Never mind about the reference. I recall that it is Dr. Brook's Lactate shuttle hypothesis.
Never mind about the reference. I recall that it is Dr. Brook's Lactate shuttle hypothesis.
Any recent updates on research done by Dr. Brookes on the lactate shuttle? I am curious about his discoveries and hypotheses. Thank you.
By the way, Phoenix, you rock when it comes to exercise physiology. Other Jack Daniels, you seem the most knowledgeable of the respondents on Letsrun.com Thank you for you input. Tom
The below is a post by JK (and reposted by Carolinarunner).
I think this is the post that young Deak may have gotten
his info from. Please comment JK or Phoenix. What is the scoop?
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Regular long runs of 2 hrs. plus or minus a few minutes
You should be running a substantial portion of many of your long runs at a pace which gives you a "full of run" feeling - strong and floating in the middle and well-trained but not strained by the end. You should also gradually pick up the pace during the last few miles of the run (but avoid STRUGGLING). This is what trains you to be able to use FT fibers at the correct time in a race (as the ST ones start to run low on fuels). It also provides the stimulus needed for your muscle fibers to store the right balance of fat and carbs. Start with picking up the pace on regular "easy" long runs at about 1-2 miles from the finish, then get to where you can comfortably do it from about 5-7 miles out.
If you're already well-trained (i.e., you've worked your way up to regular high mileage) and you run at this high-end, "train don't strain" pace, you'll usually start to recruit your FT units after about 110-115 min. You'll also have to ventilate more as a result of a gradual increase in the CO2 content of the residual volume of air in your lungs. This will train your respiratory muscles, particularly if you're gradually increasing the speed over the last several minutes.
You have to balance stimulation with adaptation or you'll go over the edge (remember, it shouldn't all be just a bunch of JOGGING on these things). Running longer than 125 min. seems to require too much recovery time to be effective as a WEEKLY long run. So I think Snell and Co. found the right distances for their long runs (20-22 miles) since they were reportedly running 5:40-6:00 per mile on most of these outings. Frank Shorter always advocating running 2 hrs. or 20 miles (whichever came first) and to go at a "comfortably fast" pace. Sound advice there.
Here is one from HADD back in NOV 2002
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And long aerobic running is the best way to do this. But note this, your body only recruits enough fibres to develop the power needed to run at the pace you are doing. Some fibres in the muscle are working flat out, while others are totally relaxed. If you want to train enough fibres, then you must go far enough that the first fibres become fuel exhausted, causing your body to rest them and recruit the next set of fibres, then the next...
As each fibre becomes fuel exhausted, it is stimulated to adapt itself so that it can do the same job BETTER next time (maybe store more fuel to last longer before exhaustion, maybe increase its enzymes to provide more energy at a faster rate...)
So, as should be obvious, one long run is better than two short ones. It is not enough to run 70mpw if it is made up of 2 x 5 miles every day. Much better to have 3 longer runs of 90 mins, with some shorter work (like runs of 60 mins) in the days in between.
Another reason for so doing (as the Japanese show us) is that our bodies will not recruit the thicker / stronger fibres until the thinner ones are exhausted... so the long runs are really necessary to get to the thicker (more powerful and usually more anaerobic) fibres. But the pace can be as slow as you want. Even 8 mins/mile is okay, just go further and further. (Note here that Paula's 3000m time improved this year after she moved up to marathon-type training)
Michelle Branch fan Fiber recruitment and adaptations 12/3/2002 1:31PM - in reply to aggie Reply | Return to Index | Report Post
During exercise, the smallest motor neurons (the ones with the lowest threshold for synaptic activation) are recruited first, as long as there is sufficient force produced to sustain the exercise. These small motor neurons innervate ST muscle fibers, while larger neurons innervate FT fibers. It follows that there is a definite hierarchy of fiber utilization during exercise, which depends on the intensity (not so much the duration) of the exercise.
