Written By: Gino Panza
There’s an old adage that says “not to beat a dead horse”, but I’m stubborn, so I’m here to wield the hammer for science one more time. On December 5th, Alex Viada posted a link to askmen.com about the elevation masks. I actually think the article is pretty good- it made me happy to read it. I really despise the mask, and I continue down the road to achieving my PhD, I’ve come to realize why I hate it so much: misleading marketing. For a long time now I have run and hid from articles regarding the mask. I could not take hearing another word about hypoxic training with the mask, and altitude this and that, followed by someone completely unqualified telling me about mitochondria and how they function.
I commented on the Facebook post regarding other mechanisms that MAY help improve performance, which I will address here. The point of this article is two-fold: 1) teach some basic physiology and responses to exercise; and 2) to explore the potential mechanisms whereby the mask may help. Please remember I am stating it may help. I hope that this article will make that clear.
For this to make sense we have to cover a few things. First are the basics on terminology for ventilation and respiration. Next, I will provide a general overview of the potential mechanism, followed by a few points that are important to this concept, and finally I will dissect a few of the articles about the training mask.
Since we are going to cover the pulmonary system and lungs, I figured I would start with the basics. Everyone uses the word respiration for breathing and moving air in and out of the lungs. That is wrong. Respiration is gas diffusion across a membrane, which is a way of saying we get oxygen into the blood and carbon dioxide out. Ventilation is the process of moving air in and out of the lungs; the two are not synonymous. Appropriate respiration depends on appropriate ventilation. I remember some of the original marketing for training masks making claims to reduce the oxygen your body brings in, simulating altitude. Sorry folks, if you take air in, it maintains the same percentage of oxygen molecules, so you really do not affect the diffusion gradient. This is where most qualified individuals argued against the masks, and I agree. However, the masks may do something else.
The potential mechanism for these masks may have to do with the work of breathing and what is termed the “respiratory steal phenomenon”.1,2 Essentially, the amount of work the ventilatory muscles must undergo to maintain oxygen and carbon dioxide concentrations in the blood becomes so high that there may be some reflexes that reroute blood flow to those ventilator muscles, thus “stealing” it from the other working muscles. This produces a scenario where we decrease oxygen delivery to the other working muscles (e.g. legs), reducing the amount of energy the muscles can create – meaning we can no longer maintain the same level of work in the muscles. However, for this to happen the ventilatory muscles must undergo a high degree of fatigue, which requires a high degree of work.
Fatigue, Work, and Blood Flow
Let’s turn to metabolism, which is actually bioenergetics – but we’ll save that for another article – and fatigue (performance). Fatigue may be defined as a loss in muscle force-generating capacity due to work, which is recovered following rest,3 or the reduction in muscle performance regardless of task outcome.4 This muscle fatigue is a result of an inability to match substrate-level phosphorylation with energy requirements, leading to intracellular hydrogen ion accumulation5 and decreased exercise sustainability.6 In other words, all those enzymes and macronutrients (yes, and micronutrients) everyone likes to clamor about – this is where they play a role. Some researchers7 have explained that all these complex intracellular cascades can “back-up”, which causes a shift in how energy is created. This back up leads to an increase in hydrogen ion concentrations inside of the muscle. Following the build-up is muscle fatigue. Improving the enzymes’ function, appropriate storage and delivery allows a muscle to meet demand (energy requirement) over long periods. The better your body is at balancing the supply and demand of exercise and intracellular processes, the better your exercise sustainability is. (Figure 1)
This process requires oxygen, which is also a “substrate” for energy creation. As work (the demand for energy) increases, so does blood flow. The more work you do, the more blood flows to the working muscles. Unfortunately, we only have a limited supply of blood (~5 liters). So, while you run/lift/bear crawl and breathe, all those muscles must receive enough oxygen to match the rate at which each cell generates energy. Working muscles require more blood flow because they are attempting to create more energy. Imagine if your ventilatory muscles, which allow you to breathe, are not effective at moving air or using oxygen to make energy. Given the amount of work they’re doing, there is a high probability they will fatigue. Think of them as “out of shape” ventilatory muscles. The ineffective energy creation causes the body to attempt to reroute blood flow to these muscles to increase the amount of oxygen available so they can continue to generate enery. If we have a limited blood supply, then the blood must come from somewhere – often enough, it comes from peripheral muscles like the legs.
