The maximum oxygen volume (VO2 max .), a quality that depends to a different extent on central factors (capacity to transport and uptake oxygen) and peripheral factors (capacity to extract oxygen and use it) but which, nevertheless, does not improve in the same order as those factors purely related to the periphery.
VO2 max shows limited improvement, and this is well documented in the scientific literature. However, other related variables such as ventilatory and, therefore, energy efficiency, or the capacity to produce energy through oxidation, have considerable room for improvement.
The example, once again, is professional athletes, whose peripheral adaptations can always be improved, no matter how good they are. So, where does this improvement come from?
One of the answers lies in the metabolic adaptations related to mitochondrial function and everything surrounding it, as well as improved functioning of metabolic pathways and their regulatory and adaptive mechanisms.
Another possible explanation lies in the composition of muscle fibers and neuromuscular function. We might also find answers that are often overlooked, for example, in the location, composition, and function of different subcellular compartments. This is where the focus shifts more specifically to the location of intramuscular triglycerides and their role in physical exercise and athletic performance.
Intramuscular triglycerides and athletes: The slice of ham
It is well known that fat, fatty acids, are stored in "droplets" (mainly triglycerides) that are related to each other in different locations throughout the human body.
The most significant numbers are found in subcutaneous regions and deep visceral adipose tissue. But also, as one would expect, within the muscles.
These triglycerides are known as Intramuscular Triglycerides (IMTG) , and their presence is due to their crucial role as an energy source during muscle contraction. This can be understood by examining a cross-section of a muscle from an elite endurance athlete (similar to a slice of ham).
What we will probably see in that cut is an image very similar to a slice of acorn-fed Iberian ham from a pig that moves freely, that runs and travels throughout its life.
It is characterized by a number of internal white lines, between the muscles, which in proportion are much greater than its content of fatty acids (white tissue) in the contour of the muscle (outside the slice, which would represent that part that we often remove from the slice before eating it).
Conversely, if we were to cut a slice of muscle from a sedentary person, we would find few or no white lines between the muscle fibers and a much larger amount of fat tissue surrounding the slice. In other words, it would be similar to a lower-quality ham from a pig that doesn't move.
This is what happens when we compare the muscles of sedentary people or those with metabolic disease, such as type 2 diabetes or obesity, with those of professional endurance athletes.
What is the difference between the two and why is this fact so important for health?
Let me introduce you to the "athlete's paradox".
When researchers have sought to explain this phenomenon, they have found that sedentary individuals or those with metabolic disease and endurance athletes show no significant differences in their TGIM content; in fact, the latter often have even higher levels. Given that TGIM levels have been negatively correlated with insulin sensitivity (higher TGIM levels correlate with lower sensitivity), these cells have always been a focus of attention when exploring the causes of such diseases. If the content is similar or even higher, and endurance athletes do not suffer from metabolic diseases (on the contrary, they are practically immune to them), what is the key to understanding this? Perhaps it lies in the location of the TGIM.
The major difference between the two populations lies in where these TGIMs are stored, in the subcellular location.
It's interesting. In sedentary people or those with illnesses, it seems that TGIM are stored mainly in the subsarcolemmal region.
In endurance athletes, it occurs in the intermyofibrillar region, primarily in type I fibers . The distribution differs between populations. Why?
Because the function of each sublocation is also different. The TGIM located between the myofibrils play a fundamental role in providing energy during contraction, and this has been documented by measuring their depletion and analyzing how these "pools" change during physical exercise.
However, in the subsarcolemmal fraction, the TGIM content does not appear to change during exercise, which suggests that its function is not energetic, but rather a regulator of the cell's energy status (related to insulin sensitivity).
Now go back to the slice of ham.
The fact that TGIM in endurance athletes is located closer to the muscle is undeniably logical. The closer, the more bioavailable. But beyond logic, it also makes metabolic sense and is supported by scientific evidence: their ability to interact with mitochondria.
