Ventilatory response to exercise of elite soccer players

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.

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Ventilatory response to exercise in subjects breathing CO2 or HeO2

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.3.746 ◽

1997 ◽

Vol 82 (3) ◽

pp. 746-754 ◽

Cited By ~ 65

Author(s):

T. G. Babb

Keyword(s):

Maximal Exercise ◽

Respiratory Mechanics ◽

Ventilatory Threshold ◽

Ventilatory Response ◽

Minute Ventilation ◽

Normal Lung ◽

Normal Lung Function ◽

Older Subjects ◽

Breathing Room ◽

Response To Exercise

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.

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Ventilation and breathlessness on maximal exercise in patients with interstitial lung disease after local anaesthetic aerosol inhalation

Clinical Science ◽

10.1042/cs0740275 ◽

1988 ◽

Vol 74 (3) ◽

pp. 275-281 ◽

Cited By ~ 32

Author(s):

A. J. Winning ◽

R. D. Hamilton ◽

A. Guz

Keyword(s):

Interstitial Lung Disease ◽

Lung Disease ◽

Maximal Exercise ◽

Ventilatory Response ◽

Minute Ventilation ◽

Statistical Significance ◽

Co2 Production ◽

Arterial Oxygen ◽

Cough Reflex ◽

Response To Exercise

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.

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Ventilatory response during exercise among chronic Chagas cardiopathy patients

Sao Paulo Medical Journal ◽

10.1590/s1516-31802006000500010 ◽

2006 ◽

Vol 124 (5) ◽

pp. 280-284 ◽

Cited By ~ 8

Author(s):

Fátima Palha de Oliveira ◽

Roberto Coury Pedrosa

Keyword(s):

Ventilatory Response ◽

Exercise Duration ◽

Peak Oxygen Uptake ◽

Cycle Ergometer ◽

Control Group ◽

Gas Exchange Parameters ◽

Peak Vo2 ◽

Ventilatory Parameters ◽

Patients With Heart Failure ◽

Patient Groups

CONTEXT AND OBJECTIVE: The change in slope of the VE/VCO2 curve with time during exercise (VE/VCO2 slope) has been recommended as a parameter for analyzing the ventilatory response during exercise among patients with heart failure of different etiologies. The aim of this work was to evaluate the ventilatory response among patients with chronic Chagas cardiopathy. METHODS: Forty-eight patients, divided into four groups according to the Los Andes clinical/hemodynamic classification, were studied. They were also classified according to peak oxygen uptake (peak VO2) for a second analysis. The results from the patients were compared with results from a control group consisting of 21 healthy male volunteers (no Chagas disease). Exercise was performed on a cycle ergometer with loads increasing at the rate of 12.5 watts/min, and exercise duration was symptom-limited. Gas concentration and flow rate data were fed into a computer, which produced a real-time report on ventilatory and gas exchange parameters (breath-by-breath). The ventilatory parameters of VE/VCO2 slope and VE/VCO2 ratio computed at different times of the test were adopted. RESULTS: Although there were no significant differences in VE/VCO2 ratio and VE/VCO2 slope when patients were grouped using the Los Andes clinical/hemodynamic classification, these parameters varied significantly when peak VO2 was used to define patient groups. CONCLUSION: Our results indicate that progressive deterioration in ventilatory response among chronic Chagas cardiopathy patients during exercise is more evident when the functional capacity (peak VO2) is reduced, than when changes are related to the Los Andes classification.

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Pulmonary gas exchange response to exercise- and mannitol-induced bronchoconstriction in mild asthma

Journal of Applied Physiology ◽

10.1152/japplphysiol.00108.2008 ◽

2008 ◽

Vol 105 (5) ◽

pp. 1477-1485 ◽

Cited By ~ 27

Author(s):

Phillip A. Muñoz ◽

Federico P. Gómez ◽

Hernán A. Manrique ◽

Josep Roca ◽

Joan A. Barberà ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Minute Ventilation ◽

