Ca mona e al Moun ain Ul ama a hon and Sa come e Dis up ion
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ORIGINAL INVESTIGATION
h p://dx.doi.o g/10.1123/ijspp.2014-0267
Moun ain Ul ama a hon and Sa come e Dis up ions o Slow Fibe s
Ge a d Ca mona, Emma Roca, Ma io Gue e o, Rose Cussó, Al edo I u ia, Lexa Nescola de,
Daniel B o ons, Josep L. Bedini, and Joan A. Cade au
Objec i e: To in es iga e changes a e a moun ain ul ama a hon (MUM) in he se um concen a ion o as (FM) and slow (SM)
myosin iso o ms, which a e ibe - ype-speci ic sa come e p o eins. The changes we e compa ed agains c ea ine kinase (CK), a
widely used ibe -sa colemma-damage bioma ke , and ca diac oponin I (cTnI), a widely used ca diac bioma ke . Me hods:
Obse a ional compa ison o esponse in a single g oup o 8 endu ance- ained ama eu a hle es. Time- ela ed changes in se um
le els o CK, cTnI, SM, and FM om compe i o s we e analyzed be o e, 1 h a e he MUM, and 24 and 48 h a e he s a o he
MUM by 1-way ANOVA o epea ed measu es o F iedman and Wilcoxon es s. Pea son co ela ion coe icien was employed o
examine associa ions be ween a iables. Resul s: While SM was signi ican ly (P = .009) inc eased in se um 24 h a e he beginning
o he MUM, FM and cTnI did no change signi ican ly. Se um CK ac i i y peak was obse ed 1 h a e he MUM (P = .002).
Mo eo e , se um peaks o CK and SM we e highly co ela ed ( = .884, P = .004). Conclusions: Since he e is e idence o muscle
damage a e p olonged moun ain unning, he inc ease in SM se um concen a ion a e a MUM could be indi ec e idence o slow-
( ype I) ibe -speci ic sa come e dis up ions.
Keywo ds: eccen ic con ac ion, c ea ine kinase, muscle myosin iso o ms
Moun ain ul ama a hons (MUM) a e compe i i e e en s
1
con-
sis ing o walking and unning on moun ain ails o e a g ea cumu-
la i e ele a ion gain and o e a longe dis ance han he a hle ic ma a-
hon (>42.195 km). Dis ance and cumula i e ele a ion gain a e he
main de e minan s o MUM di icul y. Long-dis ance ail compe i-
ions ha e isen in popula i y o e he las ew yea s.1 Howe e , he
acu e physiological esponses o ex eme endu ance e en s s ill e-
main unclea . I is known ha MUM compe i ions a e s enuous and
gene ally include nega i e slopes, so long dis ances a e un downhill.
I has been s a ed ha s enuous exe cise can esul in muscle dam-
age,2 which is pa icula ly exace ba ed i eccen ic con ac ions a e
pe o med ( o a e iew see P oske and Allen3). Downhill unning
inc eases he eccen ic componen because he peak lexion angles a e
signi ican ly g ea e , and i is a much s onge s imulus o damage
han le el o uphill unning.4 The e o e, i seems easonable o ela e
mos o he muscle damage o he nega i e-slope phases o he ail.
MUM is a g ea oppo uni y o ield-speci ic assessmen s o a physi-
ologically s ess ul compe i i e e en ha induces muscle damage.5,6
Di ec e alua ion o muscle damage in ol es his ological
examina ion o muscle issue by biopsy. Howe e , in a spo s con ex ,
he analysis o exe cise-induced muscle damage is essen ially based
on p oxy ma ke s such as measu emen s o enzyme ac i i y in blood,
especially he ac i i y o c ea ine kinase (CK). P e ious s udies
e alua ed he muscle damage induced by MUMs5,6 and e ealed la ge
inc eases in o al CK concen a ions. Howe e , CK is no a speci ic
bioma ke o skele al muscle.7 Kolle e al8 used slow ( ype I) myosin
hea y-chain (MHC) agmen s, and Melin e al9 used be a MHC as
1
Ca mona, I u ia, and Cade au a e wi h he Na ional Ins o Physical Educa ion o
Ca alonia, Ba celona, Spain. Roca is wi h he Uni e si y o Gi ona, Gi ona, Spain.
