Transcript Endurance Training & Tapering

Endurance
Training
&
Tapering
EXS 558
Dr. Moran
Wednesday November 9, 2005
Lecture Outline

Review Questions



Concurrent Training
Periodization
Endurance Training


(Chapter 9)
“Optimizing Endurance Training”
Lactic Acid Metabolism
Dalleck & Kravitz (2004)
• Tapering

“Scientific Bases for Precompetition Tapering Strategies”


Mujika & Padilla (2003)
“Physiological responses to a 6-d taper in middle-distance
runners: influence of training intensity and volume
Review Question #1
1.) For an endurance athlete why
would a concurrent resistance
training program appear to be nonbeneficial?
MacDougal et al. (1979) stated that with increased muscle
mass the productivity of mitochondria is reduced. Since
mitochondria are the workhorses of oxidative metabolism it
would appear that a resistance training program may
compromise an endurance training program.
Review Question #2
2.) Hickson et al. (1980) showed that a resistance
training program can actually ENHANCE
endurance performance. How did the authors
speculate this was possible? What types of
subjects were tested in this study?
This studies had UNTRAINED subjects perform a concurrent
training program and endurance was measured as the time to
exhaustion on a cycle and treadmill protocol. The authors
speculated that improved glycolytic enzymatic capacity and
improved NM adaptations improved endurance in these subjects.
Review Question #3
3.) With regards to trained endurance athletes, the
addition of a concurrent resistance program of 3x
a week has what effect on endurance capabilities
(performance, lactate threshold, maximal aerobic
capacity)?
The addition of a low-weight, high-repetition resistance training
program performed 3x a week has NO effect on hampering
positive endurance adaptations during a training program.
Review Question #4, 5
4.) What is the major reason why studies
investigating the addition of an endurance
training program on maximal strength
gains have been inconclusive?
These studies have used different APV and they have used two different
types of subjects: (1) untrained VS (2) trained strength athletes. With
untrained athletes a concurrent endurance program does NOT compromise
strength gains while with strength athletes the maximal strength gains are
impaired.
5.) Why are they impaired?
CHRONIC FATIGUE
Review Question #6
6.) Complete the following schematic
demonstrating the basic principle of
periodization.
Intensity High
Volume Low
PEAK
Foundation
Intensity Low
Training
Volume High
Review Question #7
7.) According to Matveyev’s training
phases which of the following is NOT
a phase of training?
a.) preparatory
b.) general
c.) competitive
d.) transition
Review Question #8
8.) According to Kraemer et al. (2003)
what model of concurrent resistance
training in collegiate women tennis
players yielded the BEST sportspecific adaptations? And why?
The nonlinear (undulating) model yielded the best specific
adaptations for these women’s players. This model worked
best b/c it allowed fluctuations on volume DURING the
competitive season to avoid any potential overtraining and
it also eliminated boredom of tennis players.
Endurance Training

Physiological Changes



Positive adaptation discussed in first half of this course (review)
COMMON THEME: improve the body’s ability to supply and
utilize ATP to power muscular exercise
What dictates endurance performance?

Genetic Contribution
• Muscle fiber type
• Maximal aerobic capacity (diminishing returns principle)

Training Status
• Lactate threshold
• Exercise economy

Acute
•
•
•
•
}
Nutrition
Rest
Hydration status
Psyche
“details”
Endurance Training
Maximal Aerobic Capacity

VO2 max


Considered most objective measure of
endurance capacity
Definition: highest rate of oxygen
consumption during maximal exercise
• As exercise intensity increases there is a “plateau-ing” of
oxygen consumption values

Improvements with training
• 15-30% ↑ over the first three months
• Could rise as much as 50% over the first 2 years

Not the best determinant of endurance
success
Endurance Training
Maximal Aerobic Capacity
Endurance Training
US XC Ski Team – Field Test for Maximal Aerobic Capacity

Purpose
•

Requirements
•
•

1 Km of consistent upgrade of 5-10%
Heart Rate monitor
Test
•
•
•
•

Determine intensity to improve maximal
oxygen uptake
10-12 runs through on the 1 Km upgrade
Increase intensity on each run by about 5-10
bpm
Average HR for last minute of each run
Calculate speed of each run
Plot
•
Speed of run vs. average HR

Similar versions for running

Conconi et al. (1982)