The most active mitochondria are located in the intermyofibrillar zone, and it is there that this interesting relationship between TGIM and mitochondria occurs. More specifically, it happens through a protein called SNAP23, which also plays an important role in the translocation of GLUT4 transporters via the insulin pathway.
Its location (different between type 2 diabetic patients and healthy individuals) has no impact on glucose absorption during exercise, but it does negatively impact absorption during rest.
This relationship between TGIM and mitochondria appears to have a functional link to energy mobilization and utilization, meaning greater bioavailability and a greater predisposition to its use. All of this, of course, is related to mitochondrial biogenesis induced by exercise itself, and therefore, its distribution is a characteristic of the athletic population.
Oxygen transport
What does all this have to do with oxygen transport and those variables that can be improved?
Understanding how O2 is transported to the mitochondria. After passing through the various physiological barriers, oxygen is finally transported to the mitochondria, and this can give us an idea of the different factors that determine its uptake and transport through the cell and into the mitochondria.
It has always been assumed that oxygen is transported passively and without major limitations.
Oxygen is a nonpolar element that shows high solubility in lipids, so it has always been suggested that these play a fundamental role in its transport.
For example, it has been shown that the lipid barriers of cells are preferred by oxygen for "traveling" throughout the cell. "Fast transport" pathways have even been proposed between the lipid layers themselves, through which oxygen could travel at a higher speed.
Among the lipids that play an important role in this creation of channels or pathways of high partial pressure of oxygen through which the element in question is transported at a higher speed, we find cholesterol or triglycerides.
Conversely, phospholipids or some proteins do not generate such channels, slowing down the passage of O2.
Therefore, taking this into account, one of the conclusions that can be drawn from the existing scientific literature on the subject is related to the transport of O2 from red blood cells to the mitochondria.
This transport appears to be faster and more efficient if it uses channels or pathways whose composition is lipid.
It is certainly a curious thing that O2 is transported faster in a fatty fluid than in an aqueous fluid or, more precisely, on a drop of fat.
Both in the membrane and in the mitochondria, transport would improve if the composition and location of the existing fatty acids were more favorable.
These adaptations are characteristic of physical exercise and play a determining role in metabolic diseases.
A closer arrangement of TGIM could ensure more efficient O2 transport by improving both the speed and, therefore, the availability for oxidation.
I have previously spoken to you about VO2 max and the peripheral factors that impact this transport and utilization.
So, the question I ask myself is whether these metabolic and peripheral adaptations associated with the composition and location of TGIM in the muscle could determine the capacity to transport oxygen and, therefore, to improve its utilization.
Training and eating to improve your TGIM
Regardless of whether we want to take this hypothesis into account, which could be an important element to improve ventilatory efficiency, or not, the role of the TGIM during endurance exercise at the bioenergetic level is well known.
It is very interesting to see how its utilization dynamics are, especially in type I fibers, during exercise at moderate intensities, since it helps us understand that TGIM are the main source of fat for skeletal muscle, as well as in recovery.
In other words, in those fat oxidation parameters that we measure when we perform metabolic tests, TGIM contribute a majority percentage. And again, that's thanks to its high bioavailability.
Furthermore, it is interesting to emphasize that its use, the use of TGIM, is regulated both internally by
- hormonal signals
- 2) signals related to the cellular environment, such as at the external level through
So, taking all this into account, especially the important bioenergetic argument, the question is:
How to train and eat to improve the composition and location of TGIM?
Training hard, but well. If we look at the history of any World Tour cyclist, we can see months in which they train from 80 to 110 hours.
Similarly, if we analyze the records of the best runners or triathletes in the world, we find weeks of >180 km or >35h, respectively.
A lot, a whole lot of time, a lot of volume.
But at what intensities?
Important. Is it possible to train 90 hours a month at high intensity? Or even at medium intensity?
No.
