Lactic acid is good? need more mitochondria?

There's been some news articles in the last month or so saying that lactic
acid is actually a very effective fuel for muscles during endurance
performance, and that many previous beliefs that lactic acid is just a waste
product, or even a poison, are mistaken. (try a Web search on "lactic acid
waste product" or "lactic acid poison")

It's tricky for me to sort out, because some of the new biochemistry
findings sound a lot like well-established old findings. And because the
researchers say that training approaches used by good coaches were on the
right track and effective even though though they were based on incorrect
biochemistry.

So any help I can get in sorting out my confusion is much appreciated.

Here's some ideas and claims I'm trying to make sense of -- are they true,
or half-true, or misunderstood?

(a) The recent biochemical finding seems to be that there is a specific path
for the mitochondria in a cell to aerobically "burn" lactic acid -- even if
the lactic acid was originally produced by anaerobic respiration elsewhere
outside the mitochondria. (My initial response is, "I should hope so. The
chemical reactions are well-described in lots of textbooks: Seems like it
would be a stupid design if our mitochondria were _not_ able to execute the
process using either glucose or lactic acid as a starting point." -- or is
there something trickier here that I'm missing?)

(b) The key limiting factor on most endurance performance is not oxygen
uptake or transport -- it's the amount and effectiveness of mitochondria. So
the critical primary goal of athletic training for endurance performance is
to build mitochondria. (? presumably then increases in oxygen uptake or
transport will soon follow as those increased mitochondria start to demand
more oxygen ?)

(c) Sometimes even if muscle cells are getting more than enough oxygen, they
still use anaerobic respiration and produce lactic acid -- because it puts
little or no burden on the limited amount of mitochondria available -- and
it's quicker. (? if the lactic acid can be transported away quickly, it
could be "burned" aerobicially by other less-critical muscles that have
currently under-utillized mitochondria available ?)

(d) Short intense interval workouts are helpful stress mainly because they
stimulate the muscles to develop more mitochondria. (not because they
directly increase oxygen uptake or central cardio-vascular capacity)

(e) Lactic acid does not "cause" pain in any simple way. This should be
obvious, since lactic acid is cleared quickly after exercise is complete,
but the pain and fatigue-feeling often endures much longer. (Unfortunately
I have not heard anyone say what else _does_ cause the short-term and
long-term pains associated with intense exercise).

Thanks for any help in sorting out the confusion.

Ken

Ken
I have studied and read a lot about this issue for years. I will attach
a recent artcile that reviewed current literature. It seems to me that
the scientist are saying that something on the order of 85% of the
limitation of VO2max is central.

I tend to beliee based on the research I have read the peripheral
limitations are of greater importance, than may currently be
recogonized. Likewise I am not sure the research upholds your statement
that short intense exercise develops more mithochondria, and enzymes.

-Statement of the Topic

The Limitation to Vo2 Max Is Central!
Introduction

Maximal oxygen uptake (VO2max) is defined as the highest rate of
oxygen, which can be taken up and utilized by the body during severe
exercise (Basset and Howley 2000).

It is frequently used as an indicator of an individual's
cardiorespiratory fitness as oxygen consumption is linearly related to
energy expenditure (Basset and Howley 2000). VO2max is commonly used in
scientific literature to evaluate changes in maximal ability to work
aerobically and in exercise prescription (Basset and Howley 2000).

To determine VO2max, incremental exercise testing is used. It is taken
as the point at which oxygen uptake peaks with additional power failing
to produce VO2 gains (Lindstedt et al 1988). Secondary criteria to
verify VO2 max include:

1. expiratory exchange ratio 1.15
2. blood lactate level 8-9 mM (Duncan 1997)

It is generally expressed in ml.kg - 1.min - 1

There has been longstanding interest in identifying physiological
factors that control VO2 max and especially debate over whether the
limitation is centrally or peripherally regulated.
Background Knowledge

In order to examine VO2max limitation an understanding of those factors
affecting O2 transport from the atmosphere to mitochondria of the
muscle must be examined.