Gue e o and Cussó a e wi h he Dep o Physiological Sciences I, Uni e si y o
Ba celona, Ba celona, Spain. Nescola de is wi h he Poly echnic Uni e si y o
Ca alonia, Ba celona, Spain. B o ons is wi h he Ca alan Spo s Council, Go e nmen
o Ca alonia, Ba celona, Spain. Bedini is wi h he Hospi al Clinic, Ba celona, Spain.
Add ess au ho co espondence o Joan Cade au a jcade au@genca .ca .
muscle- ibe -speci ic damage bioma ke s. Those g oups ound
inc eases in his p o ein in plasma a e moun ain- unning e en s.
Al hough slow ( ype I) MHC agmen s and be a MHC a e common
o skele al and ca diac muscle, he damage was mainly ela ed o slow
( ype I) ibe s o skele al muscle. Howe e , he esul s ound by
Kolle e al8 and Melin e al9 we e highly unspeci ic, since plasma
le els o MHC agmen s we e no compa ed wi h any ca diac-
speci ic bioma ke . Since i has been s a ed ha s enuous exe cise
could induce a signi ican elease o ca diac p o eins such as oponin
in o he bloods eam,10 i seems easonable o assume ha p o eins
ound in ca diac and skele al muscle, such as MHC agmen s and
be a MHC, could also be eleased om myoca dium o blood.
Recen ly, myosin iso o ms ha e been p oposed as ibe - ype-
speci ic bioma ke s o muscle damage ha would ep esen indi ec
e idence o sa come e dis up ions.11 Howe e , Ca mona e al11
obse ed selec i e elease o as myosin iso o ms (FM) a e high-
in ensi y knee-ex enso exe cise, bu no changes in slow-myosin-
iso o m (SM) se um concen a ion we e epo ed. SM is ound in bo h
ca diac and skele al muscle, and FM is cha ac e is ic o as skele al
muscle. Limb skele al muscles a e composed o slow ( ype I) and as
( ype II) ibe s,12 bu adul skele al muscles shows plas ici y and can
unde go con e sion be ween di e en ibe ypes in esponse o
exe cise.13 Endu ance a hle es end o ha e a p edominance o slow
( ype I) ibe s.14,15 Fo hese easons, we hypo hesized ha se um
inc eases in myosin iso o ms, especially in SM, in endu ance- ained
pa icipan s a e a MUM could indica e no only he ex en bu also
he ype o ibe a ec ed. Fu he mo e, in he cu en s udy, he lack
o speci ici y o SM was minimized by analyzing he changes in
se um concen a ion o ca diac oponin I (cTnI), a widely used
myoca dial-speci ic bioma ke . I has been shown ha cTnI is
eleased a e p olonged exe cise. Howe e , in con as o myoca dial
in a c ion, in which cTnI is usually o e 0.6 ng/mL and emains
s able in blood o a leas 5 days, cTnI elease a e p olonged
exe cise does no achie e such high se um le els and e u ns o
Ca mona e al Moun ain Ul ama a hon and Sa come e Dis up ion
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baseline wi hin 24 o 48 hou s.16 To he bes o ou knowledge, his is
he i s ield s udy o use a combina ion o myosin iso o ms and cTnI
o assess indi ec ly he muscle damage induced by a MUM.