Work of Breathing
A primary function of the human pulmonary system is to facilitate blood gas homeostasis at minimal metabolic cost of breathing.8 For example, as the body requires an increase in ventilation, the ventilatory musculature will require additional oxygen and substrates proportional to the increase in work. Considering that work of breathing (Wb) increases significantly with increased ventilation9,10 any perturbation that increases resistance to air flow will lead to an increase in Wb.
1) Deformation and uncoupling of the rib cage and abdominal wall, which includes changes in breathing pattern.
2) Characteristics of the ventilatory muscles
3) Airway resistance and lung tissue compliance
Under times of increased work of breathing (Wb), humans have reported decrements in oxygen uptake in working limbs and overall physical performance. The mechanisms remain largely unknown, but there are a few hypotheses.
An example: mechanical constraints such as obesity12,13 will increase the work of the ventilatory musculature, heightening metabolic demand and subsequently ventilatory muscle fatigue.14 Ventilatory muscle fatigue and the respiratory steal phenomenon11 redistribute the blood flow away from peripheral muscles (also associated with increased sympathetic outflow1 and decreases in physical performance).1,2,15
Resistance to ventilation may stem from other various factors such as mechanical resistance causing impeded airflow – 16,17 for example, something like the training mask. The measurements of mechanical constraints can be affected by postural movements between the thoracic and abdominal regions,18,19 alterations in muscle length-tension relationships of the diaphragm20 and increased resistances of the chest wall.21 The increased mechanical resistance requires additional muscle force output of the ventilatory muscles causing an increase in ventilatory muscle fatigue.22,23
The diaphragm is the first muscle activated, followed by accessory muscles, during increases in minute ventilation22 and increased work rates.24 The diaphragm is the primary generator for airflow, as the other musculature is used primarily for controlling cavity pressures,25 but accessory muscle recruitment is also required to prevent hypoventilation during times of diaphragmatic fatigue.23,26 So, if the diaphragm gets tired, the other muscles pick up the slack. If they’re not used to the work, then they may be ineffective (“out of shape”) and fatigue as well.
The stress required to induce ventilatory muscle fatigue grows when diaphragmatic force approaches 40% of maximal contraction,22 and increases with relative intensity above 85% of VO2 max.26 Studies investigating the effects of hypoxia on exercise-induced ventilatory fatigue reported significantly high Wb during hypoxia in the early and mid-stages of exercise.23 Additionally, diaphragmatic fatigue has been reported in triathletes27and moderately trained individuals.28 Babcock et al. (1995) stimulated the phrenic nerve (which controls the diaphragm) via electrical stimulation before and after heavy training. Following heavy training, individuals were no longer able to generate the same amount of force (transdiaphragmatic pressure, or Pdi, for those interested), suggesting ventilatory muscle fatigue. 23 Others have also reported diaphragmatic fatigue using electrical stimulation following heavy endurance exercise,29 as well as fatigue lasting up to at least 15 minutes post-exercise30 in both sexes.28
The redistribution of blood flow during the steal phenomenon has potential causal roots in sympathetic vasoconstriction outflow during prolonged31 and high-intensity cycling exercise.1 However, the sympathetic outflow does not always present during the steal phenomenon at submaximal exercise .15
Here is where things get tricky, and being a careful consumer of science is important.
The effect of high work of breathing may be viewed through unloading the ventilatory muscles during work, as Marciniuk et al. (1994) found. They reported decreased VO2, dyspnea (shortness of breath) and a 14% increase in endurance, but interestingly no changes in VE, VT or Bf were reported during submaximal effort.32
Here is a quick review, since I know many of you may be lost as this has been a very dense read so far. Essentially, as ventilation goes up so does the work of breathing. So, increases in ventilationà increased workàincreased oxygen demandàincrease in required blood flow (if muscles are ineffective at force production or energy production per unit force). If we alter any variable that alters ventilation, then we may potentially increase the Wb. This includes breathing patterns (which I won’t address here, but will cite9,10,33).
I can’t cover everything, but I will pick a select few articles to demonstrate some concepts. Also, I will not get into potential mechanisms of the respiratory steal phenomena, as that isn’t the focus of this article. My primary focus here is to provide evidence that something happens that changes performance.
Dempsey, citing his work with Aaron9,33, reported graphs showing VO2 cost of hyperpnea (breathing response to exercise), as a percentage of VO2 total, as the Y-axis plotted over VE (L/min). They inferred that the VO2 cost of hyperpnea ranges from about 3% to 16% of VO2 total. Additionally, a second schematic depicting VO2/ VE plotted over minute ventilation (mL-O2/L-VE over VE L/Min) reports O2 cost per liter of air breathed per minute, and this value rises curvilinearly with increasing VE. This tells us that the more we ventilate, the more Wb will rise exponentially, rather than linearly, which is extremely important.
