**3. Factors influencing respiratory muscle work during repeated-sprint exercise**

Repeated-sprints are characterised by brief 'all-out' exercise bouts of 4–15 s, separated by incomplete recovery periods of 14–30 s [29, 30]. Performance in a repeat-sprint context is therefore represented as the ability to reproduce power output after a previous bout of maximal exercise [31]. Over the course of a repeatedsprint series, there is a progressive decline in total mechanical work performed in each successive sprint. The rate of performance decline is also typically accelerated in low O2 environments [32]. Initial sprint performance is largely determined by muscular strength and power production [33], whereas the ability to resist fatigue and maintain performance is underpinned by aerobic capacity and the ability to deliver O2 to the locomotor muscles in the recovery periods between sprint recovery periods [34, 35]. Below, we outline the work load-induced physiological factors known to the work of breathing during intense intermittent exercise.

### **3.1 Metabolic determinates of repeated-sprint exercise**

Resting intramuscular stores of ATP are limited to ≈20–25 mmol·kg<sup>−</sup><sup>1</sup> of dry muscle weight, which during a sprint, can only provide energy for 1–2 s [36, 37]. As resting ATP stores become depleted, three major energy systems are responsible for ATP resynthesis. Rapid resynthesis is achieved through phosphocreatine (PCr) degradation [36]. Anaerobic glycolysis also has a large involvement in sprint metabolism [36]. Though as sprints are repeated, the relative contribution of anaerobic glycolysis towards ATP resynthesis declines [36, 37]. Conversely, aerobic metabolism has a very small role in isolated sprit performance (≈10% of total ATP production), which increases as sprints are repeated [37, 38].

Intramuscular PCr is especially important for the rapid resynthesis of ATP during explosive activities via the reversible PCr-creatine kinase pathway [39–41]. In the presence of the enzyme creatine kinase, adenosine diphosphate (ADP) is converted to ATP through the dephosphorylation of PCr to form creatine (Cr). It is estimated that during a single 6-s sprint, 50% of anaerobic ATP production is derived predominantly through PCr degradation [36]. The remaining anaerobic energy contribution during an isolated sprint is supported mainly by glycolysis (44%), and in minority by intramuscular ATP stores (6%). When sprints are repeated, the relative contribution of PCr to anaerobic ATP resynthesis increases. By the tenth 6-s sprint (each separated by 30 s passive rest), PCr degradation is estimated to account for 80% of the total anaerobic energy contribution [36]. However, intramuscular PCr stores are limited to ≈80 mmol·kg<sup>−</sup><sup>1</sup> of dry muscle weight, and after only a single 6-s sprint, stores are reduced ≈50% from baseline [36, 42]. When multiple sprints are performed, PCr depletion can be up to 75% after 5 repetitions [42], and 84% after 10 [36]. Since PCr degradation has such a large contribution to ATP resynthesis, the recovery of intramuscular stores PCr is critically important to the restoration of power output [43].

The capacity to recover PCr is limited in a multiple sprint series, largely constrained by the short recovery periods between sprints. The rate of PCr resynthesis follows an initial fast phase, followed by a second longer slow component [44]. After a single 6-s sprint, approximately 70% of PCr replenishment is achieved in the first 30 s of passive rest [42]. But as sprints are repeated and muscle stores are further depleted, PCr can only recover to 50% of resting stores after just five repetitions. When rest is extended post a repeat-sprint series, only 80% of PCr is recovered after 3 min [42], and 85% after 6 min of passive rest [45]. Though PCr degradation is an anaerobic process, PCr resynthesis is an aerobic process and is sensitive to O2 availability [43, 44, 46, 47]. When breathing a hypoxic gas mixture

**15**

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

(FIO2 = 0.10), the rate of PCr resynthesis has been demonstrated to be attenuated by 23% [46]. While breathing a hyperoxic gas (FIO2 = 1.00) enhances recovery by 20% compared with normoxia, which suggests that under normal exercise conditions PCr resynthesis is limited by O2 availability [46]. Therefore, if the work of breathing is high enough to limit locomotor muscle O2 delivery, PCr resynthesis in

The energy debt created by the rapid decrease in muscle PCr during a single sprint is met by a sizable contribution of anaerobic glycolysis to ATP resynthesis. Approximately 44% of ATP resynthesis is derived from anaerobic glycolysis during a single 6-s sprint [36]. However, the relative contribution of anaerobic metabolism declines as sprints are repeated [48]. By the tenth sprint, Gaitanos, Williams [36] estimated that glycolysis was only responsible for 16% of total anaerobic ATP production. Moreover, in four of the seven subjects, it was estimated to be zero

in the relative decrease in anaerobic glycolysis during multiple-sprint work. The most likely being the progressive depletion of muscle glycogen that is associated

inorganic phosphate, and most importantly PCr resynthesis [40, 51].

The aerobic contribution to an isolated sprint is minimal since the maximal rate of ATP resynthesis is far below the requirements of maximal sprint work [39]. In an isolated sprint, aerobic metabolism is responsible for ≈10% of total energy production [37, 48]. But as sprints are repeated, the relative increase in aerobic metabolism to total ATP turnover rate rises to compensate for reduced energy supply from anaerobic pathways [38]. Following five 6-s sprints, it is estimated the aerobic energy contribution rises to ≈40% of total ATP production [48]. The remaining 60% is derived from anaerobic pathways, predominantly PCr degradation [36, 42]. Pulmonary VO2 can fluctuate between 70 and 100% of VO2max from sprint to recovery periods in the latter stages of a repeat-sprint series [50]. When no external work is being performed (i.e., passive rest) during the recovery period between sprints, the elevated VO2 above baseline is representative of lactate metabolism, removal of

Aerobic metabolism may have a limited role in ATP formation during multiple

Muscle O2 availability during repeated-sprint exercise is critical for supporting PCr resynthesis, which underpins the capacity to maintain power out over a sprint series [36, 46]. Changes in local O2 balance (delivery vs. consumption) can

sprint work [38, 48], but is fundamental to PCr resynthesis between sprints. Compartment specific creatine kinase isozymes are located in the cytosol and mitochondrial intermembrane space, and are associated with either the ATP-consuming or -delivering process, respectively [40, 41]. In the PCr shuttle system, mitochondrial creatine kinase mediates the reaction between creatine and ATP formed by oxidative metabolism, to generate PCr and ADP [40]. Therefore, the rate at which the mitochondria can generate ATP through oxidative phosphorylation, will dictate PCr resynthesis. A positive correlation between aerobic fitness and maintaining repeat-sprint performance exists [31, 34, 52, 53]. It is likely that improvements in mitochondria function and content, that are associated with exercise training [54], underpin the correlation between aerobic fitness and repeated-sprint ability. Additionally, muscle O2 availability between sprint efforts likely affects mitochondrial oxidative phosphorylation, which would explain the connection between PCr resynthesis and O2 availability [43, 46]. Therefore, the ability to deliver O2 to the locomotor muscles during rest periods between sprints is critical to maintaining

of dry muscle weight). Many mechanisms play a role

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

repeated-sprint exercise may be impaired.