Forced Expiratory Volume ◽

Pulmonary Gas Exchange ◽

Slow Recovery ◽

Airway Narrowing ◽

Asthmatic Patients ◽

Response To Exercise ◽

Blood Flow Redistribution

Both exercise (EIB) and mannitol challenges were performed in asthmatic patients to assess and compare their pulmonary gas exchange responses for an equivalent degree of bronchoconstriction. In 11 subjects with EIB [27 ± 4 (SD) yr; forced expiratory volume in 1 s (FEV1), 86 ± 8% predicted], ventilation-perfusion (V̇a/Q̇) distributions (using multiple inert gas elimination technique) were measured 5, 15, and 45 min after cycling exercise (FEV1 fall, 35 ± 12%) and after mannitol (33 ± 10%), 1 wk apart. Five minutes after EIB, minute ventilation (V̇e; by 123 ± 60%), cardiac output (Q̇t, by 48 ± 29%), and oxygen uptake (V̇o2; by 54 ± 25%) increased, whereas arterial Po2 (PaO2; by 14 ± 11 Torr) decreased due to moderate V̇a/Q̇ imbalance, assessed by increases in dispersions of pulmonary blood flow (log SDQ̇; by 0.53 ± 0.16) and alveolar ventilation (log SDV̇; by 0.28 ± 0.15) (dimensionless) ( P < 0.01 each). In contrast, for an equivalent degree of bronchoconstriction and minor increases in V̇e, Q̇t, and V̇o2, mannitol decreased PaO2 more intensely (by 24 ± 9 Torr) despite fewer disturbances in log SDQ̇ (by 0.27 ± 0.12). Notwithstanding, mannitol-induced increase in log SDV̇ at 5 min (by 0.35 ± 0.15) was similar to that observed during EIB, as was the slow recovery in log SDV̇ and high V̇a/Q̇ ratio areas, at variance with the faster recovery of log SDQ̇ and low V̇a/Q̇ ratio areas. In asthmatic individuals, EIB provokes more V̇a/Q̇ imbalance but less hypoxemia than mannitol, primarily due to postexercise increases in V̇e and Q̇t benefiting PaO2. V̇a/Q̇ inequalities during both challenges most likely reflect uneven airway narrowing and blood flow redistribution generating distinctive V̇a/Q̇ patterns, including the development of areas with low and high V̇a/Q̇ ratios.

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Ventilatory responses to hypoxia in rats pretreated with nonpeptide NK1 receptor antagonist CP-96,345

Journal of Applied Physiology ◽

10.1152/jappl.1994.76.4.1528 ◽

1994 ◽

Vol 76 (4) ◽

pp. 1528-1532 ◽

Cited By ~ 17

Author(s):

G. T. De Sanctis ◽

F. H. Green ◽

X. Jiang ◽

M. King ◽

J. E. Remmers

Keyword(s):

Ventilatory Response ◽

Minute Ventilation ◽

Acute Hypoxia ◽

Frequency Component ◽

Nk1 Receptor ◽

Adult Rats ◽

Nk1 Receptors ◽

Before And After ◽

Sites Of Action

This study reports experiments designed to evaluate the role of neurokinin-1 (NK1) receptors for substance P (SP) in the ventilatory response to acute hypoxia. Ventilation was measured by indirect plethysmography in eight unanesthetized unrestrained adult rats before and after bolus injection of 1, 5, or 10 mg/kg (ip) of CP-96,345 (Pfizer), a potent nonpeptide competitive antagonist of the SP NK1 receptor. Ventilation was measured while the rats breathed air or 8% O2–92% N2 with and without administration of SP antagonist. Pretreatment with CP-96,345 decreased the magnitude of the hypoxic response in a dose-dependent fashion. Minute ventilation in rats pretreated with CP-96,345 was reduced by 22.1% (P < 0.05) at the highest dose (10 mg/kg), largely because of an attenuation of the frequency component. Although both control and treated rats responded to hypoxia with a decrease in duration of inspiration and expiration rats pretreated with CP-96,345 displayed a smaller decrease in inspiration and expiration than control rats (P < 0.05). We have recently shown that neuropeptide-containing fibers are important for mediating the tachypnic response during acute isocapnic hypoxia in rats. The attenuation in minute ventilation at the highest dose (10 mg/kg) is comparable in magnitude to the attenuation observed with neonatal capsaicin treatment, which permanently ablates neuropeptide-containing unmyelinated fibers. Accordingly, this previously reported role of capsaicin-sensitive nerves in the hypoxic ventilatory response of rats is probably attributable to released SP acting at NK1 receptors. One of the likely sites of action of SP antagonists is the carotid body.(ABSTRACT TRUNCATED AT 250 WORDS)

