This study evaluated the effect of inspiratory and expiratory muscle training on pulmonary function, maximal, and sub-maximal exercise performance. Specifically, how does training using a PowerLung resistive device effect exercise performance and pulmonary function in competitive marathoners and triathletes. The participants in this study (N=12) had a mean weekly aerobic training time of 7.5 hours per week of swimming, cycling, or running. Eight subjects were assigned to a PowerLung treatment group and four control subjects were given a sham device that allowed no greater than 15% resistance on inspiration or expiration. The subjects performed 30 maximal inhalation/exhalation maneuvers on their respective devices two times per day for four weeks. The subjects were tested for forced vital capacity (FVC), forced expiratory volume in one second (FEV1), FEV1/FVC ratio, forced inspiratory vital capacity (FIVC), peak inspiratory flow rate (PIFR), and peak expiratory flow rate (PEFR). Each subject was also tested for peak exhalation force test (Pex) as well as a maximal oxygen consumption (VO2max), carbon dioxide production (VCO2), tidal volume (VT), ventilation (VE), lactate threshold (LT), and respiration rate (RR). The subjects also completed weekly sub-maximal exercise test at 85% of their VO2max with exercise time, VO2, VCO2, VE, VT, and RR being measured. The data revealed that training using the Powerlung device produced significant changes in maximal VE, maximal VT, and sub-maximal VE. There were no significant effects on VO2max, sub-maximal exercise time, FVC, FEV1, FIVC, PEFR, or LT. The study revealed a 1.99 breath/minute decrease in RR coupled with a 4.93 L/min increase in VE and a .81L/breath increase in VT for the treatment group. Subjects in the treatment group also had a 28.25mm/Hg increase in Pex as compared to only a 2mm/Hg increase for the control group.

The effects of resistance training on skeletal muscle are well documented. When performed with the correct repetition scheme and load assignment, resistance training can produce skeletal muscle hypertrophy, strength, or local muscle endurance. Traditionally, strength and power athletes have used resistance training to augment sport performance while endurance athletes have avoided any type of resistance exercise believing that increased muscle would decrease aerobic performance. However, skeletal muscle controls one of the most important aspects of aerobic conditioning; air movement. The diaphragm, external and internal intercostals, scalene, and abdominal muscles (i.e. respiratory muscles) help to facilitate the increased airflow needed to fuel the increasing needs of oxygen during exercise.³ If these muscles play such a crucial role in exercise, logically one would think we should train them just as if we would any other skeletal muscle.

Devices have been manufactured that offer resistance on inhalation and exhalation and thus cause an increased strain on the respiratory muscles. This resistance has been shown to facilitate positive pulmonary function changes in people with chronic obstructed pulmonary disease (COPD). Villafranca et al.¹⁷ showed increases in maximal inspiratory pressure (PImax) after ten weeks of inspiratory muscle training using a threshold inspiratory trainer allowing 30% resistance. Likewise, Larson and Kim7 observed increases in PImax after one month of inspiratory muscle training in people with COPD.

Pulmonary resistance training has also been shown to change enzymatic profiles in sheep. Akabas et al.¹ assigned nine adult sheep to a training group and seven to a control group. The experimental group trained for twenty minutes using inspiratory flow resistance (50-100 cmH2O) five to six times per week for three weeks. In the end, biochemical changes were observed between the experimental and control group. There was a 26 percent increase in citrate synthase (CS), a 29 percent increase in ß-hydroxyacl-CoA dehydrogenase (ßHAD), and a 36 percent increase in cytochrome oxidasealso (COX) in the experimental group as compared to the control group in the diaphragm muscles. It can be concluded from this study that the aerobic enzymatic profiles increased significantly in sheep when put under inspiratory stress. An increase in aerobic enzymes during exercise in humans would equate to more efficient energy utilization of the respiratory muscles and lower fatigueability.

Data involving healthy humans using respiratory muscle training, and specifically with exercise is limited. In two separate studies, Suzuki et al.^12,13 observed changes in the rate of perceived exertion (RPE) after inspiratory and expiratory muscle training in healthy adults. Suzuki concluded that expiratory muscle training did not decrease RPE at a given work load while inspiratory muscle training did decrease RPE.

