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Completion of an Ironman triathlon results in muscle damage, indicated by reductions in muscle function and muscle soreness. However, the time course of recovery from this damage has received little attention. The purpose of this case study was to examine the time course of changes in blood markers of muscle damage and inflammation, muscle function, muscle soreness, and economy of motion following an Ironman event. An experienced well-trained male triathlete aged 35 years completed the Western Australian Ironman triathlon in 11 h 38 min 41 s (winner's time: 8 h 3 min 56 s). Before and on several occasions in the 15 days after the event, the participant performed an incremental cycling test to exhaustion, running economy test at 12 km · h (2% incline), maximal isometric knee flexion and extension at 90° knee flexion, and maximal squat and countermovement jumps. Venous blood samples and muscle soreness were also assessed. Maximal oxygen consumption, efficiency of motion, maximal muscle strength, and jump performance were all markedly reduced (4.5–54%) following the event, but returned to baseline within 15, 8, 2, and 8 days following the event, respectively. Muscle soreness and blood markers peaked 2–24 h after the race but returned to baseline within 8 days. In conclusion, although the Ironman triathlon induces marked muscle damage, a trained triathlete recovered almost completely within approximately one week, without the use of any therapeutic interventions after the event.
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Recovery following an Ironman triathlon: A case study
Kazunori Nosaka
a
; Chris R. Abbiss
a
; Greig Watson
a
; Bradley Wall
a
; Katushiko Suzuki
b
;Paul Laursen
a
a
School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, WA,
Australia
b
Faculty of Sport Sciences, Waseda University, Tokorozawa, Japan
Online publication date: 01 April 2010
To cite this Article Nosaka, Kazunori , Abbiss, Chris R. , Watson, Greig , Wall, Bradley , Suzuki, Katushiko andLaursen,
Paul(2010) 'Recovery following an Ironman triathlon: A case study', European Journal of Sport Science, 10: 3, 159 — 165
To link to this Article: DOI: 10.1080/17461390903426642
URL: http://dx.doi.org/10.1080/17461390903426642
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ORIGINAL ARTICLE
Recovery following an Ironman triathlon: A case study
KAZUNORI NOSAKA
1
, CHRIS R. ABBISS
1
, GREIG WATSON
1
, BRADLEY WALL
1
,
KATUSHIKO SUZUKI
2
, & PAUL LAURSEN
1
1
School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia, and
2
Faculty of
Sport Sciences, Waseda University, Tokorozawa, Japan
Abstract
Completion of an Ironman triathlon results in muscle damage, indicated by reductions in muscle function and muscle
soreness. However, the time course of recovery from this damage has received little attention. The purpose of this case study
was to examine the time course of changes in blood markers of muscle damage and inflammation, muscle function, muscle
soreness, and economy of motion following an Ironman event. An experienced well-trained male triathlete aged 35 years
completed the Western Australian Ironman triathlon in 11 h 38 min 41 s (winner’s time: 8 h 3 min 56 s). Before and on
several occasions in the 15 days after the event, the participant performed an incremental cycling test to exhaustion, running
economy test at 12 km × h
1
(2% incline), maximal isometric knee flexion and extension at 908 knee flexion, and maximal
squat and countermovement jumps. Venous blood samples and muscle soreness were also assessed. Maximal oxygen
consumption, efficiency of motion, maximal muscle strength, and jump performance were all markedly reduced (4.554%)
following the event, but returned to baseline within 15, 8, 2, and 8 days following the event, respectively. Muscle soreness
and blood markers peaked 224 h after the race but returned to baseline within 8 days. In conclusion, although the Ironman
triathlon induces marked muscle damage, a trained triathlete recovered almost completely within approximately one week,
without the use of any therapeutic interventions after the event.
Keywords: Muscle damage, muscle soreness, muscle strength, running economy, cycling efficiency
Introduction
The long distances that comprise an Ironman triath-
lon (3.8-km swim, 180-km cycle, 42.2-km run) create
a challenge that can induce significant physical
and psychological stress on its participants (Farber,
Schaefer, Franey, Grimaldi, & Hill, 1991; Lepers,
2008). One of the revealing signs of this physical toll is
the amount of muscle damage it inflicts. For example,
we have shown reductions in muscle strength and
jump height, together with increases in muscle
soreness, blood markers of muscle damage, and
inflammation in the 24 h following an Ironman
triathlon (Suzuki et al., 2006). While the acute phase
response has been documented, the time course of
the recovery from muscle damage induced during an
Ironman triathlon is less clear. Only Neubauer and
colleagues (Neubauer, Ko
¨
nig, & Wagner, 2008) have
outlined the recovery 1, 5, and 19 days after an
Ironman race. They showed a pronounced initial
systemic inflammatory response together with persis-
tent low-grade systemic inflammation for up to
5 days after the event, reflecting incomplete recovery.
Although all measured variables had returned to
baseline values within 19 days, a more precise under-
standing of the time course of recovery to baseline
values, together with functional measurements, is
required. It is important for sport medicine profes-
sionals to understand the recovery process associated
with this popular but challenging event.
There is also limited information available con-
cerning the effects that muscle damage and subse-
quent recovery may have on running economy and
maximal oxygen uptake (VO
2max
) after an Ironman
triathlon. It could be that running economy and
VO
2max
are reduced for several days, possibly due
to neuromuscular fatigue and/or muscle damage;
Correspondence: K. Nosaka, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, 270 Joondalup Drive,
Joondalup, WA 6027, Australia. E-mail: k.nosaka@ecu.edu.au
European Journal of Sport Science, May 2010; 10(3): 159165
ISSN 1746-1391 print/ISSN 1536-7290 online # 2010 European College of Sport Science
DOI: 10.1080/17461390903426642
Downloaded By: [Laursen, Paul] At: 17:00 1 April 2010
however, no previous studies have investigated this
response after an Ironman triathlon.
We had the opportunity to collect data on blood
markers of muscle damage and inflammation, mus-
cle function, muscle soreness, running economy, and
VO
2max
for a male triathlete while cycling, before
and for 15 days after an Ironman event. These data
show that recovery from an Ironman triathlon race
by an experienced triathlete is almost complete
within a week of finishing the event.
Methods
Participant
Our experienced male triathlete (age 35 years, body mass
75.0kg,stature1.78m,VO
2max
67.0 ml × kg
1
× min
1
)
participated in the Ironman Western Australia event
(Busselton, Western Australia) on 1 December 2006.
