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To Breathe or Not to Breathe...

To Breathe or Not to Breathe...

스포츠 생리학
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What do athletes competing in the following sports have in common Swimming, rowing, synchronized swimming, shot putting, tennis, karate, archery, discus, weight lifting, paddling, shooting and many others.

The simple answer is that, like all of us, they must breathe. However, in the case of these, and other athletes, the process of breathing is often intricately inter-twined in the activity, and in fact, the ability to breathe properly and/or to control the activity of breathing in a prescribed manner may well play a major role in their success. The following describes the functioning and limitations of the respiratory system as it pertains to exercise, and suggests a means of training the respiratory system outside of regular training.

The functional capacity of the respiratory system

The respiratory muscles, through rhythmical contraction, serve to expand and compress the chest wall to move gas in and out of the lungs [Campbell, 1970]. The resulting gas exchange serves to maintain the stability of arterial blood gasses (oxygen and carbon dioxide) and blood acidity [Powers, 1997]. Ventilation is a product of ventilatory frequency and tidal volume. Maximal breathing frequencies during exercise have been reported to be between 40-60 breaths per minute and maximal tidal volumes can range from 1.5-4.0 litres per minute [Milic-Emili, 1998], yielding the potential for ventilation in excess of 200 litres per minute during maximal exercise, an amazing feat given the size of most people’s lungs!

However, as suggested above, not all sports require the capacity of moving large volumes of air during training and competition for success, but instead require the ability of controlling the process of inspiration and expiration in order to perform accurately, or developing the capability to forcibly exhale at the point of explosive activity to increase power.

The respiratory muscles

The respiratory muscles are morphologically and functionally similar to the skeletal muscles involved in locomotion [Powers, 1997], having both strength and endurance characteristics. With skeletal muscle, strength is measured as the maximal force that can be developed; in the case of the respiratory muscles, this is assessed as the maximal static pressure developed at the mouth [Black, 1969]. Similar to skeletal muscle, the respiratory muscles exhibit endurance, which is measured as the capacity for sustaining high levels of ventilation for relatively long periods [Freedman, 1970; Shephard, 1967].

Human respiratory muscles contain a high percentage of oxidative fibres, with type I and type IIa fibres comprising 77-99% of the total fibre pool [Mizuno, 1985]. There is very limited information on the oxidative and glycolytic enzymes in human respiratory muscles [Powers, 1997].
However, from research on the rat diaphragm, it has been determined that the activity of the oxidative enzymes (i.e., Kreb’s cycle) is 35-65% greater in the diaphragm than in the locomotor muscles of similar fibre type [Grinton, 1992]. The differences between the two may be due to the chronically active nature of the respiratory muscles. For a complete review of the diaphragm muscle structure and function refer to Sieck (1988).

Control of breathing

Over the last 100 years, various authors have proposed mechanisms to explain the increase in breathing that is observed with exercise [Mateika, 1995]. Currently, most researchers have acknowledged that no single mechanism totally explains the observed responses of the respiratory system to the varying needs of exercise.

Essentially, the increase in ventilation with exercise arises as a result of the following contributions: (1) primarily initiation of the signal results from a central command region of the brain, which includes input from the areas that initiate and control the motor activity needed to perform the activity [Eldridge, 1985], (2) the signal is fine-tuned by feedback from specialized sensors (peripheral chemoreceptors), which provide information concerning the status of blood chemistry [Cunningham, 1987; Oelberg, 1998], and (3) additional feedback from active muscles concerning the frequency and degree of muscle activation [Asmussen, 1983]. For a complete review of the neural control of breathing see Feldman [1999], and for a review of the control of breathing during exercise refer to [Mateika, 1995].

Feed back control of breathing in response to changes in blood chemistry

Chemoreceptors are specialized tissues that sense changes in blood chemistry. The peripheral chemoreceptors are located in the carotid bodies at the bifurcation of the carotid artery, the major artery leading to head region, and are sensitive to the levels of various substances in the blood [Nye, 1994]. Specifically, hypoxia (lack of oxygen) acts to increase the sensitivity of the peripheral chemoreceptors to hypercapnia (increased carbon dioxide), hydrogen ion concentration (indicative of changes in the acidity of the blood), and potassium ion concentration [Mateika, 1995]. Direct estimates of the chemoreflex threshold and sensitivity by Jeyaranjan [1987] have shown that only about 20% of ventilation in heavy exercise is mediated by the peripheral chemoreflex.