(range 0–23.1 mmol ATP·kg<sup>−</sup><sup>1</sup>

with high-intensity activity [49].

maximal sprint performance [35, 47].

**3.2 Muscle oxygenation and repeated-sprint exercise**

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

(FIO2 = 0.10), the rate of PCr resynthesis has been demonstrated to be attenuated by 23% [46]. While breathing a hyperoxic gas (FIO2 = 1.00) enhances recovery by 20% compared with normoxia, which suggests that under normal exercise conditions PCr resynthesis is limited by O2 availability [46]. Therefore, if the work of breathing is high enough to limit locomotor muscle O2 delivery, PCr resynthesis in repeated-sprint exercise may be impaired.

The energy debt created by the rapid decrease in muscle PCr during a single sprint is met by a sizable contribution of anaerobic glycolysis to ATP resynthesis. Approximately 44% of ATP resynthesis is derived from anaerobic glycolysis during a single 6-s sprint [36]. However, the relative contribution of anaerobic metabolism declines as sprints are repeated [48]. By the tenth sprint, Gaitanos, Williams [36] estimated that glycolysis was only responsible for 16% of total anaerobic ATP production. Moreover, in four of the seven subjects, it was estimated to be zero (range 0–23.1 mmol ATP·kg<sup>−</sup><sup>1</sup> of dry muscle weight). Many mechanisms play a role in the relative decrease in anaerobic glycolysis during multiple-sprint work. The most likely being the progressive depletion of muscle glycogen that is associated with high-intensity activity [49].

The aerobic contribution to an isolated sprint is minimal since the maximal rate of ATP resynthesis is far below the requirements of maximal sprint work [39]. In an isolated sprint, aerobic metabolism is responsible for ≈10% of total energy production [37, 48]. But as sprints are repeated, the relative increase in aerobic metabolism to total ATP turnover rate rises to compensate for reduced energy supply from anaerobic pathways [38]. Following five 6-s sprints, it is estimated the aerobic energy contribution rises to ≈40% of total ATP production [48]. The remaining 60% is derived from anaerobic pathways, predominantly PCr degradation [36, 42]. Pulmonary VO2 can fluctuate between 70 and 100% of VO2max from sprint to recovery periods in the latter stages of a repeat-sprint series [50]. When no external work is being performed (i.e., passive rest) during the recovery period between sprints, the elevated VO2 above baseline is representative of lactate metabolism, removal of inorganic phosphate, and most importantly PCr resynthesis [40, 51].

Aerobic metabolism may have a limited role in ATP formation during multiple sprint work [38, 48], but is fundamental to PCr resynthesis between sprints. Compartment specific creatine kinase isozymes are located in the cytosol and mitochondrial intermembrane space, and are associated with either the ATP-consuming or -delivering process, respectively [40, 41]. In the PCr shuttle system, mitochondrial creatine kinase mediates the reaction between creatine and ATP formed by oxidative metabolism, to generate PCr and ADP [40]. Therefore, the rate at which the mitochondria can generate ATP through oxidative phosphorylation, will dictate PCr resynthesis. A positive correlation between aerobic fitness and maintaining repeat-sprint performance exists [31, 34, 52, 53]. It is likely that improvements in mitochondria function and content, that are associated with exercise training [54], underpin the correlation between aerobic fitness and repeated-sprint ability. Additionally, muscle O2 availability between sprint efforts likely affects mitochondrial oxidative phosphorylation, which would explain the connection between PCr resynthesis and O2 availability [43, 46]. Therefore, the ability to deliver O2 to the locomotor muscles during rest periods between sprints is critical to maintaining maximal sprint performance [35, 47].

#### **3.2 Muscle oxygenation and repeated-sprint exercise**

Muscle O2 availability during repeated-sprint exercise is critical for supporting PCr resynthesis, which underpins the capacity to maintain power out over a sprint series [36, 46]. Changes in local O2 balance (delivery vs. consumption) can

*Respiratory Physiology*

**exercise**

**3. Factors influencing respiratory muscle work during repeated-sprint** 

Repeated-sprints are characterised by brief 'all-out' exercise bouts of 4–15 s, separated by incomplete recovery periods of 14–30 s [29, 30]. Performance in a repeat-sprint context is therefore represented as the ability to reproduce power output after a previous bout of maximal exercise [31]. Over the course of a repeatedsprint series, there is a progressive decline in total mechanical work performed in each successive sprint. The rate of performance decline is also typically accelerated in low O2 environments [32]. Initial sprint performance is largely determined by muscular strength and power production [33], whereas the ability to resist fatigue and maintain performance is underpinned by aerobic capacity and the ability to deliver O2 to the locomotor muscles in the recovery periods between sprint recovery periods [34, 35]. Below, we outline the work load-induced physiological factors

known to the work of breathing during intense intermittent exercise.

