Chronic But Not Acute Oral L-Arginine Supplementation Delays the Ventilatory Threshold During Exercise in Heart Failure Patients

2005 ◽  
Vol 30 (4) ◽  
pp. 419-432 ◽  
Author(s):  
Stéphane Doutreleau ◽  
Bertrand Mettauer ◽  
François Piquard ◽  
Adrien Schaefer ◽  
Evelyne Lonsdorfer ◽  
...  

The purpose of this study was to determine, in heart failure patients (HF), whether acute or chronic L-arginine supplementation (LAS) might delay the ventilatory threshold (VT) and whether chronic LAS might reduce exercise-induced plasma lactate increase. HF patients undertook 4 cardiopulmonary bicycle exercises tests. The first 3 were maximal without (EX1), after acute (EX2), or chronic (EX3) oral LAS (6 gm twice a day for 6 weeks). The 4th test (EX4), performed after chronic LAS, was similar to the first in order to investigate the effect of chronic LAS on circulating lactate levels. Results showed that acute LAS failed to improve both submaximal and maximal exercise capacities. Similarly, maximal exercise capacity remained unmodified after chronic LAS. Nevertheless, chronic LAS delayed significantly the patients' ventilatory threshold. Thus exercise duration prior to VT increased (mean ± SEM) from 6.04 ± 0.9 to 7.7 ± 1.03 min (p = 0.04), resulting in a significant increase in oxygen uptake (1.05 ± 0.08 to 1.24 ± 0.12 L•min−1; p = 0.03), CO2 release (0.94 ± 0.10 to 1.2 ± 0.12 L•min−1; p = 0.018), minute ventilation (29.31 ± 2.8 to 34.5 ± 2.7 L; p = 0.009), and workload (60.7 ± 9.8 to 78.5 ± 10.2 watts; p = 0.034). Furthermore, chronic LAS significantly reduced the exercise-induced increase in postexercise plasma lactate concentration (−21 ± 7%). In conclusion, unlike acute supplementation, chronic LAS significantly delays the ventilatory threshold, and chronic LAS reduces circulating plasma lactate in HF patients. These data suggest that chronic LAS might improve the ability of HF patients to perform their daily-life activities. Key words: maximal exercise, heart device, vasodilator

1986 ◽  
Vol 60 (3) ◽  
pp. 777-781 ◽  
Author(s):  
J. Simon ◽  
J. L. Young ◽  
D. K. Blood ◽  
K. R. Segal ◽  
R. B. Case ◽  
...  

Six trained male cyclists and six untrained sedentary men were studied to determine whether the plasma lactate threshold (PLT) and ventilation threshold (VT) occur at the same work rate in both fit and unfit populations. The PLT was determined from a marked increase in plasma lactate concentration ([La]) and VT from a nonlinear increase in expired minute ventilation (VE) during incremental leg-cycling tests; work rate was increased 30 W every 2 min until volitional exhaustion. The trained subjects' mean VO2 max (63.8 ml O2 X kg-1 X min-1) and VT (65.8% VO2 max) were significantly higher (P less than 0.05) than the untrained subjects' mean VO2max (35.5 ml O2 X kg-1 X min-1) and VT (51.4% VO2 max). The trained subjects' mean PLT (68.8% VO2 max) and VT did not differ significantly, but the untrained subjects' mean PLT (61.6% VO2 max) was significantly higher than their VT. The trained subjects' mean peak [La] (10.5 mmol X l-1) did not differ significantly from the untrained subjects' mean peak [La] (11.5 mmol X l-1). However, the time of appearance of the peak [La] during passive recovery was inversely related to VO2 max. These results suggest that variance in lactate diffusion and/or removal processes between the trained and untrained subjects may account in part for the different relationships between the VT and PLT in each population.


1997 ◽  
Vol 82 (3) ◽  
pp. 746-754 ◽  
Author(s):  
T. G. Babb

Babb, T. G. Ventilatory response to exercise in subjects breathing CO2 or HeO2. J. Appl. Physiol. 82(3): 746–754, 1997.—To investigate the effects of mechanical ventilatory limitation on the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycle ergometry to exhaustion once while breathing room air; once while breathing 3% CO2-21% O2-balance N2; and once while breathing HeO2 (79% He and 21% O2). Minute ventilation (V˙e) and respiratory mechanics were measured continuously during each 1-min increment in work rate (10 or 20 W). Data were analyzed at rest, at ventilatory threshold (VTh), and at maximal exercise. When the subjects were breathing 3% CO2, there was an increase ( P < 0.001) inV˙e at rest and at VTh but not during maximal exercise. When the subjects were breathing HeO2,V˙e was increased ( P < 0.05) only during maximal exercise (24 ± 11%). The ventilatory response to exercise below VTh was greater only when the subjects were breathing 3% CO2( P < 0.05). Above VTh, the ventilatory response when the subjects were breathing HeO2 was greater than when breathing 3% CO2( P < 0.01). Flow limitation, as percent of tidal volume, during maximal exercise was greater ( P < 0.01) when the subjects were breathing CO2 (22 ± 12%) than when breathing room air (12 ± 9%) or when breathing HeO2 (10 ± 7%) ( n = 7). End-expiratory lung volume during maximal exercise was lower when the subjects were breathing HeO2 than when breathing room air or when breathing CO2( P < 0.01). These data indicate that older subjects have little reserve for accommodating an increase in ventilatory demand and suggest that mechanical ventilatory constraints influence both the magnitude of V˙eduring maximal exercise and the regulation ofV˙e and respiratory mechanics during heavy-to-maximal exercise.


