NIRS, Muscle Oxygenation, & Hypertrophy:
What is the Lowest Intensity You Can Use While Still Eliciting A Growth Response ?
If you accept that mechanical tension and local muscular fatigue are the two main drivers of muscle hypertrophy, any choice of training intensity represents a tradeoff between those two mechanisms. The heavier you go, the more tension you develop, but the less local muscular fatigue and subsequently metabolic stress you develop before the point of fatigue and vice versa. However, it seems that there needs to be some balance of both mechanisms to maximize growth.
When I refer to metabolic stress, i’m specifically talking about local muscle oxygen saturation, or SmO2. When we utilize oxygen at a faster rate than it is delivery there will be an impairment in the sensitivity of actin-myosin myofilaments to calcium ions, which appears to drive peripheral fatigue — peripheral fatigue will then cause increases in motor unit recruitment, which will lead to increases in mechanical tension (1,2,3). In simplistic terms: local muscle desaturation → peripheral fatigue → increased mechanical tension → hypertrophy.
So, in and of itself local muscle desaturation (metabolic stress) doesn’t appear to cause hypertrophy — it appears that it’s leading to mechanical tension which is currently believed to be the primary driver of hypertrophy. As a result, I consider metabolic stress a ‘back door’ path for hypertrophy rather than a direct causitive factor.
This points to a fundamental question about low-load training for hypertrophy: how low can you go while still eliciting a growth response?
Based on the current body of research it looks like a set performed with 30% of a 1RM provides the same stimulus for growth as a set performed with 90% of a 1RM, assuming both sets are taken to volitional failure (4,7). 30% is pretty dang light - if you back squat a respectable 500# that's only a 150# load. You'll certainly be able to tell there's something on the bar, but you can likely do 30+ reps at a steady cadence while keeping tension on the muscle.
If we can still drive hypertrophy with as low as 30% of a 1RM, can we do it with 10%? Where is the cut off point? In a study by Lasevicius et al., we are presented some evidence that the cut off likely occurs between 20% and 30% of a 1RM for most individuals (6). However, i'd wager the low end cut off may be higher than 30% for some people as well, which i'll discuss later on.
The crux now becomes figuring out what an individuals cut off point is so you can train with more specificity. If someone can only do "X" number of sets per week for a given muscle group before they push past their ability to recover it would be a shame if a handful of those sets were outside of their effective intensity range.
I believe NIRS can give us a highly effective, and minimally invasive, way of figuring this out.
What is muscle oxygenation and subsequently, what is NIRS?
Muscle oxygenation is a measurement of how much hemoglobin is carrying oxygen in the capillaries of the muscle and the subsequent transfer of oxygen to myoglobin, the oxygen carrying molecule located within the muscle. Muscle oxygenation is a localized measure that depends on level of blood flow, and changes in the hemoglobin dissociation curve. Muscle oxygenation is measured optically with near-infrared light, so it is completely non-invasive. The differing absorption spectra of the infrared light passing through the muscular tissue can be used to identify the relative amount of hemoglobin and myoglobin bound oxygen compared to the amount that is not. It is expressed as a percentage from 0 to 100 and is abbreviated SmO2.“Near-infrared light can penetrate biological tissues with less scattering and absorption than visible light and consequently offers advantages for imaging and quantitative measurements. In its simplest form, a NIRS device consists of a light-source emitting two or more wavelengths of light in the near-infrared range (650-1000 nm) into the tissue of interest and a detector placed at a known distance from the source(s). The chromophores haemoglobin (Hb) and myoglobin (Mb) are oxygen carriers in blood and skeletal myocytes respectively and their absorbance of near infrared light differs depending on whether they are in an oxygenated or deoxygenated state.” (5).
What does NIRS measure?
“NIRS measurements reflect the balance of O2 delivery to working muscles and muscle O2 consumption in capillary beds” (8).“Combining NIRS with simple physiological interventions, such as venous or arterial occlusions,allows quantitative measurements to be made from skeletal muscle. This provides a tool for assessing two major determinants of the capacity of muscles to exercise: O2 delivery and O2 utilization. The non-invasive nature of NIRS makes it an appealing technique for use in adynamic environment and for activities of daily living.” (6)
As coaches and athletes, why should we care?
