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In this chapter and in the web study guide
Energy Substrates 54
Carbohydrate 54 AU DIO FOR FIGURE 2.1 describes t h e path of the t h ree energy substrates in t he
Fat 55 b o dy.
Prote in 56
\ Controlling the Rate of Energy Production 56
AUDIO FOR FIGURE 2.2 explains t he role of enzymes.
1 ANIMATION FOR FIGURE 2.3 bre aks down a typical metabol ic pathw ay.
VIDEO 2.1 p resents Mark Hargreaves discussing the sensitivity of ATP prod u ction
to muscle activity and control of ATP production during exercise.

Storing Energy: High-Energy Phosphates 58

AUDIO FOR FIGURE 2.4 describes the structure and breakdown o f ATP.
The Basic Energy Systems 58
ATP-PCr System 59 AN IMATION FOR FIGURE 2.5 shows the reactions in the ATP-PCr syste m .
Glycolytic System 59 ACTIVITY 2.1 ATP-PCr System reviews the stages in the ATP-PCr system.
Oxidative System 61 AUDIO FOR FIGURE 2 .6 describe s th e changing leve ls of ATP and PCr du ring
maximal sprinting .
Lactic Acid as a Source of Energy
AUDIO FOR FIGURE 2.7 describes the process o f glyco lysis.
Durin g Exercise 67
ACTIVITY 2.2 Glycolytic System conside rs the main steps in t h e glycolytic system .
Summary of Substrate M etabolism 67
AUDIO FOR FIGURE 2.8 describes th e o vervi ew o f the oxi d atio n of ca rbohydrate.
AUDIO FOR FIGURE 2.9 d escribes th e Krebs cycle .
ANIMATION FOR FIGURE 2.10 shows the li nk betwee n t he Krebs cycl e and the
e lectron transpo rt cha in.
AUDIO FOR FIGURE 2.11 d e scribes th e electron transport chain.
ANIMATION FOR FIGURE 2.12 b re aks down the total e n e rgy productio n from the
oxidation of a molecule of g lucose.
ACTIVITY 2.3 Glucose O x idation d e scribes how the complete oxidation of glucose
produce s ATP, heat, wate r, and carbo n dioxide .
AUDIO FOR FIGURE 2.13 describes the com mon m etab o lic pat hways for
carbohyd rate , fat, and prote in.

Interaction of the Energy Systems 69

AUDIO FOR FIGURE 2. 14 d escribes th e re la tive e ne rgy prod u c ti o n ra te and capac ity
o f the e ne rgy system s.
ACTIVITY 2.4 ATP Prod uctio n e x p lo re s three m etho d s o f AT P produ ction , d e p e nd ing
on th e type , lengt h, an d inte nsity o f an activit y and t h e avai lability of oxygen.

The Crossover Concept 70

AUDIO FOR FIGURE 2.15 expl ains th e crossover concept.

The Oxidative Capacity of Muscle 70

nd
Enzym e Activity 71 A UDIO FOR FIGURE 2 .16 d escribes a relationsh ip between en zym e act ivity a
Fiber Type Compositi on oxid ati ve ca pa city.
and Endura nce Train in g 71
Oxyge n N eed s 72 53
In Closing 73
 ,, H itting t h e w al l" is a common expre s sion heard among marathon runn e rs . and mort· th,,n nalf o f a ll
n one lite m arathon runners report ha ving hit the wall during a marathon rega rdless of hm·, hard they
Fuel for Exe rc is e: Bioenerget ics and Musc le Me t abo li sm 55

t ra ined. T his phenomenon u sually h a ppens around mile 20 to 22. Th e runn e r's pc1c.l· .,,lov.rs consid e r-
Food intake
ably and the legs feel li ke lead. T inglin g and n u m bness are often felt in the legs a nd ar ms, and thinking oft e n
become s f uzzy and confu sed . Hitti n g th e wa ll is b asically runn ing out of avai labl e e n e rgy
T he ru nner's primary f uel sources during pro lo n ged exercise are carbohydra t es a nd fc1 s Fc1ts rrn9ht seem
t o be the log ica l first choice of fuel for e n du ra n ce events-they are ideally des igne d t o b · 0n0r CJY d nse. and
stores a re v irtu a lly unl imited. Unfortu nate ly, fat m etabolism requ ires a constant supply o f oxy qC>n, .ind delive ry Fats Carbohydrates
(triglycerides)
o f e n e rg y is s lower than that prov ided by carbo h ydrate metabolism.
Most ru nners are able t o store 2,000 to 2,200 c al o ries of g lycogen in thei r liver and rn u sck·s . 1.·.d11c. h ,s enough
to provide energ y for abo ut 20 mi (32 km) o f m oderate-pace running. Since the b o dy 1s m uch lc,c;,c;, vff1c. ,e nt at
converting fat to energy, running pace slow s a n d th e runner suffers from fatigue . Furth r m o re , c.i r hohydra t e s Glucose Amino acids
Free fatty acids + Glycerol
are t h e sole f u e l sou rce for brain function . Physiology, not coincidence, dictates why s o m a n y m zi r a th on r u nne rs
hit the w al l a t arou nd the 20 mi mark.

F FA . . Lipolys,s Z., Fal r>rotein breakdow0 Body

C h e mical r eact io n s in pla n ts (photosynthesis) c o11\·c: r1
lig ht fro m th e s un i n to stor e d c h e mi cal e n c: r gy. In
bro kl' II . S111> ... 11 ;1t<·.., ;111· 1 <l lll ]H •..,1·d 11111 11.1 1 ,h " ' , .1 1IH111.
h ~·clro g t·11. ,,x,gl'lr . ;111cl ( i 11 rl w c .1,1 · , ,I 111,,11·i 11 ) 11it1n-
pool
"'-c;; ,. stores ,,,, protein

