The maximum oxygen volume (VO 2 max), a quality that depends to a different extent on central factors (oxygen transport and uptake capacity) and peripheral factors (oxygen extraction and utilization capacity) but which, however, does not improve in the same order as those factors purely related to the periphery.
VO2 max has limited improvement, and this is well documented in the scientific literature. However, other related variables such as ventilatory efficiency, and therefore energy efficiency, or the capacity for energy production through oxidation have significant room for improvement.
The example, again, is professional athletes, whose peripheral adaptations can always be improved, even if they are good. So, where does the improvement come from?
One of the answers lies in 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 could lie in the composition of muscle fibers and neuromuscular function. We would also find answers that are often overlooked, for example, in the location, composition, and function of the various subcellular compartments. This is where the location of intramuscular triglycerides and their role in physical exercise and athletic performance begins more specifically.
Intramuscular triglycerides and athletes: The slice of ham
It is well known that fat, fatty acids, are stored in “droplets” (mainly triglycerides) that are interconnected in different locations throughout the human body.
The most representative, quantitatively, are found in subcutaneous regions and deep visceral adipose tissue. But also, naturally, within the muscles.
These triglycerides are known as intramuscular triglycerides (IMTG) , and if they're present, it's because they serve as a vital source of energy during muscle contraction. We can understand this by looking at a "cut" of muscle from an elite endurance athlete (much like a slice of ham).
What we see in that cut is probably very similar to a slice of acorn-fed Iberian ham from a pig moving freely, running and moving throughout its life.
It is characterized by a number of internal white lines, between the muscles, which are much greater in proportion to their fatty acid content (white tissue) around the muscle (outside the slice, which would represent that part that we often remove from the slice before eating it).
If, on the other hand, we cut a slice of muscle from a sedentary person, we would find few or no white lines between the muscle filaments and much more fatty tissue surrounding the slice. In other words, it's 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 diseases, 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?
I present to you the “athlete’s paradox.”
When various researchers have sought an explanation for this reality, they have found that sedentary people or those with metabolic diseases and the endurance athlete population show no significant differences in terms of IMTG content, but in fact, in many cases, the latter even have higher amounts. Considering that the amount of IMTG has been negatively linked to insulin sensitivity (the higher the IMTG, the lower the sensitivity), these have always been a focus of attention when exploring the causes of this type of disease. If the content is similar or even higher and the endurance athlete population does not suffer from metabolic diseases (on the contrary, they are perfect in this regard), where does the crux of the matter lie? Perhaps in the location.
The big difference between both populations lies in where these TGIM are stored, in the subcellular location.
It's interesting. In sedentary or ill people, it seems that IMTG is stored primarily in the subsarcolemmal region.
In endurance athletes, it is found in the intermyofibrillar region, primarily in type I fibers. The distribution varies between populations. Why is this?
Because the function of each sublocation is also different. The IMTGs located between myofibrils play a fundamental role in providing energy during contraction, as has been documented by measuring their depletion and analyzing how these pools change during physical exercise.
However, in the subsarcolemmal fraction, the IMTG content does not appear to change during exercise, suggesting 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 endurance athletes' IMTGs are found in a fraction closer to the muscle is supported by overwhelming logic. The closer they are, the more bioavailable. But beyond logic, it also makes some metabolic sense and is supported by scientific evidence: its ability to interact with mitochondria.
The most active mitochondria are found in the intermyofibrillar zone, and this is where this interesting relationship between IMT and mitochondria occurs. More specifically, it is through a protein called SNAP23, which also plays an important role in the translocation of GLUT4 transporters through the insulin pathway.
Its location (different between type 2 diabetic patients and healthy people) has no impact on glucose absorption during exercise, but it does have a negative impact on absorption during rest.
This relationship between IMTG and mitochondria appears to have a functional link to energy mobilization and utilization, that is, greater bioavailability and readiness for use. All of this, of course, is related to the mitochondrial biogenesis induced by exercise itself, and therefore, its distribution is a characteristic of the athletic population.
