I've already asked two question in this site that maybe could help you in order to make your super soldier, also, I'll explain them and try to produce more ideas:
- How to increase the efficiency of lungs;
- How to make a human that doesn't need breath;
P.S: if you or someone decide to give me an upvote for this, instead give that to JDługosz♦.
The cross-current respiratory gas exchanger in the lungs of birds. Air is forced from the air sacs unidirectionally (from right to left in the diagram) through the parabronchi. The pulmonary capillaries surround the parabronchi in the manner shown (blood flowing from below the parabronchus to above it in the diagram). Blood or air with a high oxygen content is shown in red; oxygen-poor air or blood is shown in various shades of purple-blue.
This respiratory system let birds to simulate and inhale and exhale at the same time, "basically doubling" (don't exactly) the amount of air absorbed. They have air sacs: while they inhale, the 50% of air goes to some air sacs with O2, and the another 50% is consumed and stored as CO2 in another sacs, during exhalation, the 50% of O2 in air sacs is consumed and expelled, while at the same time the 50% of C02 in air sacs is just exhaled (they are able to get oxygen even when they are exhaling, thing that we can't do).
- If you don't understand how it works, read the wikipedia's link, in this diagram wasn't show but birds also have air sacs to store air. If you keep without understanding, ask me in comments and I will try to help you. It took me a while to also understand it :).
- This system is more vulnerable to CO2 inhalation (breath faster the toxic -> die faster), also is more vulnerable to hold breath.
- Maybe they may have a hybrid mammal and bird respiratory system. Like a smaller lung, or adapted air sacs in order to also be able to absorb the storaged oxygen.
Hemogoblin, myoglobin and (2,3-BPG)
P.S: if you or someone decide to give me an upvote for this, instead you should consider give it to Aaron Barnard, P Chapman and/or elemtilas.
Futhemorer do anatomical changes we can also do some microscopic but not less important adaptations.
I am quite sure you have heard at least one time in school about this protein, it transports oxygen from the lungs to the body cells, and also transport the carbon dioxide from the body cells to the lung. Actually, people who live in high altitudes (like mountains with low oxygen) or people who smoke have an increase of this compound in their blood (red blood cells), as a response from the body to a decrease of oxygen intake: the body increase the absorbtion efficiency. You soldiers could have a higher concetration on this in blood.
High concentrations of myoglobin in muscle cells allow organisms to hold their breath for a longer period of time. Diving mammals such as whales and seals have muscles with particularly high abundance of myoglobin. Myoglobin is found in Type I muscle, Type II A and Type II B, but most texts consider myoglobin not to be found in smooth muscle.
2,3-BPG is present in human red blood cells (RBC; erythrocyte) at approximately 5 mmol/L. It binds with greater affinity to deoxygenated hemoglobin (e.g. when the red blood cell is near respiring tissue) than it does to oxygenated hemoglobin (e.g., in the lungs) due to spatial changes: 2,3-BPG (with an estimated size of about 9 angstroms) fits in the deoxygenated hemoglobin configuration (11 angstroms), but not as well in the oxygenated (5 angstroms). It interacts with deoxygenated hemoglobin beta subunits by decreasing their affinity for oxygen, so it allosterically promotes the release of the remaining oxygen molecules bound to the hemoglobin, thus enhancing the ability of RBCs to release oxygen near tissues that need it most. 2,3-BPG is thus an allosteric effector.
Emphasis mine of both quotes. Quotes from Wikipedia.
Great! Right? Well, it's quite difficult to understand, it took me around a while to understand well how it works exactly when Aaron Barnard posts it.
In other words, 2-3BPG has an affinity to red blood cell with a low amount of oxygen in their hemoglobin because they are near muscles and are releasing it. When this chemical combine with hemoglobin it decreases the affinity (ability to retain) oxygen, releasing it even faster to the muscles; oxygenating tissues and being able quicker to travel to lungs in order to re-oxygenate.
Actually, people who live in higher places have an increase in this chemical. 2,3-BPG helps the body to resist hypoxia and other oxygen privation situation or diseases.
