Generally, the pulmonary system is considered to be overbuilt for exercise at sea level (8). Respiratory muscle fatigue (RMF) occurs during sustained high-intensity (≥80% V[Combining Dot Above]O2max) exercise lasting >8–10 minutes during running (2–4,24) and cycling (7,8,21,30) in both inactive and active subjects (21). Respiratory muscle fatigue has been defined as occurring when there is a reduction in diaphragmatic or global respiratory muscle pressure, typically cited in the literature as >10% reduction from baseline (32), which has been linked to increased respiratory muscle work, decreased respiratory muscle blood flow, production of reactive oxygen species, and glycogen depletion (12,18,29). Although each of these contributes to RMF, respiratory muscle work and subsequent redistribution of cardiac output during heavy exercise are the most widely studied contributors. Specifically, Babcock et al. (4) found that unloading the respiratory muscles (by ∼50%) alleviated the diaphragmatic fatigue during heavy exercise. In addition, Babcock et al. (2) reported that subjects had to mimic ventilation at rest ∼50% higher than ventilation during heavy exercise to demonstrate diaphragmatic fatigue suggesting that the distribution of cardiac output during heavy exercise contributes to diaphragmatic fatigue as well.
However, RMF has been recently reported to occur in a shorter duration (∼3–6 minutes) after high-intensity rowing, swimming, and cycling (20,23,34). For example, Voliantis et al. reported RMF after 6 minutes of high-intensity (all-out) rowing. In addition, Lomax and McConnell found that inspiratory muscle fatigue occurred after only ∼3 minutes of high-intensity swimming at ∼90% of race pace. Therefore, it has been suggested that the earlier onset of RMF may be due to an increased work of breathing in these specific modes of exercise (16) and the higher muscle mass used in these modes of exercise (swimming and rowing). Interestingly, respiratory and diaphragmatic fatigue has recently been reported to occur after 5–7 minutes of high-intensity cycling exercise in untrained and highly active subjects, respectively (80–85% V[Combining Dot Above]O2max) (15,33). These findings of RMF after heavy cycling exercise suggest that the increase in exercising muscle mass in swimming and rowing may not contribute to the earlier onset of exercise-induced RMF. However, it is not known from these previous studies if the respiratory muscles fatigue occurs at 90% peak power in recreationally active subjects.
Although the physiological adaptations have been well documented in trained individuals, elite athletes comprise a small portion of the population, whereas inactive and recreationally active individuals comprise a much larger percentage. In the existing high-intensity interval training (HIT) literature, cardiovascular and muscular adaptations have been documented that are similar to traditional endurance training (6,13,15,19,27,35). However, less has been reported investigating various HIT protocols on the pulmonary system. The existing pulmonary literature has found that HIT increases respiratory muscle strength greater than traditional endurance training (11), which reduces postexercise RMF (10). In addition, individuals have reported that HIT at 90% of V[Combining Dot Above]O2max is more enjoyable than continuous exercise (CE) at 50% V[Combining Dot Above]O2max (5) Therefore, implementing HIT as part of a training program or normal exercise regimen may be a preferable option if physiological benefits are similar to endurance training and exercise adherence is higher. No studies, to our knowledge, have investigated repeated bouts of exercise associated with HIT and RMF, although HIT is commonly included in training programs for both recreationally active individuals and athletes.
Therefore, the purpose of this study was to (a) determine the effect of 90% peak power (∼5 minutes) of high-intensity cycling on RMF in recreationally active subjects. In addition, we wanted to (b) determine whether RMF was present during or after performing a common HIT protocol consisting of repeated bouts of exercise at 90% peak power with rest intervals added. We hypothesized that (a) high-intensity cycling exercise for ∼5 minutes would lead to RMF and that (b) RMF would be exhibited during and after high-intensity interval exercise with repeated bouts at the same intensity.
