To the best of our knowledge, this study is the first to assess the effect of IMLET on ventilatory response and VO2peak under hypoxia. We hypothesised that IMLET would improve the respiratory response and WOB under H condition, resulting in improved gas exchange. Thus, we also hypothesised that IMLET could improve VO2peak and work capacity under H condition. First, although both IMLET and ET enhanced the inspiratory and expiratory muscle strength (Table 2), we found that the magnitude of improvement in inspiratory muscle strength was greater in the IMLET group than in the ET group (Figure 2). Second, under both N and H conditions, VO2peak and Wmax increased in both training groups (Figure 3); however, VEmax increased only in the IMLET group. For exercise under H condition, although similar changes in Wmax in both training groups were seen, the magnitude of decrease in Wmax under H condition was significantly smaller in the IMLET groups (Figure 4). Our results suggest that IMLET changes the ventilatory response under H condition and suppress the extent of decrease in Wmax under H condition.
Respiratory muscle strength
Previous studies have reported that 4-10 weeks of respiratory muscle training enhances PImax by approximately 20%-30% (15, 19-21). Our IMLET caused a 44% increase in PImax, suggesting that the respiratory muscle strength improved within a short period. McEntire et al. (27) observed an increase in PImax by 28% following moderate-intensity exercise training with 15% PImax inspiratory loads, although PImax also significantly increased by 6 weeks of 30-min cycling exercise training at 70% peak work rate alone. Compared with that of McEntire et al. (27), we observed an approximately 3-time greater increase in PImax by 50% PImax inspiratory-loaded exercise training. Both McEntire et al. (27) and the present study observed an improvement of PImax in both the IMLET group and ET group. Some previous studies observed increasing respiratory muscle strength caused by strenuous exercise training itself (29-31). However, we found greater increases in PImax in the IMLET groups than in the ET group, implying that more than 50% PImax inspiratory load needs to highlight the additional influence of inspiratory load on respiratory muscle strength. Interestingly, PEmax also improved after training in both the IMLET and ET groups. Thus, it is speculated that the increase in PEmax after the training period test is caused by the exercise training per se. More likely, although we did not add expiratory load on the exercise training, the diameter becomes smaller because the subject’s mouth is squeezed to hold the inspiratory muscle trainer; thus, slight pressure may have been applied to the expiration. Increasing respiratory muscle endurance was observed in respiratory muscle training, especially with hyperventilatory training (23, 24, 26), although we did not evaluate the respiratory muscle endurance.
Effect of IMLET on normoxic exercise
With regard to exercise performance under N condition, numerous studies have observed that the exercise performance improved following the respiratory muscle training (20-22, 25, 32), while others disagreed (15, 24). Since there was no significant difference in the extent of improvement in Wmax between the IMLET group and the ET group, the improvement in Wmax caused by the exercise training would not augment, even applying an inspiratory load during the training.
Hyperventilation helps maintain SaO2 during intensive exercise even under normoxia among the subjects with exercise-induced arterial hypoxaemia (33), implying that the gas exchange partly limits the VO2peak. Some studies reported that IMT improved exercise performance related to enhanced ventilatory response (17,18). Our result of the increasing VEmax under normoxia following IMLET is consistent with those of previous studies (24, 27, 34). However, this increase in VEmax by IMLET did not contribute to the improvement of SaO2 and VO2peak, hence the exercise performance, because our subjects did not express arterial desaturation during maximal exercise. For instance, under N condition, VO2peak did not change even if subjects were breathing helium–O2 mixtures with lowered air flow resistances (35).
Effect of IMLET on hypoxic exercise
Esposito et al. (28) reported that VEmax under H condition (11% O2) was increased following IMT compared with pre-training test, which is in agreement with our results. On the contrary, Downey et al. (15) reported that VE under H condition (14% O2) during ~85% VO2peak submaximal running was reduced following IMT. This disagreement of response in VE following IMT might be due to a difference in test exercise intensity (maximal vs. submaximal). We observed that VE was not significantly different between pre- and post-exercise tests when compared with the same absolute work load (at Wmax in pre-test) (not shown in the results; 104.8±22.0 L min-1 in pre vs. 100.5±26.6 L min-1 in post; IMLET group). With this, we can speculate that an increase in VEmax after IMLET was a result of an increase in work load after IMLET.