The O2 delivery system can be viewed as including the pulmonary and
cardiovascular systems. Central physiological factors, which may affect
VO2 max limitation include:

1. pulmonary diffusing capacity,
2. maximal cardiac output,
3. O2 carrying capacity of the blood.

Peripheral skeletal muscle limitations include:

1. peripheral diffusion gradients,
2. mitochondrial enzyme levels,
3. capillary density.

Centrally Limited VO2max - Traditional View

Hill who postulated that developed the concept of maximal oxygen
uptake:

1. Oxygen uptake had an upper limit;
2. VO2 max was limited by the rate at which the cardiorespiratory
system could transport O2 to the muscles

(Bassett and Howley 2000)

The majority of the following research supports the concept that VO2max
is limited by the rate of oxygen delivery (central factors) not the
ability of the muscles to take up O2 (peripheral factors).
Pulmonary System

The ability of the pulmonary system to maintain arterial oxygen level
(% SaO2) in healthy subjects remains high even during maximal work.
Richardson et al (2000) examined whether the quadriceps are O2 supply
dependant at maximal exercise. The VO2max of the muscle group was
measured during altered inspired O2 levels (hypoxia 12%; normoxia 21%
and hyperoxia 100%). It was found VO2 max increased with increased O2
delivery. It was concluded therefore that in normal conditions of
isolated knee extension, VO2 max of trained subjects was limited not by
peripheral factors but centrally by O2 supply.

A similar study examining the effects of breathing hyperoxic gas on the
VO2max of trained athletes again demonstrated an increase in VO2max
(Powers 1989).

The rationale for the increase in VO2 max while breathing hypoxic gas
is thought to be due to an expended arterial-venous O2 difference (a-v
O2 difference). Small increases in hemoglobin (Hb) saturation and in O2
dissolved in plasma produce an increased O2 supply. Such an increase in
arterial PO2 can produce a 10% improvement in VO2max (McArdle1986).

Daniels and Oldridge (1970) likewise found that the reduced oxygen
levels at altitude compared to sea level reduced maximal aerobic power
in elite athletes.

These research studies demonstrate that a central pulmonary limitation
to maximal exercise capacity indeed exists.
Maximal Cardiac Output

Cardiac output (CO) is determined by heart rate and the quantity of
blood ejected with each stroke (stroke volume).

Hill identified maximal cardiac output as the principle factor for
individual differences in VO2 max. As maximal heart rates do not show
considerate variation in those of a similar age, differences in VO2max
have been closely related to maximal stroke volumes (Basset and Howley
2000, Bergh et al 2000).

McArdle et al (1986) conducted a study which compared maximal heart
rate, stroke volume, cardiac output and VO2max among three groups;
athletes, sedentary subjects and subjects with mitral valve stenosis.
While maximal heart rates were similar, CO was considerably higher in
the athletes due to larger stroke volumes. Those with mitral stenosis
had the lowest stroke volumes. Athletes had a 62.5% higher VO2 max than
sedatory subjects, which paralleled a 60% higher stroke volume. Similar
results were found in a study in which sedatory students put on an 8
week aerobic training program demonstrated a 35% increase in stroke
volume and a similar increase in cardiac output (McArdle et al 1986).

Such research suggests a linear relationship between oxygen consumption
and cardiac output over a wide range of submaximal exercise (McArdle et
al 1986).

Saltin and Strange (1992) again in comparing subjects post bed rest and
training found the higher VO2 max post training to be due to
differences in cardiac output.

Since there is little O2 left to be extracted from venous blood in
maximal exercise the main mechanism to increase VO2 max with training
is due to increased CO. An estimated 70-85% of the limitation to VO2
max is centrally linked to maximal cardiac output (Basset and Howley
2000).
Oxygen Carrying Capacity

The hemoglobin concentration in blood alters its O2 carrying capacity.
There is again evidence to show that by manipulating this part of the
O2 delivery system, VO2max is affected. One example occurs in a low Hb
environment, such as anaemia. In this situation there is a linear fall
in VO2 max as a function of lower Hb (Lindstedt 1988).

