scholarly journals Ventilatory response to exercise in subjects breathing CO2 or HeO2

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.

2014 ◽  
Vol 9 ◽  
Author(s):  
Adriano Di Paco ◽  
Giosuè A. Catapano ◽  
Guido Vagheggini ◽  
Stefano Mazzoleni ◽  
Matteo Levi Micheli ◽  
...  

Background: The purpose of this study was to evaluate the role of ventilatory parameters in maximal exercise performance in elite soccer players. Methods: From September 2009 to December 2012, 90 elite soccer players underwent evaluation of lung function test and ergospirometry by means of an incremental symptom-limited treadmill test. Results were analyzed according to i) maximal exercise velocity performed (Hi-M: high-performers, >18.65 km/h; Lo-M: low-performers, <18.65 km/h) and ii) usual role in the team. Results: Hi-M showed higher peak minute ventilation (V_ Epeak: 158.3 ± 19.5 vs 148.0 ± 18.54 L/min, p = 0.0203), and forced expiratory volume at first second (5.28 ± 0.50 vs 4.89 ± 0.52 liters, p < 0.001) than Lo-M, independently of playing role. Moreover, a significant correlation between peak oxygen uptake and V_ E (r = 0.57, p < 0.001) was found. Conclusions: Ventilatory response plays a role in the assessment of exercise capacity in elite soccer players.


1988 ◽  
Vol 74 (3) ◽  
pp. 275-281 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
A. Guz

1. The ventilatory response to maximal incremental exercise and the accompanying sensation of breathlessness were studied after the inhalation of 0.9% sodium chloride (saline) and 5% bupivacaine aerosols in six patients with interstitial lung disease. 2. The adequacy of airway anaesthesia induced by bupivacaine aerosol was confirmed by the absence of the cough reflex to 5% citric acid aerosol on completion of exercise. 3. All subjects first performed a trial exercise test to familiarize them with the procedure and to assess the degree of arterial oxygen desaturation on exercise. In subsequent tests, supplementary oxygen was given to maintain the saturation at 95% or above. 4. Airway anaesthesia had no effect on the ability to perform exercise as assessed by maximum workload, CO2 production or heart rate. No significant changes were seen on the pattern of breathing, minute ventilation or endtidal Pco2 on exercise. There was, however, a small but statistically significant increase in ventilation related to CO2 production (VE/Vco2) at the end of exercise. 5. There was a tendency for breathlessness to be increased by airway anaesthesia but this did not reach statistical significance. 6. These results provide no evidence that vagal afferent activity is responsible for the abnormal ventilatory response to exercise in patients with interstitial lung disease. The perception of breathlessness in these patients was not diminished by anaesthesia of the airway.


1996 ◽  
Vol 81 (5) ◽  
pp. 1978-1986 ◽  
Author(s):  
C. Tantucci ◽  
P. Bottini ◽  
M. L. Dottorini ◽  
E. Puxeddu ◽  
G. Casucci ◽  
...  

Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response to exercise in diabetic subjects with autonomic neuropathy. J. Appl. Physiol. 81(5): 1978–1986, 1996.—We have used diabetic autonomic neuropathy as a model of chronic pulmonary denervation to study the ventilatory response to incremental exercise in 20 diabetic subjects, 10 with (Dan+) and 10 without (Dan−) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan− subjects achieved lower O2 consumption and CO2 production (V˙co 2) than control subjects at peak of exercise, they attained similar values of either minute ventilation (V˙e) or adjusted ventilation (V˙e/maximal voluntary ventilation). The increment of respiratory rate with increasing adjusted ventilation was much higher in Dan+ than in Dan− and control subjects ( P < 0.05). The slope of the linearV˙e/V˙co 2relationship was 0.032 ± 0.002, 0.027 ± 0.001 ( P < 0.05), and 0.025 ± 0.001 ( P < 0.001) ml/min in Dan+, Dan−, and control subjects, respectively. Both neuromuscular and ventilatory outputs in relation to increasingV˙co 2 were progressively higher in Dan+ than in Dan− and control subjects. At peak of exercise, end-tidal [Formula: see text] was much lower in Dan+ (35.9 ± 1.6 Torr) than in Dan− (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects. We conclude that pulmonary autonomic denervation affects ventilatory response to stressful exercise by excessively increasing respiratory rate and alveolar ventilation. Reduced neural inhibitory modulation from sympathetic pulmonary afferents and/or increased chemosensitivity may be responsible for the higher inspiratory output.


