**2. Consequences of sustained respiratory muscle work during continuous exercise**

The work of breathing associated with high-intensity and maximal exercise is responsible for stealing a considerable portion of whole-body VO2, which creates an environment where the locomotor and respiratory muscles compete for O2 delivery [2, 3]. As such, respiratory muscle work, fatigue and metaboreflex are interrelated and suggested to contribute to the development of locomotor muscle fatigue, limiting one's capacity to sustain high-intensity exercise [9, 22].

An inverse relationship exists between the work of breathing and leg O2 uptake during maximal exercise [3]. To reduce the work of breathing, proportional assist ventilation (PAV) can be used to generate inspiratory pressure proportional to the effort of the patient/subject. Conversely, to elevate inspiratory muscle work, a mesh screen can be placed over the inspiratory line, or the aperture of an inspiratory port can be reduced. In one such study employing these techniques, subjects exercised at a workload sustainable for 2.5–3 min at, or near a work rate corresponding to the attainment of VO2max. The work of breathing was attenuated by 60% with PAV and increased by 95% with inspiratory loading, compared to control during the exercise bout. Elevating the work of breathing had a negligible effect on whole-body VO2. Moreover, both leg blood flow and VO2 fell compared to control exercise which coincided with an increase in leg vascular resistance. These data suggest that cardiac output did not increase to accommodate the additional muscular work [2]. It is likely that blood flow was redistributed to the respiratory muscles to support the heightened metabolic activity at the expense of the locomotor muscles [3]. When the respiratory muscles were unloaded with PAV, there was a slight increase in limb blood flow which corresponded with an increase in leg VO2. Thus, by reducing the metabolic demands of the respiratory muscles, O2 delivery to the lower limbs can be improved. Taken together, these data indicate that the

**13**

in quadriceps fatigue [25].

*The Respiratory System during Intermittent-Sprint Work: Respiratory Muscle Work…*

'normal' work of breathing incurred during high-intensity exercise may actually be a limiting factor of O2 transport to the locomotor muscle during high-intensity

Exercise intensity also plays an important role in the competition between the locomotor and respiratory muscles for available O2. While exercising at submaximal work rates (50–75% VO2max), there is a small but significant increase in whole-body VO2 in response to an elevated work of breathing [23]. Since VO2 responded proportionally to the changes in inspiratory muscle work, is has been concluded that there is enough capacity in cardiac output to increase and meet the demands of additional muscular work during submaximal exercise [3]. It is only during high-intensity exercise when cardiac output approaches maximal flow rates that competition for

Since the high work of breathing during high-intensity exercise (>80% VO2max) seems to have a limiting effect on locomotor muscle blood flow, the rate of development of peripheral fatigue is likely affected too. To examine exercise-induced quadriceps muscle fatigue, supra-maximal femoral nerve stimulation can be used to provide an objective measure of muscle force-generating capacity [24]. In one such example, peripheral muscle fatigue was assessed after exercise at a work rate corresponding to the attainment of 92% of VO2max [25]. On one occasion, subjects exercised to volitional exhaustion (13.2 min). On a separate visit, exercise at the same work rate and duration was repeated while the respiratory muscles were unloaded using PAV (56% reduction of inspiratory muscle work). Following the completion of exercise, quadriceps muscle fatigue was 8% greater when subjects were not using breathing assistance. To examine how a heightened work of breathing affects peripheral fatigue, exercise was repeated with inspiratory loading (80% increase of inspiratory muscle work) to exhaustion (7.9 min). Following the termination of exercise, the force-generating capacity of the quadriceps was 8% lower when performed with inspiratory loading compared to control [25]. These data robustly demonstrate that peripheral fatigue can be manipulated by altering the work for breathing, which suggests that respiratory muscle work is a limiting factor