Resting intramuscular stores of ATP are limited to ≈20–25 mmol·kg<sup>−</sup><sup>1</sup>

muscle weight, which during a sprint, can only provide energy for 1–2 s [36, 37]. As resting ATP stores become depleted, three major energy systems are responsible for ATP resynthesis. Rapid resynthesis is achieved through phosphocreatine (PCr) degradation [36]. Anaerobic glycolysis also has a large involvement in sprint metabolism [36]. Though as sprints are repeated, the relative contribution of anaerobic glycolysis towards ATP resynthesis declines [36, 37]. Conversely, aerobic metabolism has a very small role in isolated sprit performance (≈10% of total ATP

Intramuscular PCr is especially important for the rapid resynthesis of ATP during explosive activities via the reversible PCr-creatine kinase pathway [39–41]. In the presence of the enzyme creatine kinase, adenosine diphosphate (ADP) is converted to ATP through the dephosphorylation of PCr to form creatine (Cr). It is estimated that during a single 6-s sprint, 50% of anaerobic ATP production is derived predominantly through PCr degradation [36]. The remaining anaerobic energy contribution during an isolated sprint is supported mainly by glycolysis (44%), and in minority by intramuscular ATP stores (6%). When sprints are repeated, the relative contribution of PCr to anaerobic ATP resynthesis increases. By the tenth 6-s sprint (each separated by 30 s passive rest), PCr degradation is estimated to account for 80% of the total anaerobic energy contribution [36]. However, intramuscular PCr stores are limited

reduced ≈50% from baseline [36, 42]. When multiple sprints are performed, PCr depletion can be up to 75% after 5 repetitions [42], and 84% after 10 [36]. Since PCr degradation has such a large contribution to ATP resynthesis, the recovery of intramuscular stores PCr is critically important to the restoration of power output [43]. The capacity to recover PCr is limited in a multiple sprint series, largely constrained by the short recovery periods between sprints. The rate of PCr resynthesis follows an initial fast phase, followed by a second longer slow component [44]. After a single 6-s sprint, approximately 70% of PCr replenishment is achieved in the first 30 s of passive rest [42]. But as sprints are repeated and muscle stores are further depleted, PCr can only recover to 50% of resting stores after just five repetitions. When rest is extended post a repeat-sprint series, only 80% of PCr is recovered after 3 min [42], and 85% after 6 min of passive rest [45]. Though PCr degradation is an anaerobic process, PCr resynthesis is an aerobic process and is sensitive to O2 availability [43, 44, 46, 47]. When breathing a hypoxic gas mixture

of dry muscle weight, and after only a single 6-s sprint, stores are

of dry

**3.1 Metabolic determinates of repeated-sprint exercise**

production), which increases as sprints are repeated [37, 38].

**14**

to ≈80 mmol·kg<sup>−</sup><sup>1</sup>

be measured in real-time with near-infrared spectroscopy (NIRS) [55]. The NIRS technology relies on the relative transparency of biological tissue to near-infrared light (650–950 nm), and light absorption of deoxyhaemoglobin and oxyhaemoglobin [56]. The concentration of deoxyhaemoglobin ([HHb]) and oxyhaemoglobin ([O2Hb]) rises and falls, respectively, proportional to an increase in metabolic activity in the underlying tissue and display similar kinetics to pulmonary VO2 [50, 57]. The analysis is typically focused on [HHb] since it is less sensitive to fluctuations in total haemoglobin, is assumed to reflect venous [HHb] and thus muscular oxygen extraction, and because [O2Hb] is influenced by rapid blood volume and perfusion variations due to the skeletal muscle pump.

Because PCr resynthesis is achieved through oxidative processes [46, 58], the availability of muscle O2 during rest periods is critically important for metabolic recovery. In maximal voluntary isometric handgrip exercise, reoxygenation rate measured as the rate change of [O2Hb] during recovery was strongly correlated with the recovery of muscle PCr (*r* 2 = 0.939) [47]. Therefore, factors affecting muscle reoxygenation between sprint efforts will likely affect PCr resynthesis and repeated-sprint performance.

Vastus lateralis reoxygenation capacity can be attenuated by performing lowintensity activity (jogging/cycling) between sprint efforts [50, 59]. By reducing O2 availability, the restoration of peak cycling power and peak running speed following periods of 'active' recovery is 3–7% lower compared to passive rest. The time to exhaustion is also lowered by performing 'active' recovery when performing 15-s sprints, repeated every 15 s (745 ± 171 s vs. 445 ± 79 s; −60%) [60]. Performing active recovery between sprints, muscle tissue reoxygenation is impaired through the constant O2 uptake supporting the metabolic requirements of the active recovery. Therefore, PCr resynthesis is likely blunted because ATP from oxidative phosphorylation is devoted directly to maintain muscle contractions, rather than towards PCr resynthesis [41, 59].

The influence of limited reoxygenation on repeated-sprint ability has also been highlighted by manipulating the FIO2. When performing ten 10-s sprints with 30 s of passive rest and inspiring a hypoxic gas mixture (FIO2 = 0.13), reoxygenation was attenuated by 11% [35]. There was a ≈ 8% reduction in total mechanical work in hypoxia compared to normoxia, and the reduction in work was strongly correlated with the attenuated muscle reoxygenation (*r* = 0.78; 90% confidence interval: 0.49, 0.91). Since PCr resynthesis has similar recovery kinetics to reoxygenation [47], it is likely that muscle PCr recovery was hindered by limited O2 availability. Therefore, enhancing the capacity to reoxygenation the muscle between sprints is likely to have positive benefits for repeated-sprint ability.

There exists a positive relationship between aerobic fitness and repeated-sprint ability, which may in part be explained by superior reoxygenation capacity [31, 34, 52, 53]. After 8 weeks of endurance training, although the initial sprint performance is typically unaffected [61] (presumably because improvements in aerobic function do not support the anaerobic nature of an isolated sprint), muscle oxygenation was reported to be 152% higher prior to the commencement of the second sprint following training. Consequently, the decrement in performance within the subsequent sprint was attenuated by 26% [61]. It is likely that by improving O2 delivery to the locomotor muscle, O2 availability for oxidative phosphorylation was enhanced, and in turn, the phosphocreatine shuttle system [39, 40].

#### **3.3. Heightened inspiratory muscle work**

As described in Section 2, respiratory muscle work has been implicated as a limiting factor of limb O2 perfusion during continuous exercise [9]. However,

**17**

**Figure 1.**

*Tygon tubing to assess inspiratory mouth pressure.*

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

not translate into compromised vastus lateralis oxygenation.