"During quick, short bursts, of high intensity or high load movement such as strength training the muscle is reliant on the creation of energy molecules, ATP, from phosphocreatine (PCr), to maintain cellular energy balance. It is now known that the replenishment of this energy system is based primarily on energy synthesis from aerobic (O2consuming) means. Muscle oxygenation responds almost instantaneously with the onset of exercise, indicating that high intensity strength training is intimately tied to oxygen availability to the muscle, specifically this could represent the almost instantaneous start of replenishment of ATP via aerobic means. Therefore, monitoring oxygen consumption can be a very useful tool to aid in strength training. It should be noted that the human body can be energetically limited in the ability to combust ATP-PCR for a 1-rep max, which is independent of the Moxy-SmO2 measure that looks at replenishment. Therefore, Muscle Oxygen Consumption measures may be limited for a 1-rep max, but become exponentially more useful as the rep count, and reliance on O2 consumption, goes up."
-Phillip Batterson, Moxy Monitor"On a metabolic level, if we are after producing insane amounts of work output, what we are after is the ability to dissipate heat and acid, as well as restore phosphocreatine as efficiently and quickly as possible. NIRS may in fact be a viable proxy to the latter, which has enormous potentially. NIRS is also going to show you if you are occluding and therefore not able to get waste products out of the muscle in question, again potentially huge for sports that involve chasing work capacity on repeated efforts or even hypertrophy, but probably not as huge for sprint and powerlifting athletes."
-Dr. Ben House, Functional Medicine Costa Rica
When using a NIRS to monitor blood flow & tHB reactions, I see three types of trends: compression outflow and return, venous occlusion and release, and arterial occlusion and release. For all intents and purposes, we're primarily concerned with this first two.[For an in depth explanation of this concept click HERE]
A compression reaction is when muscle tension squeezes blood out of the muscle. This occurs within several seconds of the onset of tension and is diminished upon the release of tension. Typically this reaction occurs at <30% of MVC, or an athletes 1RM, though i've seen a deviation of up to ~10% in either direction depending on an athletes physiological predisposition.
Venous occlusion is when muscle tension restricts the outflow of blood from the muscle. This occurs over tens of seconds to minutes and upon the release of tension blood is able to leave the muscle. Subjectively athlete's feel 'a pump' when this occurs since blood is entering the muscle and isn't escaping. In most instances, this will occur between 30-70% of MVC, or an athletes 1RM, but as with the former reaction i've seen this vary quite a bit from roughly ~25-85% of an athletes 1RM.
I find it interesting that the purported effective intensity range for hypertrophy of 30-90% 1RM largely overlaps with the %'s of an athletes 1RM where they will get venous occlusion, and arterial occlusion (>70% of a 1RM in most cases). I'd go out on a limb and speculate that the observed 'low-end' cut off range of 20-30% of an atheltes 1RM is a product of what percentage of their 1RM they transition from getting muscular compression to venous occlusion. In order to find when this transition point occurs i'll have athletes perform the following assessment with a NIRS device :
5 Air Squats
5 FS @5% 1RM
5 FS @15% 1RM
5 FS @25% 1RM
5 FS @35% 1RM
….etc.
*Note % where you see compression vs venous occlusion vs arterial occlusion.
The utility of this test is in its prescriptive qualities for strength training protocols. If you have athletes who don't respond well to traditional strength protocols, they may not be creating enough intramuscular tension relative to what their heart can push through, and as a result, they occlude at higher %’s that ‘usual’, or they may be over delivering oxygen to the muscle. As a result their strength and hypertrophy work will look much different than an athlete who occludes at lower loads.