It is usually unlikely for healthy humans to experience inspiratory loading during exercise. However, exposure to (simulated) altitude is a more common environmental condition that will increase the work of breathing compared to normoxia via stimulation of pulmonary ventilation [26, 27]. To examine the relationship between hypoxia-induced elevated work of breathing and peripheral fatigue, subjects exercised at a constant work rate (≈273 W) corresponding to 82% of VO2max in simulated altitude (fraction of inspired oxygen, FIO2 = 0.15) to exhaustion [28]. Exercise was then repeated at the same work rate for an identical duration in normoxia (≈273 W for 8.6 min). Compared to hypoxia, inspiratory muscle work was 36% less when exercising in normoxia and induced a lesser reduction in quadriceps force generation (normoxia −16% vs., hypoxia −30%). To isolate the effects of the work of breathing on peripheral muscle fatigue, subjects repeated both exercise trials (normoxia and hypoxia) using PAV. Inspiratory muscle work was nearly identical during exercise between normoxia and hypoxia with PAV, and the reduction in hypoxia-induced peripheral fatigue was attenuated relative to normoxia (normoxia −15% vs., hypoxia −22%). Combined, these data demonstrate that the development of quadriceps fatigue is accelerated in hypoxia in part due to heightened inspiratory muscle work. Moreover, this occurs at a work rate and exercise duration at which inspiratory muscle work usually does not affect quadriceps fatigue [28]. Sustained exercise ≥90% VO2max and the accompanying work of breathing may have to reach a given threshold to elicit meaningful changes

*DOI: http://dx.doi.org/10.5772/intechopen.91207*

available blood flow begins to develop [3].

of high-intensity exercise [2, 3].

exercise [3].

*The Respiratory System during Intermittent-Sprint Work: Respiratory Muscle Work… DOI: http://dx.doi.org/10.5772/intechopen.91207*

'normal' work of breathing incurred during high-intensity exercise may actually be a limiting factor of O2 transport to the locomotor muscle during high-intensity exercise [3].

Exercise intensity also plays an important role in the competition between the locomotor and respiratory muscles for available O2. While exercising at submaximal work rates (50–75% VO2max), there is a small but significant increase in whole-body VO2 in response to an elevated work of breathing [23]. Since VO2 responded proportionally to the changes in inspiratory muscle work, is has been concluded that there is enough capacity in cardiac output to increase and meet the demands of additional muscular work during submaximal exercise [3]. It is only during high-intensity exercise when cardiac output approaches maximal flow rates that competition for available blood flow begins to develop [3].

Since the high work of breathing during high-intensity exercise (>80% VO2max) seems to have a limiting effect on locomotor muscle blood flow, the rate of development of peripheral fatigue is likely affected too. To examine exercise-induced quadriceps muscle fatigue, supra-maximal femoral nerve stimulation can be used to provide an objective measure of muscle force-generating capacity [24]. In one such example, peripheral muscle fatigue was assessed after exercise at a work rate corresponding to the attainment of 92% of VO2max [25]. On one occasion, subjects exercised to volitional exhaustion (13.2 min). On a separate visit, exercise at the same work rate and duration was repeated while the respiratory muscles were unloaded using PAV (56% reduction of inspiratory muscle work). Following the completion of exercise, quadriceps muscle fatigue was 8% greater when subjects were not using breathing assistance. To examine how a heightened work of breathing affects peripheral fatigue, exercise was repeated with inspiratory loading (80% increase of inspiratory muscle work) to exhaustion (7.9 min). Following the termination of exercise, the force-generating capacity of the quadriceps was 8% lower when performed with inspiratory loading compared to control [25]. These data robustly demonstrate that peripheral fatigue can be manipulated by altering the work for breathing, which suggests that respiratory muscle work is a limiting factor of high-intensity exercise [2, 3].