1997 ◽  
Vol 83 (1) ◽  
pp. 312-316 ◽  
Author(s):  
J. S. Williams ◽  
T. G. Babb

Williams, J. S., and T. G. Babb. Differences between estimates and measured [Formula: see text] during rest and exercise in older subjects. J. Appl. Physiol. 83(1): 312–316, 1997.—Arterial[Formula: see text]([Formula: see text]) has been estimated during exercise with good accuracy in younger individuals by using the Jones equation (PJ co 2) ( J. Appl. Physiol. 47: 954–960, 1979). The purpose of this project was to determine the utility of estimating [Formula: see text] from end-tidal[Formula: see text]([Formula: see text]) or PJ co 2at rest, ventilatory threshold (V˙Th), and maximal exercise (Max) in older subjects.[Formula: see text] was determined from respired gases simultaneously (MGA 1100) with arterial blood gases (radial arterial catheter) in 12 older and 11 younger subjects at rest and during exercise. Mean differences were analyzed with paired t-tests, and relationships between the estimated [Formula: see text] values and the actual values of [Formula: see text] were determined with correlation coefficients. In the older subjects,[Formula: see text] was not significantly different from [Formula: see text] at rest (−1.2 ± 4.3 Torr), V˙Th (0.4 ± 2.5), or Max (−0.8 ± 2.7), and the two were significantly ( P < 0.05) correlated atV˙th ( r = 0.84) and Max ( r = 0.87) but not at rest ( r = 0.47). PJ co 2was similar to [Formula: see text] at rest (−1.0 ± 3.9) and V˙th (−1.3 ± 2.3) but significantly lower at Max (−3.0 ± 2.6), and the two were significantly correlated at V˙th ( r = 0.86) and Max ( r = 0.80) but not at rest ( r = 0.54).[Formula: see text] was significantly higher than [Formula: see text] during exercise in the younger subjects but similar to [Formula: see text] at rest. PJ co 2was similar to [Formula: see text] at rest andV˙th but significantly lower at Max in younger subjects. In conclusion, our data demonstrate that[Formula: see text] during exercise is better estimated by [Formula: see text] than by PJ co 2in older subjects, contrary to what is observed in younger subjects. This appears to be related to the finding that[Formula: see text] does not exceed[Formula: see text] during exercise in older subjects, as occurs in the younger subjects. However,[Formula: see text] at rest is best estimated by PJ co 2in both younger and older subjects.


1975 ◽  
Vol 38 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
L. J. Folinsbee ◽  
F. Silverman ◽  
R. J. Shephard

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.


1991 ◽  
Vol 70 (1) ◽  
pp. 223-230 ◽  
Author(s):  
T. G. Babb ◽  
R. Viggiano ◽  
B. Hurley ◽  
B. Staats ◽  
J. R. Rodarte