2000 ◽  
Vol 89 (6) ◽  
pp. 2147-2157 ◽  
Author(s):  
G. D. Pinna ◽  
R. Maestri ◽  
A. Mortara ◽  
M. T. La Rovere ◽  
F. Fanfulla ◽  
...  

In this study, we applied time- and frequency-domain signal processing techniques to the analysis of respiratory and arterial O2 saturation (SaO2 ) oscillations during nonapneic periodic breathing (PB) in 37 supine awake chronic heart failure patients. O2 was administered to eight of them at 3 l/min. Instantaneous tidal volume and instantaneous minute ventilation (IMV) signals were obtained from the lung volume signal. The main objectives were to verify 1) whether the timing relationship between IMV and SaO2 was consistent with modeling predictions derived from the instability hypothesis of PB and 2) whether O2 administration, by decreasing loop gain and increasing O2 stores, would have increased system stability reducing or abolishing the ventilatory oscillation. PB was centered around 0.021 Hz, whereas respiratory rate was centered around 0.33 Hz and was almost stable between hyperventilation and hypopnea. The average phase shift between IMV and SaO2 at the PB frequency was 205° (95% confidence interval 198–212°). In 12 of 37 patients in whom we measured the pure circulatory delay, the predicted lung-to-ear delay was 28.8 ± 5.2 s and the corresponding observed delay was 30.9 ± 8.8 s ( P = 0.13). In seven of eight patients, O2 administration abolished PB (in the eighth patient, SaO2 did not increase). These results show a remarkable consistency between theoretical expectations derived from the instability hypothesis and experimental observations and clearly indicate that a condition of loss of stability in the chemical feedback control of ventilation might play a determinant role in the genesis of PB in awake chronic heart failure patients.


1997 ◽  
Vol 29 (Supplement) ◽  
pp. 269
Author(s):  
M. S. Feigenbaum ◽  
M. A. Welsch ◽  
R. W. Braith ◽  
M. K. Worley ◽  
M. L. Pollock ◽  
...  

2006 ◽  
Vol 27 (7) ◽  
pp. 567-572 ◽  
Author(s):  
S. Doutreleau ◽  
B. Mettauer ◽  
F. Piquard ◽  
O. Rouyer ◽  
A. Schaefer ◽  
...  

1992 ◽  
Vol 73 (1) ◽  
pp. 362-367 ◽  
Author(s):  
C. C. Hsia ◽  
L. F. Herazo ◽  
R. L. Johnson

Maximal exercise performance was evaluated in four adult foxhounds after right pneumonectomy (removal of 58% of lung) and compared with that in seven sham-operated control dogs 6 mo after surgery. Maximal O2 uptake (ml O2.min-1.kg-1) was 142.9 +/- 1.9 in the sham group and 123.0 +/- 3.8 in the pneumonectomy group, a reduction of 14% (P less than 0.001). Maximal stroke volume (ml/kg) was 2.59 +/- 0.10 in the sham group and 1.99 +/- 0.05 in the pneumonectomy group, a reduction of 23% (P less than 0.005). Lung diffusing capacity (DL(CO)) (ml.min-1.Torr-1.kg-1) reached 2.27 +/- 0.08 in the combined lungs of the sham group and 1.67 +/- 0.07 in the remaining lung of the pneumonectomy group (P less than 0.001). In the pneumonectomy group, DL(CO) of the left lung was 76% greater than that in the left lung of controls. Blood lactate concentration and hematocrit were significantly higher at exercise in the pneumonectomy group. We conclude that, in dogs after resection of 58% of lung, O2 uptake, cardiac output, stroke volume, and DL(CO) at maximal exercise were restricted. However, the magnitude of overall impairment was surprisingly small, indicating a remarkable ability to compensate for the loss of one lung. This compensation was achieved through the recruitment of reserves in DL(CO) in the remaining lung, the development of exercise-induced polycythemia, and the maintenance of a relatively large stroke volume in the face of an increased pulmonary vascular resistance.


1986 ◽  
Vol 18 (supplement) ◽  
pp. S85 ◽  
Author(s):  
M. Cecca ◽  
D. MacDougall ◽  
N. Tsunoda ◽  
F. O??Hagan

1986 ◽  
Vol 18 (supplement) ◽  
pp. S12 ◽  
Author(s):  
L. S. Goodman ◽  
M. B. Walters ◽  
F. Holmvang ◽  
D. C. McKenzie

2020 ◽  
Vol 16 (4) ◽  
pp. 253-258
Author(s):  
Y. Kitaoka ◽  
K. Mukai ◽  
K. Takahashi ◽  
H. Ohmura ◽  
H. Hatta

The aim of this study was to examine the effects of lactate administration on the mRNA response of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) to acute exercise in Thoroughbred skeletal muscle. Five Thoroughbred horses performed treadmill running at 90% of maximal oxygen consumption for 2 min on two separate occasions, either after the administration of two litres of a sodium lactate solution (LAC; 500 mmol/l sodium lactate in 0.9% NaCl) or a saline solution as a control (CON; 0.9% NaCl). Lactate administration significantly elevated the peak plasma lactate concentration during exercise (16.0±2.8 mmol/l in LAC vs 10.8±2.2 mmol/l in CON). The increase in PGC-1α mRNA expression after 4 h of recovery from exercise was similar between treatments. However, there was positive correlation between exercise-induced PGC-1α mRNA response at 4 h after exercise and peak plasma lactate concentration during exercise. These results suggest that the exercise intensity-dependent adaptation of PGC-1α may be attributed, at least in part, to an increased lactate concentration.


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