Aldose reductase inhibition ameliorates pupillary light reflex and F-wave latency in patients with mild diabetic neuropathy

OBJECTIVE--The present study was conducted to investigate the effect of an aldose reductase inhibitor, epalrestat, on autonomic and somatic neuropathy at an early stage in type 2 diabetic patients by assessing the pupillary light reflex and minimum latency of the F-wave. RESEARCH DESIGN AND METHODS--A total of 30 diabetic patients with subclinical or mild diabetic neuropathy were randomly allocated to a control group (n = 15) and epalrestat (150 mg/day) group (n = 15). After 24 weeks, the pupillary light reflex test, cardiovascular autonomic function tests, and nerve conduction study were performed. RESULTS--The beneficial effect of epalrestat on the pupillary light reflex was observed in the minimum diameter after light stimuli (P = 0.044), constriction ratio (P = 0.014), and maximum velocity of constriction (P = 0.008). Among cardiovascular autonomic nerve functions, the ratio of the longest expiratory R-R interval to the shortest inspiratory R-R interval during deep breathing was significantly improved by epalrestat (P = 0.037). Minimum latencies of F-wave of median and tibial motor nerves were significantly shortened by epalrestat (P = 0.002 and P = 0.001, respectively); however, no significant effects were observed in motor or sensory nerve conduction velocity. CONCLUSIONS--These observations suggest that epalrestat may have therapeutic value at the early stage of diabetic neuropathy and that the pupillary light reflex and minimum latency of F-wave may be useful indicators of diabetic neuropathy.     

Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans.

Animal studies have demonstrated that activation of the baroreflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroreflex activation on the sympathetic response to stimulation of PC and central chemoreceptors in humans. PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal reflex control to determine the selectivity of the interactive influence of baroreflex activation. Baroreflex activation was achieved by raising mean blood pressure by greater than 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 +/- 92 to 354 +/- 107 U/min (P less than 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 +/- 45 U/min (P less than 0.05). With hypoxia during baroreflex activation with PE, SNA did not increase (50 +/- 23 U/min). During hypercapnia alone, SNA increased from 116 +/- 39 to 234 +/- 72 U/min (P less than 0.01). Hypercapnia during baroreflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroreflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroreflex and the peripheral chemoreflex may be explained by convergence of baroreceptor and peripheral chemoreceptor afferents on neurons in the medulla.     

Thermoregulatory sweating abnormalities in diabetes mellitus

A properly performed thermoregulatory sweat test (TST) can be informative in patients with diabetic neuropathy. Of 51 patients suspected of having neuropathy on the basis of a clinical examination, 48 (94%) had unequivocal abnormalities on the TST. Pathologic loss of sweating occurred distally in 65%, segmentally in 25%, and only in isolated dermatomes in 25%; 78% of patients had a combination of two or more patterns. Global anhidrosis was noted in eight patients (16%), all of whom had profound autonomic neuropathy, and in the entire group, the percentage of body surface anhidrosis correlated with the degree of clinical dysautonomia (rank correlation coefficient = 0.77; P less than 0.01). Discrete zones of anhidrosis on the thorax and abdomen were noted in patients with painful diabetic radiculopathy, and they correlated highly with thoracic paraspinal muscle fibrillation potentials. Distal loss of sweating detected on the TST was always associated with a subnormal quantitative sudomotor axon reflex response or abnormal electromyographic findings, an indication of a distal axonal neuropathy. The TST provides reliable information about the distribution of diabetic neuropathic involvement and can be especially useful in the diagnosis of truncal radiculopathy and clinically significant autonomic neuropathy.     