This was the participants eleventh Ironman triathlon
(personal best time: 10 h 14 min). Before testing, the
participant was informed of the risks associated with
the study and provided written informed consent in
accordance with the Institutional Human Research
Ethics Committee. He completed the race in 11 h 38
min 41 s, in which the swimming (1 h 7 min 3 s) and
cycling (5 h 25 min 6 s) legs were performed as
expected, but his run (5 h 6 min 31 s) was about an
hour slower than expected. This was due to fatigue
related to hyperthermia and muscle cramping near the
half-way point of the run. In total, 804 athletes
participated in the event, of whom 766 completed
the course, and the winners time was 8 h 3 min 56 s.
Our participant finished 331st, and his relative time to
that of the winner was 144%.
Experimental overview
The participant attended the laboratory one week
before (Pre 1) and on seven separate occasions in
the 15 days after the Ironman event (Figure 1). The
participant also attended a makeshift laboratory the
day before (Pre 2), and 2 and 12 h after, the event.
The variables measured during the test sessions are
outlined below.
Maximal oxygen consumption, gross cycling efficiency,
and running economy
Once before and on three separate occasions after the
Ironman event (Figure 1), the participant performed
an incremental cycling test to exhaustion and a
submaximal running economy test under controlled
laboratory conditions (20228C and 4050% relative
humidity). The incremental cycling test was con-
ducted on an electromagnetic cycle ergometer
(Velotron; RacerMate, Seattle, WA), and the running
economy test was conducted on a motorized
treadmill (JAS Fitness Systems, Carrollton, TX).
Throughout both tests, expired gases were analysed
for concentration and volume using a calibrated and
validated ParvoMedics TrueOne 2400 diagnostic
system (Sandy, UT). The exercise protocol, determi-
nation of oxygen consumption (VO
2
), and maximal
aerobic power output during the incremental cycling
test were completed as previously described (Abbiss
et al., 2008). Briefly, the participant began cycling at
100 W for 5 min, after which power output was
increased by 50 W every 5 min until the participant
reached volitional exhaustion. The metabolic cart
recorded heart rate throughout the test with the use of
a compatible heart rate monitor (Polar Electro Oy,
Kempele, Finland). Average VO
2
for the last minute
of 100, 150, and 200 W was used as steady-state
oxygen consumption for the determination of gross
cycling efficiency (Gaesser & Brooks, 1975). During
the running economy test, the participant performed
a 5-min warm-up running at 8 km × h
1
followed by
5 min at 12 km × h
1
on the motorized treadmill set
at a 2% incline (Palazzetti, Margaritis, & Guezennec,
2005). Average VO
2
(litres × min
1
) over the final
minute of the 12 km × h
1
stage was used to deter-
mine running economy. Rating of perceived exertion
(RPE) and muscle soreness (described below) were
recorded 1 min before completion of each 5-min
stage during the running economy test.
Muscle function
Muscle strength of the knee extensors and flexors,
and vertical jump height of the squat and counter-
movement jumps, were assessed as previously
described (Suzuki et al., 2006) on two separate
occasions before and on eight occasions after the
Ironman event (Figure 1). Briefly, maximal isometric
strength of the knee extensors and knee flexors was
measured using a strain gauge (BongshinLoadcell
Co. Ltd., Model DBBP 200, South Korea) attached
to a wire with a belt that surrounded the ankle joint
with the knee joint angle set at 908. Peak maximal
Figure 1. Schematic time line of measurements before and after
the Ironman triathlon event.
160 K. Nosaka et al.
Downloaded By: [Laursen, Paul] At: 17:00 1 April 2010
voluntary contraction force was displayed on a digital
indicator (Rinstrum Pty. Ltd., Model 2100EX,
Brisbane, QLD) connected to the strain gauge,
and the higher value of the two measurements was
used for further analysis. Grip strength was measured
using a Smedley grip dynamometer (Takei Scientific
Instruments Co. Ltd., Model TKK5001, Niigata
City, Japan) twice for each arm, and the higher value
was used to calculate the average value of two arms,
which was used for further analysis.
Vertical jump height of the squat jump and
countermovement jump was assessed using a leap
meter (Takei Scientific Instrument, Japan). For the
squat jump, the participant was asked to jump after
holding his knee joint at 908 for at least 2 s and
without using his arms (held on their hips). The
same arm position was used for the countermove-
ment jump, but the participant began the jump
motion from a standing position with a counter-
movement. After two practice jumps, two trials for
each jump were performed, and the higher value of
the two was used for further analysis.
Muscle soreness
Muscle soreness was assessed using a verbal rating
scale of 0 (‘‘no pain’’)to10(‘‘maximal’’) that has
been used previously (Suzuki et al., 2006). The
participant was asked to rate his subjective level
of soreness on a questionnaire sheet while actively
moving specific muscles as instructed (squat, stretch-
ing or running) or while the investigator palpated
those muscles. Muscle groups of the limbs and
trunk assessed included the deltoid, pectoralis, biceps
brachii/brachialis, triceps brachii, brachioradialis,
rectus/obliquus abdominis, quadriceps femoris, bi-
ceps femoris, gastrocnemius/soleus, and low back
muscles.
Blood sampling and analyses
Before and on 10 occasions after the Ironman event
(Figure 1), approximately 8 ml of blood were taken
from the antecubital vein via standard venepuncture
techniques. Post-race blood samples were taken
within 10 min of completing the event, with the
participant lying supine in the medical tent. The
blood samples were allowed to clot and centrifuged
for 10 min to obtain serum. Serum samples were
frozen and stored at 808C until analysis.
Serum samples were analysed for the following
markers of muscle damage and inflammation: crea-
tine kinase (CK), creatine kinasae isoenzymes (CK-
MM, CK-MB), myoglobin, lactate dehydrogenase,
alanine aminotransferase, aspartate aminotransfer-
ase, C-reactive protein, and serum amyloid protein
A. All of these variables except myoglobin and serum
amyloid protein A were analysed using an automated
analyser (Model 7450 or Model 7170, Hitachi,
Japan). Serum amyloid protein A was analysed using
a different automated analyser (Model JCA-BM21,
JOEL Ltd., Japan) and myoglobin was analysed
using ELISA (Life Diagnostics, West Chester, PA,
USA). Serum cytokine concentrations of interleukin-6
(IL-6), IL-10, and IL-1ra were measured with
ELISA kits (IL-6: Quantikine HS, R&D Systems,
Minneapolis, MN; IL-10: OptEIA, BD Biosciences,
San Jose, CA; IL-1ra: Quantikine, R&D Systems).