turn , huma n s o bta in e n e rgy b y eatin g e ith c: r p la nts o r gc:11 . T h(' fll()k ( 1il ;11 ' ' " '"' " 1l 1.1t l 111 ld ill(',( ' 1·l1 ·11H"lllS lipogenesis Protein synthesis
a n im a ls th a t feed o n p la nLs. N utrie nL<; fro m illgc:s tc:cl t()gc tl1 c 1 a n · 1t· L1 ti \'l ·h \\'(•.ii, .11 11l 1l11· 1l'l, 11, · 1111,, ick lit t h:
food s a r e p rovide d in t h e fo rm o f car b o h ydra tes, fa Ls, c 1H· 1J,~· ,,·IH· 11 b1<1 k(' 11. (:., 11 ..,c·c 11w11 1h . 11111<1 1, 11111 11,t·cl
a nd protein s. Th ese three b as ic fue ls, o r e n e rgy sub- d ir cct h · fo r n· ll11 L11 ••1w 1.11 i,,11 ,. l{.11IH ·1. 11 11· 1· 11 1·1 g, i11
strates, can ultima te ly be b roken down to r e lc:ase th e: f'ood \ .111 olcc 11 L1r IH111cl , i, c l lt' 11 1i1 .il h 11·l1·.1,1·cl \\i tlii 11
s to re d e n ergy. Each ce ll con tains c h e mical p a th \\'ays c11 1r c (' 11:-. ;11 HI t I I(' 11 .., tc , 11·cl i 11 1I w I "1 11 1 11 I I I 1<' I I i g li -1· 11- -......M
.....,e..,
ta""'b""o""li"s""
' m....-1!1...,..- • • • • •
that con vert th ese s ubs t r ates to e n e rgy th a t can th e n h e: c: q.,~· C< Jl llj)OII IIC I i11 t1 c,cl1111·d i11 ( 11.11 111 ·1 I . . 1d1· 11(1, i1l t·
FI GUR E 2 .1 Cel lu lar metabolism resu lts from the brea kdown of three fuel substrates provided by t he diet. Once each is
u sed b y th a t cell an d oth e r cells of th e b o d y, a p rocess tr ip h rn, p li;it (' (.-\T l' ) . " ·l1icl 1 i, cli -..1 11 -..-..1·cl i 11 ,kt. 1i l L1ttT converted to its usable form, it eithe r circulates in the b lood as an available "poo l" to be used for metabolism or is stored
call e d b ioenergetics. Al l o f th e c h e mical reactio n s in ill t hi s c h ;1pt cr. in the body.
th e b ody a r e coll ectively calle d metabo lism. r\ t res t, ti re <·11< · rg~· tli :,t 111<' l ,c ,ch 11<·1 ·, I, i, <kr in ·d
B ecau se a ll e n ergy eventua lly d egra d es to h c:a t, th e: a lmos t c q 11 a ll~· f'n ,111 tl l<' 1>11 ·; 1k d"" 11 l l l 1 .1 il 1, ,l 1,d r;1t es
a m o un t of e n e r gy r e leased in a bio logica l reac tion a n d Ei ts . l' r o tt·i11s ... <· 1T 1· i1 1q ><111 :111 t I 11 1ll Ii, ,11, .1-.. l' ll / \ 1111·s c;1rlio li \'( lr;11('. ar ld c;111 bl' clcplct nl d uring prolo_n gccl . TABLE 2 .1 Body Sto res of Fuels and
can b e m e a s ure d fro m th e a m o u n t of h eat p rodu cc:d . th at a id c ll<' 111 ic ;i l n·;1C'l i<1 11 , ;i 1ll l ;1-.. ... tn11 111r :il ln 1ildi11g i11t e 11 sl' i·x e r c isl'. T h us. \\T r e l\' l1t·a,·ih· rnt d 1c ta 1T Associated Energy Availability
E n ergy in b io logical syste m s is meas ured in calo rics. 13y b lo c ks 1> 111 11 s 11 ;tll y jff<i\·icl <· li 11 1<- 1· 1l<'t g\ 1., 1 111 <· L1hn- srn11 -ct·s o f's t;irc h <'s a n d si rg;i rs to ·co11 ti11 u ;tl h · rt' p knis h
Location g kcal
definitio n , 1 calorie (cal) e qu a ls th e a m o unt o f h eat li s m . D1 1ri 11 g i11t<· 11s<·. s l 1c,rt-cl1 11 ;1ti 1>1 1 11 111 , c1 1L1 1· ('ff() n . c>11 r c;1r h o ll\·d r;i tt· n ·st-r\'l.'S. \\'it h o u t aclcquatl' carbol\\·-
e n e r gy n eed ed to ra ise 1 g o f wa te r 1 °C, fro m 14 .?J °C more: c arbo lt \'C l r;it(' is 11s('cl . \\'itli I<--.., r<' li;111 c (' l l l l Li t to d ra1c i11 L1 k~· . llllrscks c all bl' ckpri H·cl or th e ir p r i111;tr~· Carbohydrate
to 15 .5 °C. I n huma n s, e n ergy is expressed in kiloca1o- g<.: n c: ra tc: ,\T l.' . I.0 11g l'r, le,, i 11t 1·11-; 1· <·:--.: <· 1 c i,l' 11 , <·s hn tlt e 11t·q2;y srn rrc('. Ft rrthc n no rc. car h o ln·clratcs arc th e 011h' Liver glycogen 1 10 451
ries (kcal) , wh e r e 1 kcal is th e e qu ivale nt of 1,000 cal. ca rho h yclra t l' a11d L, t f() r s 11s t:1 i I l('cl (' 1l<TgY 1>r 11< 11 rl'I i<i11. (' IHTg'\' so11 rn· llst'd h,· hrai11 tiss11c : therefore. sc~·(TC Muscle glycogen 500 2,050
Som etim es th e te rm Calorie (with a capi ta l C) is used c;1rho h \'( lra tt· clc plc ti<.>ll 1'l'St1 lts ill ll cgatiH ' cog111 11 ,·e
G lucose in b ody fluids 15 62
syn o n ym o u s ly wit h k il ocalo r ie, but kilocalorie is mo re:
Carbohydrate ('fl('Cl S . -. - .- Fat .. - - -
tec hnicall y and scie ntifica ll y correct. Thus, wh e n one ·- - -
T h e: a rn o 11111 <>f' ca,·bohy dratc: 11 -;('cl d11 1·i11 g ('Xt-rci se Subcutaneous and visceral 7,800 73,320
read s th a t so m eon e eats o r ex p e nds 3,000 Cal per clay,
it really m ean s th e p e rson is in ges tin g o r expe ndin g
is r e l.-i tc d 10 l>ot lt t it<· c:1 r l ><>l1 >·dr;1t<· ;1\·:1 il; d ii l i1 , · ;111 d Fat
·. . . . . - I • e ncroy use d durin ,r Intram uscu lar 161 1,513
tl1e 111 11sc k s' wt' ll-d 1·\·1·lc, 1H·d S\'S t<·1 11 I, ,r c;irl>o lt \'C li·;11t• I· ,1l s p r o\·Hk ,l b r,rc por11o n o 1 l lt t->. •
3,000 kcal p e r d ay. ,..., · B ch · stor es o f !)Otc n-
t->
Tota l 74,833
m c: 1.abolis 111. A ll c 1r l>o lt ycl r;1t<·s ;1n· 1rlt i111 ;11 (' h · c 1,11\'l-rtcd 7 ,961
Som e free e n e r gy in t h e cells is used rur growt h p ro I o 11 gecl . less i1 1t c 11sc e x e rc ise. 0 • · .'
to t.h e simple s ix-carl>o 11 s 11g;11 , g lucos e ( fig1 1r l' '.Z. l ) , <I tia l t' IHTg,· ill th e ro n n o r Et • ;11 -c s11hs ta11 11alh· brger Note. These estimates are based on a body weig ht of 65 kg (143
and repa ir t h ro u g h o u t th e b ody. S uc h p rocc:sses build · I .. t , in te r ms ol h uth lb) with 12% body fat.
monos.-icc h a r iclc (011 t'-1111it s1 1g :1r ) t li ;1t is t 1·;1 11 s p o1·t ed t I1:l ll l Il l ' l'l' Sl'l'\'(' S o f carh o 11,·t I ,I l · .
muscle ma:ss duri n g tra ini ng an d repair muscl e: dam age · . . .· T ·1 f1 j ~ ') I l) rond cs ;111
t h n> u g h t h e blood t o a ll l> <> <h · t iss 11t ·s . l ' 11dl' r r e s ti ng \\'t•rg h t and Cllt'I'",· ,1\·a rlab ilr t\'. • t - ·
a fter exe r c ise or inj ury. E n e r gy a lso is n eed e d fo r ac tive ·111 d ·1c;i t1·0 11 o l· thl' ,..,_ . . . r these two c11e roy
con dit io n s , ill gC"s tc d c <1rholt yclr;11<· is s t<>n ·d i11 111 11scles to tal h o ch s101t s O t-> .
S 11h s ta11 1i ,dh·
. m o r e c n cr<>Y
;-, , is d crin' d rrum hreakin° M
tra n s p ort of' man y s ubstances, s u c h as sodium , p o tas- clm\'11 ,1 g r am oJ' fa t ( q_ ..j. kc;1 l g ) than f'rum the -,,,me
•• .. · · '> u1 I ch · fat ). Fo r th e a,·er-
siu m , a nd calci u m io n s, across cell m e mbra n es to main-
and livc:r in t h e f<> n n <>L 1 111 on · C<> lll]> l<· x p1 ,h·s; 1c c ltar id l' so 111 t <.. s 11 1 a k;111 p<·rsoll ( l - 10 10 . . . . ..
( m1 rl tip lc: lin ke d s 11 g a r 111 okc 11 k s). g lyco gen . ( ; J\'c oge n - .II .I 1-c b och · Lit (,1d1p ost ;11n o 11 11 1 o r c.1 r b oh\'Clr;11c ( -LI kca l g ). :\<)llcthckss.
tai n h o m eostasis. M yofibri ls use energy to ca use s lid ing a g<' llllC r k -;1,rcd .1d 11 lt \\'II l 1110 .· .
is s to red i n t h <' cyto pl a s rn of' 1n11sc k c('l ls 1111 ti l tlt o se . .. . . ;-, . . Jro x irn,11e h · t\\·1tT ;1s th e r.1tc o l' e n c r gv r e lease J'rorn fat is tun slo,,· tu meet
of th e actin a nd m yosin fila m e n ts, r esu ltin g in m u scle t 1ss1 1< ). t h e (; 11 s tc,rcs \ \'Ot rl cl 1Jt •1PI · ..
cc: lls 11se it to f'o n11 1\TI'. ,\ d diti <> 11 ;d g lyco g (' ll s tored in . ... . . .. . . o res wo uld Ix ,110111 1 all or th e ('lle rg,· de 111 ;111ds or ill ll'I\Se 11\IISl'llLlr acti\'it\ .
actio n a n d force ge n e ratio n , as d escr ib e d in c h a pte r I . l.11° t , \\hc r cas th <'ctr h ()l\\ d 1,1ltS l .
t h e: li ve r is con v<'rtcd h;1 c k to g l11 c o -;<· :is 11<·<·dl' d ;111 d ,..., · • .. .. 'hblc for c cl l11Lir O t h e r l\j>CS nr Llls li lllll d in the h och "l'l'\'l' IH)ll-l'll-
tlH' s,irn t· . But Lil is less read 1h •1' ' 11 ' _. .. . .
th e n t r;-1 n s p<>rt('d l>y rite l,)1,c,d t<, :1c t i\'l· t i-;-; 11l'S . \\' lt c r c . . . ..st h e rc cl u ctc1 110111 tis l' r g,·-prud uc illg r11 11c Li <i11 s. l' h<>sph() l i pids .i n · ., k,·,
11H· t;1holrs 1n lll'c:i ust· 11 1n11sl 1II .
Energy Substrates it is 11w 1a l>o li /.c d . . .
c 1,111p I1·, forlll, tng lvcencle . l () 1 ·
. ·ts h,is rc c o111po llt'l lls.
- -\
st n 1ct 11r.tl n 1111p<11H·n1 ()!' ;d i cell 111t·11 1hrancs a1 1d lt >J'lll
M 11sclc ,111 d li , ·c·r g h ·c o g t' 11 -; 101·<·-; ;in· li 111 itl' cl. l'S j)e- . • , . ~ ... ) () 11h· I· 1-.- s ;1n· user1 p r ut cctiH· shc;1t h s ,1rcH1 n d S<lllH' b rµ;t· 111-rH·:s. Slt'rt licb
£ n erg-:.· is released wh en c h e mical bonds -th t' ho 11cl s g l\'( T rol ;11 1d free fatty ac1cls (Fh ~s · ·
th ctt h o ld ekments toge th er to form 111o lc:culcs-a rc c ia lly if Il l<' di('t ('()IJl d ill 'i ;111 i11 -.. 111'1 ic i1· 111 ;11111llll ll or :in· f'1 l1111d i11 ct·II 111t·111hr;111l'" ;111d ,dsu l111H·1i<l ll .1~
I<• frn111. \ T I' ( l i g 11r\' '.! . I ).

