Alterations in atrial natriuretic peptide gene expression during endurance training in rats.

Spontaneous and experimental rises of intracardiac pressure and/or volume increase the level of atrial natriuretic (ANP) mRNA in rat atrial tissue. There is expanding evidence that ANP synthesis is increased in the ventricle under such conditions. However, little is known with regard to the myocardial ANP synthesis response to physical training. In this study, plasma and atrial immunoreactive ANP concentrations were measured in Sprague-Dawley rats trained on a treadmill and compared to sedentary controls. Atrial natriuretic peptide mRNA was detected in the heart cavities of each group by dot-blot hybridization analysis. Physical training reduced the mean immunoreactive ANP plasma levels from 405 +/- 99 to 303 +/- 45 ng/l (p < 0.05). Immunoreactive ANP in the left atrium was depleted after endurance training, while immunoreactive ANP concentration in the right atrium was unaffected. Physical training resulted in a 70% (p < 0.01) rise in ANP mRNA of the right atrium, while no changes in the other compartments were found. These data indicate that during physical training: ANP mRNA does not increase in ventricles; despite depletion of immunoreactive ANP in the left atrium, no corresponding changes of ANP mRNA are detected; and ANP mRNA increases in the right atrium while its immunoreactive ANP does not. These findings suggest that during chronic exercise the ratio between immunoreactive ANP and ANP gene expression in the atria may be altered.

The spatial integration effect of surface electrode detecting myoelectric signal.

The spectral properties of surface electrodes used for myoelectric signal detection were investigated using both a theoretical and an experimental approach. On the basis of the theoretical model, the single surface electrode was found to act as a low pass filter depending on the electrode diameter (d) and the fiber conduction velocities (CV). Several dips in the power spectrum were also predicted for varying frequencies depending on d and CV. The mathematical expression of the surface electrode filter was highly consistent with previously demonstrated properties of the single fiber power spectrum. An experimental comparison between myoelectric signals from the vastus lateralis muscle recorded using two electrode pairs with different diameters confirmed this low pass filter effect. However, the dip phenomenon was not observed from experimental data. The practical consequences of the electrode filter effect are discussed with respect to the interpretation of changes in surface myoelectric signal spectrum, particularly when a shift toward the high frequencies is observed.

Myoelectrical and metabolic changes in muscle fatigue.

In isometric contraction-induced fatigue force loss has been related to mostly myoelectrical or intramuscular events. However, some factors potentially involved may interfere at more than one site in these events and it has proven difficult to distinguish between those influences. The study of the relationships between force generating capacity, the metabolic state of a muscle and its myoelectrical properties may therefore help broaden our understanding of the fatigue process. In order to investigate these relationships, we have evaluated changes in force-generating capacity, NMR-determined metabolic variables, and myoelectrical activity, as measured from surface EMG, simultaneously in brachial biceps muscle of healthy subjects, during different types of fatiguing isometric exercise and during recovery. Factors studied include intramuscular pH, inorganic phosphate and its diprotonated form concentrations, root-mean square and mean power frequency of the EMG power spectrum, and neuromuscular efficiency index. Results show that different mechanisms are likely to contribute to force loss in fatiguing muscle and during different phases of recovery from fatigue. Indeed, relationships between variables from the three groups differed according to exercise protocol as well as in fatiguing and recovering muscle.

EMG spectral shift- and 31P-NMR-determined intracellular pH in fatigued human biceps brachii muscle.

We have simultaneously recorded human biceps brachii intracellular pH, estimated by 31P-NMR, and EMG spectral shift, during isometric contraction and recovery in six subjects. This method allows us to concurrently study several components of muscle fatigue. The results show a clear dissociation between the recovery of intracellular pH, force-generating capacity, and the shift to low frequency of the EMG power spectrum induced by fatiguing exercise.

Saliva flow and composition in humans exposed to acute altitude hypoxia.

The effects of acute hypoxia (2 days at 4350 m) on whole saliva flow and composition were studied on 12 sea-level natives, at rest and following a maximal exercise. Exercise, performed in normoxia and hypoxia, did not induce variations in saliva flow rate, saliva potassium or alpha-amylase concentrations. In contrast, acute hypoxia did lead to an increase in mean saliva flow rate both at rest (0.63 ml.min-1 to 0.93 ml.min-1, P less than 0.01) and after exercise (0.56 ml.min-1 to 1.06 ml.min-1, P less than 0.05) and a decrease in mean saliva potassium concentration at rest (20.8 mmol.l-1 to 14.7 mmol.l-1, P less than 0.01) as well as after exercise (21.7 mmol.l-1 to 16.5 mmol.l-1, P less than 0.05). This effect might be the consequence of a hypoxia-induced stimulation of the parasympathetic nervous system.