The aim o his s udy was o in es iga e changes in se um
concen a ion o myosin iso o ms a e a MUM. SM and FM we e
compa ed wi h CK, a widely used bioma ke o exe cise-induced
muscle damage. The lack o speci ici y o SM was coun e ed wi h he
measu emen o se um cTnI concen a ion. Since he e is e idence o
muscle damage a e p olonged moun ain unning,5,6 we hypo hesized
ha a speci ic inc ease in SM se um concen a ion a e a MUM
would be indi ec e idence o slow ( ype I) - ibe sa come e damage
in endu ance- ained moun ain unne s.
Me hods
Pa icipan s
We ini ially ec ui ed 17 endu ance unne s, 14 men and 3 women.
Howe e , due o bad wea he condi ions du ing he compe i ion, only
8 subjec s decided o comple e he s udy: 7 men and 1 woman (mean
± SD; men, n = 7, 39.8 ± 3.3 y, 178.7 ± 5.2 cm, 76.9 ± 7.9 kg;
women, n = 1, 39.1 y, 173.0 cm, 67.0 kg). All o he pa icipan s we e
expe ienced whi e nonp o essional a hle es (mean aining egimen,
450.0 ± 210.31 min/wk o endu ance aining) who we e speci ically
ained o MUM. All we e heal hy and had incu ed no muscle
inju ies in he 6 mon hs be o e he s udy. To a oid bias, no
ins uc ions we e gi en abou he ype o aining pe o med he week
be o e he compe i ion, bu a hle es we e asked abou i o be e
in e p e he baseline se um le els o enzymes and con ac ile
p o eins. Physical ac i i y a e he ace was limi ed and massages
we e p ohibi ed. The s udy con o med o he Decla a ion o Helsinki
o medical esea ch, pa icipan s p o ided w i en in o med consen ,
and he esea ch was app o ed by he e hics commi ee o he Ca alan
Spo s Council (Go e nmen o Ca alonia).
Design
The s udy design used obse a ional compa ison o esponse in a
single g oup o endu ance- ained ama eu a hle es.
Me hodology
The pa icipan s an in he “Ca alls del Ven ” MUM in 2012, an
o icial compe i ion o ganized by Salomon Na u e T ails. I was a
ci cula ou e wi h an o icial leng h o 84.84 km (~85 km) and a o al
cumula i e ele a ion gain o 12,180 m. The s a o he ace was a
755 m abo e sea le el and he maximum summi achie ed du ing he
ail was 2520 m (Figu e 1). Each unne ’s a e age speed was
calcula ed acco ding o he o al dis ance un di ided by his o he
o icial ime.
<<<<<<<<<FIGURE 1>>>>>>>>>>>>>
Fou blood samples we e ob ained: 1 day be o e he
compe i ion (p e), less han 1 hou a e inishing he compe i ion
(pos ), and, because a signi ican deg ee o damage can occu du ing
he ace, 24 and 48 hou s a e he beginning o he MUM. A 5-mL
blood sample was d awn om an an ecubi al ein. Blood was allowed
o clo o 30 minu es in a ube (SST II Ad ance, Bec on Dickinson
Vacu aine Sys ems, UK) be o e being cen i uged a 3000 g o 10
minu es a 4°C. Th ee 200- L aliquo s o se um we e s o ed a –80°C
un il analysis.
CK de e mina ions we e pe o med in an Ad ia 2400 au oma ic
de ice (Siemens Medical Solu ions Diagnos ics, Ta y own, NY,
USA), and cTnI de e mina ions we e made in a Dimension Clinical
Chemis y Sys em au oma ic de ice (Siemens Heal hca e
Diagnos ics, Ta y own, NY, USA) wi h an analy ical measu emen
ange o 0.017 o 40 ng/mL. To ob ain muscle myosin-iso o m
concen a ions in se um, we de eloped an enzyme-linked
immunoso ben assay (ELISA-sandwich), which is desc ibed
elsewhe e.11 B ie ly, a calib a ion cu e was ob ained by a se ial
dilu ion om 0 o 250 ng o pu e myosin om po cine muscle
M0273, and he ELISA was comple ed by using monoclonal
an imyosin (skele al, as ) clone My-32, monoclonal an imyosin
(skele al, slow) clone NOQ7.5.4D, an imyosin polyclonal an ibody
M7523, and mouse an i-IGG linked o pe oxidase A6154 (all Sigma
Ald ich, Poole, UK). In a-assay coe icien s o a ia ion we e below
8% o FM and below 7.5% o SM. The linea i y o he FM assay
esul s was 80%, and i was 90% o he SM assay.