In addition to these blood markers, a portable
blood-gas electrolyte analyser (i-STAT Corporation,
East Windsor, NJ) was used to measure pH,
partial pressure of carbon dioxide, partial pressure
of oxygen, lactate concentration, bicarbonate, oxy-
gen saturation, sodium, potassium, chloride, urea,
glucose, haemoglobin concentration, and haemato-
crit before, immediately after, and 2, 12, and 24 h
after the race. The results of these measures are not
reported here, but haemoglobin and haematocrit
were used to calculate changes in plasma volume.
Results
Maximal oxygen consumption, gross cycling efficiency,
and running economy
Figure 2 shows changes in cycling VO
2max
, gross
cycling efficiency, and running economy before and
after the Ironman event. Both running economy
and gross cycling efficiency were reduced (6.5% and
4.5%, respectively) following the event but returned
to baseline by 4 and 8 days, respectively. Maximal
aerobic power output and VO
2max
were reduced by
8.3% (352.5 W to 332.5 W) and 9.5% at 3 days
following the event, respectively, but returned to
baseline values by day 15. Maximal heart rate
decreased by 3% (191 to 185 beats × min
1
)at
3 days following the event, but returned to baseline
by day 8 (193 beats × min
1
). Rating of perceived
exertion while running at 8 km × h
1
and 12 km × h
1
during the running economy test increased in the 48
h following the event (from 8 to 15 and 11 to 18,
respectively), but returned to baseline by day 8.
Muscle function
Maximal isometric strength of the knee extensors and
knee flexors was reduced by 50% at 2 h following the
event, and maximal grip strength was reduced by
26% at 2 h following the event. Maximal isometric
strength of the knee extensors and knee flexors and
maximal grip strength returned to baseline by 48 h
post-race. Squat jump and countermovement jump
performance also declined by 50% following the
Recovery following an Ironman triathlon 161
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event, improved by 24 h and 48 h post-event, and
returned to baseline values within 8 days (Figure 3).
Muscle soreness
Table I shows changes in soreness of several muscles
before and up to 15 days after the event. Muscle
soreness developed mainly in the lower limb
muscles. The knee extensors recorded the highest
pain at 3 days post-event, followed closely by the
ankle planterflexors, lower back, and knee flexors.
Moderate muscle soreness was reported in other
muscles, including the elbow extensors, upper
back, deltoid, and abdominal muscles. The muscle
soreness reported while running at 8 km × h
1
and
12 km × h
1
increased markedly at 48 h post-event,
but returned to baseline within 8 days.
Blood markers
Plasma volume estimated from haemoglobin and
haematocrit immediately after and 2 and 12 h after
the race was 7.9%, 4.2%, and 2.9% less than that of
the pre-race volume; however, this was not seen at
24 h post-race. Table II shows changes in blood
markers before and for 15 days after the race. The
activity of all measured enzymes increased after
the race, and peaked between 2 and 24 h post-
race. Creatine kinase isoenzymes (CK-MM, CK-
MB) peaked 2 h after the race and returned to
pre-race values within 8 days. Compared with the
large increase in creatine kinase (40-fold increase
from baseline), the magnitude of increase in aspar-
tate aminotransferase, alanine aminotransferase,
and lactate dehydrogenase was small; however, all
exceeded the normal reference range after the race.
Myoglobin showed the largest magnitude of increase
(170-fold increase from baseline), peaked immedi-
ately after the race, and returned to baseline within
8 days. Fifteen days after the race, creatine kinase
and myloglobin increased from their 8-day post-race
values, probably in response to the participants
return to training (he performed a 10-km run and
weight-lifting session 3 days before this blood
test). C-reactive protein and serum amyloid protein
A increased immediately after the race. The highest
value for C-reactive protein was observed 24 h after
the race and for serum amyloid protein A 48 h after
the race; both markers remained elevated above
Figure 2. Running economy expressed as oxygen consumption,
gross cycling efficiency, and maximal oxygen consumption during
cycling before (pre) and 3, 8, and 15 days after the Ironman event.
Figure 3. Maximal isometric strength of the knee extensors (MVC-
KE) and knee flexors (MVC-KF), grip strength, squat jump (SJ)
height, and counter movement jump (CMJ) height before and in the
15 days after the Ironman event.
162 K. Nosaka et al.
Downloaded By: [Laursen, Paul] At: 17:00 1 April 2010
baseline values 8 days post-race. Interleukin-6, IL-
10, and IL-1ra also increased after the race, peaked
immediately after to 2 h post-race, and returned to
baseline within 72 h. The decrease in plasma volume
accounted in part (i.e.B8%) for the increases in
the measures after the race, at least for 12 h.
Discussion
The present case study showed that an experienced
endurance triathlete can recover from an Ironman
triathlon event in approximately one week. In a
previous study (Suzuki et al., 2006), we investigated
nine well-trained male triathletes for changes in
muscle damage and inflammation markers before,
immediately after, and one day after an Ironman
triathlon where the average total race time was10 h.
In the present study, it took longer for the athlete to
complete the race (11 h 38 min); however, the
changes in muscle function, muscle soreness, and
blood markers immediately and one day after the race
were similar to those reported in the previous study
(Suzuki et al., 2006). Neubauer et al. (2008) recently
reported changes in blood markers of muscle damage
and inflammation immediately after and 1, 5, and
19 days after an Ironman triathlon in 42 well-trained
male triathletes (average total race time: 10 h 51 min),
and showed similar changes in creatine kinase activ-
ity, myoglobin concentration, and IL-6 and IL-10
to those in the present study. Thus, the results of
the present study would appear to represent an
accurate account of the time course of recovery of
these markers in well-trained male triathletes follow-
ing completion of an Ironman triathlon.