Cain and McConnell10 reported increased sub maximal exercise performance after respiratory muscle training. This group found decreases in blood lactate, RPE, and HR along with an increased time to fatigue after four weeks of respiratory training. Boutellier et al.³ reported similar results also after four weeks of respiratory muscle training. Hanel and Secher⁶ observed a decrease in breaths per minute and an increase in tidal volume after exercising twice a day for 28 days in ten physical education students.

The purpose of our research was to investigate the effects of respiratory muscle training using a Powerlung device on pulmonary function and exercise performance in triathletes and marathon runners. We hypothesize that the treatment group will increase pulmonary function during exercise and increase dynamic lung functions. Furthermore, we believe that the exercising group will increase sub-maximal exercise time as compared to the control group. We do not believe that the treatment group or control group will increase VO2max or change lactate threshold.

Subjects:
A total of twelve subjects (9 male, 3 female) were recruited from area triathlon and running clubs. The subjects had a mean aerobic training time of 7.5 hours per week (range; 5 – 10 hours). Eight subjects (6 male; 2 female) were assigned to a Powerlung treatment group and four subjects (3 male; 1 female) were assigned to a control group. The experimental group had the following mean physical characteristics: age 36.75 ± 8.83 years, height 174.5 cm ± 9.41, weight 72.94 kg ± 7.22. The control group’s physical characteristics were age 34.5 ± 7.05 years, height 172.8 ± 4.22 cm, and weight 71.23 ± 3.64 kg. Each subject was given an informed consent form and made aware of their right to drop out of the study at any time.

Table 1: Mean±standard deviation (SD) data of group characteristics

Maximal Exercise Testing
Each subject was given a maximal oxygen consumption test (VO2max) before and after Powerlung training. The VO2max protocol consisted of 1 ½ minute stages of work, each made successively more difficult by increasing the grade by 1%. The testing speed was constant, and was selected based on the 5K time of the subjects. The protocol had a 2-stage ramp-up to the target speed to ease the transition to the test speed. In addition to the 2-stage ramp-up built into the protocol, the subject was allowed to warmup on the treadmill as long as needed before beginning the test. The protocol continued to increase by 1% in incline until the subject reached max exercise (i.e. asked for the treadmill to be stopped or grabbed the handrail). Metabolic data was acquired using a Quinton metabolic cart (QMC). The QMC sampled from a mixing chamber every 15 seconds and provided oxygen consumption (VO2), ventilation (VE), respiratory rate (RR), volume of carbon dioxide produced (VCO2), and lactate threshold (LT). Lactate threshold was derived via the v-slope method by the Quinton metabolic software version 3.3.⁸ Heart rate (HR) was measured using a five lead electrocardiogram from a Quinton Q-4500 stress-test system.

Pulmonary Function Testing
Each subject was given a spirometry test using a ChestTest spirometer (Vaccumed, Ventura, CA) before the VO2max test both pre and post training. Each subject stood facing the spirometer and performed a maximal inhalation followed by a forceful exhalation into the tube until all air was expelled. The subject then performed a maximal inhalation to complete the maneuver. The ChestTest spirometer provided forced vital capacity (FVC), forced expiratory volume in one second (FEV1), FEV1/FVC ratio, Peak expiratory flow rate (PEFR), and peak inspiritory flow rate (PIFR).

Each subject also performed a peak exhalation force (Pex) test to determine the strength of the expiratory muscles. Force was measured using a standing mercury sphygmomanometer. The subject performed a maximal inhalation then exhaled forcefully against a closed valve. Maximal force in mmHg was recorded over a maximum of three trials. The Pex test was performed pre and post training after the spirometry test but before the VO2max test. Test retest reliability was performed on the apparatus using 8 graduate students (r = .92).

Sub-maximal Exercise Testing
One to two days after the pre VO2max test and pulmonary testing, each subject returned for a sub-maximal treadmill test. Specifically, each subject ran on the treadmill using the same protocol as performed in their maximal testing. A hold was placed on the protocol in the stage in which the subject?s steady-state VO2 = 85% ± 5%. The subject continued at this workload until failure or their VO2 exceeded 90% of maximum. The QMC was used to measure the same metabolic data as measured during the maximal test. Each subject performed a sub-maximal treadmill test weekly for a total of four weeks (e.g. five total sub-maximal tests).