So it *does* matter how fast or slow you're running as to how many FT units are recruited.
So do ST fibers fatigue during long runs, thereby necessitating more and more FT fiber recruitment? Yes, they do, but it's not as much the duration of the run that determines fiber recruitment as it is the *pace*. Why should you feature a lot of relaxed running when developing an endurance base, then? One reason is because, if you're like most runners, you will wind up producing a modicum of lactic acid if you run at a pace sufficient to mobilize your FT fibers. This will be detrimental over time and will hinder your fitness development and ability to run just below your anaerobic threshold for very long.
Your policy on most runs should be to keep lactate production as low as possible at any given time in the run. Run more gently and run longer, allowing yourself time to warm up very gradually and feel as though you're firing on all cylinders. Then you can work a little closer to your AT. As you get fitter, your "relaxed" pace will become faster without any additional effort on your part, and you will mobilize FT fibers without producing nearly as much lactate as you once did. This training will improve the ability of *both* ST and FT fiber types to cope with exercise stress by stimulating you to develop more mitochondria and surrounding capillaries.
Fiber type specific glycogen depletion is influenced by training pace or more appropriately intensity.
At ~75% VO2, rate of glycogen utilization is higher in the FT fibers is higher relative to ST fibers.
Also, the info regarding adergenic stimulation of non-contracting fibers for contributions to the Cori Cycle is interesting as I always assumed (and I realize what that gets me) that the Cori cycle pertained to active fibers. Any citations or more info on that would be appreciated.
"Michelle Branch fan" is obviously JK.
Both are a good read but depending on your background may be a bit too technical. You can also try his textbook 3rd edition which lays out the theory pretty well and gives more backgroud. Re: textbook, probably the best exercise physiology textbook out there.
Brooks GA
Lactate shuttle -- between but not within cells?
J Physiol. 2002 Jun 1;541(Pt 2):333-4. No abstract available.
PMID: 12042341 [PubMed - indexed for MEDLINE]
Brooks GA
Lactate shuttles in nature.
Biochem Soc Trans. 2002 Apr;30(2):258-64. Review.
PMID: 12023861 [PubMed - indexed for MEDLINE]
I'm no bio expert wrote:
Phoenix wrote:**Fibers do NOT have to be recruited to be glycogen depleted**
It is much more likely that the ft fibers are dumping their glycogen in the form of lactate which is then being used for fuel by the heart and st fibers when st fiber fuel is depleted.
How exactly does ft fibers 'dump glycogen in the form of lactate?' Lactate is a waste product of glycolysis when no oxygen is present, so doesn't that mean that the FT fibers are working anaerobically i.e. being recruited? And whenever there's an oxygen shortage in the muscle it stimulates adaptations. Please correct me if I'm wrong. Do you have any links or studies that show your point? Thanks!
Lactate is not a "waste product"; it is a by product and can be used as a fuel by other ogans and even by muscles.
Lactate is produced even when sufficient oxygen is present, albeit in small amounts. I would guess (based on numerous samples) that I have about 1.2 mmol/L of lactate circulating in my blood right now and I am pretty aerobic at the moment.
There is a raging argument in the scientific world on the idea of hypoxia at the muscle level. Even when running pretty hard there is a lot of oxygen present; however, the rate at which energy is being demanded exceeds the ability for "aerobic" metabolism (to use the lay term) to provide energy.
I see I see, thanks.
Also Phoenix said that glycolysis occurs in FT fibres without them actually contracting. Where does the ATP go then?
Well some ATP is used in glycolysis often called Phase 1 amount depends on whether you start with glucose or glycogen (1 and 2 ATP made respectively) and some is (2 ATP) created in Phase 2. Specific steps are not really important. ATP levels usually do not change and this of course is a good thing as the muscle cell wants to maintain the ATP/ADP ratio. So in short the ATP does not go anywhere but is available for hydrolysis in the muscle cell.
Good questions and posts.