S a is ical Analyses
The no mali y o each a iable was es ed using he Shapi o-Wilk
es . As SM and CK we e asymme ically dis ibu ed, hese a iables
we e log- ans o med be o e analysis. One-way epea ed-measu es
ANOVA was used o iden i y he e ec o ime on CK ac i i y and
SM and FM se um le els. When any signi ican main e ec s we e
ound, pai wise - es compa isons wi h a Bon e oni co ec ion we e
used. The ime cou se o changes in cTnI se um concen a ion was
e alua ed wi h he use o F iedman and Wilcoxon nonpa ame ic
es s. E ec sizes (ES) (Cohen d) we e calcula ed o de e mine he
p ac ical di e ence be ween baseline alues and se um peaks o
enzymes and p o eins. ES alues o abo e 0.8, 0.8 o 0.5, 0.5 o 0.2,
and lowe han 0.2 we e conside ed la ge, mode a e, small, and
i ial, espec i ely. Pea son co ela ion coe icien was employed o
e alua e he associa ion be ween he a iables o in e es . Da a a e
p esen ed as mean ± s anda d e o o he mean unless o he wise
s a ed. The le el o signi icance was se a P < .01. All s a is ical
analyses we e conduc ed using SPSS e sion 20.0 s a is ical-analysis
so wa e (SPSS S a is ics, IBM Co p, A monk, NY).
Resul s
The week be o e he compe i ion, pa icipan s epo ed he use o
simila aining s a egies, based on a dec ease in aining olume
(km/wk) and an inc ease in in ensi y ( unning a e age eloci y). A
he compe i ion, only 1 pa icipan inished he MUM (~85 km). The
es o he pa icipan s le he compe i ion a di e en poin s along
he ail due o bad wea he condi ions: empe a u e, ange 0.9°C o
13.1°C; ain, ange 0 o 6.1 mm/h; humidi y, ange 90% o 97%; and
wind speed (eas -sou heas ), ange 1.1 o 5 m/s. The o al dis ance
(km) co e ed and o icial ime (h:min:s) o each pa icipan who
decided o ca y on wi h he s udy p o ocol we e de e mined by he
las o icial con ol poin passed jus be o e lea ing he MUM.
Indi idual a e age speed (km/h) was calcula ed acco ding o hese
esul s (Table 1). Wi h espec o biochemical ma ke s, he a e age
se um CK ac i i y a baseline was in he clinically no mal ange (35–
175 U/L) and ose signi ican ly om 132 ± 22 U/L (p e) o a peak o
2052 ± 860 U/L (ES = 3.02) less han 1 hou a e inishing he
MUM. A e age CK se um ac i i y emained signi ican ly ele a ed 24
hou s (1345 ± 651 U/L) (ES = 2.59) a e he beginning o he
compe i ion, bu a clea dec easing end was obse ed (Figu e 2).
The only woman who pa icipa ed in he s udy un il he end and also
comple ed he whole long-dis ance ail (pa icipan numbe 7) had
he highes alues o CK in se um in all samples (Table 1). Almos all
pa icipan s we e in he clinically no mal ange o cTnI (<0.017–
0.050 ng/mL), o sligh ly abo e, in all analyzed samples (Table 1).
