European Journal of Sport Science, May 2010; 10(3): 159165

ORIGINAL ARTICLE

Recovery following an Ironman triathlon: A case study

KAZUNORI NOSAKA1, CHRIS R. ABBISS1, GREIG WATSON1, BRADLEY WALL1,

KATUSHIKO SUZUKI2, & PAUL LAURSEN1
1
School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia, and 2Faculty 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 Ironman race. They showed a pronounced initial

systemic inflammatory response together with persis-
The long distances that comprise an Ironman triath-
tent low-grade systemic inflammation for up to
lon (3.8-km swim, 180-km cycle, 42.2-km run) create
a challenge that can induce significant physical 5 days after the event, reflecting incomplete recovery.
and psychological stress on its participants (Farber, Although all measured variables had returned to
Schaefer, Franey, Grimaldi, & Hill, 1991; Lepers, baseline values within 19 days, a more precise under-
2008). One of the revealing signs of this physical toll is standing of the time course of recovery to baseline
the amount of muscle damage it inflicts. For example, values, together with functional measurements, is
we have shown reductions in muscle strength and required. It is important for sport medicine profes-
jump height, together with increases in muscle sionals to understand the recovery process associated
soreness, blood markers of muscle damage, and with this popular but challenging event.
inflammation in the 24 h following an Ironman There is also limited information available con-
triathlon (Suzuki et al., 2006). While the acute phase cerning the effects that muscle damage and subse-
response has been documented, the time course of quent recovery may have on running economy and
the recovery from muscle damage induced during an maximal oxygen uptake (VO2max) after an Ironman
Ironman triathlon is less clear. Only Neubauer and triathlon. It could be that running economy and
colleagues (Neubauer, König, & Wagner, 2008) have VO2max are reduced for several days, possibly due
outlined the recovery 1, 5, and 19 days after an 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

ISSN 1746-1391 print/ISSN 1536-7290 online # 2010 European College of Sport Science
DOI: 10.1080/17461390903426642
160 K. Nosaka et al.

however, no previous studies have investigated this The variables measured during the test sessions are
response after an Ironman triathlon. outlined below.
We had the opportunity to collect data on blood
markers of muscle damage and inflammation, mus-
Maximal oxygen consumption, gross cycling efficiency,
cle function, muscle soreness, running economy, and and running economy
VO2max for a male triathlete while cycling, before
and for 15 days after an Ironman event. These data Once before and on three separate occasions after the
show that recovery from an Ironman triathlon race Ironman event (Figure 1), the participant performed
by an experienced triathlete is almost complete an incremental cycling test to exhaustion and a
within a week of finishing the event. 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
Methods (Velotron; RacerMate, Seattle, WA), and the running
Participant economy test was conducted on a motorized
treadmill (JAS Fitness Systems, Carrollton, TX).
Our experienced male triathlete (age 35 years, body mass Throughout both tests, expired gases were analysed
75.0 kg, stature 1.78 m, VO2max 67.0 ml × kg
1 × min
1) for concentration and volume using a calibrated and
participated in the Ironman Western Australia event validated ParvoMedics TrueOne 2400 diagnostic
(Busselton, Western Australia) on 1 December 2006. system (Sandy, UT). The exercise protocol, determi-
This was the participant’s eleventh Ironman triathlon nation of oxygen consumption (VO2), and maximal
(personal best time: 10 h 14 min). Before testing, the aerobic power output during the incremental cycling
participant was informed of the risks associated with test were completed as previously described (Abbiss
the study and provided written informed consent in et al., 2008). Briefly, the participant began cycling at
accordance with the Institutional Human Research 100 W for 5 min, after which power output was
Ethics Committee. He completed the race in 11 h 38 increased by 50 W every 5 min until the participant
min 41 s, in which the swimming (1 h 7 min 3 s) and reached volitional exhaustion. The metabolic cart
cycling (5 h 25 min 6 s) legs were performed as recorded heart rate throughout the test with the use of
expected, but his run (5 h 6 min 31 s) was about an a compatible heart rate monitor (Polar Electro Oy,
hour slower than expected. This was due to fatigue Kempele, Finland). Average VO2 for the last minute
related to hyperthermia and muscle cramping near the of 100, 150, and 200 W was used as steady-state
half-way point of the run. In total, 804 athletes oxygen consumption for the determination of gross
participated in the event, of whom 766 completed cycling efficiency (Gaesser & Brooks, 1975). During
the course, and the winner’s time was 8 h 3 min 56 s. the running economy test, the participant performed
Our participant finished 331st, and his relative time to a 5-min warm-up running at 8 km × h
1 followed by
that of the winner was 144%. 5 min at 12 km × h
1 on the motorized treadmill set
at a 2% incline (Palazzetti, Margaritis, & Guezennec,
2005). Average VO2 (litres × min
1) over the final
Experimental overview minute of the 12 km × h
1 stage was used to deter-
mine running economy. Rating of perceived exertion
The participant attended the laboratory one week (RPE) and muscle soreness (described below) were
before (Pre 1) and on seven separate occasions in recorded 1 min before completion of each 5-min
the 15 days after the Ironman event (Figure 1). The stage during the running economy test.
participant also attended a makeshift laboratory the
day before (Pre 2), and 2 and 12 h after, the event.
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
Figure 1. Schematic time line of measurements before and after to a wire with a belt that surrounded the ankle joint
the Ironman triathlon event. with the knee joint angle set at 908. Peak maximal
 Recovery following an Ironman triathlon 161