54
56 Physiology of Sport a nd Exercise Fue l for Exe rcise: Bioene rgetics and Mu scle Metabolism 57

hormones o r as build i ng b l ocks of h o rm o n es, su ch as c hclllic d t <11 11 p1>1111d -... C.IH· 1111, . ii 1, ·.1111,111 , ' ", 111 1111h
estrogen and testosterone . \,·hen !11t· 1c-:tt 1i11 g 1110I,·t 111<- -.. Ii. I\< " ,1 1fli, 1<"111 111111.tl ATe ~ §ate
c n c r i-,1: 1o -.. 1: 11 1 1It l' 1•·.1< 111 111 ., , , I 1.1111 " I 1'".,, 11,111,.
l-:11/\llll"'> d<1 1111( t:1 11,t· ., < l1c-111 i, .ti I t".11 " " " l t t I l l l l l l
Protein / Enzyme
a nd do 11"1 clt-1t·1111i11t · ill<" .11111,111 11 ,,t 11,.il,lt- c1H· 1g,
Prote i n can b e u sed as a min o r en e r gy source u n ck:r
some c i rcum stan ces, but it must first b e con venccl i nto
glucose (figur e 2. 1). In th e case o f sever e encrh')' d c plc-
1ha1 is p1od 1H l'd l l\ ilw -... · 1t·.tt 11,11 i-- . l{. t1 I H·1. iii, ·, , p ,Tcl
up n·ac 1io11, !,, }o\\t' I i11 g il l<" a c ti,·;11 i n11 t · 11t · 1·t.,': 11 1.11 i , B : ,----- Enzyme 1

I
(rate limiting) + Heat
n.: q11in·cl I<> lwg i 11 1l1t· 1t·.tt 1i,111 1lig1 11, · :.! .:.!1 I
tion or starvation, protei n may even be used to gc n c r atc I
.\lll l<lllg li !Il l' l"ll/\ I1 1( " I1.llllt "'- .11, · •11111, · ( 1J ll1lll t ""\.. I
FFAs for energy. The process b y which protei n or fat is 1 By-product 1
lll O:-.l l'lld ,,·i1li i11t· -.. , ilfi , ,, ,, . f-< 11 ( "\., II II J> lt- . .Il l 1111p1111- I
con verted into g l ucose is cal l ed gluconeogencsis . T h c a 111 <: 111,·11H· 1h ;11 1>11·. 11-.-.. c).,"11 .\ 1 1' .11111 1<·lt-.1 , <·, , 1111,·d
I
I
process of converti ng protein i nto fau:y acids is termccl l" I H'l"h':. i -. ;1clt-11"-..i 1ll" 11 i1 , l 111-, pl 1.11.1" ·· lwll<"l l-. 1111\\ ll ,h
I
1 Enzyme 2
lipogenesis. Protei n can suppl y up to I 0 % o r th c c n cq.,r y .-\Tl';1-.v.
I
I + Heat
n eeded to sustain prolonged exer cise. O nly th e most B io chc 111 ic ;ti 1';11}1\, :l\ -.. 11 1.11 1t·, 1il1 111 ilw pi 11tl1H 1i1111 Negative
b asic u nits o f pro t ei n-the am i n o acids-can b c u sc cl feedback
or ;i procl11e1 111,111 ;1 , 11li-.. 11.11,· .tl11111, 1 ·" " ·"' 111\t l hC
for en er gy. A gram of pro tei n yiel d s about 4. I k cal. m11 l 1ipk -..1 ,·p-.. F:,c 11 i 11 rli , id1 1. tl -.. 1, ·p ,, 1, 1,i, .tlh t.11 - By-product 2
a l ~·1c cl b y ;1 -. pvc iii< 1· 111, 11w . I l w , 1"1111 <· . 111< 11 ·.1,i11 g
Controlling the Rate th <: ;1111011111 of t· 111, 111<· 1>1•·-...· 11 1 11 1 I ii< · .1 , 11\t l \ 1,I 1h.1t
Enzyme 3
c n z,·m c ( f<,rv :-.:;1111p l<· . I>\, l1. 111 g i 11g 1!1t· I, ·111 IH ·1. 11111,· ur
of Energy Production pl I ) rc.-.1d1.-. i 11 ;111 i 11, I ,·;1-...·d 1.11, · .,J I ll 11<1111 I 1111 111.1lill)l
+ Heat