The intermittent nature of repeated sprints is likely a key mediating factor for which O2 delivery can be maintained to both locomotor and respiratory

*Representation of how inspiratory loading was achieved [62]. A plastic disk with a 10-mm opening was placed over the inspiratory side of a two-way non-rebreathing valve (Hans Rudolph Inc., Kansas, United States of America) attached to the distal end of a bidirectional turbine and held in place by the internal ridge of a rubber tubing adaptor. A pressure transducer was attached to the saliva port of the non-rebreathing valve via* 

competition between locomotor and respiratory muscle for available cardiac output does not appear to be a significant limiting factor of performance during repeated-sprint exercise. In our recent work, we examined the influence of inspiratory muscle loading on oxygenation trends in repeated-sprint exercise [62]. Participants were asked to perform ten 10-s cycle ergometer sprints, each separated by 30 s of passive rest. Inspiratory loading was achieved by placing a plastic disk with a 10-mm opening over the inspiratory side of a two-way non-rebreathing valve (**Figure 1**). Inspiratory muscle force development (calculated as the integral of inspiratory mouth pressure, multiplied by respiratory frequency) was similar to others who have shown vastus grater lateralis muscle deoxygenation with inspiratory loading during exercise [63]. In response, whole-body VO2 measured at the mouth was elevated by 4–5% during both the sprint and recovery phases (**Figure 2**) [62]. This occurred even though total sprint work was similar between the conditions. The elevation in VO2 was likely driven by a heightened oxygen O2 uptake by the respiratory muscle to accommodate for the additional inspiratory muscle work [23, 63]. Importantly, Tissue Saturation Index (TSI = [O2Hb] ÷ ([O2Hb] + [HHb]), expressed in %) measured at the sixth intercostal space, was comparable between the conditions, which suggests that O2 supply to the respiratory muscles remained proportional to the metabolic activity. The change in inspiratory muscle work did

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

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

competition between locomotor and respiratory muscle for available cardiac output does not appear to be a significant limiting factor of performance during repeated-sprint exercise. In our recent work, we examined the influence of inspiratory muscle loading on oxygenation trends in repeated-sprint exercise [62]. Participants were asked to perform ten 10-s cycle ergometer sprints, each separated by 30 s of passive rest. Inspiratory loading was achieved by placing a plastic disk with a 10-mm opening over the inspiratory side of a two-way non-rebreathing valve (**Figure 1**). Inspiratory muscle force development (calculated as the integral of inspiratory mouth pressure, multiplied by respiratory frequency) was similar to others who have shown vastus grater lateralis muscle deoxygenation with inspiratory loading during exercise [63]. In response, whole-body VO2 measured at the mouth was elevated by 4–5% during both the sprint and recovery phases (**Figure 2**) [62]. This occurred even though total sprint work was similar between the conditions. The elevation in VO2 was likely driven by a heightened oxygen O2 uptake by the respiratory muscle to accommodate for the additional inspiratory muscle work [23, 63]. Importantly, Tissue Saturation Index (TSI = [O2Hb] ÷ ([O2Hb] + [HHb]), expressed in %) measured at the sixth intercostal space, was comparable between the conditions, which suggests that O2 supply to the respiratory muscles remained proportional to the metabolic activity. The change in inspiratory muscle work did not translate into compromised vastus lateralis oxygenation.

The intermittent nature of repeated sprints is likely a key mediating factor for which O2 delivery can be maintained to both locomotor and respiratory

#### **Figure 1.**

*Respiratory Physiology*

variations due to the skeletal muscle pump.

with the recovery of muscle PCr (*r*

repeated-sprint performance.

towards PCr resynthesis [41, 59].

positive benefits for repeated-sprint ability.

in turn, the phosphocreatine shuttle system [39, 40].

**3.3. Heightened inspiratory muscle work**

be measured in real-time with near-infrared spectroscopy (NIRS) [55]. The NIRS technology relies on the relative transparency of biological tissue to near-infrared light (650–950 nm), and light absorption of deoxyhaemoglobin and oxyhaemoglobin [56]. The concentration of deoxyhaemoglobin ([HHb]) and oxyhaemoglobin ([O2Hb]) rises and falls, respectively, proportional to an increase in metabolic activity in the underlying tissue and display similar kinetics to pulmonary VO2 [50, 57]. The analysis is typically focused on [HHb] since it is less sensitive to fluctuations in total haemoglobin, is assumed to reflect venous [HHb] and thus muscular oxygen extraction, and because [O2Hb] is influenced by rapid blood volume and perfusion

Because PCr resynthesis is achieved through oxidative processes [46, 58], the availability of muscle O2 during rest periods is critically important for metabolic recovery. In maximal voluntary isometric handgrip exercise, reoxygenation rate measured as the rate change of [O2Hb] during recovery was strongly correlated

muscle reoxygenation between sprint efforts will likely affect PCr resynthesis and

Vastus lateralis reoxygenation capacity can be attenuated by performing lowintensity activity (jogging/cycling) between sprint efforts [50, 59]. By reducing O2 availability, the restoration of peak cycling power and peak running speed following periods of 'active' recovery is 3–7% lower compared to passive rest. The time to exhaustion is also lowered by performing 'active' recovery when performing 15-s sprints, repeated every 15 s (745 ± 171 s vs. 445 ± 79 s; −60%) [60]. Performing active recovery between sprints, muscle tissue reoxygenation is impaired through the constant O2 uptake supporting the metabolic requirements of the active recovery. Therefore, PCr resynthesis is likely blunted because ATP from oxidative phosphorylation is devoted directly to maintain muscle contractions, rather than

The influence of limited reoxygenation on repeated-sprint ability has also been highlighted by manipulating the FIO2. When performing ten 10-s sprints with 30 s of passive rest and inspiring a hypoxic gas mixture (FIO2 = 0.13), reoxygenation was attenuated by 11% [35]. There was a ≈ 8% reduction in total mechanical work in hypoxia compared to normoxia, and the reduction in work was strongly correlated with the attenuated muscle reoxygenation (*r* = 0.78; 90% confidence interval: 0.49, 0.91). Since PCr resynthesis has similar recovery kinetics to reoxygenation [47], it is likely that muscle PCr recovery was hindered by limited O2 availability. Therefore, enhancing the capacity to reoxygenation the muscle between sprints is likely to have

There exists a positive relationship between aerobic fitness and repeated-sprint ability, which may in part be explained by superior reoxygenation capacity [31, 34, 52, 53]. After 8 weeks of endurance training, although the initial sprint performance is typically unaffected [61] (presumably because improvements in aerobic function do not support the anaerobic nature of an isolated sprint), muscle oxygenation was reported to be 152% higher prior to the commencement of the second sprint following training. Consequently, the decrement in performance within the subsequent sprint was attenuated by 26% [61]. It is likely that by improving O2 delivery to the locomotor muscle, O2 availability for oxidative phosphorylation was enhanced, and