If we look back at these records, we see that the distribution of intensities is very significant.
The time elapsed at low intensities (Z1-Z2) is >5 times higher than that of a medium intensity (Z3) and >10 times higher than that of high intensities (Z4-Z5).
This large volume allows them to mobilize metabolic resources related to the use of fatty acids and, more specifically, to TGIM, generating adaptations that allow them to oxidize them in the mitochondria with high effectiveness and efficiency.
And what about nutrition?
Training at low intensity does not mean that the metabolic demand is low.
Do you know at what relative intensity a professional WT cyclist reaches their ventilatory threshold 1?
At the same, or even above, that an amateur athlete can obtain their ventilatory threshold 2.
But also, did you know that one quality of these athletes is their high capacity to produce energy?
They are Formula 1 engines, so their production is extremely high, but without losing efficiency, on the contrary, improving it.
A professional cyclist can generate more energy (kcal/min) than an amateur athlete at the same intensity, and that is a very good thing (contrary to what it may seem) because it translates into more mechanical energy, into more watts.
These cyclists are better at everything: producing, spending, doing it efficiently, and creating and resynthesizing what they spend.
All of this means that, even though they train at low-to-moderate intensities for them, the metabolic stress they endure is very high.
For example, an athlete might burn around 18-20 kcal/min at a moderate intensity. Multiplying that by a 3-hour workout gives you a calculation of over 3000 kcal.
Do you understand the high demand for these athletes? How do they meet it?
One of the main factors that most determine the ability to train is ingesting a lot of energy.
These athletes certainly do.
But they also consume energy that allows them to train at high volumes under high metabolic stress. And these cyclists do this too.
They consume high amounts of carbohydrates, not only during exercise, but also outside of it (although to a much lesser extent).
Reaching consumption of more than 90 grams per hour in energy gels such as our Gel 60
[[PRODUCT:gel-60]]
But at low and moderate intensities?
Let me ask you one more thing.
How many g/min of glucose do you think one of these "engines" consumes at an intensity of VT1?
The answer is a lot, exactly >1.8-2g/min.
Therefore, glycogen and glucose oxidation is high at these intensities, however much we might want to understand this zone as a "magic zone" where only fatty acids are used.
Therefore, its replacement is crucial.
Regarding the "magic zone", we shouldn't think that carbohydrate intake limits fat oxidation, or rather, the ability to generate related adaptations, because that's far from the truth.
Athletes with higher rates of fat oxidation are those who consume the most carbohydrates, especially during exercise.
In summary.
Improving TGIM will depend largely on the volume and intensity distribution of the exercise. High volumes are associated with better adaptations. To train at these volumes, especially as the athlete's level increases, it is necessary to provide sufficient energy, and more specifically, carbohydrates, always ensuring a considerable availability of lactate and hepatic and muscle glycogen.
Literature
1.Gemmink A, Daemen S, Brouwers B, Hoeks J, Schaart G, Knoops K, Schrauwen P, Hesselink MKC. Decoration of myocellular lipid droplets with perilipins as a marker for in vivo lipid droplet dynamics: A super-resolution microscopy study in trained athletes and insulin resistant individuals. Biochim Biophys Acta Mol Cell Biol Lipids. 2021 Feb;1866(2):158852.
2.Pias SC. How does oxygen diffuse from capillaries to tissue mitochondria? Barriers and pathways. J Physiol. 2021 Mar;599(6):1769-1782.
3.Bergman BC, Goodpaster BH. Exercise and Muscle Lipid Content, Composition, and Localization: Influence on Muscle Insulin Sensitivity. Diabetes. 2020 May;69(5):848-858.
4..Morales-Alamo D, Losa-Reyna J, Torres-Peralta R, Martin-Rincon M, Perez-Valera M, Curtelin D, et al. What limits performance during whole-body incremental exercise to exhaustion in humans? J Physiol. 2015;593(20):4631-48.