To b e u sefu l , free en er gy must be re leased from c h c m - thro 11g lt 1)1 ;11 111 <·1;11>< ,Ii, I 1: 1111" ·" . . \< I, 111 i , ,11. tl h. 111.11n·
<:111.,·111t·.-. n·c p1 in· tl i1 1t· r 1111 ,I, ·, ,ti ,·, , .tl l , ·d , 11l.1c 11 11·._
i cal compo unds a t a controlled rate. Th is r at e is cl ctc r-
10 f"t 111 e1io11. -;o n , L t< 1c,r ;l\ ;1i Ltl 1ili1, 111.1\ .ti .... , .tlf,·c t
- - - - - - - - - - ~ By-product 3
mine d pri m ar ily b y two th i ngs, th e avai labi l ity or th e.:
primary substrate and en zyme activi ty. T h e avai labi lit)"
o f large amounts ofa substrate i n creases th e acti\'i ty o r
c.:11z,·111c h 111e1 i 1111 ;111cl 11 1<"1 <"f.,1 , · il w 1.11, · 111 1111·1. tl 1tll i c
rcac ti o 11 s. 0 FIGURE 2 .3 A typical metabolic pathway showing the important ro le of enzymes in controlling the rate of the reaction.
An input of energy in the form of stored adenosine triphosphate (ATP) is needed to begin the series of reactions (activation
that particul ar pathway. An abundan ce o f onc panic ular .-\ s i l l 11s1r ;11ccl i 11 fi g 11 1<· '..!. :'.. 111<·1.tf1., li 1 11. 1111,, ;I\, 1,-p i- energy), but less initial energy is needed if one or m o re enzymes are involved in th is activation step. As fue ls are subsequently
fuel (e.g. , carbohyd r ate) can cause cells to rcl )' more call ~- ha,·c 1111<· ,· 111,·11 1<· 111 :11 i-.. ,ii 1i: 111 i, ,il.11 i11 q 111 r 1:1 11 l"t' degraded into by-products along the metabolic pathway, ATP is formed. Utilization of the stored ATP resu lts in the release
o n that source th an on al t ern a ti ves. T his i n llu en cc of i n co 111ro lli11 g 111(" n·:w l i<,11 ·, 1,,·, ·1; ti ) 1.11<·. I Iii, •· I 11,·111t.·. of usable energy, heat, and the release of adenosine diphosphate (ADP) and inorganic phosphate (P.) .
substrate availab ility o n th e r ate o f m etab o lism is tc n n c d 11s11;_tll y loc 11l·cl i 11 ;1111·;1rh--;1 q , i11 1lw p :1111\\, t\ . i-, J.;. 11 ,i\,·11
the mass action effect. as l h l' r a te- limiti n g e nzy m e . Tl w ;11 1i,·i 1, <,I ;1 r.11• ·-li111-
Speci fi c protei n mol ec u l es calle d enzymes also i ti ng CllZ)"ll ll" is clc l <Tllli 11<·d I,,. Ill (" :,c, l ll ll llL tli t> ll () r In Review
co ntro l th e rate of free-e n er gy r elease. Many of th ese s11 bsta 11CTS E1r1lt c-r cl1J\,·11 1I H· 11:111 1\\·;" 111: 11 ck1-rt·: 1st·
en zym es spee d up the breakdown (catabolism ) of c nzym <: ;1C1 i Yi1 , · 1lir<H 1g l1 ncgati vl' f"l't.·d h ack. 0 Energy for ce ll metabolism is derived from three substrates in foods: carb ohydrate, fat, and protein. Proteins
provide littl e of the e n e rgy used for metabol ism under norma l conditions.
0 Within cells , the usable storage form of the energy we derive from food is the high-energy compo un d
Noncatalyzed Enzyme-catalyzed adenosi ne triphosphate, or ATP.
(no enzyme present) (with creatine kinase)
0 Carbohydrate and protein each provide about 4 .1 kcal energy p er gram, compared with about 9.4 kcal / g
for fat.
~
:::J
0
Activation 0 Carbohydrate, stored as glycogen in muscle and the liver, is more quickly accessible as an ene rgy source
a., energy
0 than either protei n or fat. Glucose, d irectly from food or broken down from stored g lycogen, is the usab le
Activation
E energy form o f c arbo hydrate.
0 _ _____Phosphocreatine
- - - - - - - - S ubstrate
a., 0 Fat, sto re d as triglycerid e s in adipose t issu e , is a n ideal storage form o f e n e rgy. Free fatty acids from the
~
iii bre a kd own of tri glycerides are converted to ene rgy.
>,
Cl
.... 0 Carbohyd ra t e stores in t h e liver and skeletal m u scle are limit ed to about 2,500 to 2, 600 kca l o f e nergy, o r
a.,
w
C: t h e equ iva lent of th e energy n eeded for abou t 40 km (25 mi) of running. Fat stores can provide more than
70,000 kcal of e n ergy.
0 Enzymes control the rate of metabolism and energy production. Enzymes can speed up the o ve ral l reactio n
Product by lowering the initia l activatio n energy and by catalyzing various steps along the pathway.
Creatine Creatine
0 Enzym es can be inhibited th roug h negative feedback of subsequent pathway by-products (or o fte n ATP),
Reaction progress slo wi ng the overa ll rate of th e reaction . This usually involves a pa rticular enzyme located early in t h e path-
F IG UR E 2.2 Enzym es co ntro l the rate o f chemical reacti o n s b y lo w e ring th e activa ti on e nerg y requ ire d t o 1n1t1 a t e th e way ca lled the rate-li miti ng enzyme.
re acti o n . In this example, the e nzyme creatin e kinase b ind s to its substrate p h osphocre atine t o in crease the r a t e o f p ro-
d u ctio n of creatine.
58 Physiology of Sport and E xerci se F ue l for E xercise: Bioenergetic s a nd Mu sc le M etabolism 59