It is well documented that muscle force and power-
generating capacity are reduced significantly in the
days following exercise resulting in muscle damage
(Byrne & Eston, 2002). The reduction in VO
2max
(Figure 2) observed following the Ironman was
coupled with a reduction in maximal aerobic power
output. At submaximal workloads, an increase in VO
2
has been reported after exercise resulting in muscle
damage. For instance, economy of motion was shown
to be reduced following 30 min of downhill running
(Braun & Dutto, 2003; Chen, Nosaka, & Tu, 2007),
a marathon (Kyro
¨
la
¨
inen et al., 2000), a competitive
duathlon (Calbet, Chavarren, & Dorado, 2001), or
120 maximal eccentric contractions (Paschalis et al.,
2005). To the best of our knowledge, ours is the
first study to examine the influence of an Ironman
triathlon on economy of motion and its time course of
recovery. Interestingly, the magnitude and duration
of the recovery running economy in the present study
was similar to that observed following 30 min of
downhill running (Chen et al., 2007). The increase
in VO
2
observed during the submaximal cycling
and running may be the result of decreased muscle
function and/or altered lower limb kinematics (Chen
et al., 2007; Saunders, Pyne, Telford, & Hawley,
2004). Indeed, the time course of recovery for the
maximal voluntary isometric contractions (Figure 3)
and biochemical muscle damage markers (Table II)
followed a similar pattern to that of running efficiency
and cycling economy (Figure 2).
The decreases in muscle function after the Iron-
man triathlon are likely due to a combination of
fatigue and muscle damage. If the decrease in
grip strength (e.g. 26% at 2 h post-race) indicates
supraspinal fatigue, then supraspinal fatigue would
appear to play a partial role in the decrease in muscle
function at least in the first 24 h post-event. A precise
time course of muscle function recovery following
an Ironman triathlon race was not made clear by
previous research (Suzuki et al., 2006). As shown
in Figure 3, knee extension and flexion isometric
strength returned to baseline after 2 days of recovery,
and vertical jump performance recovered wiuthin
8 days. Muscle soreness was also alleviated after
8 days of recovery (Table I), and most of the blood
markers of muscle damage and inflammation had
returned to baseline values by 8 days (Table II).
These findings suggest that muscle damage induced
Table I. Muscle soreness during palpitation of the indicated muscles and while running before (pre) and on nine separate occasions in the
15 days after the Ironman triathlon
Pre 2 h 12 h 24 h 2 days 3 days 4 days 5 days 8 days 15 days
Knee extensors 0 7 8 8 8 7 4 2 1 0
Knee flexors 0 5 4 3 2 1 0 1 0 0
Calf 0 6 4 4 1 1 1 1 0 0
Hip 0586222010
Lower back 0 5 6 5 4 1 0 0 0 0
Upper back 0 5 4 3 3 2 1 0 0 0
Abdominal 0 4 3 2 1 0 0 0 0 0
Shoulder 0 5 4 1 2 0 0 0 0 0
Elbow flexors 0 1 0 0 0 0 0 0 0 0
Elbow extensors 0 5 3 1 1 0 0 0 0 0
Run at 8 km × h
1
0 *** 5 * 3 ** 0
Run at 12 km × h
1
0 *** 9 * 4 ** 0
Recovery following an Ironman triathlon 163
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Table II. Changes in blood markers one week before (Pre1), 24 h before (Pre2), and on 10 separate occasions in the 15 days after the Ironman triathlon (normal reference ranges are also shown)
Normal range Pre1 Pre2 Post 2 h 12 h 24 h 2 days 3 days 4 days 5 days 8 days 15 days
CK (IU × l
1
)50230 139 164 4990 5920 5280 4590 1724 863 479 330 133 366
CK-MM (IU × l
1
)44225 135 161 4889 5800 5173 4497 1688 845 469 323 130 358
CK-MB (IU × l
1
)014 4 3 101 120 107 93 36 18 10 7 3 8
Myoglobin (ng × ml
1
) B85 27 33 4597 2937 284 279 77 83 67 58 33 52
AST (IU × l
1
)1040 28 27 136 172 191 216 148 107 75 79 33 30
ALT (IU × l
1
)545 19 18 31 32 39 47 45 44 43 75 48 25
LDH (IU × l
1
) 120245 137 137 554 497 301 330 260 216 206 204 179 153
CRP (mg × dl
1
) B0.45 0.04 0.03 0.44 0.75 0.9 0.94 0.83 0.78 0.58 0.42 0.15 0.08
SAA (mg × ml
1
) B8 4.6 2.7 59.2 109.6 558 774.5 933.6 362.7 188 92.6 26.4 8.4
IL-6 (pg× ml
1
) * 3.31 2.89 70.17 43.01 9.48 8.07 3.97 3.12 3.79 2.41 2.9 3.02
IL-10 (pg × ml
1
) * 2.57 3.28 4.82 5.32 3.42 3.8 1.93 2.09 1.88 1.86 2.06 2.02
IL-1ra (pg × ml
1
) * 497 801 17982 11957 1353 1400 1321 1229 510 442 986 694
164 K. Nosaka et al.
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by the Ironman triathlon was repaired within about a
week. This was also the case for recovery from
maximal eccentric exercise in resistance-trained in-
dividuals (Newton et al., 2008) and recovery from
downhill running (Chen et al., 2007). Kyro
¨
la
¨
inen
et al. (2000) reported that recovery from a marathon
race occurs within a week. From the present case
study, it would appear that the time taken for the
muscles to recover from an Ironman triathlon is
similar to that induced by marathon running. This
may be because most muscle damage occurs during
the run phase, and that the level of muscle damage
caused by the swimming and cycling phases is
minimal due to the lower number and intensity of
lengthening contractions.
Considering the recovery of aerobic performance
markers (VO
2max
, cycling efficiency, and running
economy), it may be theoretically possible to per-
form training at maximal intensity 2 weeks after an
Ironman triathlon race. In fact, the athlete in the
present study started training 10 days after the
race, and reported that soreness and sensations of
fatigue and tiredness during training were minimal.
Further research examining a heterogeneous sample
including slower and faster athletes is needed to
establish whether muscle damage might be different
according to fitness and/or performance level. This
case report is important because it clearly identifies
the time points to be investigated in future studies of
the time course of muscle damage and recovery from
an Ironman triathlon.
In conclusion, although the Ironman triathlon
induces a high level of muscle damage characterized
by muscle soreness, loss of muscle function, and
reductions in aerobic capacity, a well-trained triath-
lete can recover from this muscle damage within
approximately one week. Further studies incorporat-
ing large cohorts of Ironman triathletes are necessary
to confirm the findings of the present study.
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Downloaded By: [Laursen, Paul] At: 17:00 1 April 2010
... The video images shot before and after the match using handheld cameras were analyzed with the help of Kinovea, a video-based image analysis software. The video analysis was performed according to the headings in Landing Error Scoring System (LESS) (27,30) . Same rater scorred the all participant video before and after match according to LESS. ...
... Handheld cameras were fixed on the right and front sides of the jumping mat. Cameras were arranged such that they are 345 cm away from the jumping mat and camera lenses are 122 cm above the ground (27,30) . ...