Training:
For the duration of the study, the subjects were asked to maintain their present aerobic training and not to increase or decrease their training time in order to eliminate the possibility of adaptations from aerobic exercise.¹¹ Both groups performed thirty maximal inhalation/exhalation cycles on the Powerlung training device two times per day for four weeks. The device allows for varying resistance on inhalation and exhalation via hand adjusted knobs. After the first sub-maximal test, the treatment group was given the Powerlung device and instructed to perform the above-mentioned protocol as assigned by Powerlung manufacturers. The subjects were instructed to adjust the resistance to allow for the 30th breath on both inhalation and exhalation to be close to a maximal effort (i.e. 30-RM). The subjects controlled the resistance via trial and error.

In the same way, the subjects assigned to the control group were given a sham device after their first sub-maximal test. The sham device looked identical to the Powerlung device, but the chambers inside the sham device were constructed to allow a resistance no greater than 15%. The control subjects were given the same instructions as the experimental group. Neither group was informed as to which group they were assigned to until the completion of their last maximal test.

Statistical Analyses
All data was analyzed using analysis of variance (ANOVA) with repeated measures. The data was copied from a summary spreadsheet in Microsoft Excel to SPSS statistical software and the software derived all F-ratios. All significant F-ratios were analyzed using Tukey’s post hoc test and p-values represent Greenhouse-Geisser adjustment for sphericity. Anthropometric data is expressed as mean±standard deviation (SD), while all exercising and pulmonary dependent variables are expressed as mean±standard error of the mean (SEM). Percent change was calculated using Microsoft Excel with the formula: % change = [(x2 -x1) / x1] * 100.

Results are provided in Tables 2 and 3 for all maximal exercising and pulmonary function data, respectively.

Table 2: Descriptive statistics (mean±standard error of the mean (SEM)) for data at maximal exercise intensity.

PLT = Treatment ;
CON = Control ;
VO2max = Maximal oxygen consumption ;
VE = Ventilation in L/min ;
VT = Tidal volume ;
R = Respiratory rate ;
VT = Ventilatory threshold ;

Exercise Variables
The purpose of this study was to determine if pulmonary function or exercise performance could be changed by specifically training the respiratory muscles using a Powerlung resistance device. Respiration is only one component of aerobic capacity. Cardiac output is generally thought to be the major limiting factor to aerobic exercise⁸. At maximal exercise, the ventilation to perfusion ratio reaches 4.0, indicating that we are ventilating four times the volume of air then is provided to the alveoli by pulmonary blood flow¹⁰. Research shows runners with the lower ventilation responses to high exercise are both hypoxemic and more acidotic¹¹. This could be attributed to an inadequate hyperventilation, reducing CO2 exhalation and the removal of blood protons.

In a study by Boutellier et al.² on trained aerobic athletes using a respiratory resistance device different from the Powerlung, the researchers found no significant increases in either VO2max or LT during a cycle ergometer test. However, they did see an increase of sub-maximal cycling time. Like Boutellier’s group, we did not see an increase in VO2max or VT. The subjects that were tested in our study were highly trained aerobic athletes. Significant changes in VO2max with high caliber aerobic athletes are rarely seen in short durations, and are usually a function of high levels of aerobic training over a long period of time. For this reason we did not expect changes in VO2 during a four- week study.

Table 3

However, using highly conditioned aerobic athletes did create an ideal situation to control the test the Powerlung. Because our subjects had likely maximized the pulmonary adaptations elicited by aerobic conditioning alone, any changed observed in oxygen consumption or pulmonary function could be attributed to the Powerlung training.

We did expect to see changes in pulmonary function during exercise. Because the subjects had trained their pulmonary muscles, they were able to increase ventilation. The increase in VE and decrease in RR in the training group indicated that the Powerlung device increased the strength of the respiratory muscles. The increased strength of the respiratory muscles allowed the subjects to perform more work (i.e. move more air) while breathing fewer times.

Earlier work by Hanel and Secher¹² showed similar results. These investigators studied inspiratory muscle training on 20 physical education students. The students trained using a device similar to the Powerlung, but only allowed resistance on inspiration. The students trained on the device for 10 min twice per day at a progressively increasing resistance for 27.5 days. VO2max was measured via treadmill test pre- and post-training and revealed a 3 breath/min decrease at max exercise in the training group and no change in the control group. A small increase in VO2 (~2 L/min) was observed in both the training and the control group from pre to post testing. Likewise, our study revealed changes in RR with a 1.88 breath/min decrease at max exercise (Table 2). However, Hanel and Secher¹² saw a 2 L/min decrease in the treatment group after 27.5 days of inspiratory muscle training where as we saw a 4.53 L/min increase in VE post Powerlung training.