O 2 transport
What does all this have to do with oxygen transport and the variables that can be improved?
Understanding how oxygen is transported to the mitochondria. After passing through various physiological barriers, oxygen is finally transported to the mitochondria. This can give us an idea of the different factors that determine this uptake and transport through the cell and to the mitochondria.
It has always been assumed that oxygen is transported passively and without major limitations.
Oxygen is a non-polar element that shows high solubility in lipids, which is why it has always been suggested that they play a fundamental role in their transport.
For example, it has been shown that oxygen is preferred by cellular lipid barriers for "traveling" throughout the cell. "Rapid transport" pathways between the lipid layers themselves have even been proposed, allowing oxygen to travel more rapidly.
Among the lipids that play an important role in this creation of high partial pressure oxygen channels or pathways through which the element in question is transported at greater speed are cholesterol and triglycerides.
On the contrary, phospholipids or some proteins do not generate such channels, slowing down the passage of O2.
So, 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 still a curious thing that O2 is transported more quickly 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 inherent to physical exercise and play a determining role in metabolic diseases.
A closer arrangement of TGIM could ensure more efficient O2 transport, improving both the rate and, therefore, the availability for oxidation.
I previously talked to you about VO2 max and the peripheral factors that impact its transport and utilization.
Well, the question I ask myself is whether these metabolic and peripheral adaptations associated with the composition and location of IMTG in the muscle could determine the capacity to transport oxygen and, therefore, improve its utilization.
Training and eating to improve your TGIM
Regardless of whether we consider this hypothesis, which could be an important element in improving ventilatory efficiency, or not, the role of IMTG during endurance exercise at the bioenergetic level is well known.
It is extremely interesting to see how their utilization dynamics are, especially in type I fibers, during exercise at moderate intensities, as it helps us understand that IMTG are the main source of fat for skeletal muscle, as well as during recovery.
That is, in those fat oxidation parameters we measure when we perform metabolic tests, MITGs contribute a majority. And again, this is thanks to their 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
Well, 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 GIM?
Training hard, but well. If we look at the history of any World Tour cyclist, we can see months in which they train between 80 and 110 hours.
Similarly, if we analyze the records of the world's best runners or triathletes, we find weeks of >180 km or >35 hours, respectively.
A lot, a lot of time, a lot of volume.
But at what intensities?
Important. Is it possible to train 90 hours a month at a high intensity? Or even at a medium intensity?
No.
If we go back to these records we see that the distribution of intensities is very significant.
The time line elapsed at low intensities (Z1-Z2) is >5 times higher than that of 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 MITGs, generating adaptations that allow them to oxidize them in the mitochondria with high efficacy and efficiency.
And 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 has his ventilatory threshold 1?
At the same level, or even higher, than an amateur athlete can achieve their ventilatory threshold 2.
But, in addition, 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's a very good thing (contrary to what it may seem) because it translates into more mechanical energy, more watts.
These cyclists are better at everything: producing, spending, doing it efficiently, and creating and synthesizing what they spend.
All of this means that, even though they train at low-moderate intensities for them, the metabolic stress they endure is very high.
For example, an athlete might consume about 18-20 kcal/min at a moderate intensity. If you multiply this by a 3-hour workout, you can get an estimate of over 3,000 kcal.
Do you understand the high demand for these athletes? How do they meet it?
One of the main factors that most determines the capacity to train is consuming a lot of energy.
These athletes certainly do.
But also, eating an energy source that allows for high-volume training 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
But at low and moderate intensities?
Let me ask you one more thing.
How many g/min of glucose do you think a “motor” like this 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, even if we want to understand this zone as a “magic zone” where only fatty acids are used.
Therefore, its replacement is crucial.
As for 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 case.
Athletes with higher fat oxidation rates are those who consume more carbohydrates, especially during exercise.
In summary.
Improving IMTG will depend largely on the volume and intensity distribution of 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 considerable availability of lactate and liver 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.
