This is an exploratory, observational, follow-up study of 14 professional male soccer players, aged between 21 and 33 years, belonging to 2 Italian “Serie A” league soccer teams. The population was examined before the start of the championship (July 2014) and after 8 months of competition during the championship (March 2015) according to a standardized protocol consisting of clinical and functional assessment parameters. The clinical assessment included history of risk behavior and physical examination, and the functional assessment included spirometry and ergospirometry. After receiving the description of the procedures and potential risks, all subjects gave their written informed consent. The study was approved by the Internal Institutional Review Boards of both teams. All procedures performed in the study complied with the ethical standards of the Internal Institutional Review Board Committee and with the 1964 Helsinki declaration and its subsequent amendments or with comparable ethical standards.

A pneumotachograph was used to measure dynamic volume indices such as forced vital capacity (FVC) and indices derived from it such as the forced expiratory volume in 1s (FEV1) and its correlation with FVC (FEV1/FVC ratio). The observed values were expressed as a percentage of the predicted values based on the American Thoracic Society/European Respiratory Society reference values.12 For heart rate (HR) monitoring, a polar heart rate monitor was used (Polar, Kempele, Finland).

For the ergospirometric test (Vmax Encore, Yorba Linda, CA, USA), a “ramp” protocol at a constant treadmill incline (1%) (starting at 8km/h and increasing speed by 1km/h every 60s) was used. Using “breath by breath” analysis of the flows and concentrations of respiratory inhaled and exhaled gases (VO2 and VCO2) obtained via mass flow and fast-responding gas analyzers (fuel cell and infrared analyzers), the following variables were obtained: oxygen uptake (VO2) and its relationship to heart rate (oxygen pulse or VO2/HR), the derived ventilatory variables (VE and VT) and the ventilatory equivalents for O2 and CO2 (VE/VO2, VE/VCO2). The anaerobic threshold (AT or ventilatory threshold) was evaluated using non-invasive measurements of respiratory variables derived from the VCO2/VO2 slope method13 and verified against the increase in VE/VO2 without change in VE/VCO2 during exercise.14

The VO2 test was rigorously performed to verify the attainment of maximal VO2 (V′O2max), accordingly to established procedures.15

The breathing respiratory reserve (BRR) was expressed as the difference in liters between the maximum voluntary ventilation (MVV) of each athlete and ventilation achieved at peak exercise (VE peak), where the predicted MVV was defined as FEV1×40. Exercise tolerance was expressed as the maximum speed reached (maximal exercise velocity: MEV), adjusted according to a modified Kuiper's equation (Eq. (1)):

The VT inflection point of each subject was manually identified on the VT/VE graph.

All functional measurements were performed before and after 8 months of competition during the championship. Specialized sports physicians individualized the training regimens for each player. Both soccer clubs specifically requested that investigators be blinded to their physical training programs to prevent any disclosure of these regimens. All measurements were performed according to standardized criteria of the American Thoracic Society and American College of Chest Physicians (ATS/ACCP).16

We studied 14 soccer players with a normal body mass index (BMI) and no spirometric evidence of obstructive ventilatory defects.17 This sample size provides an 80% power to detect a significant difference (2-tailed, α=0.05) in V′E measured at a standardized speed (iso-speed) during incremental cardiopulmonary exercise testing, on the basis of a relevant difference in VE of ∼8–10L/min, based on the use of a standard deviation of ∼9–12L/min for V′E changes in published studies.3

Data are reported as mean±standard deviation. Baseline differences between groups were evaluated using independent sample Mann–Whitney U tests. Differences before and after 8 months of competition were evaluated using related samples Wilcoxon signed rank tests. A P-value of less than .05 was used as the threshold of statistical significance. All analyses were performed using SPSS version 21 (IBM, USA). Four main evaluation time points during the treadmill exercise were considered for comparisons between “before and after 8 months of competition”: iso-speed (16km/h), VT/VE inflection 1, VT/VE inflection 2 and peak exercise. Iso-speed (16km/h) was chosen to compare each variable of interest in each test for each athlete at a standardized stimulus “before and after 8 months of competition” to reveal the real effects of training, thus avoiding the confounding factors related to a potential amelioration in VO2 peak and MEV after 8 months of training and competition.