As described in Section 2, respiratory muscle work has been implicated as a limiting factor of limb O2 perfusion during continuous exercise [9]. However,

= 0.939) [47]. Therefore, factors affecting

2

**16**

*Representation of how inspiratory loading was achieved [62]. A plastic disk with a 10-mm opening was placed over the inspiratory side of a two-way non-rebreathing valve (Hans Rudolph Inc., Kansas, United States of America) attached to the distal end of a bidirectional turbine and held in place by the internal ridge of a rubber tubing adaptor. A pressure transducer was attached to the saliva port of the non-rebreathing valve via Tygon tubing to assess inspiratory mouth pressure.*

#### **Figure 2.**

*Sprint and recovery pulmonary oxygen uptake (VO2) expressed as a percentage of VO2peak for control (CTRL), inspiratory muscle loading (INSP), and worked matched (MATCH) exercise. The symbols represent comparisons between INSP and CTRL (\*), INSP and MATCH (#). The number of symbols; one, two, and three denote likely, very likely and almost certainly respectively, that the chance of the true effect exceeds a small (−0.2 to 0.2) effect size. Values are presented as mean ± SD. Reproduced from Rodriguez et al. [62] under a Creative Commons Attribution 4.0 licence.*

muscles. Others have demonstrated that the addition of an inspiratory load while exercising >95% VO2max, results in a decrease in limb perfusion and O2 delivery, mediated by sympathetically-activated vasoconstriction in the locomotor muscles [2, 3]. Whereas during moderate intensities (50–75% VO2max), there is no change in vascular resistance or blood flow [23]. Even though repeated-sprint exercise can elicit >90% of VO2 peak, it is not sustained throughout the entire protocol and can fluctuate between 70 and 90% of VO2max between sprint and recover phases [50, 62]. The fluctuation in metabolic demands between the phases likely minimises the potential for a competition for available cardiac output. Moreover, since VO2 was able to increase, these data highlight the capacity of the cardiorespiratory system to rapidly adjust and meet the additional metabolic demands imposed by inspiratory loading even during severe exercise [64]. In instances where blood flow is impacted by additional respiratory muscle work, there is no compensatory increase in VO2 [2, 3]. Therefore, having the capacity to increase VO2 may be a crucial factor in maintaining O2 supply to all active muscles during high-intensity exercise and, thereby, sustain prolonged periods of physical activity.

#### **3.4 Acute environmental hypoxia**

To further explore the role of O2 availability in balancing the metabolic demands of the locomotor and respiratory muscles, we asked participants to exercise in an environment where the O2 concentration had been reduced to 14.55% [65]. Participants completed the same protocol as previously described (ten 10-s sprints, 30 s of passive rest) while vastus lateralis and intercostal muscle oxygenation was assessed with NIRS. Surprisingly, there was no clear difference in repeated-sprint ability in hypoxia compared to normoxia. However, there was a clear reduction in vastus lateralis muscle oxygenation similar to previous research (**Figure 3**) [35, 66]. Ventilation patterns (respiratory frequency and inspiratory volume) and inspiratory pressure generation were similar between conditions. Therefore, the O2 cost of

**19**

**Figure 3.**

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

exercise hyperpnoea was likely similar between conditions [67]. However, there was no clear difference in respiratory muscle oxygenation ([O2Hb] and [HHb]) during exercise in hypoxia when compared to normoxia (**Figure 4**) [65]. Based on this new evidence, it appears that O2 delivery is preferentially distributed to the respiratory

*Vastus lateralis muscle oxygenation trends during repeated-sprint exercise in normoxia and hypoxia expressed as a percentage of arterial occlusion. (a) Change of vastus lateralis oxyhaemoglobin (O2HbVL); and (b) vastus lateralis deoxyhaemoglobin (HHbVL). The number of symbols (\*); one, two and three denote likely, very likely and most likely respectively, that the chance of the true effect exceeds a small (−0.2 to 0.2) effect size. Results are presented as mean ± SD. Reprinted from Rodriguez et al. [65], with permission from Elsevier.*

Locomotor muscle O2 availability during rest phases between sprints is a strong determining factor of metabolic recovery [36, 37, 44], and thus performance over multiple sprints [35]. Based on our early research, it seems that locomotor muscle O2 availability is compromised in hypoxia in favour of the respiratory muscles. Others have reported exaggerated deoxygenation of the respiratory muscles in hypoxia during voluntary isocapnic hyperpnoea [68]. However, their hypoxia gas mixture (10% O2) resulted in a lower arterial O2 saturation of 82% (estimated via pulse oximetry) compared to the average 87% in subjects of the study discussed here [65]. A hypoxic threshold may exist where respiratory muscle O2 delivery can be maintained close to the rate of that during exercise in normoxia. If arterial hypoxemia was greater, further desaturation of the respiratory muscles may have been detected. Amann et al. [28] have reported a link between inspiratory muscle

muscles to maintain the metabolic function of the respiratory muscles.

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

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

#### **Figure 3.**

*Respiratory Physiology*

muscles. Others have demonstrated that the addition of an inspiratory load while exercising >95% VO2max, results in a decrease in limb perfusion and O2 delivery, mediated by sympathetically-activated vasoconstriction in the locomotor muscles [2, 3]. Whereas during moderate intensities (50–75% VO2max), there is no change in vascular resistance or blood flow [23]. Even though repeated-sprint exercise can elicit >90% of VO2 peak, it is not sustained throughout the entire protocol and can fluctuate between 70 and 90% of VO2max between sprint and recover phases [50, 62]. The fluctuation in metabolic demands between the phases likely minimises the potential for a competition for available cardiac output. Moreover, since VO2 was able to increase, these data highlight the capacity of the cardiorespiratory system to rapidly adjust and meet the additional metabolic demands imposed by inspiratory loading even during severe exercise [64]. In instances where blood flow is impacted by additional respiratory muscle work, there is no compensatory increase in VO2 [2, 3]. Therefore, having the capacity to increase VO2 may be a crucial factor in maintaining O2 supply to all active muscles during high-intensity exercise and, thereby, sustain prolonged periods of physical