To determine the effect of mild-to-moderate airflow limitation on exercise tolerance and end-expiratory lung volume (EELV), we studied 9 control subjects with normal pulmonary function [forced expired volume in 1 s (FEV1) 105% pred; % of forced vital capacity expired in 1 s (FEV1/FVC%) 81] and 12 patients with mild-to-moderate airflow limitation (FEV1 72% pred; FEV1/FVC % 58) during progressive cycle ergometry. Maximal exercise capacity was reduced in patients [69% of pred maximal O2 uptake (VO2max)] compared with controls (104% pred VO2max, P less than 0.01); however, maximal expired minute ventilation-to-maximum voluntary ventilation ratio and maximal heart rate were not significantly different between controls and patients. Overall, there was a close relationship between VO2max and FEV1 (r2 = 0.62). Resting EELV was similar between controls and patients [53% of total lung capacity (TLC)], but at maximal exercise the controls decreased EELV to 45% of TLC (P less than 0.01), whereas the patients increased EELV to 58% of TLC (P less than 0.05). Overall, EELV was significantly correlated to both VO2max (r = -0.71, P less than 0.001) and FEV1 (r = -0.68, P less than 0.001). This relationship suggests a ventilatory influence on exercise capacity; however, the increased EELV and associated pleural pressures could influence cardiovascular function during exercise. We suggest that the increase in EELV should be considered a response reflective of the effect of airflow limitation on the ventilatory response to exercise.


1984 ◽  
Vol 56 (5) ◽  
pp. 1143-1150 ◽  
Author(s):  
M. J. Brischetto ◽  
R. P. Millman ◽  
D. D. Peterson ◽  
D. A. Silage ◽  
A. I. Pack

Studies were performed to determine the effects of aging on the ventilatory responsiveness to two known respiratory stimulants, inhaled CO2 and exercise. Although explanation of the physiological mechanisms underlying development of exercise hyperpnea remains elusive, there is much circumstantial evidence that during exercise, however mediated, ventilation is coupled to CO2 production. Thus matched groups of young and elderly subjects were studied to determine the relationship between increasing ventilation and increasing CO2 production (VCO2) during steady-state exercise and the change in their minute ventilation in response to progressive hypercapnia during CO2 rebreathing. We found that the slope of the ventilatory response to hypercapnia was depressed in elderly subjects when compared with the younger control group (delta VE/delta PCO2 = 1.64 +/- 0.21 vs. 2.44 +/- 0.40 l X min-1 X mmHg-1, means +/- SE, respectively). In contrast, the slope of the relationship between ventilation and CO2 production during exercise in the elderly was greater than that of younger subjects (delta VE/delta VCO2 = 29.7 +/- 1.19 vs. 25.3 +/- 1.54, means +/- SE, respectively), as was minute ventilation at a single work load (50 W) (32.4 +/- 2.3 vs. 25.7 +/- 1.54 l/min, means +/- SE, respectively). This increased ventilation during exercise in the elderly was not produced by arterial O2 desaturation, and increased anaerobiasis did not play a role. Instead, the increased ventilation during exercise seems to compensate for increased inefficiency of gas exchange such that exercise remains essentially isocapnic. In conclusion, in the elderly the ventilatory response to hypercapnia is less than in young subjects, whereas the ventilatory response to exercise is greater.


1999 ◽  
Vol 86 (4) ◽  
pp. 1257-1263 ◽  
Author(s):  
Web McCanse ◽  
Kyle Henderson ◽  
Tetsuya Urano ◽  
Ichiro Kuwahira ◽  
Richard L. Clancy ◽  
...  