The practice of blood doping involves artificially increasing the Hb
level by removing, storing and later infusing total red blood cells.
This can increase Hb levels by 8-20%. This increases O2 carrying
capacity and produces an increase in cardiac output, by increased blood
volume. A review of well-designed double blind experiments on blood
doping reported VO2 max improvements of 4-9% (McArdle et al 1986,
Bassett and Howley 2000). This again strengthens the evidence that
increasing O2 delivery improves VO2 max.
Periphally Limited VO2max
Skeletal Muscle Limitation

While the large body evidence presented so far would suggest a central
limitation to VO2 max there is research to suggest peripheral factors
may also play a role. These mechanisms include peripheral diffusion
gradients, mitochondrial enzyme levels and capillary density (Cain
1995, Basset and Howley 2000).
Peripheral Diffusion Gradient

Some researchers would suggest that while central mechanisms are
altered to meet the needs of the peripheral system, it is the
peripheral diffusion gradient, which may be the limiting factor.

The main resistance to O2 diffusion is at the capillary sarcolemma
interface. A study which used canine muscle to examine the effect of
experimentally manipulating the peripheral O2 perfusion gradient found
a low intracellular PO2 was required relative to blood PO2 to maintain
differsion and enhance conductance. When comparing the VO2max in
hyperoxic breathing alone and in with the presence of a drug, which
enhanced peripheral O2, diffusion found no significant difference
between the two. The conclusion drawn was again that it is not the
supply of O2 to the muscle rather than the ability of the muscle to
conduct O2 that limits VO2max (Grassi 2000). A study by Salin et al
(Basset and Howley 2000) compared VO2 max and cycle training. When
comparing a trained leg, control leg and 2 legged bicycling VO2 max was
found to be 23% higher in the trained compared to the control. They
concluded peripheral factors limited VO2 max. They later demonstrated
that this experiment was limited in using only small muscle mass as the
blood flow to quadriceps was 2.3 times higher than in whole body
exercise. The final conclusion drawn was that it was the increased
blood flow and resultant O2 delivery which constrained VO2 max and not
O2 consumption by the muscle.

Richardson (2000) also suggests maximal metabolic rate may be set not
by the mitochondrial enzyme rate but by the convective/diffusive
components of O2.

It was found PO2 was a determination of VO2 max as increased inspired
oxygen levels increased intracellular PO2. In hyperoxia the
intracellular PO2 was now in excess of mitochondrial capacity
indicating cellular metabolism, which was moving towards a change
between O2 supply and O2 demand as the VO2 max limiting factor. The
previous study by Grassi (2000) would indicate these findings to be due
to the increased O2 supply rather than a peripheral one.
Mitochondrial Enzyme levels

Mitochondria are located within muscle fibres and are the sites of O2
consumption via the electron transport chain. Much research has been
performed to examine whether mitochondrial enzyme levels are a limiting
factor for VO2 max.

Under normal circumstances oxygen uptake is matched by the demand of
the mitochondria (Lindstedt et al 1988). Aerobic training causes
mitochondria to enlarge and increase in number. Enhanced concentration
of rate limiting enzymes also occurs, which improve the muscles
capacity for aerobic production of ATP (McArdle et al, 1986).

Saltin and Strange (1992) found that even a 220% increase in
mitochondrial enzymes only demonstrated a modest VO2 max increase
(20-40%). It is argued that the increased mitochondrial enzymes
produced by aerobic training have a metabolic role in fat oxidation and
to produce less lactate. Therefore the increased enzyme activity
appears to be to improve endurance performance rather than increase VO2
max.
Capillary Density

Training produces an increase in capillary density and this increases
the capillary to muscle fibre ratio and improves O2 extraction. This is
represented as the difference between the oxygen content of arterial
and venous blood (a - v O2 difference). At rest only 5 ml of O2 in
blood is extracted from each 20 ml in 100 ml of blood, leaving 75%
still bound to haemoglobin. McArdle (1986) found following 8 weeks of
training subjects a-v O2 difference was increased by 11% with 85% of O2
extracted from blood during exercise. Saltin and Strange (1992) also
show a strong relationship between capillary fibre ratio in vastus
lateralis and VO2 max during cycling.