The 14 soccer players were non-smokers (never smokers), with normal blood hemoglobin, with no respiratory or cardiac conditions (asthma and other). None were taking medication/treatment, such inhalers or other therapies.

Anthropometric characteristics of the subjects are shown in Table 1.

Tables 2 and 3 summarize the differences observed during exercise before and after 8 months of training and competition in team 1 and team 2 and in the study population as a whole (Fig. 1). Analyzing exercise responses according to teams allowed us to better appreciate the amplitude of training- and competition-related response to exercise in each variable.

Fig. 1.

Oxygen uptake (VO2, upper left panel), heart rate (HR, upper right panel), ventilation (VE, lower left panel) and ventilatory equivalents of CO2 (VE/VCO2, lower right panel) are plotted in response to symptom-limited treadmill exercise in all study subjects before (filled circles) and after (open circles) 8 months of training and competition. The graph shows mean values at baseline (starting at 8km/h), iso-speed (16km/h), VT/VE inflection 1, VT/VE inflection 2 and peak exercise. P values before vs after training and competition at the same measurement point are shown in Tables 2 and 3. Abbreviations: L, liters; min, minutes; kg, kilograms.

(0.15MB).

There were no differences in baseline age, weight, height and BMI between teams. FEV1 increased significantly after 8 months of training and competition in team 1, but not in team 2.

Table 2 shows the cardiopulmonary measurements during incremental treadmill exercise at baseline (8km/h), at iso-speed, and at maximum exercise before and after 8 months of training and competition.

Overall, there were no differences in resting cardiopulmonary variables before and after 8 months of training and competition, except for a decrease in VE/VCO2. At iso-speed, there were overall improvements in VCO2, VE/VO2, VE/VCO2, VE and fR after 8 months of training and competition. VO2 at ventilatory threshold was comparable before training and competition between teams (59.7±4.9 vs 58.6±5.7ml/kg/min respectively, P=.7); after training and competition, VO2 at ventilatory threshold increased significantly only in team 2 (58.6±5.7 vs 72.3±5.4ml/kg/min respectively, P=.004) compared with team 1 (59.7±4.9 vs 60.8±6.8ml/kg/min respectively, P=.7). After 8 months of training and competition there were overall improvements in MEV, VO2 at ventilatory threshold, peak VO2, peak VCO2, peak fR and peak O2-pulse. These changes were driven by subjects from team 2, who showed greater improvements after 8 months of training and competition than subjects from team 1.

Individual Hey plots8 showed that VT/VE inflection point 1 was discernible in all athletes, whereas VT/VE inflection point 2 was discernible only in 11/14 athletes before training and in 12/14 after 8 months of training and competition.

When considering all subjects, VT/VE inflection point 1 occurred with greater exercise time, VO2 and VCO2 and, notably, with greater VE and VT (Table 3 and Fig. 2) after 8 months of training and competition.

Fig. 2.

Tidal volume (VT) is plotted as a function of ventilation (VE) in response to symptom-limited treadmill exercise in all study subjects before (filled circles) and after (open circles) 8 months of training and competition. The graph shows mean values at baseline (starting at 8km/h), iso-speed (16km/h), VT/VE inflection 1, VT/VE inflection 2 and peak exercise. P values before vs after training and competition at the same measurement point are shown in Tables 2 and 3. Abbreviations: L, liters; min, minutes; km, kilometers; h, hours.

(0.07MB).

Similarly, VT/VE inflection point 2 also occurred with greater exercise time, VO2, VCO2, VE and VT, but also with higher HR.