Also, remember that create 2,3-BPG consume energy (which can be used in muscles):
There is a delicate balance between the need to generate ATP to support energy requirements for cell metabolism and the need to maintain appropriate oxygenation/deoxygenation status of hemoglobin. This balance is maintained by isomerisation of 1,3-BPG to 2,3-BPG, which enhances the deoxygenation of hemoglobin. Low pH activates the activity of biphosphoglyceromutase and inhibits bisphosphoglyerate phosphatase, which leads to increases in 2,3-BPG.
Like hemoglobin, myoglobin is a cytoplasmic protein that binds oxygen on a heme group. It harbors only one heme group, whereas hemoglobin has four. Although its heme group is identical to those in Hb, Mb has a higher affinity for oxygen than does hemoglobin. This difference is related to its different role: whereas hemoglobin transports oxygen, myoglobin's function is to store oxygen [generally in muscles].
Emphasis (bold and itallic) and square brackets mine. Quotes from Wikipedia.
I have read somewhere [citation needed :(, I think wikipedia] that exist some drugs that gives us the innate ability of some mammals: increase amount of blood cells during excercise activities (the spleen in some animals -very little in humans- has the ability to store red blood cells and produce them [we lose that ability after born]) but in humans it could produce heart problems because our heat can't beat with a denser blood, we need an stronger one.
Myocyte (AKA: muscle cells)
An introduction from Wikipedia:
A myocyte (also known as a muscle cell) is the type of cell found in muscle tissue. Myocytes are long, tubular cells that develop from myoblasts to form muscles in a process known as myogenesis. There are various specialized forms of myocytes: cardiac, skeletal, and smooth muscle cells, with various properties. The striated cells of cardiac and skeletal muscles are referred to as muscle fibers.3 Cardiomyocytes are the muscle fibres that form the chambers of the heart, and have a single central nucleus.4 Skeletal muscle fibers help support and move the body and tend to have peripheral nuclei. Smooth muscle cells control involuntary movements such as the peristalsis contractions in the oesophagus and stomach.
In this link you will find a bit below a large table that explains the difference between 3 types of muscle cells. Each type of muscle cell has different characteristics, I am not a medic but after reading a bit I get to the conclusion that:
- Type I fibers (Slow Oxidative (SO)) are basically "slow" muscles... they consume less oxygen and can work without getting tired a lot more time, but they are weaker and slower.
- Type IIA fibers (Fast Oxidative/Glycolytic (FOG)) are "intermediate/fast" muscles: they consume more oxygen, are faster, a bit more stronger and can resist quite well fatigue, but not for an unlimited time (they have fewer capillaries density so I guess they resupply oxygen slower, but they store some energy inside).
- Type IIX fibers (Fast Glycolytic (FG)) are "fast and strong" muscle cells: they are fast and the strongest ones, but they lack of fatigue resistance and store a lot less oxygen and energy inside them.
Don't worry! You don't have to choose only one type of fiber! Muscles are made by a composition of X% type I, Y% type IIA and Z% of IIX, so you could archive the best combination of durability and force/speed for each muscle in their bodies!
Also, I think that people which trains doing exercise can increase the amount slow-tissue-slow-oxygen-consumption up to 90%. In this link about the Narwhal there is a comparison with Narwhal muscles and marathon people.
Blood circulation on tissues regulation
The Narwhal is a marine animal able to dive really deep (record of 1.864 metres below water) during a decent amount of time (30 minutes normally, and up to 3 hours during winter).
They are able to do this thanks to this characteristics:
- They have a high amount of myoglobin in their muscles. (Talked above about it).
- During hypoxia situation it's able to priorize the blood flow only to vital organs as brain, lungs and kidneys, reducing it oxygen consumption (non-vital organs reduce their consumption) and priorizing it to better places.
- Oposite as Dolphins, they don't have "fast-muscles", instead they use slow contraction muscles (also know as "red muscle") (87% instead of 40-50%). (Talked above about it). This kind of muscle consume less oxygen and is highly ressistent fatigue.
I found a better explanation in the Spanish link of Wikipedia so I'll try to do my best to translate it:
Lactic fermentation is done on muscular tissue when there is an intense anaerobic exercise, in other words, there isn't enough oxygen supply to muscles in order to perform aerobic respiration.