Harms et al. (1997), measuring Wb, flow rates and body cavity pressures, demonstrated reduced leg blood flow during times of increased Wb. Specifically, Wb in Joules/min decreased significantly during inspiratory assistance and increased significantly during inspiratory load, which corresponded with a significant increase and decrease in leg blood flow, respectively.1 The altered leg blood flow and changes in VO2 did not change other gas exchange parameters. However, the inspiratory load altered the pressure-volume loop in the esophagus, leading to a different breathing pattern. The researchers extended their results from another study as direct evidence of the effects of Wb on cardiac output during maximal exercise.2 In this study, cardiac output (CO) was measured via Fick method. They reported no differences in stroke volume, cardiac output, or VO2 during loaded trials, but all measures were significantly lower than control during unloaded inspiratory work at VO2 max. Additionally, oxygen utilization was not different. The results of these two studies report significant portions of cardiac output redirected towards the ventilatory muscles with a simultaneous local vasoconstriction in the leg muscles.2
Chin et al. (2007) had participants report to their lab on 12 separate occasions (let that sink in a second). Day 1 was a max test to determine their work capacity. From there, subjects underwent 6 minutes of cycling, starting at 20 watts, and then increased to 90% of their anaerobic capacity, followed by another bout at 20 watts; all bouts were 6 minutes in length. This process was done 5 times for each of two conditions: control and hyperventilation. In the latter, the subjects hyperventilated until they become basic (in terms of blood pH, not pumpkin spice lattes). Although the goal of the study was not to investigate ventilation and the potential mechanisms I have discussed so far, it did show a slower VO2 adjustment to exercise, and slower muscle oxygen utilization,34 which is not good for performance, following changes in ventilation.
Chin et al. (2010) reported hyperventilation’s association with altered VO2 – resulting in alkalosis and reduced CO2 – and a direct measure of decreased femoral artery blood flow in healthy humans. This suggested that increased ventilation did reduce the amount of blood being delivered to the working leg muscles.35 Then, in 2013, Chin et al. reported that hyperventilation (without alkalosis) may alter VO2 kinetics, but if CO2 concentrations are controlled by increasing the amount of CO2 that subjects inhaled during hyperventilation, then peripheral blood flow is restored, but still delayed.36 These data provide evidence that ventilatory muscle performance may alter integrative function and potentially performance in humans.
The last two articles I will cover quickly.
Kyroussis et al. (2000) tracked the changes in cavity pressures during constant work rate walking to fatigue in participants with chronic obstructive pulmonary disease (COPD), and reported an inability to increase absolute inspiratory pressure prior to exercise cessation while minute ventilation continued to increase.37 Interestingly, they used inspiratory assistance and reported a decrease in abdominal pressure, increased transdiaphragmatic pressure, and ultimately an increase in walking endurance.
Bye et al.(1984)24 reported diaphragmatic fatigue during CWR at 80% of work capacity on a leg cycle ergometer during ambient air breathing, then by increasing the concentration of O2 inhaled (FiO2) with a 40% O2 gas mixture. The researchers reported an increase from 5.9 to 9.8 minutes of exercise during the O2 inhalation condition, which reduces the amount of work the ventilatory muscles have to do. Additionally, they reported no decrease in the rate of perceived exertion of the study participants, which I find to be particularly interesting. Despite any physiological change, these individuals reported exercise to be less effortful. I don’t know about you, but when running gets harder, I usually want to quit faster. Quitting faster than someone else is losing (if you’re racing, anyway), and losing is not performing well.
Because this article is already lengthy, and potentially denser than anticipated, I reduced some of the content and number of articles I presented. There are a lot out there, so in my conclusion I want to be very clear.
Ventilation, which may not be the number reported in papers, does have an effect on performance. The amount you ventilate is not the same amount that reaches the level where the blood can pick up the oxygen, nor does it give you a sign of how much work the muscles are doing, and it surely does not mean it does not affect performance if two individuals report the same absolute value. In conclusion, the mask MAY help some individuals who have weak/deconditioned ventilatory muscles (or other pathologies) by assisting their ventilatory muscles and thereby reducing the amount of work the muscles undergo at a given workload. If your ventilatory muscles are trained, and not a limiting factor, the mask could be making you worse. This comes from an inability to push yourself to maximum, due to the potential mechanisms mentioned above, which results in an overall reduction of stress to the body. We all know you have to progressively stress the body to get better, so if the mask slows you down, you’re not progressing. As for oxygen content, the training mask has actually changed marketing points since last time I looked- I didn’t see any “altitude/hypoxia” comments.