*Sprint and recovery pulmonary oxygen uptake (VO2) expressed as a percentage of VO2peak for control (CTRL), inspiratory muscle loading (INSP), and worked matched (MATCH) exercise. The symbols represent comparisons between INSP and CTRL (\*), INSP and MATCH (#). The number of symbols; one, two, and three denote likely, very likely and almost certainly respectively, that the chance of the true effect exceeds a small (−0.2 to 0.2) effect size. Values are presented as mean ± SD. Reproduced from Rodriguez et al. [62] under a* 

To further explore the role of O2 availability in balancing the metabolic demands

of the locomotor and respiratory muscles, we asked participants to exercise in an environment where the O2 concentration had been reduced to 14.55% [65]. Participants completed the same protocol as previously described (ten 10-s sprints, 30 s of passive rest) while vastus lateralis and intercostal muscle oxygenation was assessed with NIRS. Surprisingly, there was no clear difference in repeated-sprint ability in hypoxia compared to normoxia. However, there was a clear reduction in vastus lateralis muscle oxygenation similar to previous research (**Figure 3**) [35, 66]. Ventilation patterns (respiratory frequency and inspiratory volume) and inspiratory pressure generation were similar between conditions. Therefore, the O2 cost of

**18**

activity.

**Figure 2.**

**3.4 Acute environmental hypoxia**

*Creative Commons Attribution 4.0 licence.*

*Vastus lateralis muscle oxygenation trends during repeated-sprint exercise in normoxia and hypoxia expressed as a percentage of arterial occlusion. (a) Change of vastus lateralis oxyhaemoglobin (O2HbVL); and (b) vastus lateralis deoxyhaemoglobin (HHbVL). The number of symbols (\*); one, two and three denote likely, very likely and most likely respectively, that the chance of the true effect exceeds a small (−0.2 to 0.2) effect size. Results are presented as mean ± SD. Reprinted from Rodriguez et al. [65], with permission from Elsevier.*

exercise hyperpnoea was likely similar between conditions [67]. However, there was no clear difference in respiratory muscle oxygenation ([O2Hb] and [HHb]) during exercise in hypoxia when compared to normoxia (**Figure 4**) [65]. Based on this new evidence, it appears that O2 delivery is preferentially distributed to the respiratory muscles to maintain the metabolic function of the respiratory muscles.

Locomotor muscle O2 availability during rest phases between sprints is a strong determining factor of metabolic recovery [36, 37, 44], and thus performance over multiple sprints [35]. Based on our early research, it seems that locomotor muscle O2 availability is compromised in hypoxia in favour of the respiratory muscles. Others have reported exaggerated deoxygenation of the respiratory muscles in hypoxia during voluntary isocapnic hyperpnoea [68]. However, their hypoxia gas mixture (10% O2) resulted in a lower arterial O2 saturation of 82% (estimated via pulse oximetry) compared to the average 87% in subjects of the study discussed here [65]. A hypoxic threshold may exist where respiratory muscle O2 delivery can be maintained close to the rate of that during exercise in normoxia. If arterial hypoxemia was greater, further desaturation of the respiratory muscles may have been detected. Amann et al. [28] have reported a link between inspiratory muscle

**Figure 4.**

*Respiratory muscle oxygenation trends during repeated-sprint exercise in normoxia and hypoxia expressed as an absolute change from baseline (horizontal line). (a) Concentration change from baseline of respiratory muscle oxyhaemoglobin ([O2HbRM]); (b) respiratory muscle deoxyhaemoglobin ([HHbRM]); and (c) respiratory muscle total haemoglobin ([tHbRM]). There was no clear effect of hypoxia on respiratory muscle oxygenation compared to normoxia. Results are represented as mean ± SD. Reprinted from Rodriguez et al. [65], with permission from Elsevier.*

work in hypoxia and the development of quadriceps fatigue during high-intensity exercise. By reducing the work of breathing with PAV, the rate of fatigue developments can be attenuated [28]. Therefore, alleviating the O2 cost of exercise hyperpnoea appears to be a pathway for enhancing limb O2 delivery and exercise capacity in humans.

**21**

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

Aside from the structural characteristics of the pulmonary system, the relative strength of the respiratory muscles is likely to have a key role in the O2 cost of exercise hyperpnoea. After 6-weeks of inspiratory muscle strength training, is has been demonstrated that ventilation O2 efficiency can be enhanced [19]. Specific training targeting the inspiratory muscles (inspiratory muscle training, IMT) typically consists of inspiring against a closed valve set to open at ≈50% of an individual's maximal inspiratory mouth pressure, repeated 30 times twice per day. Strengthening the inspiratory muscles has translated to reduced O2 cost of voluntary hyperpnoea, attenuated exercise-induced respiratory muscle fatigue, attenuated vastus lateralis and respiratory muscle deoxygenation, and improved exercise capacity [19, 67–70]. However, respiratory muscle fatigue has not been clearly demonstrated for multiple-sprint work, and therefore ergogenic benefits of respiratory muscle training for improving repeated-sprint alibility may be limited [71]. Nevertheless, evidence that IMT provides some benefit towards maintaining repeated-sprint performance exists, though the mechanisms are

After a 6-week period of IMT, repeated-sprint ability was assessed in a group of recreational sprint sports players (soccer, rugby, field hockey and basketball) [72]. Performance was assessed during fifteen 20-m sprints, which participants were allowed a maximum of 30 s rest. Following the intervention, there were no clear changes in sprint times. However, self-selected recovery time was lessened by 6.9% (range: −0.9 to 14.5%). Strengthening the inspiratory muscles presumably reduced the O2 cost of exercise hyperpnoea and blunted the respiratory muscle metaboreflex, which would, in turn, reduce O2 competition between locomotor and respiratory muscles [9, 19, 74]. Through minimising O2 competition, it is likely that the quality of metabolic recovery was enhanced with IMT, so that subjects could maintain performance with less rest between sprints [72]. But since there were no measurements of muscle oxygenation, it is difficult to separate potential changes in O2 delivery from reduced feelings of dyspnoea that is associated with respiratory