While increased pulmonary muscle function did not result in an increase in VO2, it could have benefit to longer duration exercise. The maximal treadmill test lasted on average 9-12 minutes. The test is designed to end in a relatively short period of time so that central and peripheral oxygen delivery are the limiting factors and not leg fatigue. If there are to be any changes due to pulmonary resistance training, they might be more likely to occur over a longer period than 9-12 minutes. Over the duration of a marathon or triathlon, the athletes will take thousands of breaths. This equates to a large amount of air flow and related delivery of oxygen that must be distributed to the pulmonary muscles to facilitate the mechanics of ventilation. If RR can be decreased by 2 breaths/min as seen in our study, and VE could increase or remain constant, an athlete would take significantly fewer breaths over the period of their competition. This O2 that was being distributed to the pulmonary muscles could be used by other working muscles to increase or prolong exercising performance.

Pulmonary Variables
The spirometry readings did not change significantly with Powerlung training. O’Kroy and Coast¹³ examined nineteen untrained students and randomly assigned them to either a control group, an exercising group, an inspiratory loading group, an expiratory loading group, or a hyperventilating group. The subjects trained four days/week, 20 min/day for four weeks with their assigned groups. The subjects training with inspiratory loading showed increases in MIP and MIF, while the expiratory loading group showed increases in maximal expiratory pressure (MEP) and expiratory force (MEF). The only other group showing significant changes was the hyperventilating group, which exhibited increased MEP, maximum voluntary ventilation (MVV), maximal sustained ventilation for 4 minutes (MSVV), and MIF. This research suggests resistance training offers some benefit to fatigue resistance in untrained students. The research also suggests that inspiratory muscles, like all other skeletal muscles, adapt according to the stress placed on them².

Tzelpis et al.^14,15 showed similar results in a study with nineteen untrained students using flow specific training. Tzelpis assigned the students to three specific groups: a low, medium, and high pressure groups. The high pressure group performed 30 maximal static inspiratory contractions against an occluded valve. The low pressure group performed of thirty maximal inspiratory contractions against an unoccluded valve, and the medium pressure group performed 30 maximal contractions through a 7 mm resistor tube. The results were specific to the type of training. The high pressure training groups had the highest increases in peak esophageal pressure (PESmax) and maximum inspiratory flow rate (VImax). Tzelpis et al.^14,15 concluded that the groups that trained using high pressure resistance had the greatest increases in PESmax while the groups training with higher flow rates` (i.e. low pressure group) had higher increases in VImax as compared to the other two higher pressure groups.

It is known that pulmonary muscles will adapt to aerobic exercise^9,10, so we would expect to see smaller changes in aerobic athletes as their pulmonary muscles are already developed. Hanel and Sechler¹² showed no change in FEV1, FVC, FEV1/FVC, and peak expiratory flow rate after 27.5 days of training. In the same way, Boutellier et al.² did not find changes in either peak expiratory flow rate or FEV1.

Overall, it can be concluded from our research that the Powerlung device does elicit positive changes in the pulmonary muscles. The Powerlung device increased the strength of the respiratory muscles as seen by the increase in PEX, VE and VT while decreasing RR at maximal exercise. The device did not produce a significant change in VO2max. It could be deduced that a longer training period (i.e., 8-12 weeks) might reveal more significant changes. Research with intermediate level athletes might also produce larger changes.

When doing further research with highly trained athletes, one might also consider trying different training protocols. In all forms of resistance training, not only is the intensity increased, but the overall volume and duration is also varied. Perhaps training at a higher volume (i.e. more reps) might produce more favorable metabolic changes in the respiratory muscles.

As long as athletes and scientist strive to push the limits of human performance every avenue of training will be explored. Pulmonary resistance training with athletes is still relatively new, and has seen only minimal research. As records continue to fall in the athletic world, research should continue on pulmonary resistance training along with all other aspects of exercise performance.

Funding for this study was provided by Powerlung Inc. The authors would like to sincerely thank all participants in this study and the Bay Area Triathlon Club for their advertisement.