No signi ican inc ease was seen in a e age cTnI se um
concen a ions 1 hou a e he MUM ( om 0.018 ± 0.001 ng/mL o
Ca mona e al Moun ain Ul ama a hon and Sa come e Dis up ion
Page 3 o 7
0.067 ± 0.028 ng/mL), and alues e u ned o baseline 1 day a e he
ail (Figu e 2). Howe e , he a e age alues o cTnI we e highly
biased, because pa icipan numbe 7 showed an almos 10- old
inc ease in cTnI se um concen a ion 1 hou a e he compe i ion,
which emained a ound 4- old ele a ed 24 and 48 hou s a e he s a
o he MUM (Table 1). A nonsigni ican sligh inc ease in a e age
FM se um concen a ion was obse ed 1 hou a e he compe i ion
( om 1508 ± 222 g/L o 1731 ± 204 g/L), which emained s able
un il 24 hou s a e he beginning o he compe i ion (1744 ± 250
g/L) and e u ned o baseline alues a 48 hou s (1520 ± 318 g/L)
(Figu e 1). A e age FM se um alues o all ime poin s analyzed we e
in he p e iously es ablished no mal ange (> 1000 g/L).11 Finally,
no changes in SM we e ound un il 24 hou s a e he s a o he
MUM, when SM se um concen a ion ose signi ican ly om 1443 ±
390 g/L o 3743 ± 1110 g/L (ES = 1.34). SM se um ac i i y
emained nonsigni ican ly ele a ed 48 hou s a e he ini ia ion o he
compe i ion (2828 ± 762 g/L). A e age baseline SM se um le els
we e in he no mal ange (> 2000 g/L).11 (Figu e 2). The SM se um
peak a 24 hou s a e he s a o he MUM was also highly co ela ed
wi h he CK se um peak ound 1 hou a e he compe i ion ( = .884;
P = .004) (Figu e 3). Finally, SM was no co ela ed wi h cTnI.
<<<<<<<<<TABLE 1>>>>>>>>>>>>>
<<<<<<<<<FIGURE 2>>>>>>>>>>>>>
<<<<<<<<<FIGURE 3>>>>>>>>>>>>>
Discussion
To ou knowledge, his is he i s s udy o assess he u ili y o he
myosin iso o ms SM and FM as se um biochemical ma ke s o ibe -
speci ic muscle damage induced by a MUM in expe ienced endu ance
unne s. SM and FM we e compa ed agains CK, a widely used
bioma ke o exe cise-induced muscle damage, and cTnI, a speci ic
bioma ke o ca diac damage. The no el inding o he cu en s udy
was ha only SM se um le els we e signi ican ly aised, while FM
se um le els emained almos unal e ed a e he MUM compe i ion.
Ano he ema kable inding was ha CK and SM se um peaks we e
highly co ela ed.
In he absence o myoca dial in a c ion, muscle inju y, o
disease, la ge and ime-sus ained inc eases in blood CK ac i i y ha e
been widely accep ed as a bioma ke o muscle damage.17 As
expec ed, he MUM induced la ge inc eases in CK se um le els, up o
an almos 16- old ise 1 hou a e he compe i ion. Signi ican CK
se um inc eases in heal hy and well- ained pa icipan s ha e been
p e iously documen ed a e MUM compe i ions.5 La ge a iabili y in
se um CK concen a ions among pa icipan s is common and has been
p e iously desc ibed in expe ienced ul ama a hone s a e 24 hou s
o eadmill unning18 and a e a 166-km MUM.6 The eason o his
a iabili y s ill emains unclea , bu i has been sugges ed ha
suscep ibili y is mainly ela ed o geno ype cha ac e is ics.19 The CK
se um peak 1 hou a e he MUM and i s eco e y o e he ollowing