The effectiveness of IMT on repeat-sprint ability and run time to exhaustion at 100% of the speed obtained during a maximal incremental exercise test has also been assessed in a group of professional female soccer players [73]. Repeated-sprint ability was assessed with six 40-m sprints (20 m + 180° turn +20 m) with 20 s of passive rest between sprints. Vastus lateralis and intercostal muscle oxygenation was only examined during the time-to-exhaustion trials. There was no significant difference between the groups in repeated-sprint ability (*P* > 0.05). However the effect size for performance decrement was slightly larger in the IMT group post intervention (Cohen's *d* = 0.84 vs. 0.16). Similar, both placebo and experimental groups improved time to exhaustion with no significant difference between groups, but the effect size in the IMT group was larger (Cohen's *d* = 0.74 vs. 0.46). Specific training of the respiratory muscles, therefore, may only provide negligible/small performance benefits beyond professional soccer periodised training. Performance benefits were partly attributed to a blunted increase in respiratory muscle [HHb], with a concurrent increase in vastus lateralis [O2Hb] [73]. In terms of the athlete's ability to preserve repeat-sprint performance, the IMT group also showed the greatest improvement in the capacity to maintain sprint time over multiple sprints. The blunted respiratory muscle metaboreflex in the exhaustion test may have also occurred during the repeated-sprint test. However, without muscle oxygenation measurements during the sprint trials, it is unclear if there were any changes to O2

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

**3.5 Respiratory muscle training**

unclear [72, 73].

muscle training [69, 72].

availability after training.

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

### **3.5 Respiratory muscle training**

*Respiratory Physiology*

**20**

in humans.

*[65], with permission from Elsevier.*

**Figure 4.**

work in hypoxia and the development of quadriceps fatigue during high-intensity exercise. By reducing the work of breathing with PAV, the rate of fatigue developments can be attenuated [28]. Therefore, alleviating the O2 cost of exercise hyperpnoea appears to be a pathway for enhancing limb O2 delivery and exercise capacity

*Respiratory muscle oxygenation trends during repeated-sprint exercise in normoxia and hypoxia expressed as an absolute change from baseline (horizontal line). (a) Concentration change from baseline of respiratory muscle oxyhaemoglobin ([O2HbRM]); (b) respiratory muscle deoxyhaemoglobin ([HHbRM]); and (c) respiratory muscle total haemoglobin ([tHbRM]). There was no clear effect of hypoxia on respiratory muscle oxygenation compared to normoxia. Results are represented as mean ± SD. Reprinted from Rodriguez et al.* 

Aside from the structural characteristics of the pulmonary system, the relative strength of the respiratory muscles is likely to have a key role in the O2 cost of exercise hyperpnoea. After 6-weeks of inspiratory muscle strength training, is has been demonstrated that ventilation O2 efficiency can be enhanced [19]. Specific training targeting the inspiratory muscles (inspiratory muscle training, IMT) typically consists of inspiring against a closed valve set to open at ≈50% of an individual's maximal inspiratory mouth pressure, repeated 30 times twice per day. Strengthening the inspiratory muscles has translated to reduced O2 cost of voluntary hyperpnoea, attenuated exercise-induced respiratory muscle fatigue, attenuated vastus lateralis and respiratory muscle deoxygenation, and improved exercise capacity [19, 67–70]. However, respiratory muscle fatigue has not been clearly demonstrated for multiple-sprint work, and therefore ergogenic benefits of respiratory muscle training for improving repeated-sprint alibility may be limited [71]. Nevertheless, evidence that IMT provides some benefit towards maintaining repeated-sprint performance exists, though the mechanisms are unclear [72, 73].

After a 6-week period of IMT, repeated-sprint ability was assessed in a group of recreational sprint sports players (soccer, rugby, field hockey and basketball) [72]. Performance was assessed during fifteen 20-m sprints, which participants were allowed a maximum of 30 s rest. Following the intervention, there were no clear changes in sprint times. However, self-selected recovery time was lessened by 6.9% (range: −0.9 to 14.5%). Strengthening the inspiratory muscles presumably reduced the O2 cost of exercise hyperpnoea and blunted the respiratory muscle metaboreflex, which would, in turn, reduce O2 competition between locomotor and respiratory muscles [9, 19, 74]. Through minimising O2 competition, it is likely that the quality of metabolic recovery was enhanced with IMT, so that subjects could maintain performance with less rest between sprints [72]. But since there were no measurements of muscle oxygenation, it is difficult to separate potential changes in O2 delivery from reduced feelings of dyspnoea that is associated with respiratory muscle training [69, 72].

The effectiveness of IMT on repeat-sprint ability and run time to exhaustion at 100% of the speed obtained during a maximal incremental exercise test has also been assessed in a group of professional female soccer players [73]. Repeated-sprint ability was assessed with six 40-m sprints (20 m + 180° turn +20 m) with 20 s of passive rest between sprints. Vastus lateralis and intercostal muscle oxygenation was only examined during the time-to-exhaustion trials. There was no significant difference between the groups in repeated-sprint ability (*P* > 0.05). However the effect size for performance decrement was slightly larger in the IMT group post intervention (Cohen's *d* = 0.84 vs. 0.16). Similar, both placebo and experimental groups improved time to exhaustion with no significant difference between groups, but the effect size in the IMT group was larger (Cohen's *d* = 0.74 vs. 0.46). Specific training of the respiratory muscles, therefore, may only provide negligible/small performance benefits beyond professional soccer periodised training. Performance benefits were partly attributed to a blunted increase in respiratory muscle [HHb], with a concurrent increase in vastus lateralis [O2Hb] [73]. In terms of the athlete's ability to preserve repeat-sprint performance, the IMT group also showed the greatest improvement in the capacity to maintain sprint time over multiple sprints. The blunted respiratory muscle metaboreflex in the exhaustion test may have also occurred during the repeated-sprint test. However, without muscle oxygenation measurements during the sprint trials, it is unclear if there were any changes to O2 availability after training.

The few studies demonstrating enhanced repeated-sprint performance following IMT [72, 73] support the notion that respiratory muscle work plays a negative effect on high-intensity intermittent exercise. Training the respiratory muscles can reduce the O2 cost of exercise hyperpnoea [19], and attenuate blood flow competition between the locomotor and respiratory muscles [70, 74]. However, there remains a very limited understanding of the role exercise hyperpnoea plays during repeated-sprint exercise. Research still needs to answer if the enhanced repeatedsprint ability following respiratory muscle training is derived from improved skeletal muscle oxygenation kinetics.