voluntary contraction force was displayed on a digital amyloid protein A were analysed using an automated
indicator (Rinstrum Pty. Ltd., Model 2100EX, analyser (Model 7450 or Model 7170, Hitachi,
Brisbane, QLD) connected to the strain gauge, Japan). Serum amyloid protein A was analysed using
and the higher value of the two measurements was a different automated analyser (Model JCA-BM21,
used for further analysis. Grip strength was measured JOEL Ltd., Japan) and myoglobin was analysed
using a Smedley grip dynamometer (Takei Scientific using ELISA (Life Diagnostics, West Chester, PA,
Instruments Co. Ltd., Model TKK5001, Niigata USA). Serum cytokine concentrations of interleukin-6
City, Japan) twice for each arm, and the higher value (IL-6), IL-10, and IL-1ra were measured with
was used to calculate the average value of two arms, ELISA kits (IL-6: Quantikine HS, R&D Systems,
which was used for further analysis. Minneapolis, MN; IL-10: OptEIA, BD Biosciences,
Vertical jump height of the squat jump and San Jose, CA; IL-1ra: Quantikine, R&D Systems).
countermovement jump was assessed using a leap In addition to these blood markers, a portable
meter (Takei Scientific Instrument, Japan). For the blood-gas electrolyte analyser (i-STAT Corporation,
squat jump, the participant was asked to jump after East Windsor, NJ) was used to measure pH,
holding his knee joint at 908 for at least 2 s and partial pressure of carbon dioxide, partial pressure
without using his arms (held on their hips). The of oxygen, lactate concentration, bicarbonate, oxy-
same arm position was used for the countermove- gen saturation, sodium, potassium, chloride, urea,
ment jump, but the participant began the jump glucose, haemoglobin concentration, and haemato-
motion from a standing position with a counter- crit before, immediately after, and 2, 12, and 24 h
movement. After two practice jumps, two trials for after the race. The results of these measures are not
each jump were performed, and the higher value of reported here, but haemoglobin and haematocrit
the two was used for further analysis. were used to calculate changes in plasma volume.