48 hou s we e also consis en wi h p e ious s udies.6 Howe e , CK
le els p o ide a g oss indica ion o muscle- ibe damage, because
hey canno iden i y he magni ude o damage20 o he ype o ibe s
a ec ed.7
Al hough di ec e idence o muscle damage is his ological,
o ce-gene a ing capaci y is conside ed a eliable and alid ma ke o
muscle damage.21 I has mo eo e been demons a ed ha unning a
MUM induces la ge dec eases in he knee-ex enso o ce-gene a ing
capaci y (a 35% dec ease a e a 166-km MUM), which a e ela ed o
a igue and muscle damage.6 Fu he mo e, di e en s udies ha e
ecen ly p oposed sa come e p o eins such as oponin as p oxy ibe -
ype-speci ic bioma ke s o muscle damage.7,22 Acco ding o he
obse ed ime cou se, molecula mass, and ibe compa men in
which hese p o eins a e loca ed, hei ele a ion in se um sugges s
mo e se e e damage, signi ying sa come e damage.22 As ibe - ype-
speci ic sa come e p o eins, SM and FM could allow o indi ec
diagnosis o sa come e damage and he ype o ibe a ec ed.11
Because MUM unning has been demons a ed o induce muscle
damage,6 he signi ican inc eases in SM se um concen a ion seen 24
hou s a e he s a o he MUM sugges ed selec i e slow ( ype I)
ibe damage, and due o i s ele a ed molecula weigh (493 kDa) and
i s ibe in asa come ic compa men aliza ion, inc eased se um SM
could indica e sa come e dis up ions o hose ibe s. Mo eo e , since
cTnI showed a nonsigni ican se um inc ease 1 hou a e he
compe i ion and e u ned o almos baseline alues 24 hou s a e he
beginning o he MUM, SM se um inc eases in heal hy indi iduals
can be mainly ela ed o skele al-muscle slow- ibe damage, a he
han myoca dial damage. Fu he mo e, he e was no s a is ical
ela ionship be ween SM and cTnI. Howe e , u he esea ch is
needed on cTnI and he dis ance o ul aendu ance e en s, because he
only pa icipan who comple ed he whole MUM (pa icipan numbe
7) showed he highes inc eases in cTnI in e e y sample analyzed
a e he compe i ion.
No changes in FM se um concen a ion we e seen a e he
MUM, which indica es ha he as ibe s su e ed no damage o , a
leas , less damage han he slow ibe s. Ce ainly, i has been p o ed
by his ology ha as ibe s a e mos suscep ible o eccen ic
con ac ions,23 and downhill unning, which is a mainly eccen ic
ac i i y, induces muscle damage.4 Howe e , since endu ance unne s
ha e g ea e le els o slow ( ype I) ibe s,14,15 i is easonable o
assume ha slow ( ype I) ibe s a e p edominan ly ec ui ed and
damaged du ing a MUM. Howe e , he hypo hesis ha a MUM also
induces as ( ype II) - ibe damage canno be comple ely uled ou
because CK is non– ibe - ype-speci ic. Mo eo e , baseline FM se um
le els we e o e he p e iously desc ibed no mal ange,11 a
phenomenon ha can be a ibu ed o he ype o aining (highe
in ensi y and less olume) pe o med by he unne s he week be o e
he ace, bu his is only specula ion. Fu u e s udies in his a ea should
ca e ully analyze he aining s a egies used he week be o e he
compe i ion.