It could be suggested this represented improved peripheral factors
previously limiting VO2max. It is suggested however that this training
effect improves O2 delivery by enhancing mean transit time to maintain
or expand O2 extraction (a-v O2 difference) even at high blood flow
rates. This again suggests a central O2 delivery limitation not a
peripheral one.
Conclusion

There is undeniable scientific evidence to support the conclusion that
it is the ability of the cardiorespiratory system to deliver O2 to the
muscles and not the ability of the mitochondria to consume O2 that is
the limitation to VO2 max. This relates to healthy subjects performing
maximal, large muscle mass exercise (Saltin and Strange 1992; Basset
and Howley 2000; Richardson 2000).

Basset and Howley (2000) identify maximal cardiac output as the major
factor limiting VO2 max during bicycling and running tests. There is no
single central limiting factor to VO2 max. Just as O2 delivery involves
an integrated pathway, any factor which reduces the delivery of O2 to
the mitochondria, will limit VO2 max (Basset and Howley 2000;
Richardson 2000).
Clinical Implications

If indeed the limitation to VO2 max is in the delivery of O2 how can
this knowledge be utilised to increase an individual's capacity for
aerobic work? It should be noted that endurance is not only limited by
VO2 max but also by factors such as lactate threshold and the efficient
use of the three energy systems.
Aerobic Training

Aerobic training was found to improve O2 delivery by increasing stroke
volume and thus cardiac output by 50-60% above resting in trained
athletes.

Improved a-v O2 difference is achieved by an increased mitochondria
size and number, increased rate limiting enzymes and capillary density
(Basset and Howley 2000).

An 8 week training program using large muscle mass could produce a 35%
increase in VO2max (McArdle et al 1986)
O2 inhalation

There was not found to be any ergonomic value in breathing O2 pre or
post exercise with regard to improving VO2 max or in increased removal
of blood lactate (McArdle et al 1986).
Anaemia

As Hb levels affect O2 carrying capacity an anaemic state can
significantly affect the aerobic capacity of an individual. Early
detection and correction is therefore vital.
Blood Doping

An endurance athlete who won gold at 1976 Montreal Olympics was alleged
to have used this illegal technique. While there is conflicting
evidence blood doping while generally thought to increase VO2 max by
5-13%, reduced sub maximal HR and blood lactate levels for standard
tasks and improved endurance performance at altitude and at sea level.
It poses serious side effects however including venous thrombosis and
pulmonary embolism via increased platelet viscosity. (McArdle et al
1986)
Respiratory and Cardiac Disease

Both respiratory and cardiac disease alter O2 supply to working muscle
and will alter an individuals ability to work aerobically. Such
conditions and those taking medication, which may alter cardiac or
respiratory function, must be identified by those prescribing exercise
programmes.
References

Bassett DR and Howley ET (2000)
Limiting factors for maximum oxygen uptake and determinants of
endurance performance. Medicine and Science in Sports and Exercise
32:70-84.
Bergh U, Ekblom B, Astrand P (2000)
Maximal oxygen uptake "classical" versus "contemporary" viewpoints.
Medicine and Science in Sports and Exercise 32:85-88
Cain SM (1995)
Mechanisms which control VO2 near VO2max: an overview. Medicine and
Science in Sports and Exercise 27 (1):60-64.
Daniels J and Oldridge N (1970)
The effects of alternate exposure to altitude and sea level on
world class and middle distance runners. Medicine and Science in Sports
and Exercise 2:107-112.
Grassi B (2000)
Skeletal muscle VO2 on-kinetics: set by O2 delivery or by O2
utilization? New insights into an old issue. Medicine and Science in
Sports and Exercise 32:108-115.
Lindstedt SL, Wells DL, Jones JH, Hopprter H and Thronson HA (1988)
Limitations to aerobic performance in mammals: interaction of
structure and demand. International Journal of Sports and Medicine
9:210-217.
McArdle WD, Katch FI and Katch VL (1986)
Exercise Physiology. (2nd ed.). Philadelphia: Lea and Febiger.
Powers SK, Lawler J, Dempsey JA, Dodd S and Landry G (1989)
Effects of incomplete gas exchange on VO2max. Journal of Applied
Physiology 66:2491-2495.
Richardson RS (2000)
What governs skeletal muscle VO2max? New evidence. Medicine and
Science in Sports and Exercise 32:100-107.
Richardson RS, Harms CR, Grassi B and Hepple RT (2000)
Medicine and Science in Sports and Exercise 32:89-93
Saltin B and Strange S (1992)
Maximal oxygen uptake: "old" and "new" arguments for a
cardiovascular limitation. Medicine and Science in Sports and Exercise
24:30-37.
Wagner PD (1995)
Muscle O2 transport and O2 Dependent control of metabolism.
Medicine and Science in Sports and Exercise 27 (1):47-53.