Experimental Approach to the Problem
Each subject visited the laboratory 7 times within a 2-week period and 48 hours between visits. Subjects were instructed to not exercise within 24 hours of each testing sessions, and at least 48 hours was given between all HIT and CE trials. For all testing sessions, subjects were instructed to not consume caffeine or alcohol within 12 hours or exercise within 24 hours. The familiarization day and additional trials were scheduled at subjects preferred between 7 AM and 7 PM, which remained as consistent as possible per the subjects and investigators schedules. Subjects were instructed to drink water normally and not eat within 2 hours of the testing session. The study was powered to detect a 10% reduction in PIMAX that has been reported in the literature after HIT in other exercise modalities (power = 0.80). On the first visit, subjects' height and weight were recorded, standard pulmonary function tests (PFTs) were administered, and an incremental test to exhaustion was performed. The following day, subjects returned to the laboratory to complete familiarization trials with maximal inspiratory and expiratory mouth pressure (PIMAX and PEMAX) measurements to ensure tests could be performed correctly. The subject performed PIMAX and PEMAX tests until maximal mouth pressure and lung volume measurements were consistently within 10% of each other. The order in which subjects completed the CE and HIT trials were randomized through coin flips for CE vs. HIT, and furthermore for PIMAX vs. PEMAX. Every subject completed the HIT protocol twice (measuring PIMAX and PEMAX on separate days) and 3 CE trials. PIMAX and PEMAX were measured pre- and post-HIT and CE trials as well as during the HIT protocol.
Eight healthy men (age range 19–24 years) were recruited from the Kansas State University campus and volunteered to participate in the research study. Subjects were college aged and moderately active, although not competitively trained. Activity level was determined through physical activity screening questions on the medical history questionnaire. All were free of acute or chronic diseases determined through the medical history questionnaire. Written informed consent was obtained from each subject, and all procedures were approved by the Institutional Review Board for Research Involving Human Subjects (#6460) at Kansas State University, Manhattan, Kansas, and conformed to the Declaration of Helsinki. Subject characteristics, PFTs, and V[Combining Dot Above]O2max data are shown in Table 1. All subjects were moderately active but not competitively trained. Subjects' completed both HIT and CE protocols at 90% peak power, determined from the V[Combining Dot Above]O2max test. No subjects significantly desaturated during exercise. Subjects' pulmonary function was not different (p > 0.05) from predicted reference values (17).
The incremental test to exhaustion (25 W·min−1) for determination of V[Combining Dot Above]O2max was performed on a cycle ergometer (Sensormedics 800). Subjects were instructed to maintain a pedal frequency of 60–80 revolutions per minute. Breath-by-breath metabolic and ventilatory data were recorded on a metabolic cart and analyzed continuously during exercise (Sensormedics 229; Sensormedics Corp., YorbaLinda, CA, USA). Heart rate (HR) was recorded through polar HR monitors, and rating of perceived exertion was recorded the last 5 seconds of each stage using the modified Borg rating scale (1–10). A pulse oximeter (Datex-Ohmeda 3900P, Madison, WI, USA) was used to determine arterial saturation (SpO2). Power output was recorded every minute on the cycle ergometer, and peak power was recorded at V[Combining Dot Above]O2max. Termination of the test occurred when the subject was unable to maintain a pedal cadence of 60 rpm. The subject completed an additional trial 15 minutes after the initial max test at 105% peak power to validate V[Combining Dot Above]O2max (28).
Pulmonary function was assessed using standard PFTs. Maximum flow-volume loop was used to determine peak expiratory flow, forced expiratory flow in 1 second, forced vital capacity, and forced expiratory flow at 25–75% of vital capacity. Pulmonary function tests were performed according to ATS/ERS guidelines (25) (Sensormedics 229; Sensormedics Corp.). Pulmonary function tests were performed until at least 3 flow-volume loops were within 10% of one another, and then 3 closest were averaged and used for analysis (11,30). Respiratory muscle strength was measured using PIMAX and PEMAX (Sensormedics 229, Sensormedics Corp.). PIMAX was measured from residual volume and PEMAX was measured from total lung capacity (ATS/ERS Statement of Respiratory Muscle Testing, 2002). Maximal pressures and lung volume measurements were taken after PFTs, with the average of the closest 3 (within 10%) used in the analysis (11,30). Taking the closest measurements within 10% is more stringent than the current ATS guidelines.
The CE protocol was performed on an electronically braked cycle ergometer (Sensormedics 800). Seat height was kept the same for all exercise testing sessions. Every subject completed 3 CE trials at 90% of peak power determined through final workload in the V[Combining Dot Above]O2max test to assess respiratory muscle strength. Each subject completed PIMAX and PEMAX measurements before warming up for 3 minutes at 50% peak power. Subjects were instructed to ride until exhaustion, and the test was terminated when subjects could not maintain a pedal cadence of 60 rpm for 5 seconds. PIMAX and PEMAX measurements were performed immediately after termination of the exercise bout. Heart rate was recorded every minute of exercise to ensure it was ≥85% of HR at V[Combining Dot Above]O2max. Each subject completed 3 trials to ensure consistency, and time to exhaustion was not different between trials. PIMAX or PEMAX values were averaged over the 3 trials for statistical analysis.