Due o i s mainly sa coplasmic loca ion, CK is hough o
indica e inc eased memb ane pe meabili y a e memb ane
dis up ions a ea ly ime poin s24 and he pe oxida ion o memb ane
lipids caused by an inc ease in eac i e oxygen species and he
ac i a ion o ion (Na+ and Ca2+) channels o se e al days a e
exe cise.25 The peak alue o CK se um was ound 1 hou a e he
MUM. This could be explained by he long du a ion o he
compe i ion, causing a signi ican deg ee o memb ane damage
du ing he un.26 I has been demons a ed ha he esealing o
a i icially p oduced memb ane dis up ions occu s in less han a
minu e,27 bu CK e lux may occu du ing he un due o a con inuous
p ocess o memb ane dis up ion ollowed by apid esealing. The CK
se um peak pos -MUM and i s eco e y kine ics o e he ollowing 2
days we e consis en wi h p e ious s udies.6 Ne e heless, he a e age
1-hou pos -MUM CK se um peak was lowe han ha ound a e
longe dis ance aces.28 In his espec , and acco ding o Waskiewicz
e al,28 since he olume o exe cise inc eases he me abolic demands
o in acellula Ca2+,26 and i is associa ed wi h muscle-damage
indices, i seems easonable o assume ha augmen ed memb ane
pe meabili y is ela ed o he dis ance co e ed, as can be seen in Table
1. While pa icipan s 2 and 3, who comple ed 26 km, showed mild
inc eases in se um CK ac i i y pos -MUM, pa icipan 7, he only one
who comple ed he whole MUM (~85 km), p esen ed he g ea es
inc eases in CK se um ac i i y a e he compe i ion. In con as ,
Ca mona e al Moun ain Ul ama a hon and Sa come e Dis up ion
Page 4 o 7
exe cise in ensi y, exp essed as a e age speed (km/h) a which he
pa icipan s an he MUM, showed no end, since pa icipan s le he
compe i ion a di e en poin s along he ou e (see Table 1). Fu he
esea ch wi h a la ge sample is he e o e needed in his a ea o cla i y
he ela ionship be ween biochemical ma ke s o muscle damage and
bo h dis ance (km) and a e age speed (km/h).
Myosin iso o ms ha e a di e en se um ime cou se han CK.11
Sa come e-p o ein u no e is longe han ha o sa coplasm
p o eins,29 so he SM se um peak 1 day a e he MUM can be
explained by he inc eased ac i i y o calpain 2 days a e exe cise.30
Calpain is a Ca+2-dependen p o ease. The long du a ion o he MUM
may ha e led o la ge inc eases in in acellula Ca+2 du ing he un,
which would accele a e calpain deg ada ion and lead o he signi ican
inc eases in SM se um 1 day a e he MUM. Calpain emo es
myosin om he ilamen ous s uc u e o he sa come e.31 A his
ime, inc eased memb ane pe meabili y due o he ac i a ion o
s e ch-ac i a ed ion channels25 could lead o a elease o la ge
p o eins in o he in e s i ium. Once in he in e s i ial space, p o eins
a e mainly anspo ed ia he lympha ic sys em in o he bloods eam,
because he capilla y memb anes in skele al muscle a e almos
impe meable o p o eins.7–32 The muscle- ibe compa men in which
SM is loca ed and i s complex deg ada ion p ocess could explain he
delayed inc eases in se um o SM.
Finally, CK and SM se um peaks occu ed wi h 1-day
di e ence bu we e s ongly co ela ed. Memb ane damage could
accompany sa come e dis up ions, due o he igh connec ion
be ween myo ib ils, cy oskele on, and memb anes.33 The e o e, i
seems ha memb ane damage could be ela ed o subsequen ibe
sa come e dis up ion o slow ibe s.
P ac ical Implica ions
The cu en s udy shows ha SM could p o ide indi ec in o ma ion
abou ibe - ype-speci ic sa come e damage 1 day a e a MUM, and
since he se um peak o myosin iso o ms is no eached un il 1 day
a e a MUM, hey could be used in diagnoses ha a e no made
immedia ely a e he compe i ion. Al hough ibe speci ici y canno
be de e mined by CK, i s se um ac i i y 1 hou a e a MUM seems o
be ela ed o he subsequen SM se um esponse. MUM aine s and
unne s should be awa e ha he o al dis ance co e ed could be
ela ed o muscle damage, and sha p SM se um inc eases sugges ha
a longe eco e y may be needed. Fu he esea ch ega ding MUM
dis ance co e ed, aining and pe o mance a iables, and damage
deg ee in lic ed o skele al-muscle slow ( ype I) ibe s is needed.