Jim:

Wow. Nice review article, but where did it come from? Pretty well
covers the coventional wisdom.

Ken:

Yes, we've known that lactate is a great fuel for the muscles, but ya
gotta have the oxygen to use it. Remember, it's only produced (in
quantity) when the muscle is called upon to produce more work than it
can "aerobicaly" with the oxygen supply available. It's all about
oxygen delivery.

And no, lactate isn't "cleared" rapidly after the cessation of
exersize. This was proven to me with lactate testing at a ski clinic.
We measured resting lactate, then did a 10K (skiing) time trial, and
measured lactate again. (High, as you might guess) We then ate lunch
and rested an hour or two, and then rechecked lactate. The lactate was
higher than the original resting level. We then went out for a very
easy ski, about 40 minutes while keeping our heart rates about 15 BPM
less than our "lactate balance point", or lactate threshold. (We knew
this from testing days earlier.) We then rechecked lactates, which
were lower than before the easy ski.

The explaination is that we still had lactate sitting in our cells and
in our blood from the all-out time trial, even after resting, and that
it was burned more efficiently with our easy ski, making sure that lots
of oxygen was available for the muscles to use to burn it.

Makes sense?

Randy

Ken Roberts wrote:
There's been some news articles in the last month or so saying that lactic
acid is actually a very effective fuel for muscles during endurance
performance, and that many previous beliefs that lactic acid is just a waste
product, or even a poison, are mistaken. (try a Web search on "lactic acid
waste product" or "lactic acid poison")

It's tricky for me to sort out, because some of the new biochemistry
findings sound a lot like well-established old findings. And because the
researchers say that training approaches used by good coaches were on the
right track and effective even though though they were based on incorrect
biochemistry.

So any help I can get in sorting out my confusion is much appreciated.

Here's some ideas and claims I'm trying to make sense of -- are they true,
or half-true, or misunderstood?

(a) The recent biochemical finding seems to be that there is a specific path
for the mitochondria in a cell to aerobically "burn" lactic acid -- even if
the lactic acid was originally produced by anaerobic respiration elsewhere
outside the mitochondria. (My initial response is, "I should hope so. The
chemical reactions are well-described in lots of textbooks: Seems like it
would be a stupid design if our mitochondria were _not_ able to execute the
process using either glucose or lactic acid as a starting point." -- or is
there something trickier here that I'm missing?)

(b) The key limiting factor on most endurance performance is not oxygen
uptake or transport -- it's the amount and effectiveness of mitochondria. So
the critical primary goal of athletic training for endurance performance is
to build mitochondria. (? presumably then increases in oxygen uptake or
transport will soon follow as those increased mitochondria start to demand
more oxygen ?)

(c) Sometimes even if muscle cells are getting more than enough oxygen, they
still use anaerobic respiration and produce lactic acid -- because it puts
little or no burden on the limited amount of mitochondria available -- and
it's quicker. (? if the lactic acid can be transported away quickly, it
could be "burned" aerobicially by other less-critical muscles that have
currently under-utillized mitochondria available ?)