Quantitative evaluation of diabetic autonomic neuropathy by using heart rate variations: relationship between cardiac parasympathetic or sympathetic damage and clinical conditions

It was previously suggested that respiratory heart rate (HR) variations were predominantly affected by the parasympathetic nerve and HR increase to standing was predominantly affected by the sympathetic nerve. To compare parasympathetic and sympathetic nerve function in diabetics, these two tests were performed in 95 diabetics and 38 controls by use of an instantaneous-HR-change continuous recorder. All subjects were between 40 and 59 years-old. As indices of autonomic nerve function, the mean difference between maximal and minimal HR during deep breathing (delta I-E) and the HR increase on standing (delta HR) were determined. The mean delta I-E and delta HR in the diabetics were 9.4 beats/min and 15.1 beats/min, respectively. These values were significantly lower than those in the controls (delta I-E 14.4, delta HR 20.5 beats/min). delta I-E correlated negatively to duration of diabetes and mean fasting blood glucose during the last 6 months in the diabetics, but delta HR did not correlate to them at all. Diminished delta I-E was found in the patients with insulin treatment, retinopathy or persistent proteinuria. Diminished delta HR, however, was found only in the patients with long-standing complicated diabetes. Thus, both cardiac parasympathetic and sympathetic nerve function were significantly impaired in the diabetics as compared with the controls and that parasympathetic nerve damage occurred early whereas sympathetic innervation was preserved.     

Peripheral nerve conduction studies and bulbocavernosus reflex in the investigation of impotence

Patients with erectile dysfunction underwent sensory and motor conduction and bulbocavernosus reflex tests to determine the incidence of peripheral nerve involvement. Of a total of 111 patients, abnormal sensory conduction was found in 87 (78%), abnormal motor conduction in 56 (50%), and abnormal bulbocavernosus reflex in 40 (36%). Most of these patients had other medical problems. Objective evidence of peripheral nerve involvement helped in the management of these patients.     

Effects of nasal continuous positive airway pressure on awake ventilatory responses to hypoxia and hypercapnia in patients with obstructive sleep apnea

This study was aimed to examine the short- and long-term effects of nasal continuous positive airway pressure (CPAP) on the chemosensitivity to hypoxia and hypercapnia in the patients with obstructive sleep apnea (OSA). Awake ventilatory responses to hypoxia and hypercapnia were examined in 28 patients (3 female) with moderate to severe OSA. All these tests were examined before and after 2 weeks of nasal CPAP. In 10 patients these tests were repeated after 3-6 months of nasal CPAP. All were also tested for spirometry and arterial blood gas analysis. Patients were middle-aged (48.9 +/- 9.9 years) and their mean apnea-hypopnea index was 58.3 +/- 20.4/hour. After 2 week of nasal CPAP, PaO2 significantly increased (77.7 +/- 11.8 vs. 84.6 +/- 9.8 mmHg) and PaCO2 significantly decreased (44.9 +/- 3.8 vs. 42.3 +/- 3.7 mmHg). The ventilatory response to hypoxia significantly decreased (0.80 +/- 0.51 vs. 0.61 +/- 0.51 liter/min/%) whereas the ventilatory response to hypercapnia significantly increased after 2 weeks (1.47 +/- 0.73 vs. 1.80 +/- 0.76 liter/min/mmHg). Similar findings were also observed after 3-6 months of nasal CPAP in 10 OSA patients. Nasal CPAP treatment can alter the ventilatory responses in patients with OSA.     

Complications: neuropathy, pathogenetic considerations.

The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy, often accompanied by autonomic neuropathy. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration, segmental, and paranodal demyelination and blunted nerve fiber regeneration. In both humans and laboratory animals, this progressive nerve fiber damage and loss parallels the degree and/or duration of hyperglycemia. Several metabolic mechanisms have been proposed to explain the relationship between the extent and severity of hyperglycemia and the development of diabetic neuropathy. One mechanism, activation of the polyol pathway by glucose via AR, is a prominent metabolic feature of diabetic rat peripheral nerve, where it promotes sorbitol and fructose accumulation, myo-inositol depletion, and slowing of nerve conduction by alteration of neural Na(+)-K(+)-ATPase activity or perturbation of normal physiological osmoregulatory mechanisms. ARIs, which normalize nerve myo-inositol and nerve conduction slowing, are currently the focus of clinical trials. Other specific metabolic abnormalities that may play a role in the pathogenesis of diabetic neuropathy include abnormal lipid or amino acid metabolism, superoxide radical formation, protein glycation, or potential blunting of normal neurotrophic responses. Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency and nerve hypoxia that may contribute to nerve fiber loss and damage. Although major questions about the pathogenesis of diabetic neuropathy remain unanswered and require further intense investigation, significant recent progress is pushing us into the future and likely constitutes only the first of many therapies directed against one or more elements of the complex pathogenetic process responsible for diabetic neuropathy.     