Hormonal and metabolic changes during exercise in cirrhotic patients.

The metabolic response to exercise was compared in 10 cirrhotic patients (P) in a stable clinical condition and in 6 sedentary, age-matched, normal subjects (C) performing 32 minutes of treadmill exercise with the same constant workload corresponding to three to four times their resting oxygen uptake. Taking indirect calorimetry as reference, respiratory exchanges indicated that cirrhotic patients consumed carbohydrates almost exclusively, unlike the normal controls, who consumed lipids and glucids in about the same proportions (RQ: 0.98 +/- 0.04 v 0.87 +/- 0.04, P less than .0001). In the patients, this carbohydrate path of exercise metabolism lowered glycemia from the resting value of 5.23 +/- 0.16 mmol/L to 4.03 +/- 0.37 mmol/L (P less than .0001) and raised the plasma lactate concentration from 2.08 +/- 0.24 mmol/L at rest to 3.48 +/- 0.32 mmol/L at the eighth minute of exercise (P less than .001), thus suggesting defective liver glyconeogenesis. Fatty free acids and glycerol remained almost constant during exercise, whereas catecholamines increased. Insulin levels were high in patients at rest (67.1 +/- 14.5 U/mL v 15.1 +/- 3.5 U/mL); they declined sharply at the onset of exercise but nevertheless remained high compared to those observed in the controls (P less than .0001). Glucagon increased in exercising patients from 88.3 +/- 21.3 pg/mL to 127.4 +/- 30.6 pg/mL (NS). Esterified plasma carnitine declined in the patients from 13.0 +/- 2.2 mumol/L to 8.6 +/- 1.5 mumol/L (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sustained exercise on pulmonary clearance of aerosolized 99mTc-DTPA.

The effects of intensive prolonged exercise on the pulmonary clearance rate of aerosolized 99mTc-labeled diethylenetriaminepentaacetate (99mTc-DTPA) and pulmonary mechanics were studied in seven healthy nonsmoking volunteers. 99mTc-DTPA clearance and pulmonary mechanics (lung volumes and compliance) were assessed before and after 75 min of constant-load exercise performed on a treadmill, corresponding to 75% of maximal O2 uptake. Because both clearance measurements were made in similar conditions of pulmonary blood flow, respiratory rate, and tidal volume, changes in clearance rate can be assumed to represent changes of alveolar epithelial permeability. After exercise, total, apical, and basal clearance were significantly increased (P less than 0.01, 0.05, and 0.05, respectively) and the increases in total clearance and tidal volume observed during exercise were significantly correlated (P less than 0.05). In contrast, no significant change was found in pulmonary mechanics. These results show that prolonged intensive exercise induces an increase in epithelial permeability, which appears to be related to the mechanical effects of sustained increased ventilation. Because no change was evidenced in pulmonary volumes or in lung elasticity, our results suggest that this increase may result from alteration of the intercellular tight junctions rather than from a surfactant deficiency.

Surface EMG power spectrum and intramuscular pH in human vastus lateralis muscle during dynamic exercise.

The relationship between intramuscular pH and the frequency components of the surface electromyographic (EMG) power spectrum from the vastus lateralis muscle was studied in eight healthy male subjects during brief dynamic exercise. The studies were carried out in placebo control and metabolic alkalosis induced by oral administration of NaHCO3. At the onset of exercise, blood pH was 0.08 units higher in alkalosis compared with placebo. Muscle lactate accumulation during exercise was higher in alkalosis (32 +/- 5 mmol/kg wet wt) than in placebo (17 +/- 4 mmol/kg wet wt), but no difference in intramuscular pH was found between the two conditions. The EMG power spectrum was shifted toward lower frequencies during fatigue in the control condition (10.1 +/- 0.9%), and these spectral shifts, evaluated from changes in the mean power frequency (MPF) of the EMG power spectrum, were further accentuated in alkalosis (19 +/- 2%). Although the changes in frequency components of EMG correlated with muscle lactate accumulation (r = 0.68, P less than 0.01), no direct relationship with muscle pH was observed. We conclude that alkalosis results in a greater reduction in MPF associated with a higher muscle lactate accumulation. However, the good correlation observed between the two variables is not likely causative, and a dissociation between intramuscular pH and the increase in the low-frequency content of EMG power spectrum appears during muscle fatigue.