To determine when RMF occurred, an HIT protocol was used to determine at what time the fatigue occurred. The HIT protocol was performed on an electronically braked cycle ergometer (Sensormedics 800). The HIT protocol was performed twice by the subject with PIMAX measured one visit and PEMAX measured during the other visit. PIMAX or PEMAX were assessed before the warm-up. Subjects warmed up for 3 minutes at 50% of peak power determined from the final workload in the V[Combining Dot Above]O2max test. Each subject completed a modified HIT protocol at seven 1-minute intervals at 90% peak power with 2 minutes of rest (11). PIMAX or PEMAX was measured during the 2-minute resting period, and the closest 3 measurements (within 10%) were averaged and used for data analysis. PIMAX and PEMAX were assessed immediately after completion of the final interval (within 30 seconds). To measure these correctly and accurately within the 2-minute rest intervals, it was necessary to assess them on separate visits. After each exercise interval, subjects put in the mouthpiece immediately, so the investigator could view several tidal volume loops and ensure all tests were performed at residual volume for PIMAX and total lung capacity for PEMAX. After the investigator viewed normal tidal volume loops, the subjects were instructed to perform the maximal mouth pressure. They were given ∼10–15 seconds in between every maneuver so the investigator could monitor normal tidal breaths. Therefore, performing ∼3–4 measurements for either PIMAX or PEMAX used most of the 2-minute rest intervals. Heart rate was recorded in the final 10 seconds of each interval to ensure it was ≥85% of HR at V[Combining Dot Above]O2max.
Data analysis was performed using the SigmaStat program (Jandel Scientific Software). Data are expressed as mean ± SD. Changes in respiratory muscle strength between baseline and end exercise were assessed using a 2 (time) × 2 (condition) analysis of variance (ANOVA) to determine differences between the HIT (PIMAX and PEMAX) and CE. A repeated-measures ANOVA used to determine differences between respiratory muscle strength assessed after every one minute of exercise in both HIT protocols. Significance was set at p ≤ 0.05 for all analyses.
Respiratory Muscle Strength
Subjects cycled for 5 ± 1 minute for the CE protocol. PIMAX and PEMAX were not different (p > 0.05) preexercise between the HIT and CE protocol. Postexercise PIMAX and PEMAX were not different (p > 0.05) compared with baseline for the CE trial (Figure 1). Postexercise PIMAX and PEMAX were not different (p > 0.05) compared with baseline for the HIT trial (Figure 2). Table 2 displays respiratory muscle strength assessed at each stage of the HIT protocol. There were no differences (p > 0.05) in respiratory muscle strength assessed after each stage.
The major finding in this investigation was that RMF did not occur after heavy intensity exercise at 90% peak power (∼5 minutes) in recreationally active males. In addition, we did not find RMF during or after the repeated bouts of exercise in the HIT protocol. These findings suggest that heavy cycling exercise at a high intensity for a short duration or repeated bouts is not sufficient for the development of RMF in moderately active males.
Respiratory muscle fatigue has consistently been reported after high-intensity (>80% V[Combining Dot Above]O2max) sustained (>8–10 minutes) running and cycling (2–4,7,8,21,24,30). However, recently Vogiatzis et al. reported diaphragmatic fatigue after 5 minutes of cycling at ∼85% peak power in active individuals. Interestingly, studies using high-intensity swimming and rowing have reported RMF after ∼3–6 minutes of exercise (20,23,34). In this study, neither ∼5 minutes of continuous high-intensity cycling nor seven 1-minute intervals at 90% peak power resulted in RMF in moderately active subjects. This study in combination with previous studies suggests that the modes of exercise using more muscle mass (e.g., swimming and rowing) may lead to an earlier onset of RMF compared with cycling for a shorter duration (<8 minutes) at high intensities. Babcock et al. (2,4) demonstrated that both work of breathing and the redistribution of cardiac output contribute to exercise-induced RMF. Lomax and McConnell (23) have suggested that respiratory mechanics during swimming may lead to higher work of breathing. In addition, swimming and rowing use more muscle mass during high-intensity exercise compared with cycling, which would lead to higher cardiac output redistribution. Therefore, it is likely that the greater muscle mass (and therefore cardiac output redistribution) used in swimming and rowing contributed to the earlier onset of RMF.