Effect of liver failure on the ventilatory response to hypoxia in man and the goat.

1. The ventilatory responses to transient and steady-state hypoxia were measured in ten patients with hepatic cirrhosis and in ten healthy control subjects. Successive measurements of these responses were also obtained in six goats before and after the experimental production of liver failure. Changes in the effect of steady-state hypoxia on the ventilatory response to hypercapnia were evaluated by successive studies in another goat. 2. In spite of a respiratory alkalosis during liver failure, the response to transient hypoxia was greater in the patients than in the control subjects. This response was increased after the onset of liver failure in all the goats. 3. In healthy humans and goats the responses to transient and steady-state hypoxia were similar in magnitude. During liver failure there was a disparity between the size of these responses, since the ventilatory increment evoked by steady-state hypoxia was unchanged in spite of the increase in response to transient hypoxia. Steady-state hypoxia consistently enhanced the ventilatory response to hypercapnia in a healthy goat, but frequently depressed the response to hypercapnia during liver failure. 4. The findings suggest that liver failure heightens the sensitivity of the peripheral chemoreceptors to the hypoxic stimulus, but may increase the tendency of the medullary centres to become depressed in hypoxia.     

Detection of autonomic sympathetic dysfunction in diabetic patients. A study using laser Doppler imaging

OBJECTIVE: To study signs of the disturbed reflex autonomic sympathetic nerve function in type 1 and type 2 diabetic patients. RESEARCH DESIGN AND METHODS: Measurements were made on 15 type 1 (duration 13-32 years) and on 50 recently diagnosed type 2 diabetic patients (duration 3-4 years). The vasoconstrictor responses in the distal phalanx of the middle finger (locally heated to 40 degrees C) to the cooling of the contralateral arm were measured using Laser Doppler Imaging (LDI). A vasoconstriction index (VAC) was calculated taking age into account and was compared with reference values obtained in 80 control subjects. The diabetic patients were also studied with deep-breathing tests (i.e., the heart-rate variation expressed as the expiration-to-inspiration [E/I] ratio, a test of parasympathetic nerve function). RESULTS: The vasoconstrictor responses to indirect cooling (VAC) were significantly reduced in the fingers of the diabetic patients, both type 2 (0.77 +/- 0.02 V; P < 0.01) and type 1 (0.83 +/- 0.04 V; P < 0.001), compared with the healthy control subjects (0.65 +/- 0.01); the age-corrected VAC (VACz) was slightly more impaired in type 1 than in type 2 diabetic patients. The frequency of an abnormal VACz corresponded well to the frequency of an abnormal E/I ratio in type 1 diabetic patients (approximately 50%), whereas the frequency of an abnormal VACz was significantly higher than an abnormal E/I ratio among type 2 diabetic patients (11/50 vs. 4/50; P < 0.05). CONCLUSIONS: Both type 1 and type 2 diabetic patients have impaired cutaneous blood flow regulation. The VAC index seems to be a promising tool for detection of subclinical changes in autonomic sympathetic function.     

Quantitative evaluation of diabetic autonomic neuropathy by using heart rate variations--determination of the normal range for the diagnosis of autonomic neuropathy

Heart rate (HR) variations--in supine resting position, during deep breathing and on standing--were measured in 162 healthy subjects and 168 diabetics by use of an instantaneous-HR-change continuous recorder. As indices of HR variations, the standard deviation of the HR at rest (SD of HR), the mean difference between maximal and minimal HR during deep breathing (delta I-E) and the HR increase on standing (delta HR) were determined. In healthy subjects, the values for each test declined with age and the log-transformed data fitted the linear regression. The 90% confidence limits were calculated for the normal range and the values below normal range were defined as abnormal. In diabetics, the incidence of abnormal response were 19% in the SD of HR, 38% in the delta I-E and 22% in the delta HR. The delta I-E was the most sensitive index for the autonomic neuropathy. The delta HR was considered to be able to detect the different mechanisms of neural reflexes because of the poor correlation between the delta HR and the respiratory HR variations. The present studies suggested that delta I-E and delta HR should be measured at the same time to evaluate the autonomic neuropathy.     