(d) Short intense interval workouts are helpful stress mainly because they
stimulate the muscles to develop more mitochondria. (not because they
directly increase oxygen uptake or central cardio-vascular capacity)

(e) Lactic acid does not "cause" pain in any simple way. This should be
obvious, since lactic acid is cleared quickly after exercise is complete,
but the pain and fatigue-feeling often endures much longer. (Unfortunately
I have not heard anyone say what else _does_ cause the short-term and
long-term pains associated with intense exercise).

Thanks for any help in sorting out the confusion.

Ken

Hi Ken,

I just became aware of these articles a few days ago, and after reading
a few, my carefully crafted bubble-world of understanding how LT
relates to sustainable pace has been shattered.

I am busy trying to determine what this information means for me in
practice. For bicycle time-trials I have been using my measured LT of
163 HR to pace myself. However, in group start races I often have my HR
way above that and even feel good for extended periods at 173 or so.
and I se short bursts of 185. Sort of like this second wind some of the
articles mentioned.

I am very confused. If lactic acid is in the bloodstream and is
available for mitochondria to use, is this so that less stressed
muscles can use it thus "saving" oxygen for the muscles doing the real
work?

Is it possible that my apparent increase in tolerance of lactic acid
while on a bike between last year and this year is from increased
mitochondria in my upper body from skiing?

As I understand things, LSD type training encourages mitochondria
development. Is this the case? So a training program would include LSD
to develop mitochondria for the purpose of being able to make use of
lactic acid, and intervals would be for the purpose of increasign the
pump-volume, and long above LT intervals would be for th epurpose of
accostoming the body to using lactic acid. Doe sthis make sense?

Joseph

Joseph wrote
If lactic acid is in the bloodstream and is available for
mitochondria to use, is this so that less stressed muscles
can use it thus "saving" oxygen for the muscles doing the real work?

I think that's part of the debate. It gets more complicated because
different types of muscle fibers are specialized for more or less emphasis
on mitochondria. So the recent 3rd edition of Bicycling Science by
D.G.Wilson speculates on page 61 that one purpose of short bursts of
standing pedaling on a bicycle might help by mobilizing stored glycogen in
FG ("fast-twitch") fibers and send the resulting lactic acid to fuel
glycogen-depleted SO ("slow-twitch") fibers. The new thinking is that one of
the positive advantages of lactic acid as fuel is that it's easy to move it
around (unlike glycogen).

a training program would include LSD to develop mitochondria
for the purpose of being able to make use of lactic acid, ...

I think everybody agrees that Long Slow Distance is good for building
mitochondria (and other critical peripherial infrastructure).

... and intervals would be for the purpose of increasing the pump-volume

That sounds like the old-school interpretation of short-interval workouts.
An emerging interpretation is that the short intervals _also_ build
mitochondria.

But I think both the old and new schools agree that short-interval workouts
for peaking are good (provided your body is prepared to handle them without
damage). I think the new school is saying something like:
"short-interval training works because it builds up mitochondria, and the
oxygen demand from those increased mitochondria stimulates central
cardio-vascular adaptations like increased stroke volume." So it's partly an
argument about whether the Central adaptation is primary + direct versus
secondary + indirect.

As long as you do the workout, does it matter which theory is correct?

To me it matters, because if I believed only the old-school theory, I would
not do any short-interval workouts (like 4 minutes and less) -- because I
don't have any skiing or bicycling goals that require for sprints or
peak-VO2max performance.

Ken

Lots of helpful findings in that article Jim posted titled "The Limitation
to VO2max is Central".

But my main concern is not with VO2max, it's with endurance performance. The
article seems to be aware of the difference, and even says, "the increased
[mitochondrial] enzyme activity appears to be to improve endurance
performance rather than increase VO2max". Sounds like agreement with the
"new school" interpretation of endurance performance.

Jim wrote
I am not sure the research upholds your statement
that short intense exercise develops more mithochondria

It's not my statement. I just found it at the end of a May 16 article on
www.nytimes.com. I was actually surprised by the claim by a biochemist that
short-interval workouts for "peak" training would result in additional
increase in my mitochondria mass.