Feedback control of breathing in response to the activity of the working muscles

In addition to the chemoreceptors, specialized cells (Glogi tendon organs and muscle spindles) within the skeletal muscles provide feedback concerning the muscular activity, including the amount of force, the frequency of activation, and the stretch imposed on the muscles, through afferent nerve fibres. These nerves in the muscles are sensitive to lactic acid and potassium, two metabolites that are produced during exercise. Therefore, afferent feedback (both chemical and mechanical) from exercising limbs may be a contributor to the drive to breathe during exercise. For a complete review, please refer to Kaufman and Forster [1996].

The impact of limitations in respiratory muscle functioning on exercise performance

The ventilatory system has not been traditionally viewed as a limiting factor during exercise: “Actually, a healthy individual tends to over breathe in relation to oxygen consumption during heavy exercise. Even during maximal exercise, a considerable breathing reserve exists because pulmonary minute ventilation represents only 60-85% of a healthy persons maximum capacity for breathing.” [McArdle, 1991]. However recent research has questioned this notion. During exercise there is an increased work of breathing, exercise-induced arterial hypoxemia, respiratory muscle fatigue, and dyspnoea, each of which may result in a limitation to exercise performance [Bye, 1983].

The work of breathing

Work is performed when a force moves a point of application through a distance, i.e., W = Fd. In the case of a fluid system, such as air, the force is measured in terms of pressure difference and the displacement in terms of volume change, i.e., W = PV. With increasing ventilation, the work required to inspire is increased. While expiration is initially a passive process due to the elastic recoil of the lungs and the fall of the rib cage, it becomes an active process at higher ventilations as the muscular effort is needed to expel the air quickly; this adds to the work of breathing [Dodd, 1988].

The work of breathing is of importance as the relationship between ventilation and energy requirement is not a straight line, but exhibits a curve of increasing slope. Therefore, as exercise intensity increases, so does the total metabolic cost of ventilation [Otis, 1977]. This increases the total metabolic cost of the activity, as well as creates a competition for blood flow between the respiratory and locomotor muscles that may well result in a decreased exercise performance [Harms, 1997]. Indeed, there may be a “critical ventilation” where further increases in ventilation will not result in more oxygen available to the working muscles of locomotion [Otis, 1977]. Thus, as exercise intensity increases, greater and greater proportions of the increase in total body oxygen consumption are made up of increases in the oxygen requirements of the respiratory muscles [Dempsey, 1996].

Respiratory muscle work does not compromise peripheral blood flow and oxygen delivery during submaximal exercise [Wetter, 1999]. However, it has been shown that the respiratory muscles and the locomotor muscles compete for blood flow during intense exercise, under conditions of peak respiratory muscle work and peak whole body cardiac output. The respiratory muscles require a substantial portion of the total cardiac output during intense exercise up to 10% in the moderately trained and 15% in the highly trained [Aaron, 1992]. Harms [2000] and St Croix [2000] have demonstrated that a significant inverse relationship exists between the work of the breathing and blood flow to the legs, indicating that that the work of breathing during maximal exercise compromises locomotor muscle perfusion, and hence the delivery of oxygen to the working locomotor muscles. Several factors have been forwarded to explain the observed increase in the work of breathing during exercise, including an increased duty cycle, an increased contraction frequency, and an increased tidal volume.

Duty cycle - the importance of the duty cycle concerns the proportion of the total time for a single breath that is required for the process of inspiration. Decreasing the inspiratory time in relation to total breathing cycle time increases the work of breathing.

Muscle contraction frequency the importance of contraction frequency is easy to understand in that the more often the muscles contract, the higher will be the metabolic cost.

Tidal volume - tidal volume (the amount of air taken in with each breath) increases as exercise intensity increases (at least in the initial stages) [Campbell, 1970]. This can present several issues that can increase the work of breathing during exercise, including increasing the need to actively expand the chest. These greater tension requirements would require increased muscle activation, and therefore, an increased metabolic cost [Whitelaw, 1983].