Cardiovascular reflex evaluation for detecting autonomic neuropathy in chronic dialysis patients

3 cardiovascular reflexes were tested in 25 patients on regular haemodialysis: measurement of the beat-to-beat variation in heart rate in the supine position and during deep breathing, measurement of heart rate response to change in posture (30:15 ratio). 8 patients (32%) had abnormal results in at least two of the tests, 3 patients (12%) had abnormal results in all 3 tests. Beat-to-beat variation was found to be the most sensitive test, the heart rate difference during deep breathing showing a direct correlation to the nerve conduction velocity of the peroneal nerve. Hence, a common cause can be postulated in the pathogenesis of the autonomic lesions and the sensorimotor polyneuropathy in the patients under investigation. Furthermore, the group with the most severe radiological calcification due to M?nckeberg's medial sclerosis had a significantly lower mean heart rate difference during deep breathing than the group with no radiological calcification. A similar correlation between autonomic neuropathy and M?nckeberg's medial sclerosis has recently been described in diabetic patients.     

The ventilatory response in severe metabolic acidosis.

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH less than 7-10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH less than 7-10 were judged to have "appropriate hypocapnia", and fifteen had "submaximal hypocapnia". Thirteen of the latter fifteen had circulatory failture and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate greater than 9 mmol/1. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.     

Clinical significance of chemosensitivity in chronic heart failure: influence on neurohormonal derangement, Cheyne-Stokes respiration and arrhythmias

Increased chemosensitivity has been observed in HF (heart failure) and, in order to clarify its pathophysiological and clinical relevance, the aim of the present study was to investigate its impact on neurohormonal balance, breathing pattern, response to exercise and arrhythmic profile. A total of 60 patients with chronic HF [age, 66+/-1 years; LVEF (left ventricular ejection fraction), 31+/-1%; values are means+/-S.E.M.] underwent assessment of HVR (hypoxic ventilatory response) and HCVR (hypercapnic ventilatory response), neurohormonal evaluation, cardiopulmonary test, 24-h ECG monitoring, and assessment of CSR (Cheyne-Stokes respiration) by diurnal and nocturnal polygraphy. A total of 60% of patients had enhanced chemosensitivity. Those with enhanced chemosensitivity to both hypoxia and hypercapnia (i.e. HVR and HCVR), compared with those with normal chemosensitivity, had significantly (all P<0.01) higher noradrenaline (norepinephrine) and BNP (B-type natriuretic peptide) levels, higher prevalence of daytime and night-time CSR, worse NYHA (New York Heart Association) class and ventilatory efficiency [higher VE (minute ventilation)/VCO(2) (carbon dioxide output) slope], and a higher incidence of chronic atrial fibrillation and paroxysmal non-sustained ventricular tachycardia, but no difference in left ventricular volumes or LVEF. A direct correlation was found between HVR or HCVR and noradrenaline (R=0.40 and R=0.37 respectively; P<0.01), BNP (R=0.40, P<0.01), N-terminal pro-BNP (R=0.37 and R=0.41 respectively, P<0.01), apnoea/hypopnoea index (R=0.57 and R=0.59 respectively, P<0.001) and VE/VCO(2) slope (R=0.42 and R=0.50 respectively, P<0.001). Finally, by multivariate analysis, HCVR was shown to be an independent predictor of both daytime and night-time CSR. In conclusion, increased chemosensitivity to hypoxia and hypercapnia, particularly when combined, is associated with neurohormonal impairment, worse ventilatory efficiency, CSR and a higher incidence of arrhythmias, and probably plays a central pathophysiological role in patients with HF.     