Maybe it depends on what is meant by "short intense exercise". I was
thinking of work intervals of less than 4 minutes. Like some coaches
advocate doing 4 hard work intervals of 3:00 minutes each. Or I've seen
suggested for deleveloping Central CV capacity doing short work intervals in
the range of 40 to 80 seconds, with shorter rests in between.

If those are not effective for longer endurance performance like a 50km ski
race, please let me know, and I'll stop doing them.

Ken

Ken Roberts wrote:
Joseph wrote
If lactic acid is in the bloodstream and is available for
mitochondria to use, is this so that less stressed muscles
can use it thus "saving" oxygen for the muscles doing the real work?

I think that's part of the debate. It gets more complicated because
different types of muscle fibers are specialized for more or less emphasis
on mitochondria. So the recent 3rd edition of Bicycling Science by
D.G.Wilson speculates on page 61 that one purpose of short bursts of
standing pedaling on a bicycle might help by mobilizing stored glycogen in
FG ("fast-twitch") fibers and send the resulting lactic acid to fuel
glycogen-depleted SO ("slow-twitch") fibers. The new thinking is that one=
of
the positive advantages of lactic acid as fuel is that it's easy to move =
it
around (unlike glycogen).

That is a very interesting theory. If true, it may help me a great
deal. Often when I am struggling to not get dropped on a hill (on a
bike or skis) I concentrate all my effort on as smooth and "regular" as
possible power transmission. Remain seated (cycling) and try to be as
efficient as possible in the hopes that I won't loose contact before
the crest. But maybe what I should do is a last-ditch effort monster
standing stomp to get the juices flowing, which I do not do now for
fear of blowing up.

... and intervals would be for the purpose of increasing the pump-volume

That sounds like the old-school interpretation of short-interval workouts.
An emerging interpretation is that the short intervals _also_ build
mitochondria.

But I think both the old and new schools agree that short-interval workou=
ts
for peaking are good (provided your body is prepared to handle them witho=
ut
damage). I think the new school is saying something like:
"short-interval training works because it builds up mitochondria, and the
oxygen demand from those increased mitochondria stimulates central
cardio-vascular adaptations like increased stroke volume." So it's partly=
an
argument about whether the Central adaptation is primary + direct versus
secondary + indirect.

As long as you do the workout, does it matter which theory is correct?

To me it matters, because if I believed only the old-school theory, I wou=
ld
not do any short-interval workouts (like 4 minutes and less) -- because I
don't have any skiing or bicycling goals that require for sprints or
peak-VO2max performance.

Knowing which theory it is matters for me too for precisely the same
reason. 99% of my interest is in raising my sustainable sub-maximal
power output. While I do enjoy sprinting, I have no plans to train
specifically for doing so. My body is by nature suited to sprinting
such that I am automatically pretty good and only people who train
specifically for sprints are able to (occasionaly) beat me (speaking of
course about people with a similar level of conditioning). But what
really interests me is things like Birkebeinerrennet, Vassal=F8pet, and
similar yet longer cycling events.

An ideal training plan for me in terms of what would be fun and doable
would be 80% LSD at 75% of LT and 20% at 105% of LT. Dropping
structured intervals would be nice. Not because I want to avoid the
discomfort, but more because it is a hassle to deal wth the logistsics
of finding a suitable place, timing the intervals, timing the recovery,
etc. When I ride or ski, I just want to get into a groove.

Joseph

Joseph wrote
when I am struggling to not get dropped on a hill I
concentrate all my effort on as smooth and "regular" as
possible power transmission. Remain seated (cycling) ...

I think the real lesson here is the biochemistry and physical transport is
so complicated, and there's so many strategy mixes available to our body,
that there's little point in trying to calculate some optimal theory of
how to climb hills. Better to actually try out some personal time trials
using different mixes of techniques and turnover frequencies and see which
mixes are obviously better or obviously worse in objective timing results.

try to be as efficient as possible

If your objective is to avoid using extra energy, a simpler strategy is to
skip all the pedaling, and stay home and "remain seated" while just watching
TV.