A few things to consider (in no particular order):
The Cori Cycle is not to be considered with the lactate shuttle. One contribution of Brooks pertinent to the current discussion is the idea that mitochondria metabolize lactate directly. Older dogma stated that mitochondria metabolize pyruvate rather than lactate.
There is a difference between gluconeogenesis and glyocneogenesis (glycogen synthesis). Skeletal muscle is capable of glyconeogenesis from lactate but is not capable of gluconeogenesis. The liver is capable of gluconeogenesis from lactate (and also protein). Thus circulating lactate can:
1) Go to the liver and be converted to glucose and glycogen.
2) Go to skeletal muscle and be converted to glycogen.
3) Go to skeletal muscle and be directly metabolized by mitochondria.
4) Go the heart or other tissues to be used directly as fuel. The heart can metabolize a considerable amount of lactate directly.
Glycogenolysis occuring in skeletal muscle without contraction:
1) Epinephrine released from the adrenal medulla acts on Beta-2 Adrenergic receptors. Epenephrine acts through the cAMP PKA pathway.
For those interested in the biochemistry
Epenephrine interaction witht the Beta-2 adrenergic receptor causes a release of the Gs protein from its beta and gamma subunits. The released Gs subunit activates adenylate cyclase. Adenylate cyclase hydrolyzes and converts ATP to cyclic AMP (cAMP). cAMP activates PKA which catalyzes phosphorylation of phosphorylase kinase. Phosphorylase kinase catalyzes phosphorylation of phosphorylase b to phosphorylase a. Phosphorylase a causes glycogenolysis.
2) Where does the ATP go? All cells require ATP to live. Some or all of this ATP is likely consumed by normal cell processes necessary to live. The rate of lactate release by these fibers under the influence of epinephrine is much less that the lactate released during hard anaerobic exercise. However over hours it is enough to significantly deplete muscle glycogen. In glycogen depletion studies using hard anaerobic work glycogen in the fast twitch fibers is significantly depleted in a matter of minutes.
3) Hypoxia in skeletal muscle can activate ATP generating pathways but this is NOT the normal mechanism during exercise. A major mechanism is the increase in the AMP/ATP ratio in the cell. Hypoxia will cause a rise in AMP but so will muscle contraction in the absence of hypoxia. A rise in the AMP/ATP ratio activates the AMP-activated protein kinase which is a known signaling molecule for mitochondrial biogenesis. It is also very likely that the calcium released by muscle contraction also plays a signaling role here through yet to be completely elucidated mechanisms.
4) I've read one interesting study by a researcher currently active in my own area of study where rats were demedullated. That is their adrenal medullas, the part that releases epinephrine, were removed. After the surgery that ran for a long time on the treadmill (I don't remember the length of time.) Control rats were run for the same duration. The normal rats showed some glycogen depletion during the latter stages of the run in their white (IIb) fibers as expected. The demedullated rats showed NO glycogen depletion in their white fibers! They couldn't release epinephrine into the blood because their adrenal medullas were removed. No epinephrine meant no glycogen release from the unrecruited white fibers. Both groups showed significant glycogen depletion in their slow fibers becuase those fibers were actively recruited during exercise unlike the fast fibers. The normal rise in blood lactate associated with prolonged running was NOT observed.
J Appl Physiol. 1985 Feb;58(2):544-8.
Epinephrine is unessential for stimulation of liver glycogenolysis during exercise.
Carlson KI, Marker JC, Arnall DA, Terry ML, Yang HT, Lindsay LG, Bracken ME, Winder WW.
5) A couple standard physiological principles would have to be violated for the fast twitch fibers to be recruited on long runs:
1) All motor units have a threshold of depolarization. Lower threshold units (I) are recruited first followed by IIa, and then IIb. For fast fibers to be recruited the ordered wiring and firing of the nervous system would have to be turned on its head. There is no physiological explanation of how this might occur.