... The jumping was demonstrated to each participant and those who needed were allowed to try it beforehand. The participants were not commanded in any manner during the practice, and the jumping protocol was repeated three times in a row (27,30) . ...
Article
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Introduction: Insufficiencies in landing biomechanics and neuromuscular fatique that induced from sportive activities are risk factor for sport injuries. The combination of these factors increases the risk of sports injuries. Aim of the study was to evaluate the effec-tivness of soccer match induced fatigue on landing biomechanical parameters and neuromuscular performance. Materials and methods: Eighteen young professional male soccer players were included the study. Fatigue level was assessed with the Borg Rate of Perceived Exertion and Pain Scale (BRPEPS). Neuromuscular function measured using a force platform during drop jump test. The Landing Error Scoring System (LESS) was used for infucient of landing biomechanics. The night before the offical match when players were not tired was selected for the pre-match test. The post-match test was conducted in two hours following the end of the match. Results: The difference of pre and post match the BRPEPS was statistically significant (p0.05). There were no statistically significant differences between pre-match and post-match neuromuscular performance values. However, pre-match and post-match LESS scores were statistically significant different(p0.05). Conclusion: It was concluded thatfatigue that occurs in a soccer match disrupts landing biomechanics. Impairment of landing biomechanics doesn’t releated with neuromuscular function, but reduction of postural control, proprioceptive acuity and neromuscular control may affect landing biomechanics.
... Training volumes in the 8 weeks preceding each of the races included in this study are presented in figure 1. grade systemic inflammation up to 5 days post-race, reflecting incomplete recovery, but all variables returned to baseline levels by 19 days after the race. however, it is not clear from their study when the triathletes recovered from the race completely. in a case study, Nosaka et al. 3 examined a triathlete who completed an Ironman race in 11 hours 38 minutes, and showed that running economy and gross cycling efficiency, muscle function (e.g. maximum knee flexion and extension isometric strength, vertical jump performance), lower extremity muscle soreness and increased blood markers of muscle damage and inflammation all returned to baseline by 8 days post-race. ...
... This is in line with previous results obtained on lower caliber athletes. [1][2][3] Blood samples were not taken immediately before and after the races, so the actual changes in these blood markers are not known. it should be also noted that the blood sampling time varied (5, 6 or 8 days post-race) among the races. ...
... however, based on the values measured 5 to 8 days after racing, it can be assumed that the changes were not much different from those reported in non-elite athletes, for whom the time course of changes in several blood variables were reported after ironman distance triathlon races. [1][2][3] Thus, it appears that the recovery from ironman distance racing is not vastly different between this elite and non-elite triathletes. ...
Article
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To understand the recovery of a top triathlete from Ironman distance triathlon races and the timing of training resumption, this study followed an elite male triathlete for 4 years and examined blood parameters after 6 Ironman triathlon races, in which he finished either first (3 races) or second (3 races), with finishing times of 8:00:21 to 8:49:38 (hours:minutes:seconds). The blood was taken either 5, 6 or 8 days after each triathlon race without any training sessions or recovery interventions after the race until the blood sampling. The blood analyses consisted of full hematology including red cell count and differential leucocyte counts (neutrophils, lymphocytes, monocytes, eosinophils, basophils), full iron status (serum iron, total serum capacity, transferrin, saturation index, and ferritin) and general biochemistry (glucose, urea, creatinine, total proteins, aspartate transaminase [AST], alanine transaminase [AST], creatine kinase [CK]). No abnormal values were found for hematology and full iron status. CK activity exceeded the normal reference range (32-162 IU/L) after 3 races that he finished second (Roth 2007: 255 IU/L; Frankfurt 2008: 413 IU/L; Frankfurt 2009: 308 IU/L), but the blood samples were taken at 5 days after the two Frankfurt races and were not different from the athlete's normal training values. AST and ALT activities were also slightly elevated after the two Frankfurt races (2008: 57 IU/L, 61 IU/L; 2009: 43 IU/L, 46 IU/L). It appears that despite slightly elevated CK activity, this elite triathlete recovered from Ironman distance triathlon races within approximately one week and could therefore resume full training within that time frame.
... One of the revealing signs of the physical toll placed on the long distance triathlete is the degree of muscle damage it inflicts. This has been characterized by muscle soreness, loss of muscle function, and reductions in aerobic capacity (Suzuki et al., 2006;Nosaka et al., 2010). For example,Suzuki et al. (2006)showed reductions in muscle strength and jump height, with accompanying increases in muscle soreness, blood markers of muscle damage, and inflammation in the 24 h period following an Ironman triathlon. ...
... Of course, significant muscle damage occurs irrespective of training level, and may actually be higher in well trained athletes due to the higher run speeds, greater muscle mass engaged, and reduced amount of walking relative to less trained triathletes. Regardless, a well-trained triathlete can recover from this muscle damage within approximately one week (Nosaka et al., 2010). ...
Article
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Laursen PB. Long distance triathlon: demands, preparation and performance. J. Hum. Sport Exerc. Vol. 6, No. 2, pp. 247-263, 2011. The rise in worldwide popularity of long distance triathlon racing comes with it an increased interest into how to train and prepare optimally for such an event. This paper examines the physiologic and bioenergetic demands of long distance triathlon racing, including energy requirements, muscle damage consequences, thermoregulatory demands and water turnover rates. In response to these physiological challenges, the second part of the paper describes the training goals and race practices that may assist to minimize these disturbances, in turn, optimizing performance and health for the long distance triathlete. Some of these race strategies include appropriate pacing, ensuring adequate fluid and carbohydrate consumption, acclimating to the heat, and consuming caffeine in appropriate quantities.
... Concerning triathlon and duathlon races [24-28], muscle damage and inflammation were more pronounced, and acute kidney injury was also observed [24,27]. On the other hand, time course changes in inflammatory markers were examined in longer duration and the recovery and revealed that the triathlete recovered almost completely within approximately one week using inflammatory markers [28]. However, typical inflammatory markers such as C-Reactive Protein (CRP) were not sensitive enough in case of exercise, but some cytokine responses to exercise were more exaggerated in urine [2,26]. ...
... A large percentage of those surveyed opted to rely on their own custom designed self-report forms rather than those that have been used in Fatigue was also commonly assessed by respondents via tests of functional performance, with maximal jump assessments most popular within this category. Vertical jumping in particular has been touted as a convenient model to study neuromuscular function and has been used in a multitude of studies investigating the time course of recovery from fatiguing training or competition [9,40,60,64,109,148,177,198,218,246,282,300]. The utility of vertical jumps as a practical measure of neuromuscular fatigue is reflected by the adoption of such testing procedures in the high performance sporting environment. ...
