Can You Assess Mitochondrial Function With NIRS?
Mitochondria have several roles, including cell growth and differentiation, apoptosis, and cellular signaling, but are most known for their metabolic capability to generate chemical energy in the form of ATP. As a result, Mitochondria play a crucial role in cellular function and, subsequently, performance. Any alteration in mitochondrial structure or function can either increase or decrease mitochondrial respiration capacity, impacting energy production, among other functions.
In skeletal muscle, mitochondria generate most of the fuel required for contractile activity and physical functioning, and the number and function of mitochondria are related to exercise performance. Because of the importance of mitochondrial function on health and physical performance, the development of novel, cost-effective methodologies to study mitochondrial health is critical.
The mitochondria’s capacity for oxidative phosphorylation is typically measured indirectly as mitochondrial oxygen consumption, which can be done with a series of in vitro (in a test tube), in vivo (in the body) tests. Two problems exist with these approaches:
(1) they can be very invasive and can expose tissues to non-physiological conditions, and
(2) they can be incredibly expensive. As a result, these types of approaches can have limited translational significance, especially when the goals to assess changes in mitochondrial density and function for athlete performance.
Recent advances in NIRS have resulted in developing novel techniques for assessing muscle oxygen consumption (mVO2), an index of mitochondrial respiratory capacity. For this reason, NIRS can be used as a novel non-invasive way to measure skeletal muscle mitochondrial function. To do this, NIRS is used in conjunction with a rapid cuff inflation system (used to block oxygen delivery and venous return) to measure skeletal muscle oxygen consumption changes. The cuff blocks arterial inflow and allows one to isolate oxygen consumption from oxygen delivery, whereas not using the rapid cuff represents the difference between oxygen consumption and delivery. Since mitochondrial function changes over time with training, this type might be used to track these changes in a non-invasive way on the training floor over long time frames, which can be a useful metric for coaches or athletes doing physiologically guided training.
In the picture at the top of this article, we have an athlete’s pre-post test from 8 weeks of repeat desaturation training.
Repeat desaturation training is designed to increase capillarization, increase oxygen utilization, mitochondrial biogenesis, and intra-muscular coordination. Below you’ll find an auto-regualted and NIRS guided version of the workout performed in this intervention:
(Running time on 45:00 Clock) As many rounds of…..
10 sec AB at 75% max watts
Rest 1 min b/w bouts
*terminate workout when you begin to compensate biomechanically (shifting or changing movement pattern to accommodate for fatigue), breathing cannot get back down to baseline during rest/hyperventilation is induced, you can no longer elicit the Rx’d power output, or quality of work significantly drops off.
(Running time on 45:00 Clock) As many rounds of…..
10 sec AB at 75% max watts
Rest 1 Minute b/w sets
*The session terminates when O2 cannot be depleted to the extent of previous sets, you cannot reach a THb and Smo2 recovery baseline during rest, you can no longer hit the rx’ed wattage, you compensate biomechanically, or effort needed to sustain intensity begins to exponentially increase from set to set.
My speculation is that the increased magnitude and rate of oxygen utilization (and smaller area under the curve) from the pre-training → post-training intervention represents an increase in mitochondrial density and enzyme concentration. More research needs to be done in this area before making any claims with a greater degree of certainty, but it may be worth investigating.
