) (standard deviation of mean R-R intervals) and frequency domain (FD) methods. The power spectral components were expressed as absolute (a) and normalized units (nu) at low (LF) and high (HF) frequencies and as the LF/HF ratio. Control (C) condition: HRV in TD (Y: 108, MA: 96 ms; P<0.05) and FD -LFa, HFa -was significantly higher in young (1030; 2589 ms 2 /Hz) than in middle-aged men (357; 342 ms 2 /Hz) only during sleep (P<0.05); posttraining effects: resting bradycardia (P<0.05) in the awake condition in both groups; V . O 2 increased for both groups at anaerobic threshold (P<0.05), and at peak condition only in young men; HRV in TD and FD (a and nu) was not significantly changed by training in either groups. The vagal predominance during sleep is reduced with aging. The resting bradycardia induced by short-term APT in both age groups suggests that this adaptation is much more related to intrinsic alterations in sinus node than in efferent vagal-sympathetic modulation. Furthermore, the greater alterations in V . O 2 than in HRV may be related to short-term APT.

The purpose of the present study was to determine if autonomic heart rate modulation, indicated by heart rate variability (HRV), differs during supine rest and head-up tilt (HUT) when sedentary and endurance-trained cyclists are compared. Eleven sedentary young men (S) and 10 trained cyclists (C) were studied. The volunteers were submitted to a dynamic ECG Holter to calculate HRV at rest and during a 70º HUT. The major aerobic capacity of athletes was expressed by higher values of V. O 2 at anaerobic threshold and peak conditions (P < 0.05).At rest the athletes had lower heart rates (P < 0.05) and higher values in the time domain of HRV compared with controls (SD of normal RR interval, SDNN, medians): 59.1 ms (S) vs 89.9 ms (C), P < 0.05. During tilt athletes also had higher values in the time domain of HRV compared with controls (SDNN, medians): 55.7 ms (S) vs 69.7 ms (C), P < 0.05. No differences in power spectral components of HRV at rest or during HUT were detected between groups. Based on the analysis of data by the frequency domain method, we conclude that in athletes the resting bradycardia seems to be much more related to changes in intrinsic mechanisms than to modifications in autonomic control. Also, HUT caused comparable changes in sympathetic and parasympathetic modulation of the sinus node in both groups.

We investigated the effects of aerobic training on the efferent autonomic control of heart rate (HR) during dynamic exercise in middleaged men, eight of whom underwent exercise training (T) while the other seven continued their sedentary (S) life style. The training was conducted over 10 months (three 1-h/sessions/week on a field track at 70-85% of the peak HR). The contribution of sympathetic and parasympathetic exercise tachycardia was determined in terms of differences in the time constant effects on the HR response obtained using a discontinuous protocol (4-min tests at 25, 50, 100 and 125 watts on a cycle ergometer), and a continuous protocol (25 watts/min until exhaustion) allowed the quantification of the parameters (anaerobic threshold, V . O 2 AT; peak O 2 uptake, V . O 2 peak; power peak) that reflect oxygen transport. The results obtained for the S and the T groups were: 1) a smaller resting HR in T (66 beats/min) when compared to S (84 beats/min); 2) during exercise, a small increase in the fast tachycardia (∆0-10 s) related to vagal withdrawal (P<0.05, only at 25 watts) was observed in T at all powers; at middle and higher powers a significant decrease (P<0.05 at 50, 100 and 125 watts) in the slow tachycardia (∆1-4 min) related to a sympathetic-dependent mechanism was observed in T; 3) the V. O 2 AT (S = 1.06 and T = 1.33 l/min) and V . O 2 peak (S = 1.97 and T = 2.47 l/min) were higher in T (P<0.05). These results demonstrate that aerobic training can induce significant physiological adaptations in middle-aged men, mainly expressed as a decrease in the sympathetic effects on heart rate associated with an increase in oxygen transport during dynamic exercise.

This article reviews studies performed since 1975 on the occurrence of central and peripheral neurological manifestations in low-level lead exposure. The review shows that in many workers exposed to lead who present indications of both biological effects and exposure below the limits established by the Brazilian laws, abnormalities are found in peripheral nerve conduction velocity and also in several central nervous system functions. The study thus suggests that the threshold values used in Brazil to confirm lead poisoning should be revised.

Fourteen normal subjects were submitted to isometric exercise (IE), dynamic exercise (DE) and a combination of the two (IE + DE). The main purpose of the present study was to use IE as a means of evaluating the mechanism of the heart rate (HR) increase induced by DE. To this end, the magnitude of the IE (handgrip) was standardized so as to cause an elevation of HR almost exclusively by vagal withdrawal: IE was performed using a dynamometer strain-gauge system with a linear response at 75% of maximum voluntary contraction (MVC) for 10 s, repeated at 1 min intervals. The change in HR evoked by IE under control conditions was compared with that evoked during DE, and during the corresponding recovery period. DE was performed by the legs, with the subject in the seated position for 4 min, at workloads of 55 and 105 watts, separated by a rest period. In the combined protocol, IE was performed at the beginning of DE, as well as at 1, 2 and 3 min during DE, and at 0, 1, 2, 3 and 5 min during recovery period. The following results were obtained: (1) IE associated with DE always induced smaller increase in heart rate than IE alone, and this effect was more marked at 105 than at 55 W; this finding suggested a workload-dependent vagal withdrawal at the very beginning of DE that was sustained until the end of effort.(ABSTRACT TRUNCATED AT 250 WORDS)