This study has certain limitations that must be acknowledged. First, lack of measurement of PaCO2 and VD/VT during exercise prevented us from reaching a definite conclusion on the relative contributions of these different factors to improved ventilatory demand and efficiency during exercise in our athletes after 8 months of training and competition. Second, the lack of respiratory mechanics-related pressure measurements, the absence of dynamic lung volume measurements during exercise, and the lack of measurements of locomotor muscle oxygenation and lean body mass prevented us from reaching a definite conclusion on the relative contribution of these different factors to the improved ventilatory profile/behavior during exercise in our athletes after 8 months of training and competition. However, it should be noted that these choices were largely justified by the exploratory nature of the study, our efforts to restrict the study to observational data, the tight time schedule imposed by each football club on each athlete (these soccer players had “no time” to come to our laboratory and perform a complete study involving measures of inspiratory and expiratory pressure, lactates and so on; therefore, the investigators had to conduct exercise testing in their respective football clubs. This was done as rigorously as possible, given the time restraints and limited equipment). Last but not least, investigators were blinded to the physical training program used by each soccer team (as specifically requested by each football club to prevent disclosure of these regimens). This was an important limitation, given that the ventilatory improvement seen cannot be attributed to any particular exercise protocol; this, therefore, greatly limits the applicability, feasibility and potential benefits of these protocols in patients with cardiorespiratory disorders.

To the best of our knowledge, this is the first study to report the effects of 8 months of training and competition on the ventilatory profile response to treadmill exercise in elite soccer athletes. The ventilatory effects were more pronounced than the effects on the cardiovascular and metabolic systems in these athletes. As such, this study paves the way for training programs that focus more on recording and assessing ventilatory profile response and breathing activity than heart rate, lactic threshold and other metabolic variables that may not change significantly. The subjects included in this study were elite athletes who started the training season with an above-normal cardiovascular and metabolic capacity. However, as observed, the benefits to the ventilatory system were largely out of proportion to those obtained by the cardiovascular and metabolic systems.

The lung plays a fundamental role in exercise performance in patients with ventilatory limitations. This is quite often neglected in athletes (except for those presenting with exercise-induced bronchospasm), in healthy subjects and in some patients suffering from cardiorespiratory disorder such as CHF and PAH, because it is erroneously believed that the ventilatory system has enough “reserve” to cope with exercise. This may not, in fact, be the case in some healthy asymptomatic subjects and in some endurance athletes, in whom expiratory flow limitation and diaphragm fatigue can impair exercise performance as much as dynamic lung hyperinflation and mechanical constraints on tidal volume expansion can impair exercise performance in patients with cardiovascular and respiratory disorders.

Despite this, ventilatory response to exercise has never been considered a crucial tool for assessing performance. Further evidence of this is shown by a PubMed search using the terms “Exercise, Athletes, Heart”, which retrieved 1536 studies in the last ten years, compared to 157 studies retrieved when “Heart” is replaced with “Lung”. In addition, attention is almost always focused on the lung as a “gas exchanger” rather than on the “ventilatory response to exercise”.

In light of this, the assessment of ventilation, its response and profile/behavior to exercise using measurements derived from tidal breathing and respiratory frequency (such as cardiopulmonary exercise testing) could perhaps complement heart rate-based training programs, provide a simple, accurate picture of the status of the respiratory system, and help reveal the mechanisms behind improved exercise performance in elite athletes. This should also prompt respiratory physicians focused on respiratory pathophysiology to (1) address the important question of whether ventilatory changes during exercise represent a physiological mechanism for the improvement seen in patients after pulmonary rehabilitation; (2) attach more importance to the role the ventilatory system may play in some patients in whom it is not thought (erroneously) to contribute to exercise limitation.

Further studies are required to determine whether evaluation of the ventilatory response to exercise could give insight into the potential improvement of technical, tactical, psychological and athletic skills in these elite athletes.30

In summary, this is the first study to demonstrate that an improved ventilatory profile response after training likely contributes to the greater exercise performance observed in our soccer athletes, despite no significant changes in heart rate at a given speed and a negligible improvement in VO2 and MEV after 8 months of training and competition.