One exampl e o f a s u bs ta n ce that may acc u1111ila1c cbrd cc n 1cl iti<J 11,. 1>111 p11,,i li h 111 , ,., I 11 1-. , .ti I w1 1111 ,It- 111 :{. Tlw ox icLt tin· S\'Stc m ( oxicbt in· ph osphor\'la - inc r eased :\DP concen tr a tion c nh a n ces c r eatinc kinase
and feed back to d ec r ease e n zvme ' acti\·it\·
.
\,·oitld hl' . \T p ()I g I l'. 11 l. I \\ i I I I i II I I It' ( (' 11 J . I I I"' I ( . I II I' ( .... I l It' \ I p 1irn1 ) aniYiL\', a 11cl PC:r is catab o li zecl Lo fo rm add itional .-\TP.
t h e e ncl product o r th e pathwa)'; a n o th e r \,·o iilcl bL· 10 a d c n osine d ip h o:-, p h a tl' (. \ D P ) .111d I' , ti ~ 111 , · :.! l /,1. .-\s exerc ise p r ogresses and aclclitio nal ATP is g-e n e ratecl
Till · fir,1 t\,·o s\·s 11·111s c;111 ;1ct in th e absence o r ox\·ge n
ATP a nd its breakdown producL-;, A DP and inorga ni c To g l"ll (' J,111 · .\ "I I'. . 1 p'111, pl 1.11, · ~ •.,1q 1 1, .,d dnl tn b\'. th e ot h er t\,·o en e r oyn . S\'Sle
. m s -t he o.
rrh ·colnic
. and
;111 d ;1rv _joi11th· tt-r111 c d an aerobic m e ta b o lism . Th e
phospha te. If the goals of a m e tabo li c p a thway arc w 1ltc n ·bt i\l·h l<>\\ ·1·111·1g \ , , 11 , q,11 11 11<I. \Ill'. 11 1 .1 1• • •11<·,, oxiclatin: sys1c111s-c r ea1ine kin ase actiYity is inhibi te d .
tl ,ird s \·,11· 111 rl'Cp 1ircs ()x,·ge n ancl therefore com prises
form a chem ical produ c t a nd r elease free e n e rgy in call('d p h o:-, p h o rylati o 11 . l l1i , 1111,1 1·-,-, 11·1111 111 ·, .1 • ,11i-.. 1< l- This p rocess o f' breaking dm\"11 PCr Lo a ll m,· fo rm a-
ac nibic m etabo lis m .
the fo rm o f ATP, it m a kes sense that a n alrnncl,111Ct· or l"J;tl1lt- ;1111c, 11111 1111·111 ·1g\ . '--,11 111t · \ (I', ... '._;("11< "1 .111 ·d 1111!t·- tio n o r ATP is r apid a nd c an b e accomplish ed \,·i1hou1
e ith e r t h a t e ncl product o r ATP wou ld keel bac k I<> s low Pl' Jldt"J ll CJ( () X\g('JI ,l\,1il.tl,il1 1\ , .11 1< ! ., ,., It 111< ' 1.tl >• ,1,., , 11 , ... , Ill\' s pcc i;tl s tru c tures wi t hin th e cel l. Th e ..\.TP-PCr

further pro ducti o n a nd r e lease, res p ec Li\·e ly. c a lkd ..,11li-, 11;1 t\'- lt-\(· I 111t,,-..1il1111 \ l. 11 1, 11 1. < >1!11 ·1 \ I l 1 -p 1c>- ATP-PCr System s\·st c 1n is class iri c cl a s su b st ra te- lc\T l m e t a b ol is m.
d11 c i11g n ·;1< tic, 11, ( cl i-..c '' "" ' " l. 111 ·1 111 1lw , l1.q11 1·1 1 • 111111 A lth o u g h it can act in th e presence or oxyge n . th e
0 VIDEO 2.1 Presents Mark Harg reaves d iscuss-
ing the sensit iv ity of ATP production t o muscl e
wi1ho11t c,X\gl" tt . " !iii,· , 1ill 111l1< ·1-, "' c 11 1 ,,1 1! 1 111 <' .11 cl nf
ox~ g t·11. a p i CH 1·" c .tilt-cl o x icLtti \'l • p ho,plinr· ~·la t io n .
Till · , i111pl1·,t or till· l' lllTgY S\'Sll'lllS IS the ATP-PCr
syste m . s lto\,·11 in lig 11 rt· '.Z.:->. 111 ;1clcl i1io n 10 storin g ,1
\'('J'\' Sltl;tll ,llll Ollllt or ;1detH1si11e Lripho ~phatc (ATP )
process docs n ot requi r e ox\·g en.
Duri11g the fi rst k\,· seco n ds or in tense musc ular
activity and control of ATP produ ctio n during . \_.., , II< ) \\' I l i II t ig II I l. '.! .:\. . \ I I' I ... t' I I 111< ' I I t I ' " 11 \ I ) I ' . I II d ac ti\·it\·. s u ch a s sprinting ...\.TP is mai n ta ine d at a rel-
clin -c th·. ev ils C<l lJLli11 ;11 wthl'r hi g h -t·nl' f).,"· p hosp h a te
exercise. P, \'i;1 pl1C"-j>lt<1J\l;1tio11 .1 , 1111 ·1, .11 , · 11111 1-. , ·11 cl11\\ tl 111 111 a ti\'e h · constant le\'e l. b ut P C:r decli n es ste adih· a s i t is
11 1<1lt- n tl l· tltat s to r es l'tll'rg, · c tl kcl phospho crealine
hid 1>~-prc,cl 111 i-.. ;11 \ ; 11 i11 11, ,,, . ,,, .ti, 111 ..: .1 11 1, ·1.t!H d1< l'·'th- ( P C 1·: so 11 1t·1i 1111·s ctlkcl cn·;tli11 t· p h os ph atl' ) . T his used to replenish th e depicted .-\TP (see figu r e 2.o ) . .-\1
Storing Energy: High-Energy \,·a~·. Tl ll · -.tc, 1;1g 1· I< 11 111 , ,I 1· 111 · 1g \ . . \ I I'. , . 11 1 , , , I 1-, , · , 111< · 111 h s i111pk p;1tltw;t\' i11,·oh·('S clo11atio 11 or a P, rrom PC:r lO e xhallst io n . hmH'H' r. b oth ..\.TP an d P Cr le\'els are Im,·
rdl"a..,l"frt'l"< ll ll '-;d >l<·1· 11t ·1g \ ,, !1<"111 1, Tcl, ·cl.1 , 111 , 1llll l" a n d arc u nab le to pro Yidl' e n c rg, f'or f'unh e r mus cle
Phosphates a g ai11 l>ro kt' 11 cl<>\\·11 i,,, ., .\ I >I' .111<1 I' .
.-\1)1' to 1'C1n11 .- \TP. l' 11likl' \,·h;ll occurs \1·ith the li mi ted
co111r;1nio n and re laxa tion. T hus. th e capaciLY LO main-
f'rn· h. · ;1\·;1 il; tl1k .\Tl' i11 tht· c l'II. l'IJl• r noy . released b\· . the
The imme diate !)' ava ila ble so urce of e n ergy for a lmos t lin·akclo\,·11 o f' I' ( :r is 1101 din·nh· u sed !'o r cellular "·ork. ta in AT P k ·,-cls \,·ith t h e nH: 1-g-:, from PCr is limite d .
a ll bod il y fun ctio n s, in cluding musc le contrac tion , i:-. l11 stc;1cl . it n·gl'Jt l-r;1t l'S .-\TP 1;1 rn a i111;1in a rdatiYc h · The c ombination o r ..\.TP and PCr stor es can s u stain
ATP. An ATP m o lecul e ( fig ure 2 .4a) is composed or The Basic Energy Systems crn 1st;111t s1q >ph· 11 1Hkr rl'sti n g co11d i1 ions. the musc les· energy n eeds f'o r onh· ~ to I :1 s duri n g
a d e n osine (a molecul e o fad e nine j o ine cl Lo a moleu tl c Cell -; ca 11 , 1c,n· c, 111\ \ t·1·\ li11 1it 1·cl .,11 1, 11 11 11-.. , ,t \II' .11 1d Tit,· r l'k;1sc of' l' ll l'rg-Y f'ro1 n PC:r is ca tal ~·zecl h\' th e an all-out sprint. Be\'011d t hat tim e . muscles must reh·
of ribose) combin e d with thre e in organ ic phosph a te lllll'il ('() Jl',l,lllth· g1· 11<-i;1( <· Ill ' \\ . \ 11' tc • }ll • 1\ icl 1· l ttTcl1·d l'll/\'tlll' c re atin c kinase . \d1 ic h ,\C ts 011 PC r to sqJarate 011 oth er p1·occsscs fo1· ..\.TP fo rm atio n: g lycolnic and
(P) gro ups. Ade nin e is a n itrogen-conLaining base , a nd c 11 t-rh". l11r ;ill ct' ll1tl ;11 111t·Ltl1c, li,111. i11, l11d i 11 g 111 11,t· k I' ' f'rrn11 c r l';ll i11 l'. T hl' l' llt'l'•r\' rl'lc;ised ca n then be used oxicLitin· path\,·a\·s.
n .
r ibose is a fi ve-carbon s u gar. W h e n an AT P m o lec ule
is co mbined with wa ter ( h )'drol )'sis) and acted o n by
c o 111 rac ti o11. c :(' 11',g( "lll'r;1tt · .\' I I' 1l11 , 111g l1 .I ll\ •H it' ,i i l l l l '
a c o111hi11;11ic>1 1 c>I ) 1l1n·t· 1111·LtlJCdi< p,1tll\, .t \,:
[Cl ;1dcl ;1 I' 1nokc11k to ;11 1 :\DP 111olcculc. form ing AT P.
'
.- \ s c lll' rg-Y is n ·k;1sl·d f'rorn .-\TP b \· th e spl i11i ng of' a
. Glycolytic System
th e enzym e ATPase, th e last phos ph ate gro up splits phosp lt ;1tt· group. Cl'!ls can pn·\·c n .t ATP ck plctio n b\· T h e ..\.TP-PCr s\'stc m has a limited capac it, to generate
away, r a pidly r e leasin g a la rge amount o r rree e n e rgy hn·a k i1w cln\\"11 P( :r. 1J r o\·idi11•r encroy a n d P I to r c-l'o r m
,-, t"') \l , ATP for e n crg,·. lasting onh· a rew secon ds. The second
(approx ima te ly 7.3 kca l per m o le o r ATP uncl c r sta n- :\Tl' rrn111 :\ D I'. me th od or ATP prod u ction in\'Ol\'es th e li be r atio n or
Follo\\'i 11g th e prin c iples of' 11 cgatin· f"ccdbac k and encr t,
oy, thrmwh th e brcakdm\"11 (" h-sis .. ) of g.... lucose. T h is
t, .
r;1 1c-li1 ni1i11 g t' ll /.\'llll'S discussed c ;1rli c r. crcat in e kinase S\'Stem is call e d th e g h -col\'lic sYste m because it entai ls
Adenine . ' . . .
NH2
I
ac t i\·i ty is c11 lia11 ced whl' ll crn1cc111ra ti ons oL\DP or P, glyco lys is. th e b rcakd o\\'n or g lucose t h rn llg h a path\,·a\
i11 c rl'ase. and is i11hihitcd \\'hl'11 AT P con cent r ations 1ha1 im·oln·s a se quence ofgh nil\'Li c en zq nes. Gh·c n l\'s is
;,:N_ C _...,..C~ N
i11 crl',ISl' . \\'he n i111c11 sc exercise is initiated. the s m a ll
H- c ( II I ;11no111 11 o f' a\·;1i la hk ATP in lll llsclc cells is broke n
N- c ,
N
-::?c , H
100
High-energy bond clm,·11 for imn1t·d i,1 tl' l'ne r,r\·. n. .
\'iclditwn
.-\DP and P•. T h e
80
H H ~
,,,p. , I I ~o e...,
~ ATP
H-C H (-C - Creatine (1)
:::, 60
\I I ro ~ PCr
C-C H >
I l"H Cl
C: 40
OHOH Phosphocreatine .:;
Inorganic phosphates (PCr) en
Ribose