Conclusions
In summa y, since he e is e idence o muscle damage a e
p olonged moun ain unning, an inc ease in SM se um concen a ion
a e a MUM could be indi ec e idence o selec i e slow ( ype I) -
ibe -speci ic sa come e dis up ions.
Acknowledgmen s
This s udy was suppo ed by he Ins i u Nacional d’Educació Física de
Ca alunya (INEFC), he Gene ali a he Ca alunya (2014SGR/1629). Ge a d
Ca mona is he ecipien o a p edoc o al ellowship om he Agency o
Managemen o Resea ch and Uni e si y G an s (AGAUR) (Gene ali a de
Ca alunya).
The au ho s would e y much like o hank he 7 compe i o s who ook
pa in he whole esea ch p ocess.
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Figu e 1 — Al i ude p o ile o he en i e moun ain ul ama a hon and he dis ance scale.

Ca mona e al Moun ain Ul ama a hon and Sa come e Dis up ion
Page 6 o 7
Figu e 2 — Changes in (a) se um concen a ion o c ea ine kinase (CK)
(n = 8), (b) slow myosin (SM) (n = 8), and (c) skele al-muscle as
myosin (FM) (n = 7) 1 day be o e he compe i ion (p e), less han 1 hou
a e inishing he compe i ion (pos ), and 1 and 2 days a e he moun ain
ul ama a hon. Da a a e no malized (mean ± s anda d e o o he mean)
o p e-moun ain-ul ama a hon alues (100%). **Signi ican ly di e en
om p eexe cise alue a P < .01.
Figu e 3 — Associa ion be ween se um c ea ine kinase (CK) (na u al
log) peak ac i i y 1 hou a e inishing he long-dis ance ail compe i ion
(pos ) and slow myosin (SM) (na u al log) peak concen a ion 24 hou s
a e he s a o he moun ain ul ama a hon (n = 8). , Pea son
co ela ion coe icien .
Ca mona e al Moun ain Ul ama a hon and Sa come e Dis up ion
Page 7 o 7
Table 1 Concen a ions o Se um C ea ine Kinase, Slow Myosin, and Ca diac T oponin I 1 Day Be o e he Compe i ion (P e), Less Than 1
Hou A e Finishing he Compe i ion (Pos ), and 24 and 48 Hou s A e he Beginning o he Moun ain Ul ama a hon o Each Pa icipan
C ea ine Kinase (U/L)
Slow Myosin ( g/L)
Ca diac T oponin I (ng/mL)
Pa icipan
Gende
km
Time (h:min:s)
A speed (km/h)
P e
Pos
24 h
48 h
P e
Pos
24 h
48 h
P e
Pos
24 h
48 h
1
M
41
09:39:18
4.25
70
793
933
611
856
703
1674
1333
0.017
0.029
0.017
0.017
2
M
26
06:47:33
3.83
108
363
356
214
811
920
1741
1832
0.017
0.022
0.017
0.017
3
M
26
06:47:16
3.83
156
350
196
126
628
505
1233
963
0.017
0.040
0.017
0,017
4
M
41
09:10:12
4.47
74
2691
1118
468
3097
3159
9812
5543
0.018
0.034
0.017
0.018
5
M
53
10:26:24
5.08
173
856
553
259
842
1225
1928
1162
0.017
0.029
0.017
0.017
6
M
53
12:09:28
4.36
179
2542
1156
531
3338
3205
4553
3979
0.017
0.079
0.017
0.017
7
F
85
11:48:48
7.26
233
7643
5819
2722
988
1404
6999
6361
0.027
0.260
0.115
0.101
8
M
53
12:09:32
4.36
59
1175
626
288
984
1400
2007
1454
0.017
0.043
0.017
0.017
Abb e ia ions: M, male; F, emale; km, kilome e s o moun ain ul ama a hon comple ed; A , a e age.