This becomes very apparent when working with high level Crossfit competitors. At the elite level, we see two distinct types of physiological limitations, both of which come with distinct global adaptation trends. On the one hand we have respiratory limited athletes who present with great cardiac outut and mitochondrial / capillary density, but with a weak respiratory system. As a result of having excellent cardiac output, and less local muscle tension, these athletes usually get compression, venous occlusion, and arterial occlusion at higher %'s of their 1RM's compared to the prototypical figure out <30%, 30-70%, and >70% 1RM respectively. On the other hand, we have delivery limited athletes who present with great mitochondrial and capillary density, but have weak cardiac output. For these athletes increased blood pressure limits blood flow resulting in a low oxygen environment in the muscle, and failure when their heart can't 'break' the blockages. Whereas respiritory limited athletes occlude at higher than expected %'s of their 1RM's, delivery limited athletes occlude at lower than expected %'s. Consequently delivery limited Crossfit athletes get far more hypertrophy when performing sport specific work than respiratory limited athletes. To go over some specific figures, if we place a delivery limited athletes low cut off at ~25% of their 1RM for hypertrophy and a respiritory limited athlete cut off at ~35% then they would need 100# and 140# on the bar to do an effective sets of hypertrophy training on a squat assuming both of them can squat a modest 400#.
Below I've posted a NIRS graph comparing a delivery and respiratory limited athletes going head to head in a Crossfit metcon. Despite the fact that the workout was the same, and their scores were similar, they had completely different reactions inside the muscle. If we look at the respiratory limited athlete's oxygen desaturation trend on the bottom, we see a nice linear trend. Inside the muscle it almost looks like they were performing a cyclical test, like a 2k. If we look at the delivery limited athlete's desaturation trend, on the other hand, we see a lot of peaks and valleys, and their blood flow trend was equally as erratic as they cut off blood flow when alternating movements and occluded the working muscle when under load. It's no wonder they put on so much muscle mass when doing sport specific work as the blood flow and oxygenation trends inside the working muscle aren't dissimilar from what we'd observe in an athlete doing circuit training work on machines or KAATSU, and the total weekly volumes likely surpass 20 sets per muscle group which amount to a potent growth stimulus.
With everything in this article being said, we should take into consideration that NIRS has yet to be validated as a tool we can use to guide hypertrophy training, My hope is not to sway anyone, but instead to provide potential uses for this technology as I believe it has the potential to answer a number of unanswered questions posed by the current body of research.
Work Cited:
1. Allen D. G., Lamb G. D., Westerblad H. (2008). Impaired calcium release during fatigue. J. Appl. Physiol. 104 296–305. 10.1152/japplphysiol.00908.20072. Drouin, Patrick & Kohoko, Zach & Mew, Olivia & Lynn, Mytchel & Fenuta, Alyssa & Tschakovsky, Michael. (2019). Fatigue-Independent Alterations in Muscle Activation and Effort Perception During Forearm Exercise: The Role of Local Oxygen Delivery. Journal of Applied Physiology. 127. 10.1152/japplphysiol.00122.2019.
3. Fitts R. H. (2008). The cross-bridge cycle and skeletal muscle fatigue. J. Appl. Physiol. 104 551–558. 10.1152/japplphysiol.01200.2007
4. Jenkins, Nathaniel & Housh, Terry & Cochrane, Kristen & Bergstrom, Haley & Hill, Ethan & Smith, Cory & Buckner, Samuel & Cramer, Joel & Schmidt, Richard & Johnson, Glen. (2015). Neuromuscular adaptations after 2- and 4-weeks of 80% versus 30% 1RM resistance training to failure. The Journal of Strength and Conditioning Research. In Press. 10.1519/JSC.0000000000001308.
5. Jones S, Chiesa ST, Chaturvedi N, Hughes AD. Recent developments in near-infrared spectroscopy (NIRS) for the assessment of local skeletal muscle microvascular function and capacity to utilise oxygen. Artery Res. 2016;16:25–33.
6. Lasevicius, T., Ugrinowitsch, C., Schoenfeld, B.J., Roschel, H., Tavares, L.D., Souza, E.O., Laurentino, G.C., & Tricoli, V. (2018). Effects of different intensities of resistance training with equated volume load on muscle strength and hypertrophy. European journal of sport science, 18 6, 772–780 .
7. Schoenfeld, B.J., Peterson, M.D., Ogborn, D.I., Contreras, B., & Sonmez, G.T. (2015). Effects of Low- vs. High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men. Journal of strength and conditioning research, 29 10, 2954–63 .
8. Ufland P, Lapole T, Ahmaidi S, Buchheit M. Muscle force recovery in relation to muscle oxygenation. Clin Physiol Funct Imaging. 2012;32(5):380–387.