When lactic acid is acumulated on muscular cells it produce symptoms of muscular fatigue. Some cells, like eritrocites (red blood cells) hasn't mitochondrias so they are forced to get energy using lactic fermentation. On the contrary, the parenchyma die quickly because it doesn't do fermentation, and it only energy source is aerobic respiration.
In other words, when there isn't enough oxygen in your body, your muscular cells switch to an anaerobic respiration: lactic fermentation. The problem is that the lactic acid... is acid, and your body doesn't like acid (acidosis). So your cells try to expulse that acid and send it to the bloodstream, the problem is that our cells aren't able to expulse it with enough fast, and it acumulate inside them, producing pain. Your super soldiers could have better bodies modified to be able to use it more frequently without problems.
I won't explain the citric acid cycle nor this one (because I am not a biologist and they are too large), but I'll try to give basic explanation to you:
Glycolysis: 1 Glucose + 2 ATP + 2 ADP + 2 P + 2 NAD+ → 2 pyruvate + 4 ATP + 2 NADH + 2H+ + 2 H2O
1 Pyruvate + 1 NAD+ + CoA → 1 Acetyl-CoA + NADH + CO2 + H+
- Citric Acid Cycle: 1 Acetil-CoA + 3 NAD+ + FAD + GDP + Pi + 2 H2O → CoA-SH + 3 (NADH + H+) + FADH2 + GTP + 2 CO2
- Several more steps (8?) with GTP and NADH (also with FADH2?) → TOTAL NET → 29.85 ATP to 30 ATP, with a theorical max of 36 ATP. (Biology isn't exactly, it's random).
Lactic acid fermentation 1 Pyruvate + NADH → Lactic acid + NAD+ + 2 ATP
- So 2 ATP from Glycolysis + 2 ATP from Lactic fermentation → 4 ATP instead of around 29.85 - 30 ATP. Obviously Krebs Cycle (citric acid cycle) is better, but it needs oxygen, that is why our body only use it on emergency (low O2), your soldiers will need to eat more calories due to the low efficiency of fermentation.
Looks this cute lactic acid fermentation animation:
Edit: @Demigan pointed in comments:
FYI, lactic acid does not damage the cells. It has long been thought so as whenever lactic acid was present so did muscle pains, but tests showed that your cells suffer no ill effects from the lactic acid, it just happens to coincide with the work you did and because of that the amount of pain you might experience. Unfortunately, it's rather hard changing something relatively minor that is being used in textbooks and sports everywhere.
So I have read a bit more and I found also something similar, I put a quote because I didn't understand it enough in order to take my own conclusions:
In 2004 Robergs et al. maintained that lactic acidosis during exercise is a "construct" or myth, pointing out that part of the H+ comes from ATP hydrolysis (ATP4- + H2O → ADP3- + HPO2-4 + H+), and that reducing pyruvate to lactate (pyruvate- + NADH + H+ → lactate- + NAD+) actually consumes H+. Lindinger et al. countered that they had ignored the causative factors of the increase in [H+]. After all, the production of lactate- from a neutral molecule must increase [H+] to maintain electroneutrality. The point of Robergs's paper, however, was that lactate- is produced from pyruvate-, which has the same charge. It is pyruvate- production from neutral glucose that generates H+:
- Glucose + 2 NAD+ + 2 ADP3- + 2 HPO2-4 → 2 pyruvate- + 2 H+ + 2 NADH + 2 ATP4- + 2 H2O
Subsequent lactate− production absorbs these protons:
- 2 pyruvate- + 2 H+ + 2 NADH → 2 lactate ion- + 2 NAD+
- Glucose + 2 NAD+ + 2 ADP3- + 2 HPO2−4 → 2 pyruvate- + 2 H+ + 2 NADH + 2 ATP4− + 2 H2O → 2 lactic ion− + 2 NAD+ + 2 ATP4− + 2 H2O
Although the reaction glucose → 2 lactate- + 2 H+ releases two H+ when viewed on its own, the H+ are absorbed in the production of ATP. On the other hand, the absorbed acidity is released during subsequent hydrolysis of ATP: ATP4− + H2O → ADP3− + HPO2−4 + H+. So once the use of the ATP is included, the overall reaction is:
- Glucose → 2 pyruvate- + 2 H+
The generation of CO2 during respiration also causes an increase in [H+].