Exercise-induced compromise of oxygen uptake at the lung

The idea that the lung may not be capable of maintaining adequate blood oxygen levels during intense exercise was first suggested by Dempsey [1986]. Essentially, this situation occurs when there is a decrease in arterial blood oxygen levels of more than 10% below normal due to insufficient oxygen being taken up by the blood at the lungs. The impact of the blood not being able to take up sufficient oxygen is obvious oxygen consumption will be compromised [Dempsey, 1999]. It has now been documented that this phenomenon occurs during intense exercise in a significant number of normal healthy subjects [Dempsey, 1999], and in nearly all highly trained endurance athletes [Durand, 2000].

Respiratory muscle fatigue

Much like skeletal muscle, the respiratory muscles are subject to fatigue [Farkas, 1996]. Skeletal muscle fatigue has been defined as a reversible reduction in the force/velocity generating capacity of a muscle [Noakes, 2000]. Perret [2000] has shown that respiratory muscle performance is reduced after exercise, regardless of the preceding exercise intensity, and suggestive that respiratory muscle performance may well be compromised to one degree or another in situations with multiple events without sufficient recovery time [Martin, 1982].

The exact mechanism by which respiratory muscle fatigue occurs is still unresolved. Two factors in particular have been correlated with the development of respiratory muscle fatigue the level of aerobic power reached during the exercise, and the peak pressure required compared to the maximal capacity of the muscle [Mador, 1991]. This suggests that inspiratory force generation plays a significant role in fatigue, and that factors related to exercise intensity (such as competition for blood flow, and production of metabolites) also play a role [Johnson, 1996].

Exercise training results in several positive adaptations that impacts respiratory muscle fatigue, such as an increased oxygen uptake capability [Noakes, 2000], an improved efficiency during both maximal and prolonged submaximal exercise [Metzger, 1986], and an increased storage of substrates in the muscle [Metzger, 1986]. Further, the utilization of substrates becomes more efficient, and it is possible that, with training, the respiratory muscles enhance their ability to use lactate as a substrate [Spengler, 1999]. Any training-induced reduction in the work of breathing would, theoretically, decrease respiratory muscle fatigue.

Dyspnoea the feeling of breathlessness

Dyspnoea can be described as the conscious sensation of breathlessness produced by changes in thoracic displacement or respiratory muscle force during breathing that causes an individual to alter the depth of a breath or the level of ventilation [Altose, 1985].

The physiological purpose of dyspnoea may be to protect and limit strain on the respiratory muscles and to prevent the development of respiratory muscle fatigue [Altose, 1985]. During either high duration or high intensity exercise there may be considerable strain placed on the respiratory muscles. In this case, the sensation of dyspnoea may limit the ability of an individual to continue to perform the exercise at the required intensity. The sensations associated with dyspnoea seem to be influenced by individual behavioral styles, personality, and emotional state [Cherniack, 1987].

Exercise training reduces the sensations of dyspnoea via several possible mechanisms: (a) a depression of the activity of the chemoreceptors reduces the level of respiratory activity, and therefore, decreases the sensation of dyspnoea, (b) Wells [1999] has shown that exercise training attenuates the peripheral chemoreflex response to exercise, and (c) specific respiratory muscle training to increase the maximal strength and pressure producing capacity of the respiratory muscles.

Respiratory muscle training

Respiratory muscle training may be an effective intervention that could address the limitations imposed by the respiratory system. Research in this area has demonstrated that the respiratory muscles do adapt to specific respiratory muscle training and to whole body exercise training. Controversy exists about the transfer of respiratory muscle training effects to performance of whole body exercise and about the effects of the different modes of respiratory muscle training.

Like skeletal muscles, the training of the respiratory muscles follow the established principles of training [Powers, 1990]. The respiratory muscles adapt specifically to the training stimulus to which they are exposed be that high pressure (increased strength), high flow (increased velocity of shortening), or high repetition (increased endurance) [Leith, 1976]. Not surprisingly, high-pressure training yields improvements in the pressure generating capacity, and high-flow training programs improve the ability to create higher rates of high flow [Tzelepis, 1999]. The respiratory muscles increase their endurance in response to high repetition, low-pressure training.

