INBAR, O., P. WEINER, Y. AZGAD, A. ROTSTEIN, and Y. WEINSTEIN. Specific inspiratory muscle training in well-trained endurance athletes. Med. Sci. Sports Exerc., Vol. 32, No. 7, pp. 1233-1237, 2000.
Purpose: It has been reported that arterial O2 desaturation occurs during maximal aerobic exercise in elite endurance athletes and that it might be associated with respiratory muscle fatigue and relative hypoventilation. We hypothesized that specific inspiratory muscle training (SIMT) will result in improvement in respiratory muscle function and thereupon in aerobic capacity in well-trained endurance athletes.
Methods: Twenty well-trained endurance athletes volunteered to the study and were randomized into two groups: 10 athletes comprised the training group and received SIMT, and 10 athletes were assigned to a control group and received sham training. Inspiratory training was performed using a threshold inspiratory muscle trainer, for 0.5 h·d-1 six times a week for 10 wk. Subjects in the control group received sham training with the same device, but with no resistance.
Results: Inspiratory muscle strength (PImax) increased significantly from 142.2 ± 24.8 to 177.2 ± 32.9 cm H2O (P < 0.005) in the training but remained unchanged in the control group. Inspiratory muscle endurance (PmPeak) also increased significantly, from 121.6 ± 13.7 to 154.4 ± 22.1 cm H2O (P < 0.005), in the training group, but not in the control group. The improvement in the inspiratory muscle performance in the training group was not associated with improvement in peak V̇Emax, V̇O2max, breathing reserve (BR), or arterial O2 saturation (%SaO2), measured during or at the peak of the exercise test.
Conclusions: It may be concluded that 10 wk of SIMT can increase the inspiratory muscle performance in well-trained athletes. However, this increase was not associated with improvement in aerobic capacity, as determined by V̇O2max, or in arterial O2 desaturation during maximal graded exercise challenge. The significance of such results is uncertain and further studies are needed to elucidate the role of respiratory muscle training in the improvement of aerobic-type exercise capacity.
Afundamental question in exercise physiology concerning the factor(s), which limits maximal oxygen uptake (V̇O2max), is still unresolved. However, growing evidence indicates that in trained athletes, oxygen delivery to the muscles limits the V̇O2max during heavy exercise (1,33,35). O2 delivery depends on blood flow, arterial O2 saturation, and hemoglobin concentration. Traditionally, it was claimed that arterial O2 saturation does not decline markedly in healthy individuals exercising at sea level, even at maximal effort (1,37,39). However, there are reports in the literature which suggest that arterial hypoxemia may occur during heavy exercise in healthy individuals with a high V̇O2max (11,17,23,32). Aerobic performance of highly trained individuals may, therefore, be limited by this arterial hypoxemia.
Four possible mechanisms of exercise-induced hypoxemia have been proposed: 1) venoarterial shunt, 2) ventilation-perfusion inequality, 3) hypoventilation, and 4) diffusion limitations (13,31,36,39). It seems that venoarterial shunt does not play an important role in exercise-induced arterial hypoxemia, because oxygen breathing during heavy exercise was found to correct such hypoxemia (13,34). It was suggested that ventilatory capacity might play a role in the development of hypoxemia during maximal effort in highly trained endurance athletes (17,19,20,31). In a previous study performed by our group (17), we studied well-trained athletes during graded maximal aerobic exercise while breathing atmospheric air, normoxic helium, and oxygen-enriched mixture. It was concluded that the observed arterial O2 desaturation is secondary to a relative hypoventilatory response and may limit V̇O2max and aerobic performance at high work levels. It has also been shown that respiratory muscle fatigue occurred after both voluntary hyperpnea (2) and marathon running (20) in normal humans. Moreover, in at least one study (18), it was reported that increasing the stimulus to breathe during maximal exercise by inducing either hypercapnia or hypoxemia, but without parallel physiological modification in the respiratory system, failed to increase V̇E, V̇O2, as well as inspiratory or expiratory pressure.
Although there is ample evidence that inspiratory muscles' ability to generate force may be reduced, especially at work rates associated with high ventilatory requirements (19), it is well established that respiratory muscles can be trained like other skeletal muscles (4,29), both in healthy subjects and in patients with dyspnea (23,27,28,34,38). We, therefore, hypothesized that if respiratory constraints resulting in a relative hypoventilation plays a role in arterial O2 desaturation at high work levels, then specific respiratory muscle training might result in improvement in exercise performance and in aerobic capacity in well trained endurance athletes.