Thesis
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With improving professionalism of sports around the world, the volume and frequency of training required for competitive performances at the elite level has increased concurrently. With this amplification in training load comes an increased need to closely monitor the associated fatigue responses, since maximising the adaptive response to training is also reliant on avoiding the negative consequences of excessive fatigue. The rationale for the experimental chapters in this thesis was established after considering survey responses regarding current best practice for monitoring fatigue in high performance sporting environments (Chapter 3). On the basis of the results, vertical jump assessments were selected for further investigation regarding their utility in determining neuromuscular fatigue responses. Outcomes from the subsequent series of studies aimed to provide practitioners working in high performance sport with guidelines for using vertical jumps to monitor athletic fatigue. The results from Chapter 4 indicate using the mean value of at least six jumps enhances the ability to detect small but practically important changes in performance from week to week. This study also highlighted large differences (4-6%) in morning and afternoon performance, indicating that the time of day performance is assessed needs to be accounted for when monitoring changes in jump performance. Chapter 5 explored the theory that the time of day effect observed in Chapter 4 can be explained by internal temperature differences. This theory was supported by demonstrating that an extended warm-up period can negate differences in jump performance in the morning and the afternoon. Researchers who are unable to standardise the time of day that assessment occurs are able, therefore, to control for performance differences by manipulating the warm-up protocols. The third study examined changes in vertical jump performance over a three month training period and produced several novel outcomes. A major finding was that unloaded jumps were more sensitive to neuromuscular fatigue during intensive training than loaded jumps (Chapter 6). Furthermore, this set of results showed that all subjects changed their jump technique via a reduction in the amplitude of the countermovement when they were highly fatigued. Using the same data, an analysis was performed to quantify individual differences in within-subject variation (Chapter 7) during normal and intensive training. These results provided the first indication that within-subject variability in vertical jump performance is substantially different between individuals and between different training phases, an important consideration for interpreting the practical importance of performance changes. In Chapter 8 the relationship between vertical jump performance and electrically elicited force of the knee extensors was examined to better understand the mechanism(s) of changes in jump performance associated with neuromuscular fatigue during intensive overload training. The results showed that the fatigue assessed by vertical jump performance was likely not only peripheral in origin as previously suggested by other authors. Further research is required to further understand the mechanisms of reduced performance during overload training, although the preliminary evidence presented implicates central mechanisms. To conclude the thesis, the findings presented in the experimental chapters are summarised, with a series of practical recommendations for using vertical jumps to monitor athletic fatigue presented.
... Fatigue was also commonly assessed by respondents via tests of functional performance, with maximal jump assessments most popular within this category. Vertical jumping in particular has been touted as a convenient model to study neuromuscular function and has been used in a multitude of studies investigating the time course of recovery from fatiguing training or competition (3, 8, 11, 15, 21, 27, 32, 36, 41, 44, 47, 53). The utility of vertical jumps as a practical measure of neuromuscular fatigue is reflected by the adoption of such testing procedures in the high performance sporting environment. ...
Article
Full-text available
BSTRACT Research has identified a plethora of physiological, biochemical, psychological and performance markers that help inform coaching staff about when an athlete is in a state of fatigue or recovery. However use of such markers in the regular high performance training environment remains undocumented. To establish current best practice methods for training monitoring, 100 participants involved in coaching or sport science support roles in a variety of high performance sports programs were invited to participate in an online survey. The response rate was 55% with results indicating 91% of respondents implemented some form of training monitoring system. A majority of respondents (70%) indicated there was an equal focus between load quantification and the monitoring of fatigue and recovery within their training monitoring system. Interestingly, 20% of participants indicated the focus was solely on load quantification, while 10% solely monitored the fatigue/recovery process. Respondents reported that the aims of their monitoring systems were to prevent overtraining (22%), reduce injuries (29%), monitor the effectiveness of training programs (27%), and ensure maintenance of performance throughout competitive periods (22%). A variety of methods were used to achieve this, based mainly on experiential evidence rather than replication of methods used in scientific publications. Of the methods identified for monitoring fatigue and recovery responses, self-report questionnaires (84%) and practical tests of maximal neuromuscular performance (61%) were the most commonly utilised.
Article
Endurance exercise induces notable acute hormonal responses on the gonadal and adrenal hormones. The purpose of this study was to assess the changes in salivary testosterone (Ts), salivary cortisol (Cs) and T/C ratio during long-distance triathlon. Ten well-trained male triathletes participated in the study and were assessed for hormonal changes at four time-points (pre-competition, post-swimming, post-cycling, and post-running phases). Ts decreased from pre-competition to post-swimming (from 93.37 pg/mL to 57.63 pg/mL; p < .01) and increased during two other parts of the competition to almost pre-competition values (cycling: 79.20 pg/mL, p = .02; running: 89,66 pg/mL, p = .04, respectively). Cs showed a similar behavior; decreasing in the post-swimming phase (1.74 pg/mL) and increasing in the other transitions (post-cycling: 7.30 pg/mL; post-running: 13.31 pg/mL), with significant differences between pre-competition and post- competition values (p = .01). Conversely, T/C increased significantly from pre-competition to post-swimming phase (p = .04) to later decrease until the end of the competition. Overall, T/C significantly decreased (p < .05). In conclusion, during an Ironman triathlon, hormone values fluctuate in response to the demands of the competition. Ts and Cs decrease after-swimming, increase after-cycling and reach the maximum values after-running. T/C reflects overall catabolic status.
Article
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Published information on aspects related to muscle damage and running economy is both limited and contradictory. To contribute to the current debate, we investigated the effects of an eccentric exercise session on selected muscle damage indices in relation to running economy using 10 (mean age 23 +/- 1 years) healthy male volunteers. The eccentric exercise session consisted of 120 (12 x 10) maximal voluntary repetitions by each randomly selected leg at the angular velocity of 1.05 rad . s (-1). Muscle damage (creatine kinase, delayed onset muscle soreness, range of movement, and eccentric, concentric and isometric [at 60 degrees and 110 degrees knee flexion] peak torque) and running economy (oxygen consumption, pulmonary ventilation, respiratory exchange ratio and breaths per minute during treadmill running at 133 and 200 m . min (-1)) indicators, were assessed pre-, 24-, 48-, 72- as well as 96-h after exercise. All muscle damage indicators revealed significant changes at almost all time-points of assessment compared to pre-exercise data (p < 0.05). However, none of the running economy parameters disclosed any significant change throughout the study (p > 0.05). It was concluded that changes in muscle damage and muscle performance as measured in this study are not reflected by concomitant alterations in running economy at submaximal intensities.