Quote from Wikipedia. I've replaced some complex chemical formulas to its chemical names.
Did you still remember all that I've said about the lactic acid fermentation, this is why I was talking about it:
The Cori cycle (also known as the Lactic acid cycle) [...] refers to the metabolic pathway in which lactate produced by anaerobic glycolysis in the muscles moves to the liver and is converted to glucose, which then returns to the muscles and is metabolized back to lactate.
Our muscles cells are too focused on "being" muscles and so they aren't able to get energy efficiently and quickly, so they centralized part of this task to the liver.
Basically our muscles consumes glucose and produces lactic acid, which is send to the liver and is returned into glucose (with a slightly net energy loss) in order to be re-sent to muscles again.
If you don't understand this picture you can go to the Spanish Wikipedia, they have a more colorful version of it :) (If you want I can edit it with paint).
Muscular activity requires ATP, which is provided by the breakdown of glycogen in the skeletal muscles. The breakdown of glycogen, a process is known as glycogenolysis, releases glucose in the form of glucose-1-phosphate (G-1-P). The G-1-P is converted to G-6-P by the enzyme phosphoglucomutase. G-6-P is readily fed into glycolysis, [...] a process that provides ATP to the muscle cells as an energy source. During a muscular activity, the store of ATP needs to be constantly replenished. When the supply of oxygen is sufficient, this energy comes from feeding pyruvate, one product of glycolysis, into the Krebs cycle.
Emphasis and adaptation mine.
But, what happens if you don't have enough oxygen? Muscles consumes around 7 to 40 times more glucogen and oxygen during activity [spanish Wikipedia]. Obviously, the lactic acid fermentation which produces a lesser amount of energy without oxygen (Also regenerate NAD+ making easier the glycolysis). That is the first part of the Cori cycle.
Instead of accumulating inside the muscle cells, lactate produced by anaerobic fermentation is taken up by the liver (using the delivered by the bloodstream). This initiates the other half of the Cori cycle. In the liver, gluconeogenesis occurs. From an intuitive perspective, gluconeogenesis reverses both glycolysis and fermentation by converting lactate first into pyruvate, and finally back to glucose. The glucose is then supplied to the muscles through the bloodstream; it is ready to be fed into further glycolysis reactions. If muscle activity has stopped, the glucose is used to replenish the supplies of glycogen through glycogenesis.
Remember that as I said before, this is an inefficient cycle, but at least it helps the muscles:
Overall, the glycolysis part of the cycle produces 2 ATP molecules at a cost of 6 ATP molecules consumed in the gluconeogenesis part. Each iteration of the cycle must be maintained by a net consumption of 4 ATP molecules. As a result, the cycle cannot be sustained indefinitely. The intensive consumption of ATP molecules indicates that the Cori cycle shifts the metabolic burden from the muscles to the liver.
- Glucose + 2ADP → 2 lactic acid + 2H+ + 2ATP + 2H20 (muscle)
- 2 lactic acid + 6 ATP + 4 H20 --> glucose + 6ADP (liver)
- Net energy loss: 4 ATP
Luckily, if you finish your activity, this cycle becomes more efficient:
The cycle is also important in producing ATP, an energy source, during muscle activity. The Cori cycle functions more efficiently when muscle activity has ceased. This allows the oxygen debt to be repaid such that the Krebs cycle and electron transport chain can produce energy at peak efficiency
The Spanish wikipedia said that you can get painfully tired of doing exercise because our liver isn't enough fast to do all these reactions, so some of the lactic acids get involuntary stored in muscular cells producing acidosis. Maybe having a bigger liver (or several small in strategic locations) can help our mucles. Or maybe increasing the activity of the adrenal gland to produce more adrenaline hormone which activates the Cori cycle in the liver (Futhemorer to glucagon).
Futhemorer the Cory Cycle there is very other similar cycle called Cahill, it isn't used when the body is doing activity, it's used when you are starving, so muscles start feeding with amino-acids to keep working and the liver regen them. I can post information about it if you think you could use also that.
P.S: If you have any question ask in comments. I don't bite and I love this!