®
-+-~
(1)
a:
20
Adenosine

0
0 Inorganic phosphates 0 2 4 6 8 10 12 14
ATPase Time (s)
Adenosine ~ ®
~
Adenosine ~ + + FIGURE 2.6 C hanges i n type 11 (fast- twit ch) ske leta l
m uscle adenosin e triphosphate (AT P) an d phosphocreatine

~
FIGURE 2.4 (a) The structure of an adenosin e triphosphate (ATP) m o lecu le , sh o w ing t he h igh -e n e rg y p h o sph a t e b o nd s.
0 FIGURE 2.5 In the ATP-PCr system , adenosine t rip hos-
phate (AT P) can be recreated via the binding of an ino rg anic
phosphate (P) to adenosine d iphosphate (ADP) w it h the
(PCr) d u ri ng 14 s o f m axima l muscu lar effort (sp ri nting).
A lt hough ATP is being used at a very h,gh rat e , t he energy
from PCr is used to synthesize ATP, 1nit1ally pre ve nting the
(b) Wh en t h e th ird phosphate on the ATP molecu le is sep a rat ed fro m ad enosine by th e ac ti o n o f adenos 1n e triphospha t a se energy d e rived from t h e breakd o wn of p hosp hocreat1ne ATP level from decreasin g . Ho we ve r, at exh austion , bo th
(PCr). AT P and PCr levels are low.
(ATPase), energ y is re leased .
60 Physiology of Sport and Exe rcise Fuel for Exercise: Bioe nergetics and Muscle Meta bol is m 61

