Training to "breathe better"

Can training to breathe more efficiently help you as an athlete in your sport? Like many things, it depends. Here is a paper and experiment we conducted, minus any statistical analysis, where we attempted to answer that exact question.

Pulmonary ventilation is a process involving the lungs and the exchange of carbon dioxide and oxygen between the alveolar air and the blood. For the purpose of this paper, pulmonary minute volume, or rate of pulmonary ventilation (VE), which is measured in L·min-1, was measured and calculated by multiplying frequency of breathing by tidal volume. Tidal volume is the amount of air moved in and out of the lungs in a normal inspiration and expiration and is measured in litres. VE is important when speaking about exercise because it is related to the rate of a person’s consumption of oxygen(VO2) and production of carbon dioxide(VCO2). VO2 and VE are related linearly when exercise is maintained at a steady state, however when exercise intensities exceed aerobic metabolism’s ability to re-synthesize ATP by reducing oxygen, the body is unable to use as much oxygen, and the relationship changes. During this time, the body begins to rely more on anaerobic glycolysis to produce adequate energy to re-synthesize ATP, and excess lactate is produced in the system. The body buffers lactic acid with sodium bicarbonate which in turn gives off carbon dioxide as a bi-product. Respiratory exchange ratio (RER) is the ratio between VCO2 and VO2 and provides an indication of the substrate being utilized for energy at that given time. When anaerobic glycolysis takes over for aerobic metabolism, RER exceeds 1.0 because expired carbon dioxide plus the amount of carbon dioxide produced in metabolism exceeds the amount of oxygen being utilized. In the atmosphere, the air is made up primarily of the three gases nitrogen, oxygen and carbon dioxide. Each makes up a percent of the atmosphere approximately equal to 79.04%, 20.93%, and 0.03%, respectively. Expressed as fractions of the inspired air we breathe, we term these values FIN2, FIO2, and FICO2. After air enters our lungs and gas exchange occurs, the fractions of these gases changes in expired air, and is measured as fractions termed FEN2, FEO2, and FECO2. These values help us determine the amount of oxygen and carbon dioxide utilized by the body.

From rest to low intensity exercise, mainly the aerobic metabolic system is being utilized, thus the muscles are requiring more oxygen, and are extracting more oxygen from the blood, resulting in a lower FEO2 and a higher FECO2 because carbon dioxide is a bi-product of this metabolism (Skinner & McLellan, 1980). During this time, there is also a linear increase in VE, heart rate, VCO2 and VO2. Other evidence that aerobic metabolism is used during this time is that the RER is between 0.7-0.8, indicating free fatty acids (FFA) are the primary fuel source (Skinner & McLellan, 1980). As exercise continues to increase in intensity, glycolysis is used more extensively, and acidity from hydrogen ions (H+) increase. H+ is buffered by bicarbonate in the blood which then dissociates to produce CO2. Heart rate, VCO2 and VO2 continue to increase while VE rises because the respiratory center stimulates the breathing center in an attempt to remove the extra CO2. As exercise progression continues, ventilation rate changes so that tidal volume increases while breathing frequency only increases slightly. This is when deep breaths are taken in order to maximize oxygen uptake and utilization in the muscle (Mateika & Duffin, 1995). During higher intensities at non-steady rate exercise, VE rises disproportionately with O2 consumption because there is an excess production of CO2(Mateika & Duffin, 1995). Also during this time, breathing frequency increases in attempt to eliminate the increased carbon dioxide production from dissociation of lactate.

This lab was performed at sub-maximal effort, thus aerobic metabolism was being used at all times during this exercise. Glycolysis likely supplemented aerobic metabolism, thus accounting for many of the physiological changes to anaerobic metabolism. One way to determine if anaerobic glycolysis is used is by blood lactate measures. Other factors such as increases in VE, VCO2 and VO2 are indications of this switch to anaerobic metabolism. Since this energy system requires less oxygen from each breath, FEO2 should increase, and FECO2 should not decrease (Skinner & McLellan, 1980).

With a further increase in intensity to about 65-90% VO2max , heart rate and VO2 continues near maximum work loads and begin to plateau, (although not all healthy individuals demonstrate a plateau). At this point, ventilation increases disproportionately to both oxygen uptake and carbon dioxide elimination, and is marked by a further increase in blood lactate measures (Mateika & Duffin, 1995). Blood lactate measures during this time normally increase from a level of 4mmol/L (Skinner & McLellan, 1980). There is a continued increase in the pulmonary ventilation, and hyperventilation occurs, which still cannot compensate for the simultaneous increases in blood lactate. Hyperventilation is when there is an increase in breathing rate while taking short shallow breaths (Skinner & McLellan, 1980). It appears that it cannot compensate readily, and thus there is a drop in FECO2 while at the same time FEO2 rises.