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In a comparison of traditional and theoretical exercise efficiency calculations male subjects were studied during steady-rate cycle ergometer exercises of "0," 200, 400, 600, and 800 kgm/min while pedaling at 40, 60, 80, and 100 rpm. Gross (no base-line correction), net (resting metabolism as base-line correction), work (unloading cycling as base-line correction), and delta (measurable work rate as base-line correction) efficiencies were computed. The result that gross (range 7.5-20.4%) and net (9.8-24.1%) efficiencies increased with increments in work rate was considered to be an artifact of calculation. A LINEAR OR SLIGHTLY EXPONENTIAL RELATIONSHIP BETWEEN CALORIC OUTPUT AND WORK RATE DICTATES EITHER CONSTANT OR DECREASING EFFICIENCY WITH INCREMENTS IN WORK. The delta efficiency (24.4-34.0%) definition produced this result. Due to the difficulty in obtaining 0 work equivalents, the work efficiency definition proved difficult to apply. All definitions yielded the result of decreasing efficiency with increments in speed. Since the theoretical-thermodynamic computation (assuming mitochondrial P/O = 3.0 and delta G = -11.0 kcal/mol for ATP) holds only for CHO, the traditional mode of computation (based upon VO2 and R) was judged to be superior since R less than 1.0. Assuming a constant phosphorylative-coupling efficiency of 60%, the mechanical contraction-coupling efficiency appears to vary between 41 and 57%.
Article
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The present study was designed to investigate interactions between running economy and mechanics before, during, and after an individually run marathon. Seven experienced triathletes performed a 5-min submaximal running test on a treadmill at an individual constant marathon speed. Heart rate was monitored and the expired respiratory gas was analyzed. Blood samples were drawn to analyze serum creatine kinase activity (S-CK), skeletal troponin I (sTnI), and blood lactate (B-La). A video analysis was performed (200 frames x s(-1)) to investigate running mechanics. A kinematic arm was used to determine the external work of each subject. The results of the present study demonstrate that after the marathon, a standardized 5-min submaximal running test resulted in an increase in oxygen consumption, ventilation, and heart rate (P < 0.05), with a simultaneous decrease in the oxygen difference (%) between inspired and expired air, and respiratory exchange ratio (P < 0.05). B-La did not change during the marathon, while sTnI and S-CK values increased (P < 0.05), peaking 2 h and 2 days after the marathon, respectively. With regard to the running kinematics, a minor increase in stride frequency and a similar decrease in stride length were observed (P < 0.01). These results demonstrate clearly that weakened running economy cannot be explained by changes in running mechanics. Therefore, it is suggested that the increased physiological loading is due to several mechanisms: increased utilization of fat as an energy substrate, increased demands of body temperature regulation, and possible muscle damage.
Article
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In this study, we assessed the effect of exercise-induced muscle damage on knee extensor muscle strength during isometric, concentric and eccentric actions at 1.57 rad x s(-1) and vertical jump performance under conditions of squat jump, countermovement jump and drop jump. The eight participants (5 males, 3 females) were aged 29.5+/-7.1 years (mean +/- s). These variables, together with plasma creatine kinase (CK), were measured before, 1 h after and 1, 2, 3, 4 and 7 days after a bout of muscle damaging exercise: 100 barbell squats (10 sets x 10 repetitions at 70% body mass load). Strength was reduced for 4 days (P< 0.05) but no significant differences (P> 0.05) were apparent in the magnitude or rate of recovery of strength between isometric, concentric and eccentric muscle actions. The overall decline in vertical jump performance was dependent on jump method: squat jump performance was affected to a greater extent than countermovement (91.6+/-1.1% vs 95.2+/-1.3% of pre-exercise values, P< 0.05) and drop jump (95.2+/-1.4%, P< 0.05) performance. Creatine kinase was elevated (P < 0.05) above baseline 1 h after exercise, peaked on day 1 and remained significantly elevated on days 2 and 3. Strength loss after exercise-induced muscle damage was independent of the muscle action being performed. However, the impairment of muscle function was attenuated when the stretch-shortening cycle was used in vertical jumping performance.
Article
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Running economy (RE) is typically defined as the energy demand for a given velocity of submaximal running, and is determined by measuring the steady-state consumption of oxygen (V̇O2) and the respiratory exchange ratio. Taking body mass (BM) into consideration, runners with good RE use less energy and therefore less oxygen than runners with poor RE at the same velocity. There is a strong association between RE and distance running performance, with RE being a better predictor of performance than maximal oxygen uptake (V̇O2max) in elite runners who have a similar V̇O2max. RE is traditionally measured by running on a treadmill in standard laboratory conditions, and, although this is not the same as overground running, it gives a good indication of how economical a runner is and how RE changes over time. In order to determine whether changes in RE are real or not, careful standardisation of footwear, time of test and nutritional status are required to limit typical error of measurement. Under controlled conditions, RE is a stable test capable of detecting relatively small changes elicited by training or other interventions. When tracking RE between or within groups it is important to account for BM. As V̇O2 during submaximal exercise does not, in general, increase linearly with BM, reporting RE with respect to the 0.75 power of BM has been recommended. A number of physiological and biomechanical factors appear to influence RE in highly trained or elite runners. These include metabolic adaptations within the muscle such as increased mitochondria and oxidative enzymes, the ability of the muscles to store and release elastic energy by increasing the stiffness of the muscles, and more efficient mechanics leading to less energy wasted on braking forces and excessive vertical oscillation. Interventions to improve RE are constantly sought after by athletes, coaches and sport scientists. Two interventions that have received recent widespread attention are strength training and altitude training. Strength training allows the muscles to utilise more elastic energy and reduce the amount of energy wasted in braking forces. Altitude exposure enhances discrete metabolic aspects of skeletal muscle, which facilitate more efficient use of oxygen. The importance of RE to successful distance running is well established, and future research should focus on identifying methods to improve RE. Interventions that are easily incorporated into an athlete’s training are desirable.