Systemic O2 transport during maximal exercise at different inspired [Formula: see text]([Formula: see text]) values was studied in sodium cyanate-treated (CY) and nontreated (NT) rats. CY rats exhibited increased O2affinity of Hb (exercise O2half-saturation pressure of Hb = 27.5 vs. 42.5 Torr), elevated blood Hb concentration, pulmonary hypertension, blunted hypoxic pulmonary vasoconstriction, and normal ventilatory response to exercise. Maximal rate of convective O2 transport was higher and tissue O2extraction was lower in CY than in NT rats. The relative magnitude of these opposing changes, which determined the net effect of cyanate on maximal O2 uptake (V˙o 2 max), varied at different [Formula: see text]:V˙o 2 max(ml ⋅ min−1 ⋅ kg−1) was lower in normoxia (72.8 ± 1.9 vs. 81.1 ± 1.2), the same at 70 Torr [Formula: see text] (55.4 ± 1.4 vs. 54.1 ± 1.4), and higher at 55 Torr[Formula: see text] (48 ± 0.7 vs. 40.4 ± 1.9) in CY than in NT rats. The beneficial effect of cyanate on V˙o 2 max at 55 Torr [Formula: see text] disappeared when Hb concentration was lowered to normal. It is concluded that the effect of cyanate on V˙o 2 maxdepends on the relative changes in blood O2 convection and tissue O2 extraction, which vary at different [Formula: see text]. Although uptake of O2 by the blood in the lungs is enhanced by cyanate, its release at the tissues is limited, probably because of a reduction in the capillary-to-tissue[Formula: see text] diffusion gradient secondary to the increased O2 affinity of Hb.


1985 ◽  
Vol 59 (4) ◽  
pp. 1040-1045 ◽  
Author(s):  
W. A. LaFramboise ◽  
D. E. Woodrum

Diaphragmatic electromyogram (EMG) was obtained in eight 48-h-old unanesthetized monkeys while breathing air and then either of two different hypoxic gas mixtures (12 or 8% O2 in N2) for 5 min. Minute ventilation (VI) rose significantly above control levels by 1 min of hypoxemia while animals were breathing either of the hypoxic gas mixtures as tidal volume (VT) and slope and rate moving average EMG increased. The relative gains in VI were associated with comparable increases in diaphragmatic neural activity per minute (EMG/min = peak EMG X frequency) during this early phase of hypoxemia. VI subsequently fell to control levels (inspired O2 fraction = 12%, arterial PO2 = 23 +/- 3 Torr) or significantly below (inspired O2 fraction = 8%, arterial PO2 = 18 +/- 0.4 Torr) by 5 min of hypoxemia, secondary to changes in VT. Despite the decline in VI, slope and rate moving average EMG, and EMG/min remained statistically above control values by 5 min of hypoxemia, although there was a trend for EMG/min to decrease slightly from the 1-min peak response. These findings demonstrate that hypoxic-induced depression of neural input to the diaphragm is not independently responsible for the biphasic nature of the newborn ventilatory response, although it cannot be ruled out as a contributor. The fall in inspiratory volumes despite constant elevated EMG activity suggests the presence of a change in respiratory mechanics and/or an impairment in diaphragmatic contractile function without offsetting neural compensatory activity.


1981 ◽  
Vol 51 (5) ◽  
pp. 1169-1174 ◽  
Author(s):  
W. A. LaFramboise ◽  
T. A. Standaert ◽  
D. E. Woodrum ◽  
R. D. Guthrie

End-expiratory airway occlusions were performed in eight unanesthetized premature newborn monkeys during acute hypoxemia to investigate mechanisms involved in the newborn's biphasic ventilatory response to hypoxia. Two-day-old monkeys demonstrated an immediate increase in minute ventilation (VI) and a decrease in PaCO2 followed within 5 min by a return of VI and PaCO2 to base-line levels. The decline in VI was associated with a decrease in tidal volume (VT) and inspiratory flow (VT/TI) and an increase in respiratory frequency. Occlusion pressures (PO.2) remained elevated throughout the hypoxic stimulus, and end-expiratory lung volume increased during the late response. “Effective” impedance (P0.1/V0.1, P0.2/V0.2, etc.) and “effective” elastance (Pmax/VT) were also elevated. At 21 days of age, the monkeys demonstrated a sustained ventilatory response as VI, VT, VT/TI, and P0.2 remained elevated throughout the period of hypoxemia. End-expiratory lung volume increases as on day 2, but effective impedance and effective elastance did not change. These data suggest that the biphasic response to hypoxia in the newborn may result from a change in respiratory timing and an alteration in respiratory mechanics and is not due to a decrease in central respiratory drive.


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