The purpose of this experiment was to investigate the relationship among the variables discussed above, namely pulmonary ventilation (VE), oxygen consumption, carbon dioxide production, and the fractions of these values (FEO2 and FECO2 ) and how they change from rest and in response to aerobic exercise on a cycle ergometer.

The exercise tests performed both pre and post respiratory fatiguing protocol showed minimal changes in perceived dyspnea and leg pain. Subjects in fact rated dyspnea lower for a given power output after fatigue, indicating that the subjects could possibly have needed a more straining fatigue protocol than was given to see a change. Hart et al. (2001) cites that Powerbreathe systems, when used as per the manufactured instructions for a healthy population (30 max voluntary ventilations from RV to TLC) were not sufficient to induce fatigue. Although their study was relatively small (n=12), perhaps it held true to these findings. Another study (Mador & Acevedo, 1991), presented that inspiratory muscle fatigue occurred when respiratory muscles were exposed to a great enough load for a long enough period of time. In this case, dyspnea and leg discomfort scores changed minimally during the exercise tests, and all four subjects reached the same power outputs after the fatigue protocol as before, so there was probably not enough muscle fatigue induced to see large changes. A possible reason for the lower ratings of dyspnea post-fatigue could be the learning effect of doing the same tests one-week prior, and knowing what to expect; subsequently perceiving less effort.

For self-reported leg discomfort (Figure 1B), although the increase was minimal, there was a slightly higher rating (0.5 at max) of overall leg discomfort. When performing highly fatiguing muscle contractions of the respiratory musculature, there will be local metabolites produced (such as lactate (Bailey et al., 2010)), as well as muscle deformation, stimulating group III and group IV afferent activity (Dempsey, Sheel, St Croix, & Morgan, 2002),. This activity causes vasoconstriction in inactive skeletal muscles and local vasodilation, increased blood flow and decreased vascular resistance in areas where metabolites are being produced (Dempsey et al., 2002). At the same time, central command increases vasoconstriction and reduces cardiac outflow by resetting the baroreceptors set point. This rise in muscle sympathetic nervous activity (MSNA) that happens during exercise, is potentially the muscle metaboreflex responding to the steady increases in metabolites with the exercise (Dempsey et al., 2002). This local vasoconstriction could cause pain and discomfort, and could be the reason why subjects had slightly more leg discomfort after the respiratory fatigue test (Dempsey et al., 2002). As mentioned by Dempsey et al. (2002), the magnitude of the muscle metaboreflex is proportional to the size of the muscle contracting, which in this case was a small muscle mass, accounting for the increase in leg discomfort post-fatigue and no increases in dyspnea after fatigue.

EILV is expected to increase with increasing exercise intensity and EELV is expected to drop slightly with increasing exercise intensity as tidal breaths increase and plateau at high exercise intensities where thereafter breathing frequency accounts for the largest rise in ventilation (Johnson, Weisman, Zeballos, & Beck, 1999; Martin, B. J., Stager, 1981; Miller et al., 2005). These trends were certainly demonstrated amongst the four subjects, however the magnitude of the EILVs, which were >85% TLC as a collective, encompass a mild to moderate ventilatory constraint (Dempsey et al., 2002; Johnson et al., 1999). This constraint occurs at the higher ranges of EILV because as it approaches TLC, lung compliance falls and increases the elastic load on the inspiratory muscles causing increased work (Johnson et al., 1999). EELV decreased slightly more post fatigue than the pre-fatigue protocol, but was within normal ranges (< rest, normal) to assume no EELV limitation occurred in subjects overall (Johnson et al., 1999). The decrease in EELV usually occurs in the absence of a respiratory limitation, as it is a sign the expiratory muscles are activating more so that TV’s can stay in the linear portion of the chest compliance curve, minimizing work and optimizing diaphragm muscle length for elastic force generation (at high intensities)(Johnson et al., 1999).

A typical response of healthy subjects to exercise is increasing tidal breath loops towards the maximum FV envelope boundary in increments outward with little overlap of loops and without reaching the borders of the maximum loop(Wanger et al., 2005). A constraint is observed where two subjects FV loops at submax exercise show a slight hyperinflation (increasing EELV at higher exercise intensities), which produces more work on the muscles used for breathing (Johnson et al., 1999), but is not reflected in the dyspnea scores. Subject 1 shows a slight hyperinflation at maximal exercise intensities both pre and post fatigue, which did not effect his dyspnea rating or power output at exhaustion. Subject 4 shows some dynamic hyperinflation at lower exercise intensities both pre and post fatigue, which seem to dissipate at her higher exercise intensities. Her dyspnea rating was not higher at these lower power output (not pre nor post fatigue), and she still managed to complete the same power output at exhaustion, meaning that the respiratory fatiguing protocol likely did not cause more hyperinflation of her lungs.