Jones, A and Doust, J (1995) Lack of
reliability in Conconi's heart rate deflection
point. International Journal of Sports
Medicine, Vol 16, pp 541-544.
Deflection point
Endurance Training
Muscle Fiber Type


Slow-twitch (type I) fibers
Long-distance runners  ~70%
(some > 92%)






Greater capillary density
Greater mitochondrial content
Increased oxidative enzymes
Positive correlation between % of
ST fibers and best 6 mile
performance
Good Article
Difficult to switch fibers from type
II  type I
 Endurance training will
transfer some % of fiber
subtypes to become more
oxidative (Ch. 1)
Frank Shorter: 1972 Olympic
marathon champion
Endurance Training
Lactate Threshold

Blood Lactate Concentration

Rest & steady-state exercise: a good balance between production and

When exercise intensity is increased to a point the removal (clearance) of
lactate is not adequate
removal



•
Onset of blood lactate accumulation (OBLA)
Anaerobic Threshold
Lactate Threshold
This point is described at the % of VO2 max where it occurs
Endurance Training
Lactate Threshold (LT)


Best predictor of endurance success
LT is used as part of the exercise prescription


Exercise intensity is set right above or below this
point of lactate accumulation
Pattern of LT is similar between trained and
untrained individual


Untrained: OBLA at 55% of max VO2
Trained: OBLA at 80-90% of max VO2
• Due to a blunted catelcholamine response
• Increased ability to deliver and extract oxygen
• Increased lactate utilization

Figure 9.3
Endurance Training
Lactate Threshold (LT)
Endurance Training
Improving Lactate Threshold

Steady-State Training (“tempo runs”)
• Performed as close to LT as possible
• Duration will change depending on:
• Training status
• Type of endurance activity
• Distance of goal event

(i.e. cycling vs running)
Interval Training
• Short duration training above the LT
• Rest intervals allow lactate [ ]s to return to
near-normal before the next interval
Endurance Training
Exercise Economy

Definition: describe oxygen consumption required to run
at a given velocity
• Explains differences in performance with runners of similar
VO2 max


Biomechanics will influence economy of both cycling and
running
Other factors influencing exercise economy




Body temperature
Wind resistance
Weight
Daniels 1985
Endurance Training
Monitoring Intensity

Heart Rate



Close relationship with HR and oxygen consumption
(Fig 9.5)
Regardless of age, conditioning level, or gender this
relationship between VO2 max and HR is maintained
Rating of Perceived Exertion (RPE)
Borg Scale (RPE)
6 No exertion at all
7 Extremely Light
9 Very Light
11 Light
13 Somewhat Hard (70% of max HR)
15 Hard (heavy)
17 Very Hard
19 Extremely Hard
May not be the best indicator
for exercise intensities
between 50-80%.
Abstract
Lactic Acid Metabolism
LDH
Lactate Dehydorgenase (LDH): catalyzes the interconversion of
pyruvate and lactate.
Lactic Acid Metabolism



Lactate produced and released from tissue even with adequate
oxygen (LDH always present)
Several tissues beside muscle produce lactate (skin, liver, heart,
renal, RBCs)
Lactate constantly released into and taken up from blood:
“turnover” (~75%)


Even oxidized within the heart! (Good Introduction in the article)
Lactate can serve as oxidative energy substrate (gluconeogenesis)
or be incorporated in AA’s or proteins (~25%)
• LA taken up by liver and used as building block to make liver glycogen

“Lactate Shuttle” – lactate produced in myofibers with ↑ rates of
glycolysis used as ENERGY by nearby or remote cells with ↑
oxidative capacity
• Never gets in blood so blood lactate NOT affected
Endurance training improves muscle capacity for lactate utilization and increases
membrane transport of lactate probably via an increase in Type I monocarboxylate
transport protein (MCT1) and perhaps other MCT isoforms as well.
Lactate Shuttle
Illustration of the essential
elements of the recently introduced
intracellular lactate shuttle (red) in
comparison to the more well-known
malate-aspartate and glycerolphosphate NAD+/NADH shuttles
(blue). LDH, lactate
dehydrogenase; MCT
(monocarboxylate transporter) ,
monocarboxylate transporter; ETC,
electron transport chain; Shuttles,
malate-aspartate and glycerolphosphate NAD+/NADH shuttles.
The H+ ions for pyruvate and
lactate are inserted to emphasize
that the MCT symports a proton;
the same MCT carrier can transport
both pyruvate and lactate. Note
that the mitochondrial LDH may
actually be in the intermembrane
space of the mitochondria and on
the outer surface of the inner
membrane. Note also that
operation of the intracellular lactate
shuttle delivers both reducing
equivalents and substrate for
oxidation to mitochondria. The
shuttle explains
Endurance training improves muscle capacity for lactate intracellular
utilizationlactate
and increases
HLa production and accumulation
membrane transport of lactate probably via an increase in
Type I monocarboxylate
under aerobic exercise conditions.
transport protein (MCT1) and perhaps other MCT isoforms as well.
Lactic Acid Metabolism (con’t)