Muscle soreness
Results
Muscle soreness was assessed using a verbal rating
scale of 0 (‘‘no pain’’) to 10 (‘‘maximal’’) that has Maximal oxygen consumption, gross cycling efficiency,
been used previously (Suzuki et al., 2006). The and running economy
participant was asked to rate his subjective level
Figure 2 shows changes in cycling VO2max, gross
of soreness on a questionnaire sheet while actively
cycling efficiency, and running economy before and
moving specific muscles as instructed (squat, stretch-
after the Ironman event. Both running economy
ing or running) or while the investigator palpated
and gross cycling efficiency were reduced (6.5% and
those muscles. Muscle groups of the limbs and
4.5%, respectively) following the event but returned
trunk assessed included the deltoid, pectoralis, biceps
to baseline by 4 and 8 days, respectively. Maximal
brachii/brachialis, triceps brachii, brachioradialis,
aerobic power output and VO2max were reduced by
rectus/obliquus abdominis, quadriceps femoris, bi-
8.3% (352.5 W to 332.5 W) and 9.5% at 3 days
ceps femoris, gastrocnemius/soleus, and low back
following the event, respectively, but returned to
muscles.
baseline values by day 15. Maximal heart rate
decreased by 3% (191 to 185 beats × min
1) at
Blood sampling and analyses 3 days following the event, but returned to baseline
by day 8 (193 beats × min
1). Rating of perceived
Before and on 10 occasions after the Ironman event
exertion while running at 8 km × h
1 and 12 km × h
1
(Figure 1), approximately 8 ml of blood were taken
during the running economy test increased in the 48
from the antecubital vein via standard venepuncture
h following the event (from 8 to 15 and 11 to 18,
techniques. Post-race blood samples were taken
respectively), but returned to baseline by day 8.
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
Muscle function
for 10 min to obtain serum. Serum samples were
frozen and stored at
808C until analysis. Maximal isometric strength of the knee extensors and
Serum samples were analysed for the following knee flexors was reduced by 50% at 2 h following the
markers of muscle damage and inflammation: crea- event, and maximal grip strength was reduced by
tine kinase (CK), creatine kinasae isoenzymes (CK- 26% at 2 h following the event. Maximal isometric
MM, CK-MB), myoglobin, lactate dehydrogenase, strength of the knee extensors and knee flexors and
alanine aminotransferase, aspartate aminotransfer- maximal grip strength returned to baseline by 48 h
ase, C-reactive protein, and serum amyloid protein post-race. Squat jump and countermovement jump
A. All of these variables except myoglobin and serum performance also declined by 50% following the
162 K. Nosaka et al.

Figure 3. Maximal isometric strength of the knee extensors (MVC-

KE) and knee flexors (MVC-KF), grip strength, squat jump (SJ)
Figure 2. Running economy expressed as oxygen consumption, height, and counter movement jump (CMJ) height before and in the
gross cycling efficiency, and maximal oxygen consumption during 15 days after the Ironman event.
cycling before (pre) and 3, 8, and 15 days after the Ironman event.
24 h post-race. Table II shows changes in blood
event, improved by 24 h and 48 h post-event, and markers before and for 15 days after the race. The
returned to baseline values within 8 days (Figure 3). activity of all measured enzymes increased after
the race, and peaked between 2 and 24 h post-
race. Creatine kinase isoenzymes (CK-MM, CK-
Muscle soreness MB) peaked 2 h after the race and returned to
Table I shows changes in soreness of several muscles pre-race values within 8 days. Compared with the
before and up to 15 days after the event. Muscle large increase in creatine kinase (40-fold increase
soreness developed mainly in the lower limb from baseline), the magnitude of increase in aspar-
muscles. The knee extensors recorded the highest tate aminotransferase, alanine aminotransferase,
pain at 3 days post-event, followed closely by the and lactate dehydrogenase was small; however, all
ankle planterflexors, lower back, and knee flexors. exceeded the normal reference range after the race.
Moderate muscle soreness was reported in other Myoglobin showed the largest magnitude of increase
muscles, including the elbow extensors, upper (170-fold increase from baseline), peaked immedi-
back, deltoid, and abdominal muscles. The muscle ately after the race, and returned to baseline within
soreness reported while running at 8 km × h
1 and 8 days. Fifteen days after the race, creatine kinase
12 km × h
1 increased markedly at 48 h post-event, and myloglobin increased from their 8-day post-race
but returned to baseline within 8 days. values, probably in response to the participant’s
return to training (he performed a 10-km run and
weight-lifting session 3 days before this blood
Blood markers test). C-reactive protein and serum amyloid protein
Plasma volume estimated from haemoglobin and A increased immediately after the race. The highest
haematocrit immediately after and 2 and 12 h after value for C-reactive protein was observed 24 h after
the race was 7.9%, 4.2%, and 2.9% less than that of the race and for serum amyloid protein A 48 h after
the pre-race volume; however, this was not seen at the race; both markers remained elevated above
 Recovery following an Ironman triathlon 163