2) When fibers contract they have to regenerate their ATP supply. Fast twitch fibers lack the metabolic characteristics that would enable them to do this aerobically. They are too big, too thick, have too little mitochondria, too little myoglobin, etc.
I'm tired of writing!
Oops I meant 1 or 2 ATP used in phase 1 of glycolysis, depending on whether you start with glucose or glycogen. Sorry for the confusion.
Nice job with the physiology of glycolysis generation of ATP. I am glad to see a thoughtful response to the topic of using fast twitch fibers during long slow runs. I was certain that fast twitch could not be activated at low intensities. I sure there had to be another explanation as to why those fast twitch fibers showed glycogen depletion. Now I know: Lactate Shuttle processing. Thanks!
So, I am following correctly; The below are NOT true? Thanks in advance.
--\\\"train don\\\'t strain\\\" pace, you\\\'ll usually start to recruit your FT units after about 110-115 min
--- If you want to train enough fibres, then you must go far enough that the first fibres become fuel
exhausted, causing your body to rest them and recruit the next set of fibres, then the next...
---so the long runs are really necessary to get to the thicker (more powerful and usually more anaerobic) fibres
---nd you will mobilize FT fibers without producing nearly as much lactate as you once did. This training will
improve the ability of *both* ST and FT fiber types to cope with exercise stress by stimulating you to develop
more mitochondria and surrounding capillaries.
observer wrote:
So, I am following correctly; The below are NOT true? Thanks in advance.
--\"train don\'t strain\" pace, you\'ll usually start to recruit your FT units after about 110-115 min
This is false. The fast twitch fibers are not recruited. They do become glycogen depleted. This effect occurs later in well trained runners.
observer wrote:
--- If you want to train enough fibres, then you must go far enough that the first fibres become fuel
exhausted, causing your body to rest them and recruit the next set of fibres, then the next...
This is false for the same reason. If you go far enough they dump their fuel via the epinephrine mediated glycolysis (I don't know that I would call this the lactate shuttle though.)
observer wrote
---so the long runs are really necessary to get to the thicker (more powerful and usually more anaerobic) fibres
This statement may be true. It is likely that glycogen depletion itself is a signal for some sort of adaptation. However, running 5 minutes at VO2max pace will deplete IIb fibers a lot more than a 2 hour run will. Real world experience shows the long run to be important. I don't think we really understand what is going on here. I would really like to biopsy some mega mileage Japanese runners who run a lot of their stuff at super slow paces and see if they have selective slow twitch fiber hypertropy or some other strange adaptation.
[/quote]observer wrote
---nd you will mobilize FT fibers without producing nearly as much lactate as you once did. This training will
improve the ability of *both* ST and FT fiber types to cope with exercise stress by stimulating you to develop
more mitochondria and surrounding capillaries.[/quote]
Could you clarify the context of this statement? I'm not quite sure what it means as written.
Thanks a bunch for your answers Phoenix. They dispelled alot of my misconceptions.
One more question: So if FT fibers are not recruited during long runs will they be recruited at all during a marathon? (the speed of which shouldn't be drastically faster than long runs)
great thread. thanks.
I want throw something out that has bugged me for a long time about this topic.
Long runs do NOT improve basic sprint speed. If they did, Mo Greene would be doing 20-milers. In some quarters FT recruit is actually trumpeted in this manner, and it drives me nuts. Many other factors (mechanics, powers, range of motion, etc) go into sprint speed that are far more important.
There are tons of reason to do regular long runs that are also proportionate to your total mileage, and they are one of many elements that belong in a balanced training plan. But don't kid yourself into thinking that they improve your sprint speed. If want to improve speed, then add sprint training, weights, plyos, etc.
It should also be added that the concept of long runs improving basic speed only applies to athletes in a program which has specific basic speed workouts.
The concept is such that Snell could kick bettern than anyone in his 800m/1500m Oly finals because of all the endurance training he had done.