Is it possible that my apparent increase in tolerance of lactic
acid while on a bike between last year and this year is from
increased mitochondria in my upper body from skiing?

Not my first guess. I'd guess that the most critical factor in operating
successfully at higher levels of lactic acid production is _transport_ :
moving the excess lactic acid quickly out of the muscle fibers that are
producing it. Which points to the importance of building capillary density.
(Which contradicts the focus on mitochondria in recent announcements this
biochemist -- but does explain why altitude training and EPO are so
effective for endurance performance, by increasing the transport capacity of
capillaries).

Of course it couldn't hurt to have more mitochondria available elsewhere in
the body -- I'm just not sure if there's a shortage of them, or if you can
mobilize them to "burn" lactic acid when there's nothing additional useful
for them to do with it. But then maybe that's the point of some of those
"wasted" motions which the second-tier regional "experts" are forever
pointing out as flaws in the technique of the world champions -- to mobilize
otherwise irrelevant mitochondria to "clear" excess lactic acid.

I haven't heard whether elite endurance athletes develop increased
capability in the _liver_ to recycle lactic acid (back into glucose). It's
rather inefficient from an energy utilization perspective -- but so what,
that's what energy drinks are for.

For bicycle time-trials I have been using my measured LT
of 163 HR to pace myself. However, in group start races
I often have my HR way above that and even feel good for
extended periods at 173

I'd guess that relying too much on heart rate as a measure of what's
happening in your muscle fibers and peripheral transport gradients is going
to yield all kinds of spurious "phenomena" that need to be explained.

There's some web page where Stephen Seiler lists at least five different
ways that heart rate shows spurious observations that have no basis in the
what's happening with effective muscular propulsion.

Ken

Reading this as far as I can comprehend, rings a bell with me.
In mountainbiking, there's this thing called singlespeeding. I'm honoured to
be 2003 and 2005 Dutch Champ with that.
On some types of courses. With short climbs and long flats, singlespeeds are
stunningly fast. And as the rider, you get the impression you're just doing
what's required to keep going, or not to be dropped.
With just one gear ratio, climbs are hard (low rpm, lots of anaerobic
strangth required), flats are hard (spinning out, not able to get power
down). Climbs you attack to get them over with, and hopefully not be forced
to walk. Flats, you spins till it hurts, and coast (recover) till you slow
back down to the comfort zone, and spin back up.
After a SS race I'm much much much more tired than with gears (forced to
give my all, all the time), but specific parts of courses it's just a really
FAST way to get cross country.

This whole new look at lactic acid might offer answers WHY singlespeeds are
fast. Singlespeeders even win races overall, and it's not even rare anymore.

When I first had a lactate test, I was just getting into serious cycling
training. I was a rookie.
I had a lactate peak of 3.3 or so, around 165-170bpm. LT was 182-185 back
then, and I recorded 1.1 in that zone. So near LT heartrate, my body
actually cleaned up the built up lactate somehow.
When I trained by myself, the 165-170 zone was NOT fun. Hurt like hell. It
was an undertrained zone for me, so I worked on it with 10-15min intervals.
If I'd push on to higher heartrates, it would be like a relief "ah, that's
better!".
Before I got to train seriously, I did weekly sunday rides over marked
courses, 40-60km most of the time. Flat out. Mostly flat. strong
competition, so I really had to dig deep. In those days I could get that
famous rush of being in pain, but loving it, going a notch faster still. I
lost that feeling since. And I lost the speeds I could generate. But now I
can climb steeps hills, back then I had to use the smallest gear to get up a
fly-over, while my weight never changed much.
But especially, for fun I often trained on 5km time trails. A 620m course
with 2 corners that forced me to lift off just a bit. I kept attacking my
own best times, and got good at it. Immense pain, obviously. My trainer
figured that way of training made me so fast, and so clean of lactate at the
LT heartrate.

snip!

If you train lactate training then you also adapt to this via enzymes
and musclefiber composition etc with all the pro and cons that follows.
One bad thing is the limited storage of carbohydrates.


What are these pros and cons? And what do you mean by lactate
training?

Joseph