Consideration of the principle of training specificity is important in the design of respiratory muscle training protocols. Important qualitative differences in respiratory muscle loading can be achieved by means of different devices and breathing strategies [Belman, 1994]. Further, it is possible to create tailored training regimens that range from pure loads, combinations of flow and pressure loads, predominantly flow loads, all through a variety of repetitions. Two main types of respiratory muscle training have been described: (a) inspiratory and expiratory resistive training (accomplished by application of a threshold loading device, or breathing through a tube with a diameter less than the trachea), and (b) iso-capnic hyperpnoea, i.e., increasing ventilation while maintaining the same level of carbon dioxide, which is accomplished by maintaining a high ventilation for an extended period of time while breathing through a specific circuit.

Physiological effects of respiratory muscle training

Threshold loaded resistive training has been shown to increase both strength (defined as the ability to generate high pressures) and endurance (defined as the ability to generate and maintain high levels of ventilation). The duration of the resistive training protocols have ranged from 4-11 weeks. The training used in these studies generally consisted of breathing against a load equal to 15-50% of maximal inspiratory pressure for between 5-20 minutes, 4-5 times per week.

Research on resistive training of the respiratory muscles has shown that there is an improvement in maximal inspiratory pressure (improvements range from 8-57% [Sheel, 2002], and changes in pulmonary function, with some studies reporting improvements in vital capacity and total lung volumes of 3-5%, and in peak inspiratory flow.

The improvements in respiratory muscle strength arise due to a) an increased voluntary neuromuscular drive and co-ordination (timeframe of days) [Almasbakk, 1996], b) an increased neural adaptation (timeframe of 0-4 weeks) [Moritani, 1993], and c) changes in the contractile proteins and muscle hypertrophy (timeframe of 3+ weeks) [Bishop, 1999]. Increases in respiratory muscle strength have been associated with decreased perceptions of dyspnoea [Jones, 1985].

Several studies have shown that resistance training has resulted in an improvement in the endurance characteristics of the respiratory muscles. While this may seem counterintuitive, Coast [1988] has demonstrated that 4.5 minutes of resistive loaded breathing (55-60% of maximal developed pressure) at a breathing frequency of 18 breaths per minute, and a duty cycle of 0.5, resulted in significant improvements in cardiac output and oxygen consumption.

It remains controversial as to whether the improvements in respiratory muscle performance outlined above are transferable to exercise performance. Research in this area is limited. To date, the results of studies using respiratory muscle resistive training have been equivocal, with some showing improvement in performance [rowing: Volianitis, 2001 and cycling: Romer, 2002], and others no change in performance [running: Inbar, 2000; Williams, 2002; or cycling: Sonetti, 2001]. While it is not completely clear why there are differences in the results of these studies, the more recent studies have been better designed using large groups of subjects, and including a control (sham-training) group.

Respiratory muscle training using iso-capnic hyperpnoea - iso-capnic hyperpnoea training has been shown to increase respiratory muscle endurance capacity (defined as the power to sustain high levels of ventilation for relatively long periods of time). The duration of the training protocols has been in the range of 4-6 weeks. Again, the transfer of these improvements to whole body exercise is controversial with several authors demonstrating improvements in exercise endurance [cycling: Boutellier, 1992, 1998; Spengler, 1999; Markov, 2001; Stuessi, 2001] and others reporting no changes [cycling: Morgan, 1987; Fairbarn, 1991; Sonetti, 2001; Williams, 2002].

In those papers that do demonstrate improvement in exercise performance, the improvements have been attributed to decreased blood lactate levels (possibly due to (a) working muscles producing less lactate because of an overall reduced energy demand due to less respiratory work, or (b) trained respiratory muscles use more lactate as fuel for their own activity), lower exercise ventilation, decreased respiratory muscle fatigue [Powers, 1997], and a decreased sensation of dyspnoea [Killian, 1988].

There have been no studies to date on the effect of training on the expiratory muscles. All of the research summarized herein has focused on the effect of training on the inspiratory muscles, perhaps due to the preconception that expiration is a predominantly passive process [Duffin, 2000].

Research in this area remains controversial due to the lack of proper experimental design (mainly a lack of adequate control groups and small sample sizes). In addition, it is possible that in the studies where there was no transfer of training effect, that the breathing patterns chosen for respiratory muscle training were not applicable to the breathing patterns used during the activity, or that the training impulse was not adequate to stimulate adaptation to the extent that would be of benefit during maximal endurance exercise. However, several conclusions can be drawn concerning the benefits from iso-capnic hyperpnoea training: a) a reduced blood lactate levels, b) a decreased exercise ventilation, c) an increased fatigue resistance of the respiratory muscles, and d) a decreased sensation of dyspnoea.