#### **3.6 Evidence for hyperventilation**

Hyperventilation is demarcated when alveolar ventilation disproportionally rises relative to CO2 production causing a decrease in the pressure of alveolar CO2, and an increase in the pressure of alveolar O2 [75]. Hyperventilation readily occurs during high-intensity exercise and can constrain a fall in arterial O2 and pH [75, 76]. Though this was not directly examined in our research [62, 65], some evidence of hyperventilation occurring during repeated-sprint exercise was present. As depicted by the data of a representative subject (**Figure 5**), the partial pressure of end-tidal oxygen (PETO2) and carbon dioxide (PETCO2) rose and fell respectively from baseline over the course of the repeated-sprint protocol [62]. The wave-like pattern in PETO2 and PETCO2 appears to be linked to the phase of the protocol (sprint vs. rest) and occurs at exercise onset. This pattern is suggestive of a locomotor respiratory coupling, in which breathing frequency matches the cadence of locomotor exercise [77].

Further new evidence of hyperventilation comes from our recent hypoxia research [65]. Arterial hypoxemia is a potent stimulus of ventilation [26–28]. However, as we reported, there was no clear difference in either inspiratory volume, respiratory frequency or inspiratory mouth pressure during the repeatedsprint protocol. One may argue that participants were already operating at their

#### **Figure 5.**

*Partial pressure of end-tidal oxygen (PETO2) and carbon dioxide (PETCO2) recorded on a breath-by-breath basis during repeated-sprint exercise. Data are from a single subject collected as part of the study by Rodriguez et al. [62] during the control exercise condition. The exercise protocol consisted of ten 10-s sprints, separated by 30 s of passive rest so that a sprint commenced every 40 s. The grey shaded area represents the 2-min baseline period observed prior to the commencement of warm-up.*

**23**

**Author details**

Ramón F. Rodriguez1

, Robert J. Aughey1

2 Department of Kinesiology, University Laval, Quebec, Canada

\*Address all correspondence to: francois.billaut@kin.ulaval.ca

provided the original work is properly cited.

1 Institute for Health and Sport, Victoria University, Melbourne, Australia

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

and François Billaut1,2\*

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

upper limits of ventilation, and thus arterial hypoxemia could not have had an additive effect. Although appealing, such hypothesis requires additional work to determine the influencing factors of exercise hyperpnoea over a variety of sprint

The findings of our research do not support heightened inspiratory muscle work as being a limiting factor in vastus lateralis muscle oxygenation in normoxia. The intermittent nature of repeated-sprint activity is likely a key mediating factor for which O2 delivery can be maintained to both the locomotor and respiratory muscles. Moreover, reducing the relative intensity of exercise hyperpnoea through inspiratory muscle training shows limited benefits for enhancing repeated sprint ability. Inspiratory muscle work appears to play a more influential role under conditions of arterial hypoxemia. Our research showed that locomotor muscle oxygenation can be compromised through preferential O2 delivery to the respiratory muscles. It is yet to be seen if inspiratory muscle training could be of benefit to exercise under these

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

durations.

conditions.

**4. Conclusion**

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

upper limits of ventilation, and thus arterial hypoxemia could not have had an additive effect. Although appealing, such hypothesis requires additional work to determine the influencing factors of exercise hyperpnoea over a variety of sprint durations.

## **4. Conclusion**

*Respiratory Physiology*

skeletal muscle oxygenation kinetics.

**3.6 Evidence for hyperventilation**

cadence of locomotor exercise [77].

*period observed prior to the commencement of warm-up.*

The few studies demonstrating enhanced repeated-sprint performance following IMT [72, 73] support the notion that respiratory muscle work plays a negative effect on high-intensity intermittent exercise. Training the respiratory muscles can reduce the O2 cost of exercise hyperpnoea [19], and attenuate blood flow competition between the locomotor and respiratory muscles [70, 74]. However, there remains a very limited understanding of the role exercise hyperpnoea plays during repeated-sprint exercise. Research still needs to answer if the enhanced repeatedsprint ability following respiratory muscle training is derived from improved

Hyperventilation is demarcated when alveolar ventilation disproportionally rises relative to CO2 production causing a decrease in the pressure of alveolar CO2, and an increase in the pressure of alveolar O2 [75]. Hyperventilation readily occurs during high-intensity exercise and can constrain a fall in arterial O2 and pH [75, 76]. Though this was not directly examined in our research [62, 65], some evidence of hyperventilation occurring during repeated-sprint exercise was present. As depicted by the data of a representative subject (**Figure 5**), the partial pressure of end-tidal oxygen (PETO2) and carbon dioxide (PETCO2) rose and fell respectively from baseline over the course of the repeated-sprint protocol [62]. The wave-like pattern in PETO2 and PETCO2 appears to be linked to the phase of the protocol (sprint vs. rest) and occurs at exercise onset. This pattern is suggestive of a locomotor respiratory coupling, in which breathing frequency matches the

Further new evidence of hyperventilation comes from our recent hypoxia research [65]. Arterial hypoxemia is a potent stimulus of ventilation [26–28]. However, as we reported, there was no clear difference in either inspiratory volume, respiratory frequency or inspiratory mouth pressure during the repeatedsprint protocol. One may argue that participants were already operating at their

*Partial pressure of end-tidal oxygen (PETO2) and carbon dioxide (PETCO2) recorded on a breath-by-breath basis during repeated-sprint exercise. Data are from a single subject collected as part of the study by Rodriguez et al. [62] during the control exercise condition. The exercise protocol consisted of ten 10-s sprints, separated by 30 s of passive rest so that a sprint commenced every 40 s. The grey shaded area represents the 2-min baseline* 

**22**

**Figure 5.**

The findings of our research do not support heightened inspiratory muscle work as being a limiting factor in vastus lateralis muscle oxygenation in normoxia. The intermittent nature of repeated-sprint activity is likely a key mediating factor for which O2 delivery can be maintained to both the locomotor and respiratory muscles. Moreover, reducing the relative intensity of exercise hyperpnoea through inspiratory muscle training shows limited benefits for enhancing repeated sprint ability. Inspiratory muscle work appears to play a more influential role under conditions of arterial hypoxemia. Our research showed that locomotor muscle oxygenation can be compromised through preferential O2 delivery to the respiratory muscles. It is yet to be seen if inspiratory muscle training could be of benefit to exercise under these conditions.

## **Author details**

Ramón F. Rodriguez1 , Robert J. Aughey1 and François Billaut1,2\*

1 Institute for Health and Sport, Victoria University, Melbourne, Australia

2 Department of Kinesiology, University Laval, Quebec, Canada

\*Address all correspondence to: francois.billaut@kin.ulaval.ca

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