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The aim of the study was to verify whether an overloaded training (OT) in triathlon deteriorates running kinematics (RK) and running economy (RE). Thirteen well-trained male long-distance triathletes (age: 28.1 +/- 4.3 yrs; V.O (2max): 65.0 +/- 3.1 ml O (2) . min (-1) . kg (-1)) were divided into two groups: completed an individualized OT program (OG; n = 7) or maintained a normal level of training (NT) (CG; n = 6) for a duration of 3 weeks. Every week, each triathlete completed a standardized questionnaire to quantify the influence of training loads on mood state. To reach OT, total training load (h . 3 wk (-1)) was increased by 24 %; swimming and cycling total volumes were increased by 46 and 57 %, respectively, but the distance run was not modified in order to limit the risk of injuries. RK and RE were determined on treadmill test at 12 km . h (-1) before and after the 3 weeks. The 3-week swimming and cycling OT in triathlon was sufficiently stressful to alter mood state but not to deteriorate the running kinematics and economy parameters in our previously well-trained male long-distance triathletes.
Article
To examine the improvement in swimming (3.8 km), cycling (180 km), running (42.2 km), and overall performances at the Hawaii Ironman Triathlon of elite males and females between 1981 and 2007. Trends across years, gender differences in performance times in the three disciplines, and overall winning times of the top 10 males and females were analyzed. Overall performance time in the ironman decreased rapidly from 1981 but has remained stable since the late 1980s. From 1988 to 2007, linear regression analysis showed that change in swimming, cycling, running, and total performance for both males and females was less than 1.4% per decade, except for females' running time, which decreased by 3.8% per decade. Since 1988, the mean (SD) gender differences in time for swimming, cycling, running, and total event were 9.8% (2.9), 12.7% (2.0), 13.3% (3.1), and 12.6% (1.3), respectively. After an initial phase of rapid improvement of performances during the 1980s, there was a relative plateau, but at least in running and cycling, there were small improvements. Over the last two decades, gender difference in swimming remained stable while it slightly increased in cycling and decreased in running. The gender difference in ironman total performance is unlikely to change in the future.
Article
We analyzed metabolic parameters in 11 volunteers after each segment of an endurance triathlon and, in a separate year, analyzed similar parameters in eight volunteers during 6 d of recovery following completion of an endurance triathlon. After the 2.4-mile ocean swim, serum lactate tripled, and albumin and muscle enzymes were increased. After the 112-mile bicycle ride, mild dehydration occurred, and muscle enzymes and uric acid levels increased markedly. Serum lactate was elevated over baseline but was lower then after the swim. After the 26.2-mile run, dehydration and muscle damage progressed; serum triglycerides dropped by 50%. Serum lactate remained elevated, but less than after either of the other segments. During recovery, muscle enzymes continued to rise and peaked (creatine phosphokinase on the day following the triathlon at 4920 +/- 685 U.ml-1; range 1321-16,746); creatine phosphokinase and lactate dehydrogenase remained significantly elevated at the end of the recovery period. Total protein and albumin decreased, suggesting alterations in their synthesis or their utilization for tissue repair. Serum cholesterol levels fell significantly until the 4th d. Serum triglycerides slowly increased to baseline over 4 d, suggesting their use as energy substrate during recovery. Thus, competition in an endurance triathlon causes skeletal muscle injury that appears early, increases as the triathlon progresses, and is still apparent even 6 d after completion of the triathlon. Changes in plasma proteins and lipid suggest that energy substrate utilization is shifted as the triathlon progresses and as the body repairs itself following completion of the event.
Article
The main purpose of this study was to test the effects of a duathlon competition on running economy. METHODS. A prospective study. University. Participants: nine male and six female physical education students, which mean (SEM) age was 24.0 (1.3) years. Subjects participated in two competitive duathlons: D1 and D2 (5 km running + 16 km cycling + 2 km running). Before D1, an incremental exercise test on the treadmill was performed to determine the V O2max, the running speed at exhaustion (vmax), and the V O2, as well as the running speed (u) attained at the first and second ventilatory threshold (V O2V T1, uV T1, V O2V T2, uV T2). Two days later running economy (RE1) was assessed at four different speeds corresponding to 58, 63, 67 and 71% of the umax. During the following six weeks the subjects trained 4 days a week, running all them 210 km in total. At the end of the training program the incremental exercise test and the duathlon competition were repeated (D2). Two and seven days after the second duathlon running economy was measured again (RE2 and RE3, respectively). Small, but significant improvements were observed in duathlon performance, V O2max, umax, uV T1, V O2V T2 and uV T2, after training. Two days after D2 the oxygen cost of running was approximately 5% higher than seven days after D2 (p < 0.001). The respiratory exchange ratio increased by approximately 0.04 units between RE2 and RE3 (p < 0.001). However, the increase in fat oxidation in RE2 only accounted for approximately 20% of the extra oxygen cost of running (RE2 vs RE3). No significant differences across tests were observed for ventilation (V E), heart rate, V CO2 and V E/V CO2. This study shows that two days after a duathlon competition running economy is impaired, however, seven days after the competition the oxygen cost of running is restored.
Article
Delayed onset of muscle soreness (DOMS) is a common response to exercise involving significant eccentric loading. Symptoms of DOMS vary widely and may include reduced force generating capacity, significant alterations in biochemical indices of muscle and connective tissue health, alteration of neuromuscular function, and changes in mechanical performance. The purpose of the investigation was to examine the effects of downhill running and ensuing DOMS on running economy and stride mechanics. Nine, well-trained distance runners and triathletes participated in the study. Running economy was measured at three relative intensities [65, 75, and 85% of maximal aerobic capacity ( VO(2peak))] before (RE1) and 48 h after (RE2) a 30-min downhill run (-10%) at 70% VO(2peak). Dependent variables included leg muscle soreness, rate of oxygen consumption ( VO(2)), minute ventilation, respiratory exchange ratio, lactate, heart rate, and stride length. These measurements were entered into a two-factor multivariate analysis of variance (MANOVA). The analysis revealed a significant time effect for all variables and a significant interaction (time x intensity) for lactate. The energy cost of locomotion was elevated at RE2 by an average of 3.2%. This was coupled with a significant reduction in stride length. The change in VO(2) was inversely correlated with the change in stride length ( r= -0.535). Lactate was significantly elevated at RE2 for each run intensity, with a mean increase of 0.61 mmol l(-1). Based on these findings, it is suggested that muscle damage led to changes in stride mechanics and a greater reliance on anaerobic methods of energy production, contributing to the change in running economy during DOMS.