In addition, subjects in the previously cited studies which showed RMF postexercise in cycling have been either highly active or untrained. We wanted to elucidate the physiological responses to very high-intensity cycling, with and without repeated bouts, in recreationally active individuals. This may then have greater real-world practical applications for coaches, trainers, and sports practitioners working with moderately active subjects, who represent a larger part of the overall population than untrained individuals or elite athletes. The V[Combining Dot Above]O2max of our subjects was ∼3.3 L·min−1 and were at ∼270 W at 90% peak power, whereas the subjects who exhibited RMF in Vogiatzis study were at ∼4.2 L·min−1 and ∼290 W. Although they had higher overall aerobic capacity, elite athletes are capable of exercising at higher intensities that is closer to their maximum aerobic capacity. In Vogiatzis study, subjects were stopped at 5 minutes, whereas the subjects in our study reached volitional fatigue at ∼5 minutes. Although subjects showed RMF at 5 minutes in Vogiatzis study, subjects were highly trained endurance cyclists and may have been able to exercise longer. In addition, these investigators specifically assessed diaphragmatic fatigue, whereas we assessed global RMF. Currently, the literature is inconclusive on whether or not RMF affects exercise performance.
Repeated bouts of exercise with rest intervals were also used to investigate RMF in a common HIT protocol (1-minute exercise: 2 minutes of rest). To our knowledge, no previous studies have investigated RMF during and after repeated bouts of exercise at 90% of peak power. One possible reason we did not find RMF is the rest intervals in the HIT protocols allowed for the respiratory muscles to recover and delay the onset of fatigue. This is not likely and only supported by 1 study, to our knowledge, that showed that respiratory muscles can recover from fatigue in 1.5 minutes postexercise (22). The majority of research studies show a reduction in maximal mouth pressures beyond 10 minutes after exercise until exhaustion in moderately active subjects (26). Future studies should investigate the number of repeated bouts that can be performed in recreationally active individuals for the greatest performance and fitness benefits without the pulmonary system as a limitation.
Bilateral phrenic nerve stimulation has previously been the gold standard for assessing diaphragmatic fatigue, and gastric pressures have been used to assess abdominal fatigue (31). In this study, maximal mouth pressures were used to measure RMF. Although an indirect assessment of respiratory muscle strength, these pressures are accepted by the American Thoracic Society as a validated method to assess RMF (1). To ensure consistency, lung volume measurements were made and evaluated for every trial, and tests were performed in triplicate. The number of trials of maximal mouth pressures was kept ≤3 before and after, and in between every interval because this has been shown to reduce both subject variability (34) and not cause RMF. Also, subjects completed a familiarization day for both PIMAX and PEMAX to ensure that they could produce maximal mouth pressures consistently within 10% of one another.
Previous research has established that RMF occurs in as little at ∼3 minutes of high-intensity swimming and rowing exercise due to greater cardiac output redistribution and ventilatory demands that are used in these sports. Interestingly, RMF has been reported to occur in as few as 5 minutes in highly trained male cyclists and ∼7 minutes in untrained males. Although mode of exercise and exercise duration may help to elucidate when RMF occurs, this is the first study to investigate high intensity (90% peak power) and short duration (∼5 minutes) of CE, and a matched HIT session on RMF in recreationally active subjects. Future research should further investigate the optimal work: rest ratio in which benefits in respiratory muscle strength are documented and RMF does not limit exercise tolerance to possibly implement in training programs.
In recreationally active individuals, a common HIT protocol of 1 minute of work to 2 minutes of rest at 90% peak power does not cause RMF. A similar protocol used previously in our laboratory has been reported to have greater increases in respiratory muscle strength than a traditional endurance training protocol (11), which leads to less exercise-induced RMF (10). In addition, there has been greater reported exercise adherence and enjoyment in HIT protocols than traditional endurance training (5). With these findings previously and our work, which shows a common HIT protocol does not cause RMF, the sports practitioner, physical trainer, or fitness professional making an exercise prescription for the client should consider implementing HIT training into the exercise regimen for the recreationally active individual who wants a consistent training program.
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