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Ventilatory response to exercise in diabetic subjects with autonomic neuropathy

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.5.1978 ◽

1996 ◽

Vol 81 (5) ◽

pp. 1978-1986 ◽

Cited By ~ 20

Author(s):

C. Tantucci ◽

P. Bottini ◽

M. L. Dottorini ◽

E. Puxeddu ◽

G. Casucci ◽

...

Keyword(s):

Respiratory Rate ◽

Autonomic Neuropathy ◽

Ventilatory Response ◽

Minute Ventilation ◽

Control Subjects ◽

Inhibitory Modulation ◽

End Tidal ◽

And Control ◽

Response To Exercise ◽

Maximal Voluntary Ventilation

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.

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Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.3.1383 ◽

1988 ◽

Vol 65 (3) ◽

pp. 1383-1388 ◽

Cited By ~ 16

Author(s):

J. I. Schaeffer ◽

G. G. Haddad

Keyword(s):

Ventilatory Response ◽

Minute Ventilation ◽

Severe Hypoxia ◽

Moderate Hypoxia ◽

Arterial Blood Gas ◽

Arterial Blood ◽

Before And After ◽

The Relationship ◽

Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

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Cardiorespiratory and sensory responses to exercise in adults with mild cystic fibrosis

Journal of Applied Physiology ◽

10.1152/japplphysiol.00692.2015 ◽

2015 ◽

Vol 119 (11) ◽

pp. 1289-1296 ◽

Cited By ~ 9

Author(s):

Bradley S. Quon ◽

Sabrina S. Wilkie ◽

Yannick Molgat-Seon ◽

Michele R. Schaeffer ◽

Andrew H. Ramsook ◽

...

Keyword(s):

Cystic Fibrosis ◽

Tidal Volume ◽

Minute Ventilation ◽

Inverse Correlation ◽

Peak Oxygen Uptake ◽

Forced Expiratory Volume ◽

Dynamic Hyperinflation ◽

Expiratory Flow Limitation ◽

Lung Volumes ◽

Therapeutic Trials

The purpose of this study was to evaluate cardiorespiratory fitness and reasons for exercise curtailment in a contemporary adult cystic fibrosis (CF) cohort with mild lung disease. Adults with mild CF ( n = 19, forced expiratory volume in 1 s = 95 ± 17% predicted) were age-, sex-, ethnicity-, and body mass index-matched to healthy controls ( n = 19) and underwent a detailed cardiopulmonary cycle exercise test. While CF subjects had a reduced peak oxygen uptake compared with controls, the values were normal when expressed as %predicted in 14/19 (74%) of subjects. Both groups demonstrated a normal cardiovascular limitation to exercise and stopped exercise primarily because of leg fatigue. Despite not being exercise-limited by respiratory factors, there was some evidence of ventilatory abnormalities as patients with mild CF had increased end-inspiratory lung volumes and reached an inflection/plateau in tidal volume relative to minute ventilation at lower exercise intensities compared with controls. Subjects with CF were not more likely to demonstrate expiratory flow limitation compared with controls and did not have evidence of dynamic hyperinflation during exercise. Despite increased end-inspiratory lung volumes and an earlier tidal volume inflection/plateau, CF subjects did not experience higher levels of dyspnea. In an exploratory analysis, a significant inverse correlation was observed between sweat chloride and peak work rate. Adult CF subjects with relatively well preserved spirometry have normal exercise performance relative to reference values and are primarily limited by nonrespiratory factors. However, ventilatory abnormalities were detected even in this mild CF cohort and should be evaluated in future therapeutic trials focused on disease-modifying therapies in mild CF.

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