is a more comple x pathway than the ATP-PC:r syste m. Clu co-.t· a << 111111 h l, 11 .d ,, 1111 • 1•1 ', "' .di 'llc!,ll' < 11- g h-co g l' tl. ( ;hT <>gt·n is s~·nthcs ized fro m g lucose by a rate-limiting e nzym es. PFK catalyzes an e arly s tep in
a nd the seq uence o f steps involved in this process is c ubti n g in till' l>lc H,cl . l'.l< >< ><I ~ 111 , .,,, . , , 1111, ·, 1,.,,11 tht• pn,n·ss c tl kcl g h -cogl' n es is and is sto red in the li,·e r the p athway. th e co n \'ersio n of fructose-6-ph o spha te
presented in figure 2.7. dig c -.1i o 11 o f 1;11lic,IJ\cl1,11t · .11 1< l 1lw l ,1, ·.1~1l,,,, 11 , ,I lt\t'I <>r in 111t1sc lt- until IH'l'dcd. :-\t th at time. the g l\'cogcn Lo fructose-1.6-diphos phate. Inc reasing ADP and P ,
i-. l>rnkt'II clo,,·11 to g h1 cosc-l-ph o sphate. \\·hic h e nters con ce ntratio n s e nhan c e PFK acti\'i ty and th e refore
1hl' g hn,h s is p;1 1!i,,·a,·. a process terme d glycogcno lysis . speed 11p g lycolysis, while e le\'ate d ATP conce ntrations
D slow glyco lysis by inhibiting PFK. Additio n a lly. because
Glucose lkforl' t·ithcr g h1coSL' o r g ln .- ogen can be used to
--~--z;.,. . . . .,.-AD_P____ Gluoosrr:hate G lucose 1-phospha te - - - Glycogen
g l·1H-r;1tt· t· 1H· r)-,':'· it 111t1s1 he conn: rted to a co m po und the g lycolytic path\\'ay feeds into the Krebs cycle for
c;1 ll <"d gh1 cos l·-l ►-phosphatc. Fn·n though the goal of additional c n c rgy production whe n oxygen is present
g h·coh·sis is to n·k;1sl' .-\TP. the con nTsion ofa m o lec ule ( discussed later). products or the Kre bs cycle . especially
of g h1cost· 10 g l11 cosL·-b-phosp h a1e rcci uires th e cxpe n- citrate and h ydrogen ions. likewise fe e dback to inhibit
PFK.
~~6-p ho:hate clitt1r<" or input or <>IH' :\Tl' 111olec11k. In the CO!l\'Cr-
A muscle fiber's rate or entTg,· use during e x e rcise
si<>1 1 o f ghTog<" n . g l11 cosL"-ll-ph osp h at L' is fo rm ed from
g lt1c<>sc- l -p lll>sph;11c "·it h<>111 this cnc.-r1--,"· expenditure. can bc '.200 tim es gre ater th a n a t rest. The ATP-PCr a nd
ADP-1 1
Fructose 1, 6-diphosphate
Clyc<1h·s is l<"c hni c;tlh· begins 01HT 1hc g lt1cose-h-ph os-
plt;1t<· is 1·o n11t'd.
( ;hToh'sis rl'q11in·s I{) to l '.Z l"n1.n11atic reactions for
g lycolytic syste m s alone ca nnot suppl y a ll the nee d e d
e n e rgy. Funhennore. t h e se two syste ms are not capable
of suppl ying a ll or th e e n ergy n eeds for a ll-out a c ti,itT
t IH· hrl'akdo\,·n of ,rh·coo·L·n :-. . n to J)\Tll\'ic
. acid. whi c h is lasting more th a n 2 min o r so. Prolonged exercise re lies
tl H· n co nn-rtl'cl to lacti c ;tei d ..-\II steps in the pat lnrny o n the third e n e rg,· system . th e oxida ti,·e sys tem.
;1 11cl ;di ofthl' l'n1.\'11H·s i1 1\'olH·d operate ,,·ithin th e ce ll
D cytopbsrn. TIH· 11<·1 g;1i n from th is process is 1 moles
In Review
(11101 ) ol .-\TI' f'on11t'd for l';1ch 1110k of o-iffotren
~ . n broken
Dihydroxyacetone phosphate
clow11. If g lt tcost· is used instl'ad of g l\'cogen. the g;1in 0 The formation of ATP provides cells wit h a
2(3-phosphogtyceraldehyde) high-energy compound for storing and, when

F::::.
is 011ly '.2 11101 o f :\Tl' lwca11sc I 1110 1 \,·as used for the
('Oll\'t'l'Si<>11 or gl 11 cos(' to gl 11 COSl'-li-phosph;lll'. b roken down, releasing ene rgy. It serves as the

NADHN:::11 ° 1 w
This l' IH'I').\"'. s, ·stt·m oh\'io 11sl~· docs not prod11cc L1rge
an1011111s of' :\TP. Dt'spite this limitatio n . the co111bincd
;1ct io11s of the ATl'-1'( :rand g h Tolytic s,·stc m s al lm,· the
immediate source of energy for most body fun c-
tions, including muscle contraction.
0 Adenos in e triphosphate is generated t h rough

101~~
2(1, 3-diphosphoglycerate)
11111sc k s to gt·rn·r;1tc force l'H'n when the ox~·gcn supply three primary energy systems:
is li111il(•d . These two s\'stcms predomi n a te during th e
ADP l'arly 111i11111t·s o f' lti g h -int e n sit\' exercise.
1. The ATP-PCr system
2. The glycolytic system
t\ 11 o t lit'!' 111 ;1jor lin1itatio11 . or a n ;1erobic g lycolysis
2(3-phosphoglycerate) is 1h;11 it c11 1st's an accu1111tlation or lactic acid in the 3. T h e oxidative system
111t1scks ;111 d hoch· (lt1 ids. Clycoh·sis produces pyruvic O In the ATP-PCr system, P, is sepa rated from PCr
To electron To electron ;1cid . This proct'SS docs n ot require ox,·gcn . but the through the action of creatine kinase. The P, can
transport
chain 11 ° l l
2(2-phosphoglycerate)
transport
chain
prt'S('llCe or ox~·ge11 de termines the fate or the pHtl\-ic
;1cid. 'v\'itho111 oxygen present. the pyrtt\'ic acid is co n-
then combine with ADP to form ATP using the
energy released from the breakdown of PCr. Th is

H,o-1 l l~H,o
nT tl'd din·ct lv to bctic acid. an ,1c id with th e c hemi cal system is anaerobic, and its main fu n c tion is t o
for1111rl;1 ( ) 1,:0 1 that quick!\' dissociates. forming lac- maintain ATP levels early in exercise . The energy
tatl'. Th(' terms /1vn11 1ic (/(id a nd /1_\T/(11(1/(', and /o!'lir (/(id yield is 1 mol of ATP per 1 mol of PCr.
D ;111cl lru-tolt' , arc ol'ten u sed interc hangeably in e xe rcise O The glyco lytic system involves the process of
2(phosphoenolpyruvate) physiolog,·. 111 l'ach case. the acid form of the m olecule glycolysis, through whic h glucose o r glycogen

1 ~ l ~~
is re lati vely 11nstahlc ;11 11o rn1 ;tl boch· pH a n d rapidly
is broke n down to pyruvic a c id . Whe n g lycolysis
loses a h ydroge n ion. Th e re main in g n1 o leculc is more
o ccurs witho ut o xyge n , t he pyruvic a c id is con-
correct ly c dkcl pnu\'atc or J,1ct;it e . Lac tate c;111 itself
ve rte d to la c ti c a c id . On e m o le o f gl u cose yields
he a so11rc<.· of l'nerg-v as discussed la1 c 1· in this c h apte r.
2 mol ATP, but 1 mol glycoge n y ie ld s 3 m o l AT P.
Lactic acid ~ 2(pyruvate) ~ Lactic acid In all-0111 sprint l'\T 11ts lasti n g I or 2 min. the
0 The ATP-PCr and glycolytic systems a re major
ckn1,111ds on the g lvcolvtic system are hig h , and muscle
Net gain contributors of energy du ring short-burst a ct iv ities
Net gain lactic acid COIH'l'tllrations c,1n inc re ase from a resting
(starting from (starting from \';tl11<· or about ] llllllol / kg or musck to more than '.2!"> lasting up t o 2 min and during the early min utes
glucose) muscle glycogen) of longer high - intensity e x e rcise.
ll111101 / kg. This aciclilic1tion o f m 11 sc k lihcrs inhibits