Lactate exchange can occur between:






Active  Inactive Myofibers (same muscle)
Active  Inactive Muscles (X-training effect)
• The Journal of Physiology workers from two different
laboratories (Rasmussen et al. 2002; Sahlin et al.
2002) dissent from the refined concept, but do agree 'it
is well documented that lactate can be released by one
muscle and oxidized by another muscle'
Blood  Muscle
Active Muscle  Liver
Active Muscle  Heart (sink for lactate, b/c of H-LDH)
Within cytosol of same cell, [lactate] ↑ away from
mitochondria and ↓ [lactate] close to mitochondria.
Lactic Acid Metabolism (con’t)

Exercise Conditions
• At beginning of exercise muscle becomes site
of net lactate release

Net release of lactate UNDERESTIMATES lactate
production by muscle
• Initial rate of release depends upon mass of
active muscle
• With ↑ exercise intensity, VO2 in linear manner
but lactate ↑ in curvilinear fashion
• Primary reason for sharp in lactate production
is stimulation of sympathetic nervous system

Catelcholamines stimulate glycolysis but not
oxidative enzymes, also ↓ splanchic blood flow (↓
uptake by liver and kidneys)
Lactic Acid Metabolism (con’t)

Fiber Type Differences
• During exercise lactate produced by FT fibers
can either diffuse directly or via blood into ST
fibers which can take it up and oxidize it
• Concurrently some FOG fibers can release
lactate while others consume it
• FT fibers have greater capillarity than needed
for oxidative capacity, may be more important
for lactate than oxygen transport
• LDH profile strong predictor of whether fiber
will be net producer or net consumer
Post-Exercise Lactate Metabolism

Since 1928 it has been known that
blood [lactate] ↓ more quickly with
ACTIVE than PASSIVE recovery


Due to ↑ blood flow to removal centers and
↑ energy demand
Is there an optimal training
intensity?

Rate of blood lactate decline ↑ along with
intensity up to a critical point
Tapering

Tapering Phase: final period of training before most important
competition
• Still remains more of an art rather than an informed science
• “Scientific Bases for Precompetition Tapering Strategies”





Mujika & Padilla (2003)
Aim of Tapering: reduce psychological and physiological effects of
everyday training with the thought that performance can be
maximized over a short time frame
Reduction of Training Load: the extent with which load can be
reduced is of greatest concern so that detraining does not occur
Reduction of Training Intensity: the most effective tapering
involved a HI-Intensity and LO-volume approach
Reduction of Training Frequency: for highly trained individuals
training frequency should remain normal to avoid a “loss of feel”
Tapering (con’t)



Muscle Fiber: type IIa (FOG) more affected than
type I fibers (Trappe et al. 1998)
Duration of Taper: the optimal time frame has not
been established
Type of Taper
• Linear
• Exponential
 Slow Decay
 Fast Decay
• Step
*Only 1 study has looked at the performance effects
of different types of taper. A fast experimental
produced the best performance increases in a
group of triathletes
Tapering (con’t)

Mujika et al. (2002): resting testosterone increases
following a 6-day taper improving the anabolic:catabolic
ratio
Tapering Strategy
Minimize fatigue without compromising fitness
Maintain Training Intensity (middle distance taper)
Reduce Training Volume by 60-90%
Maintain Training frequency at >80%
Individual taper duration between 4 and 28 d
Use progressive, nonlinear taper designs
Expect performance improvements of ~3% (range 0.5-6%)
Tapering
Mathematical Modeling