When visually inspecting the loops, even at maximum exercise, there should still be room to increase both volume and flow in the maximum FV envelope, yet the exercising loops for subject 1 and 4 (for expiratory and inspiratory reserve) seem to enclose on, touch or even overlap the max IC loop. According to Johnson et al. (1999), if a FV loop at an exercise intensity touches or overlaps with the expiratory flow volume loop for >40% of that tidal volume, then it is considered an expiratory flow limitation. In subject 1, >80% of her maximal exercise intensity tidal volume was surpassing her max FV maneuver at rest, so in both pre and post fatigue protocols, she was experiencing a large expiratory flow limitation, whereas subject 1 showed <10% overlap. This was possibly due to her asthma. According to Kosmas et al (2004), expiratory flow limitation and dynamic hyperinflation is common in asthmatics with no exercise-induced asthma, and may contribute to a decreased exercise capacity. Another possibility is that in fit, young athletes, although normal lung function is observable, expiratory flow limitation can be apparent (Johnson et al., 1999). Although normally, people adopt a breathing pattern to avoid high lung volumes, when high levels of ventilation (seen in athletes) occur at max intensities, this could imply a high inspiratory demand near capacity, reducing inspiratory reserves, but allowing for needed breathing compensations (Johnson et al., 1999).

Inspiratory flow limitations are usually due to a limitation in the inspiratory muscles(Johnson et al., 1999), which in these young trained subjects was not likely a factor. These results may be due to only one trial of max IC’s taken, whereas usually in the literature there are three or more trial conducted to get a more accurate estimate of the max FV loop (Johnson et al., 1999; Quanjer, Tammeling, Pedersen, Peslin, & Yernault, 1993). Because of this, sometimes the exercising FV-loops shown exit the max FV envelope where there was probably no true limitation. Another potential for the error was that the data collection methods were new to the lab technicians, and problems during data collection could have occurred.

In endurance sports especially, the athlete’s VO2max is of interest as it relates to performance (Basset, D.R., Howley, 1999) although it is not the only factor determining performance. VO2max is a product of the athlete’s cardiovascular output and arteriole-venous difference in oxygen content which sets the upper limit for an athlete’s performance ability (Astrand, P-O., Saltin, 1961; Basset, D.R., Howley, 1999; Ferretti, 2014; Hill & Lupton, 1923). Through training, improvements in exercise tolerance can increase VO2max, speed at thresholds, speed of VO2 kinetics, and reduce the slow component amplitude, in order to enhance performance by reducing the fatigue process (Bailey et al., 2010). During highly intense exercise, the respiratory muscles can consume around 14-16% of the total cardiac output as well as 10-15% of the total VO2, therefore potentially limiting oxygen delivery to the large working muscles through the metaboreflex previously discussed (Bailey et al., 2010; Dempsey et al., 2002). Mcclaran, Harms, Pegelow, & Dempsey (2015) explain that fit women (versus fit men and generally unfit people) have a greater prevalence of expiratory flow limitation (during heavy exercise), a relative hyperinflation, higher breathing frequency, and that they come closer to their ventilatory reserve than the less fit women, increasing the overall cost of breathing during intense exercise. An acute increase in EELV decreases inspiratory muscle length, increases the work and oxygen cost of breathing, and decreases inspiratory muscle endurance time, as previously discussed (Johnson et al., 1999). So, ventilatory fatigue in a female endurance athlete limit performance, perhaps more so than a male and than an untrained counterpart. This could be trained so that the O2 cost of ventilation can decrease as a contributor to total demand of the exercise (Bailey et al., 2010).

In conclusion, it appears that respiratory muscle training, or training in general would decrease the contribution of the respiratory muscles’ contribution to the total VO2, and potentially lower the energy cost of the exercise contribution from respiratory muscles, potentially increasing O2 delivery to working muscles through less muscle metaboreflex.


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Dempsey, J. a, Sheel, a W., St Croix, C. M., & Morgan, B. J. (2002). Respiratory influences on sympathetic vasomotor outflow in humans. Respiratory Physiology & Neurobiology, 130, 3–20. doi:10.1016/S0034-5687(01)00327-9

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