The R3 component of the electrically elicited blink reflex is present in patients with congenital insensitivity to pain

To clarify whether the R3 component of the electrically elicited blink reflex is a nociceptive response we studied two patients with congenital insensitivity to pain due to the impaired development of Aδ and C nerve fibers (hereditary sensory and autonomic neuropathy types III and IV). We postulated that if the R3 component is a nociceptive reflex, it should be absent in these patients. The R3 responses were elicited in both sides in both the patients at all intensities, strongly suggesting that the R3 component of the blink reflex is not a nociceptive response.     

Breathlessness during different forms of ventilatory stimulation: a study of mechanisms in normal subjects and respiratory patients

This study investigates the mechanisms underlying the perception of breathlessness induced by hypoxia and hypercapnia in both naive normal subjects and patients with respiratory mechanical problems. In normal subjects separately receiving both oscillating hypercapnic and hypoxic ventilatory stimulation, equivalent peak stimulus intensities in end-tidal gas were associated with a 'damped' ventilatory response when the frequency of stimulation was increased. A concomitant fall in peak breathlessness levels on a visual analogue scale was recorded in each case. In normal subjects and patients, the voluntary copying of a ventilatory pattern recorded during oscillating hypercapnic stimulation was associated with a marked diminution or complete absence of breathlessness despite equivalent levels of peak ventilations achieved. Voluntary copying of hypercapnic stimulated ventilation was not associated with any demonstrable change in the distribution of muscle movements between the chest wall and abdomen. These results suggest that the intensity of breathlessness depends on the level of effective reflex stimulation of the respiratory-related neurones in the medulla. They cannot be explained solely in terms of perception of afferent neural information arising from either chemoreceptors or respiratory mechanoreceptors.     

Role of blink reflex in diagnosis of subclinical cranial neuropathy in diabetic mellitus type II

BACKGROUND AND OBJECTIVES: Peripheral neuropathy (PN) is one of the late complications of diabetes mellitus. Cranial nerves III, VII, and V are among the most commonly affected in diabetic patients. Traditional electrodiagnosis (Edx) studies are a useful method for diagnosis of PN and symptomatic cranial neuropathy, and may not be useful for detecting subclinical involvement of cranial nerves. The main objective of this study is to evaluate the role of blink reflex (BR) for early diagnosis of cranial neuropathy in diabetic patients with PN. DESIGN: A prospective study was performed on NIDDM patients with PN. One hundred eighty-eight subjects were included in our study in which 142 acted as healthy subjects and 46 as diabetic patients. Patients were excluded with prior history of cranial nerve lesions, stroke, or any other disease with polyneuropathy or drug-induced neuropathy. Routine nerve conduction studies were performed, and only patients with PN were included in this study. RESULTS: Abnormalities were found in 54.4% of patients. R1, IR2, and CR2 were prolonged relative to the healthy group. Statistically there was no significant difference in R/D ratio of patients (P=0.201). Also, there was a positive correlation between R1, IR2, and CR2 latencies with duration of diabetes and severity of polyneuropathy, but not for R/D. The greatest correlation was shown in R1 latency (69.9% abnormality). CONCLUSION: BR is a noninvasive and very useful method for the evaluation and diagnosis of subclinical cranial nerve involvement in diabetic patients.     

Baroreceptor reflex is suppressed in rats that develop hyperalgesia behavior after nerve injury

The baroreceptor reflex buffers autonomic changes by decreasing sympathetic activity and increasing vagal activity in response to blood pressure elevations, and by the reverse actions when the blood pressure falls. Because of the many bidirectional interactions of pain and autonomic function, we investigated the effect of painful nerve injury by spinal nerve ligation (SNL) on heart rate (HR), blood pressure (BP) and their regulation by the baroreceptor reflex. Rats receiving SNL were separated into either a hyperalgesic group that developed sustained lifting, shaking and grooming of the foot after plantar punctate nociceptive stimulation by pin touch or a group of animals that failed to show this hyperalgesic behavior after SNL. SNL produced no effect on resting BP recorded telemetrically in unrestrained rats compared to control rats receiving either skin incision or sham SNL. However, two tests of baroreceptor gain showed depression only in animals that developed sustained hyperalgesia after SNL. The animals that failed to develop hyperalgesia after SNL were found to have elevations in HR both before and for the first 4 days after SNL, and HR variability analysis gave indications of decreased vagal control of resting HR and elevated sympatho-vagal balance at these same time intervals. In human patients, other research has shown that blunted baroreceptor reflex sensitivity predicts poor outcome during conditions such as hypertension, congestive heart failure, myocardial infarction, and stroke. If baroreceptor reflex suppression is also found in human subjects during chronic neuropathic pain, this may adversely affect survival.     