As a young researcher with no skin or money in the game, I’m okay with being a little more bold with my statements and here is one: There is an obvious effect on performance when ventilation, and more appropriately, ventilatory muscle work, is perturbed. Period. The arguments and ambiguity, I think, come from statements of how it happens. There are plenty of papers that show when the Wb changes, performance does too. The problem is much of it comes from when the ventilatory muscles are relieved of their work, but then the performance measures change. Secondly, performance is typically measured by a change in VO2, not always by a task (see earlier definition of fatigue). The arguments for performance usually boil down to mechanisms, which aren’t usually the key focus for a coach or athlete. In summary, the research is unclear on the mechanisms of ventilation and its potential effect on performance. A potential mechanism is sympathetic nervous system activation leading to systemic vasoconstriction, reducing the blood flow and oxygen delivery to the muscle. There is a large difference between “altered ‘things’ regarding breathing and performance” and HOW some of these potential mechanisms are implicated. Be careful what you read, be clear in what you say, and ask for clarity when you’re learning.
About the Author
Gino Panza currently does programming and walking training for individuals with incomplete spinal cord injury, and his area of focus is ventilatory performance.
Facebook: Gino Severio
1 Harms CA, Babcock MA, McClaran SR, Pegelow DF, Nickele GA, Nelson WB et al. Respiratory muscle work compromises leg blood flow during maximal exercise. J Appl Physiol Bethesda Md 1985 1997; 82: 1573–1583.
2 Harms CA, Wetter TJ, McClaran SR, Pegelow DF, Nickele GA, Nelson WB et al. Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise. J Appl Physiol Bethesda Md 1985 1998; 85: 609–618.
3 NHLBI Workshop summary. Respiratory muscle fatigue. Report of the Respiratory Muscle Fatigue Workshop Group. Am Rev Respir Dis 1990; 142: 474–480.
4 Bigland-Ritchie B, Woods JJ. Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle Nerve 1984; 7: 691–699.
5 Keyser RE. Peripheral fatigue: high-energy phosphates and hydrogen ions. PM R 2010; 2: 347–358.
6 Grassi B, Rossiter HB, Zoladz JA. Skeletal Muscle Fatigue and Decreased Efficiency: Two Sides of the Same Coin? Exerc Sport Sci Rev 2015.
7 Randle PJ, Garland PB, Hales CN, Newsholme EA. The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1963; 1: 785–789.
8 Dempsey JA, Smith CA. Pathophysiology of human ventilatory control. Eur Respir J 2014; 44: 495–512.
9 Aaron EA, Johnson BD, Seow CK, Dempsey JA. Oxygen cost of exercise hyperpnea: measurement. J Appl Physiol Bethesda Md 1985 1992; 72: 1810–1817.
10 Coast JR, Rasmussen SA, Krause KM, O’Kroy JA, Loy RA, Rhodes J. Ventilatory work and oxygen consumption during exercise and hyperventilation. J Appl Physiol Bethesda Md 1985 1993; 74: 793–798.
11 Dempsey JA, Harms CA, Ainsworth DM. Respiratory muscle perfusion and energetics during exercise. Med Sci Sports Exerc 1996; 28: 1123–1128.
12 Dempsey JA, Reddan W, Balke B, Rankin J. Work capacity determinants and physiologic cost of weight-supported work in obesity. J Appl Physiol 1966; 21: 1815–1820.
13 Dempsey JA, Reddan W, Rankin J, Balke B. Alveolar-arterial gas exchange during muscular work in obesity. J Appl Physiol 1966; 21: 1807–1814.
14 Lourenço RV. Diaphragm activity in obesity. J Clin Invest 1969; 48: 1609–1614.
15 Wetter TJ, Harms CA, Nelson WB, Pegelow DF, Dempsey JA. Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise. J Appl Physiol Bethesda Md 1985 1999; 87: 643–651.
16 Johnson BD, Saupe KW, Dempsey JA. Mechanical constraints on exercise hyperpnea in endurance athletes. J Appl Physiol Bethesda Md 1985 1992; 73: 874–886.
17 Glenny RW. Determinants of regional ventilation and blood flow in the lung. Intensive Care Med 2009; 35: 1833–1842.
18 Hart N, Laffont I, de la Sota AP, Lejaille M, Macadou G, Polkey MI et al. Respiratory effects of combined truncal and abdominal support in patients with spinal cord injury. Arch Phys Med Rehabil 2005; 86: 1447–1451.