Effects of propranolol and pindolol on plasma ANP levels in humans at rest and during exercise.

In attempt to elucidate whether the beta-adrenoceptor is involved in the control of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP level was measured at rest, in recumbent and upright positions, and during graded maximal ergocycle exercise in nine healthy male subjects (23 +/- 0.5 years of age) treated for 3 days with nonselective beta-blockers propranolol (150 mg/day) or pindolol (15 mg/day) or with placebo. The effects of beta-blockers, which differ by their hemodynamic actions at rest because of the intrinsic sympathomimetic activity of pindolol, were compared. Maximal O2 consumption (VO2max) during beta-blockade was not significantly different from the placebo value. Resting heart rate was not affected by pindolol treatment but was decreased with propranolol (-10 beats/min). Both beta-blockers caused a reduction in heart rate at all the exercise intensities. Mean blood pressure was not affected by beta-blockade at rest but was significantly reduced during exercise. During placebo treatment, plasma ANP increased in response to exercise intensities greater than 65% of VO2max. At 100% VO2max plasma ANP was nearly doubled (101.5 +/- 14 pg/ml) compared with the basal value in upright position (56.6 +/- 15 pg/ml). beta-Blockade caused a marked elevation in plasma ANP at all the levels of activity. Despite different hemodynamic responses to pindolol and propranolol, both beta-blockers produced similar increases in the basal level of plasma ANP. These rises were maintained in the course of exercise tests, and no significant difference was found between propranolol and pindolol. We conclude that beta-adrenoceptor mechanisms are not directly responsible for tonic and exercise-induced ANP secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of hypoxia-induced decrease in human cardiac response to isoproterenol infusion.

A decrease in heart rate response to isoproterenol (IP) infusion has been previously described in humans exposed to acute (2-3 days) or chronic (21 days) exposure to altitude hypoxia (J. Appl. Physiol. 65: 1957-1961, 1988). To evaluate this cardiac response in subacute (8 days) hypoxia and to explore its reversal with restoration of normoxia, six subjects received an IP infusion under normoxia (condition N), after 8 days in altitude (4,350 m, condition H8), on the same day in altitude after inhalation of O2 restoring normoxic arterial O2 saturation (SaO2, condition HO), and 6-11 h (condition RN) and 4-5 mo (condition ND) after the return to sea level. Cardiac chronotropic response to IP, evaluated by the mean increase in heart rate from base value (delta HR, min-1), was lower in condition H8 [mean 30 +/- 13 (SD)] than in condition N (50 +/- 14, P less than 0.03); it was slightly higher in condition HO (38 +/- 14) or condition RN (42 +/- 15) than condition H8 but still significantly different from condition N (P less than 0.03), despite normal values of SaO2. delta HR in condition ND (55 +/- 10) returned to base N value. These findings confirm the hypothesis of a hypoxia-induced decrease in cardiac chronotropic function. Two possible mechanisms are suggested: an O2-dependent one, rapidly reversible with recent restoration of normoxia, and a more slowly reversible mechanism, probably a downregulation of the cardiac beta-receptors.

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude.

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.

[Effect of beta-adrenergic receptors blockade on auricular natriuretic factor, aldosterone and renine blood activity during physical exercise]. / Effet du blocage des récepteurs beta-adrénergiques sur le facteur natriurétique auriculaire, l'aldostérone et l'activité rénine plasmatique, au cours d'un exercise physique.

Physical exercise stimulates the renin-angiotensin-aldosterone system. However several factors affect the control of mineralocorticoid secretion. In this study, eight healthy volunteers performed maximal exercise on cycle ergometer after being pretreated for 3 days with placebo (P) or with a non selective beta-blocker (B) (pindolol 15 mg/day). Plasma reinin activity (PRA), aldosterone (ALD), atrial natriuretic factor (ANF), and kalemia (K+) were measured at rest (R) and during exercise until exhaustion (E). (table; see text) These results confirm the role of beta-adrenoceptor activation in the increased PRA during exercise. It appears an exercise-induced increase in plasma ANF which was more elevated in subjects treated with pindolol, but which had no inhibitory effect on ALD secretion in theses conditions. K+ rose during exercise and this hyperkalemia tended to be higher with a beta-blocker. It is suggested that K+ elevation counterbalance both PRA decrease and ANF increase to be responsible for the absence of change in plasma ALD during beta-blockade.