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 2h 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 0 5 8 6 2 2 2 0 1 0
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

baseline values 8 days post-race. Interleukin-6, IL- has been reported after exercise resulting in muscle
10, and IL-1ra also increased after the race, peaked damage. For instance, economy of motion was shown
immediately after to 2 h post-race, and returned to to be reduced following 30 min of downhill running
baseline within 72 h. The decrease in plasma volume (Braun & Dutto, 2003; Chen, Nosaka, & Tu, 2007),
accounted in part (i.e. B8%) for the increases in a marathon (Kyröläinen et al., 2000), a competitive
the measures after the race, at least for 12 h. duathlon (Calbet, Chavarren, & Dorado, 2001), or
120 maximal eccentric contractions (Paschalis et al.,
2005). To the best of our knowledge, ours is the
Discussion first study to examine the influence of an Ironman
The present case study showed that an experienced triathlon on economy of motion and its time course of
endurance triathlete can recover from an Ironman recovery. Interestingly, the magnitude and duration
triathlon event in approximately one week. In a of the recovery running economy in the present study
previous study (Suzuki et al., 2006), we investigated was similar to that observed following 30 min of
nine well-trained male triathletes for changes in downhill running (Chen et al., 2007). The increase
muscle damage and inflammation markers before, in VO2 observed during the submaximal cycling
immediately after, and one day after an Ironman and running may be the result of decreased muscle
triathlon where the average total race time was 10 h. function and/or altered lower limb kinematics (Chen
In the present study, it took longer for the athlete to et al., 2007; Saunders, Pyne, Telford, & Hawley,
complete the race (11 h 38 min); however, the 2004). Indeed, the time course of recovery for the
changes in muscle function, muscle soreness, and maximal voluntary isometric contractions (Figure 3)
blood markers immediately and one day after the race and biochemical muscle damage markers (Table II)
were similar to those reported in the previous study followed a similar pattern to that of running efficiency
(Suzuki et al., 2006). Neubauer et al. (2008) recently and cycling economy (Figure 2).
reported changes in blood markers of muscle damage The decreases in muscle function after the Iron-
and inflammation immediately after and 1, 5, and man triathlon are likely due to a combination of
19 days after an Ironman triathlon in 42 well-trained fatigue and muscle damage. If the decrease in
male triathletes (average total race time: 10 h 51 min), grip strength (e.g. 26% at 2 h post-race) indicates
and showed similar changes in creatine kinase activ- supraspinal fatigue, then supraspinal fatigue would
ity, myoglobin concentration, and IL-6 and IL-10 appear to play a partial role in the decrease in muscle
to those in the present study. Thus, the results of function at least in the first 24 h post-event. A precise
the present study would appear to represent an time course of muscle function recovery following
accurate account of the time course of recovery of an Ironman triathlon race was not made clear by
these markers in well-trained male triathletes follow- previous research (Suzuki et al., 2006). As shown
ing completion of an Ironman triathlon. in Figure 3, knee extension and flexion isometric
It is well documented that muscle force and power- strength returned to baseline after 2 days of recovery,
generating capacity are reduced significantly in the and vertical jump performance recovered wiuthin
days following exercise resulting in muscle damage 8 days. Muscle soreness was also alleviated after
(Byrne & Eston, 2002). The reduction in VO2max 8 days of recovery (Table I), and most of the blood
(Figure 2) observed following the Ironman was markers of muscle damage and inflammation had
coupled with a reduction in maximal aerobic power returned to baseline values by 8 days (Table II).
output. At submaximal workloads, an increase in VO2 These findings suggest that muscle damage induced
 164
K. Nosaka et al.
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 2h 12 h 24 h 2 days 3 days 4 days 5 days 8 days 15 days

1
CK (IU × l ) 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
 Recovery following an Ironman triathlon 165

by the Ironman triathlon was repaired within about a and ambient temperature on muscle fatigue development in
week. This was also the case for recovery from endurance-trained male cyclists. Journal of Applied Physiology,
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