19 Estenne M, De Troyer A. Mechanism of the postural dependence of vital capacity in tetraplegic subjects. Am Rev Respir Dis 1987; 135: 367–371.
20 Winslow C, Rozovsky J. Effect of spinal cord injury on the respiratory system. Am J Phys Med Rehabil Assoc Acad Physiatr 2003; 82: 803–814.
21 Scanlon PD, Loring SH, Pichurko BM, McCool FD, Slutsky AS, Sarkarati M et al. Respiratory mechanics in acute quadriplegia. Lung and chest wall compliance and dimensional changes during respiratory maneuvers. Am Rev Respir Dis 1989; 139: 615–620.
22 Bellemare F, Grassino A. Effect of pressure and timing of contraction on human diaphragm fatigue. J Appl Physiol 1982; 53: 1190–1195.
23 Babcock MA, Johnson BD, Pegelow DF, Suman OE, Griffin D, Dempsey JA. Hypoxic effects on exercise-induced diaphragmatic fatigue in normal healthy humans. J Appl Physiol Bethesda Md 1985 1995; 78: 82–92.
24 Bye PT, Esau SA, Walley KR, Macklem PT, Pardy RL. Ventilatory muscles during exercise in air and oxygen in normal men. J Appl Physiol 1984; 56: 464–471.
25 Romagnoli I, Gigliotti F, Lanini B, Bianchi R, Soldani N, Nerini M et al. Chest wall kinematics and respiratory muscle coordinated action during hypercapnia in healthy males. Eur J Appl Physiol 2004; 91: 525–533.
26 Johnson BD, Babcock MA, Suman OE, Dempsey JA. Exercise-induced diaphragmatic fatigue in healthy humans. J Physiol 1993; 460: 385–405.
27 Boussana A, Matecki S, Galy O, Hue O, Ramonatxo M, Le Gallais D. The effect of exercise modality on respiratory muscle performance in triathletes. Med Sci Sports Exerc 2001; 33: 2036–2043.
28 Ozkaplan A, Rhodes EC, Sheel AW, Taunton JE. A comparison of inspiratory muscle fatigue following maximal exercise in moderately trained males and females. Eur J Appl Physiol 2005; 95: 52–56.
29 Mador MJ, Dahuja M. Mechanisms for diaphragmatic fatigue following high-intensity leg exercise. Am J Respir Crit Care Med 1996; 154: 1484–1489.
30 Mador MJ, Magalang UJ, Rodis A, Kufel TJ. Diaphragmatic fatigue after exercise in healthy human subjects. Am Rev Respir Dis 1993; 148: 1571–1575.
31 Dempsey JA, Amann M, Romer LM, Miller JD. Respiratory system determinants of peripheral fatigue and endurance performance. Med Sci Sports Exerc 2008; 40: 457–461.
32 Marciniuk D, McKim D, Sanii R, Younes M. Role of central respiratory muscle fatigue in endurance exercise in normal subjects. J Appl Physiol Bethesda Md 1985 1994; 76: 236–241.
33 Aaron EA, Seow KC, Johnson BD, Dempsey JA. Oxygen cost of exercise hyperpnea: implications for performance. J Appl Physiol Bethesda Md 1985 1992; 72: 1818–1825.
34 Chin LMK, Leigh RJ, Heigenhauser GJF, Rossiter HB, Paterson DH, Kowalchuk JM. Hyperventilation-induced hypocapnic alkalosis slows the adaptation of pulmonary O2 uptake during the transition to moderate-intensity exercise. J Physiol 2007; 583: 351–364.
35 Chin LMK, Heigenhauser GJF, Paterson DH, Kowalchuk JM. Pulmonary O2 uptake and leg blood flow kinetics during moderate exercise are slowed by hyperventilation-induced hypocapnic alkalosis. J Appl Physiol Bethesda Md 1985 2010; 108: 1641–1650.
36 Chin LMK, Heigenhauser GJF, Paterson DH, Kowalchuk JM. Effect of voluntary hyperventilation with supplemental CO2 on pulmonary O2 uptake and leg blood flow kinetics during moderate-intensity exercise. Exp Physiol 2013; 98: 1668–1682.
37 Kyroussis D, Polkey MI, Hamnegård CH, Mills GH, Green M, Moxham J. Respiratory muscle activity in patients with COPD walking to exhaustion with and without pressure support. Eur Respir J 2000; 15: 649–655.