A respiratory muscle training protocol (Wells, 2003)

An inspiratory and expiratory resistance loading technique was implemented for the respiratory muscle training protocol. To this end, a commercially available resistance training device the Power Lung ™ (Power Lung Inc., www.powerlung.com) was used.

The PowerLung ™ is a pressure resistance device that requires continuous application of pressure throughout inspiration and expiration for the spring-valve to remain open and for flow to be generated. The pressures required to generate flow through the device, settings 1-6 for inspiration and 1-3 for expiration, have been determined, as well as the flow-pressure characteristics of the device.

Participants (competitive swimmers) were required to perform the respiratory muscle training before each swim training session (approximately 10 swim training sessions per week). Each training session required the participants to inspire and expire a number of times against a resistance equal to a fixed percentage of their maximal developed pressure. Participants were instructed to initiate each breath from the end of a maximal expiration and to inhale as completely as possible. Breathing frequency was limited to 6-8 breaths per minute to prevent hyperventilation and hypocapnia. A duty cycle of 3 seconds for inspiration and 3 seconds for expiration was maintained for all training. The participants performed the training in a standing position, with a partner who “spotted” them to monitor adherence to the protocol and to ensure the participant’s safety. The coach was asked to keep a participation record to monitor adherence to the protocol.

In the first 6-week period, Group 1 performed respiratory muscle training and Group 2 performed the same training program using a sham trainer. The subjects that used the sham trainer were told that the device was a hypoxic endurance trainer designed to lower the amount of oxygen that was getting into their lungs. The groups performed the training according to the protocol described in Table 1. Note the pressure values for the sham training group were estimated based on the flow resistance of the sham trainers.

In the second 6-week period, Group 2 trained with the complete PowerLung ™ trainers and performed the same training protocol as described above for Group 1. Group 1 was asked to perform more intense respiratory muscle training in the second 6-week training phase: 1 set of 15 repeats at 60% of maximal pressure before each swim training session. After each swim training session they were asked to perform 1 set of 12-15 repetitions at 70% maximal pressure, 1 set of 10-12 repetitions at 80% maximal pressure, and 1 set of 6-8 repetitions at 90% maximal pressure. The rest interval between sets was 2 minutes for both groups, and the duty cycle remained at 3 seconds for inspiration and 3 seconds for expiration. Subjects were provided with the settings for their PowerLung ™ devices that would enable them to train at the appropriate intensity.

The results of the study showed that resistive respiratory muscle training improved: (a) pulmonary function, as evidenced by increases in vital capacity and forced volumes, and (b) ventilatory endurance, seen as improvements in both inspiratory and expiratory muscle functioning during a sustained ventilatory capacity test. These changes in various dynamic measurements of lung function would benefit the endurance athlete in maintaining optimal gas transport and exchange during exercise, and the improved muscle strength of the respiratory muscles would support the forcible exhales often used by athletes during explosive type movements.

Interestingly, there was a decrease in the sensitivity of the peripheral chemoreceptors, but, as this was not statistically different compared to the sham training, the desensitization cannot be attributed directly to the resistive respiratory muscle training program. The importance of the desensitization of the chemoreceptors is that athletes involved in those activities requiring breath holding, such as synchronized swimming, or extreme control of breathing during an activity, such as archery or shooting, would experience a decreased drive to breathe, which would allow a longer performance time.


Previously, the well developed structures and functioning of the lung has led researchers to suggest that the lung presents no real limitation to performance. This review has presented evidence quite to the contrary, including support that strongly suggests that improvements in pulmonary function alone can lead to improvements in exercise performance. This being the case, the use of resistance respiratory training as an adjunct to regular exercise training may well prove advantageous to performance. Presented herein is a description of a program of resistive respiratory muscle training using a commercially available training device.

References are available upon request.

For information concerning the material in this paper, please contact: Greg Wells at 이 이메일 주소가 스팸봇으로부터 보호됩니다. 확인하려면 자바스크립트 활성화가 필요합니다..

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