It is usually unlikely for healthy humans to experience inspiratory loading during exercise. However, exposure to (simulated) altitude is a more common environmental condition that will increase the work of breathing compared to normoxia via stimulation of pulmonary ventilation [26, 27]. To examine the relationship between hypoxia-induced elevated work of breathing and peripheral fatigue, subjects exercised at a constant work rate (≈273 W) corresponding to 82% of VO2max in simulated altitude (fraction of inspired oxygen, FIO2 = 0.15) to exhaustion [28]. Exercise was then repeated at the same work rate for an identical duration in normoxia (≈273 W for 8.6 min). Compared to hypoxia, inspiratory muscle work was 36% less when exercising in normoxia and induced a lesser reduction in quadriceps force generation (normoxia −16% vs., hypoxia −30%). To isolate the effects of the work of breathing on peripheral muscle fatigue, subjects repeated both exercise trials (normoxia and hypoxia) using PAV. Inspiratory muscle work was nearly identical during exercise between normoxia and hypoxia with PAV, and the reduction in hypoxia-induced peripheral fatigue was attenuated relative to normoxia (normoxia −15% vs., hypoxia −22%). Combined, these data demonstrate that the development of quadriceps fatigue is accelerated in hypoxia in part due to heightened inspiratory muscle work. Moreover, this occurs at a work rate and exercise duration at which inspiratory muscle work usually does not affect quadriceps fatigue [28]. Sustained exercise ≥90% VO2max and the accompanying work of breathing may have to reach a given threshold to elicit meaningful changes in quadriceps fatigue [25].

*Respiratory Physiology*

muscles.

O2 supply to vital organs [4, 9–11]. Additionally, when the metabolic demands of multiple muscle groups are high, and cardiac output is nearing maximal flow rates, competition for available blood flow can arise between muscle groups. One such example is the interplay between limb locomotor musculature and the respiratory

become a limiting factor of exercise capacity [2, 9, 19–21].

**continuous exercise**

**2. Consequences of sustained respiratory muscle work during** 

limiting one's capacity to sustain high-intensity exercise [9, 22].

The work of breathing associated with high-intensity and maximal exercise is responsible for stealing a considerable portion of whole-body VO2, which creates an environment where the locomotor and respiratory muscles compete for O2 delivery [2, 3]. As such, respiratory muscle work, fatigue and metaboreflex are interrelated and suggested to contribute to the development of locomotor muscle fatigue,

An inverse relationship exists between the work of breathing and leg O2 uptake during maximal exercise [3]. To reduce the work of breathing, proportional assist ventilation (PAV) can be used to generate inspiratory pressure proportional to the effort of the patient/subject. Conversely, to elevate inspiratory muscle work, a mesh screen can be placed over the inspiratory line, or the aperture of an inspiratory port can be reduced. In one such study employing these techniques, subjects exercised at a workload sustainable for 2.5–3 min at, or near a work rate corresponding to the attainment of VO2max. The work of breathing was attenuated by 60% with PAV and increased by 95% with inspiratory loading, compared to control during the exercise bout. Elevating the work of breathing had a negligible effect on whole-body VO2. Moreover, both leg blood flow and VO2 fell compared to control exercise which coincided with an increase in leg vascular resistance. These data suggest that cardiac output did not increase to accommodate the additional muscular work [2]. It is likely that blood flow was redistributed to the respiratory muscles to support the heightened metabolic activity at the expense of the locomotor muscles [3]. When the respiratory muscles were unloaded with PAV, there was a slight increase in limb blood flow which corresponded with an increase in leg VO2. Thus, by reducing the metabolic demands of the respiratory muscles, O2 delivery to the lower limbs can be improved. Taken together, these data indicate that the

The respiratory muscles perform work to overcome the elastic recoil of the lungs and chest, resistance from turbulent and viscous airflow through the respiratory tract and tissue deformation [12]. As pulmonary ventilation (VE) rises, there is an exponential increase in the work being performed by the respiratory muscles [12, 13]. This ventilation-induced rise in work of breathing is caused by two factors; (1) dynamic hyperinflation to accommodate greater expiratory flow rates [14], and (2) progressive increase in the contribution of the expiratory muscles to breathing [15]. As the lungs and chest are progressively stretched to accommodate the increasing volume of inhaled air and end-expiratory lung volume is reduced, the contribution of elasticity in these tissues to the work of breathing increases [16, 17]. Accompanying the changes in work of breathing with VE, there is a certain O2 cost of exercise hyperpnoea [13, 18]. By mimicking the ventilation pattern (respiratory frequency and tidal volume) obtained during exercise while at rest, it is possible to estimate the proportion of whole-body VO2 that is devoted to the respiratory muscles. During moderate exercise, the O2 cost of breathing accounts for 3–6% of the total whole-body VO2. During high-intensity exercise, the relative contribution of exercise hyperpnoea to whole-body VO2 is estimated increases to 10–15% and can

**12**