A high VE under H condition appears to be beneficial for minimising the reduction in VO2peak (4, 5), while WOB and oxygen cost of breathing should be higher with an increase in VE (6) compared with those under N condition. Further, higher WOB would elicit respiratory muscle fatigue (36, 37). Accordingly, we hypothesised that the benefit of IMLET would be emphasised under hypoxic exercise condition rather than under normoxic exercise condition. Previous studies have reported that the IMT did not change the VO2peak under H condition (15, 28). We observed an increase in VO2peak in both training groups following the training period. Similar to the N condition, we cannot deny that the increase in VO2peak under the H condition was caused by the exercise training itself. Interestingly, VO2peak increases without any increase in SaO2 in both groups after training, which indicates that the magnitude of increase in VE after IMLET is inadequate for improving the alveoli gas exchange. Thus, the increase in VO2peak may be the result of exercise training causing circulatory function and peripheral adaptation. In fact, %dVO2peak under H condition did not change even after IMLET. We should speculate one possibility that increase in VEmax by IMLET was a result of an increase in exhaustion intensity by the training.
High VE under H condition leads to higher O2 cost in respiratory muscles with an increase of inspiratory flow resistive work and expiratory flow limitation (36). This would lead to a compromised blood flow to active muscles during heavy exercise (8, 9). Recently, we have reported that in exhaustive incremental running, higher VEmax and exercise performance without any change in VO2peak under hypobaric normoxic condition (492 mmHg with 32.2% O2 gas inhalation) than under normobaric normoxic condition (760 mmHg) and estimated respiratory muscle VO2 reduced by 23% under hypobaric normoxic condition, suggesting that lower air density-related reduction of respiratory load affects exercise performance (38). Further, Downey et al. (15) reported that during 85% VO2peak running under H condition (14% O2), VO2 and cardiac output reduced after IMT. In line with this, we hypothesised that if IMLET reduced WOB against hyperventilation, the reduction in exercise performance under H condition would be attenuated. Our results that %dWmax was significantly smaller after training in the IMLET group partly supports the hypothesis that IMLET increased oxygen transport, such as increased blood flow to active muscles. Further, our result of an increase in VEmax without any significant increase in WOB under H condition following IMLET, not seen in the ET group, implies that the participants can more hyperventilate with similar ventilatory effort after IMLET. Indeed, PEFR and VT at post-training test were higher than those at pre-training test, implying that breathing pattern is altered and increased with elastic work (i.e., recoiled energy work by chest wall inflation). However, we must emphasise the fact that WOB increased by 16% after IMLET. It is suspected that reduced %dWmax after IMLET is a result of reduced limb muscle fatigue due to unloading at submaximal intensity; eventually, the distribution of blood flow in the whole body VO2 at maximal intensity was not different before and after training. Further investigation is warranted to clarify this point.
This study has some limitations. Firstly, we did not fully record subject’s daily workout habits. However, subjects were instructed not to change their usual daily activities and not to participate in strenuous exercises. In addition, subjects belonged to the university track club, and similar exercise training was performed in both the IMLET group and ET group, except that in the laboratory. Secondly, subject’s fitness level and daily sports modality could have influenced our results. Further, the subjects with highest aerobic power tend to express the greatest decrease in VO2pwak under H condition (5). When dividing the subject’s groups, we ensured that the modalities of sports engaged are the same, and no significant difference was found in VO2peak at the pre-training period between the training groups. Thirdly, exercise training was held only for 20 min per day. If the training duration is longer, the outcome between the ET groups and IMLET group may be different. However, the subjects were close to exhaustion by completing 20 min of exercise with the inspiratory load. Thus, subjects of the IMLET group may not be able to exercise further. Finally, the small number of subjects may have biased our conclusion. However, the minimum sample size was calculated from our study (power = 90%, α= 0.05). The minimum sample sizes were estimated to be 5, 9, 8, and 8 for PImax, VO2peak, VEmax, and Wmax under H condition, respectively. Further, data collection needs to clarify the effect of IMLET on hypoxic exercise.