中枢传导时间在糖尿病中枢神经病中的意义

目的 测定糖尿病患者的中枢传导时间以观察糖尿病患者中枢神经病变以及糖尿病中枢神经病变与周围神经病变的关系.方法 对86例糖尿病患者进行躯体感觉诱发电位检查,并获得中枢传导时间（CCT）：N11-N20峰间期;对86例患者进行神经传导检查,并据此分为周围神经传导正常组、周围神经传导检查异常组,并将两组CCT进行比较.结果 糖尿病患者CCT 8.1 7±1.10ms,与正常人CCT 7.70ms比较,P〈0.01,差异具有显著性;周围神经传导正常组103例与周围神经传导异常组64例CCT进行比较,P〉0.05,差异无统计学意义.结论 糖尿病患者可出现中枢神经系统病变,且其发生与周围神经病变不全相关.     

Reflex sweating in patients with spinal cord injury: a review.

Sweat glands derive their innervation from the sympathetic nervous system. The spinal sympathetic structures that are located in the intermediolateral areas extend from T1-L2 segments and are under the control of hypothalamic centers. Cord transection abolishes the supraspinal control of sudorimotor function. Since sympathetic innervation does not follow a clear segmental distribution, normal sweating may be preserved at a higher or lower level than skin sensation. Nonthermoregulatory reflex sweating is an indication of unchecked spinal cord facilitation and is precipitated by afferent stimuli from bladder, rectum, and various other sources. It is usually a manifestation of mass reflex or autonomic crisis and occurs particularly in cervical or high thoracic lesions. Transection below T8-T10 is not accompanied by reflex sweating. The phenomenon of thermal relfex sweating is controversial. Although some aspects of nonthermoregulatory reflex sweating are still unclear, proper immediate and continuing preventive management will reduce the incidence of this and other autonomic manifestations. Chemical sympathectomy should be a last resort in case of emergency or when the source of facilitation cannot be ascertained.     

Suppression of heart rate variability after supramaximal exertion

Wingate test is short anaerobic exercise, performed with maximal power, whereas aerobic exercise at 85% maximal heart rate (HR(max)) may be performed for long period. Sustained HR elevations and changes in autonomic activity indices have been observed after latter kind of exercise. Several studies reported reduction in mean interval between consecutive R peaks in ECG (RRI) 1 h after Wingate test; however, underlying changes in autonomic activity remain elusive. In eight young males, RRI and heart rate variability (HRV) were measured daily over two 5-day trials. Subjects exercised on third day of each trial, measurements were taken 1 h after (i) two consecutive 30-s bouts of Wingate tests or (ii) after a 30-min exercise at 85% HR(max), with subjects in supine rest and breathing either spontaneously or at controlled rates of 6 and 15 breaths / min. RRI was significantly shorter after Wingate and submaximal exercise, reduction of high- and low-frequency components of HRV attained reliability only after Wingate tests. This pattern remained preserved for three modes of breathing: spontaneous, 6 and 15 breaths /min. After 24 and 48 h, no exercise effects were traceable. We hypothesize that (i) anaerobic exertion is followed by sustained inhibition of vagal activity, (ii) parasympathetic system plays dominant role in mediating suppression of high- and low-HRV frequency components during postexercise recovery, (iii) degree of alteration of autonomic activity caused by anaerobic and strenuous aerobic exercise may be similar and (iv) normalization of vagal activity precedes normalization of sympathetic cardiac nerves activity during final stage of postexercise recovery.