+2~ ~ +3~~~ flrrth <"r gl~TogT 11 breakdown because it impa irs g l\'CO·
lytic t'tll:y111 c h111ction. In addition. the acid decreases
Oxidative System
till' filw rs· c;1ki11111-hi11din g capac it\' and tlt11s 111a,·
FIGURE 2.7 The de rivation of e ne rgy (ATP) b y glycolys is . G lyco lys is invo lves the b re a kdown o f o ne g lu cos e (s ix -c a rbon) i111pnlt- 11111sclt- <"<>11tr;1ctio11. The lin,tl S\"S ll'lll or cl'l lt1L1 r t'll<' I).!,"\ pr!ldU L'tiun is th l'
m o lec u le to two t hre e-ca rb o n mo lecules o f pyruvic acid . The process can b egi n with e it h e r g lu cose c 1rc ul a t1 ng 111 th e b lood Tit!' 1a1t·-li111 i1 i11 g t·11 1,·111 t· in 1'1t· ,,·l\'col\'lic p,11'1- oxidative syste m . Th is is I hl' Ill( 1st n >Ill pk, ( ii IIH' 1h rt' t '
o r g lycogen (a c ha in of g lucose molecules, th e sto ra ge form o f g lucose in m uscle a nd live r) N o t e tha t th e re a re ro ug hly 1O "·
w: 1\ is phos phofruc tokinas c ( PFK) . L.ikc :il111()s l ,il l <"11<'1).!', s,·s1t· 111:-. ;111d ,1111' ,1 hricl tl\·t-r,ic,, i:- p r,,,idn l
sep a rate step s in this a naero bic p roce ss, and the net re sult is the generation o f e ithe r two o r th ree AT P m o lec u le s, d e p e nd ing
on whet he r g lu co se o r glyco g en is the initial substrate .
62 Physiology of Sport and Exe rcise Fu e l for Exe rc ise: Bi oe n erget ics a n d Mu sc le M e t a bolism 63

h ere . The p rocess by which the body breaks dmrn loc a li /l"cl l<1\\ ;11 cl 1!1t· 1w1 i pl11"1 \ , ,I 1111", , ·II lw111· li 1, 1he G lyco lysis 111 c:1rboh\'Clr:11c 1m·1abo lis m. ;-, <Tl\'c
' . o h. ·sis Pyruvate
substrates with the a id of oxyg e n Lo ge n e rate e n crgv is mu -,c k fi b l·J I )\ upti111i / i11 ~ " ' ' t.:•·11 d.-11\<·r \ 1, , ,1 1,1.1111 pl ;1\, ;1 ro le i11 /111//, ;111 ;1l· ruhi c ;111d ;1t·rohi c .-\TP prod1 1c-
called cellular r espiration. Because oxyge n is re quire d . hig h llll"ta b , ,l i< J; l(("-. .' I l, 1\\l"\ (' I, l1 .I\ III '..! 1!1 , · 11111, .. li ,1 11- r N A D+
t irn1. T Iil' prc,n·ss of" g h ·coh·sis is the sa m e regardlc.:ss
this is an a e robic process. U nlike the a nae r obic pro- clria l<1c11 c cl :111111111I tl1<· p 1·11pl1 <' 1\ " ' t lw « · II .tl, t1 ol \,·lll'1 l1 l·r ox,·gt· 11 is pn·sl· nt. Tlil' prese 11ce of oxygen
in c n ·a~t·-, RC)~ p111d11< ti,111 lw, .111 , <· .,f 1l11 ·11 ,. , 111 1,1 111· CO2 ,...,.-r,._-NADH
duction of ATP that occurs in th e c yto plas m o f th e cel l. clt·tt·rr t1 i11l"~ 01 11'· tlil' fatl' o f" thl· c11d p r odu c t . p,-r11,·ic
the oxidative p rodu ction of ATP occ urs within spec ia l lo o xygl'J l. ·1 !t 1i-.. . 111it11< l1<111d11. 1 1,· 11 d '" lw d 1, t1 rl111tl'd :ic id . R<"l':111 tli ;11 ;11 1;1l-rohic g l~-col~·sis prod11n·s bctic
c e ll organ e lles calle d mitoc hondria. In musc les, th e se 11 011111 1i(<1n11h :11<1ll11CI till" 1111r-..1Cl1 · ., f ilw, , ·II . d1 ·1w1ul - Acetyl CoA
:1c id ;111cl <ll1h- tlirel' lll'l 111oks of".-\T P p c: r mole o f' g h·-
a re adjacent to th e m yo fibrils and a r c a lso sc aue r c d i11g <Ill ta p ill;11\ l<H :11i,H1. 1.1tltn 1l1. 111 11!' 111 ~ 1·\1 ·11h c1>g< ·11 . or t\\'() ll('t 111u k s ur .-\TP per Jll()lt- or gl u cose.
through o ut th e sar cop las m (see fi g ure 1.3 ) . s pac ed. T hi, I()< :iti()JJ i, ()pti111.tl f.,, 111. 11111.1111111 ~ hi g h 111 th l' prl·st· 11 n· 01· <>X~)-~l·n. lH J\\T\'l'r. the P>Tu\·ic a c id
111 <.: tabo lic 1a tc , \,·l1 ilt- 111i11i111i/i11 ~ 11 ,h. f.,, 111, 1t·.1,111 g H,0 CoA ~
The total number, or density, o f mitoc h ond ri a with i11 i~ c, >11\'('J't('cl i11to :1 comp<H111cl ca lled acetyl cocnzyrne
a muscle fiber is dete rmined b y iL5 demand for AT P ROS prod11< 1i1>11 . \\Iii< l1 <.11 1 ll<' g .111 \ , · h .tf l, ·, 1 ill<' , <" II. A (ace tyl CoA) . ~ e Citrate
production , b ut the precise loca tion o f these miLOchcrn- \lt1-,c lt· -, 11l·<·cl ;1 , 11 ·;1ch ,111 q1 h "' , ·11 , ·1~ ' 1,,, 1111ti 11 - Oxaloacetate synthase ~
K rebs Cycle Onc l' funnl'd. ;1ce1d Co..\ e n ters the

f
dria within th e cell is dete rmined by oxyge n cliffus io 11 . 1101l',h· procl11< <' rill' 1<>1 «· 11 1"<'11<-d d 111111 g }., 11 l,.!-t<·1111 NADH ~ Aconitase
Each individua l muscle fiber has a n optimal distribu- .tt'li,·it~·. l ' 11li kl' \\ l1 ;11 l1 .1 111 ><·11 , \\ ir Ii ,I ll. I (" ! " " ' ' \ n•
0 Kre bs cycl e (:tlso c:tlkd thl' citric ,1cid c~-ck or tric>·clic Malate
;1c icl n ·ck ) . ;1 c0111pkx sl'ril's o f c h l'mictl reac tions that NAO+ dehydrogenase lsocitrate
tio n of mitochondria within th e cell t h at a llows for a prod11ctio11. till' " x icl :1 1i \(· " ' 11·111 i , ' ' " " 1" 111111 <>tl .
n ear maximal r ate o f ATP pro du c tion wh ile e xposing but it has ;i 1111 1< l1 l:1 1g <"r c·rll"r g \ -1>1 • ,d11 , 111 g , ·'I'·" 11 ,. ' l l pl'nnit till" c rn11pl1·tt· oxidatio11 oLlt'L' t~·I C:o.-\ (see figure Malate Ao~

1
a<.: robi c 11 w 1,di<l li, 11 1 i, ti ll' 111 i111. t1\ 1111 · tl1<1d ,,I , ·1ll" I ).! \ '.! .q). R,·c:111 th;1t fo r <'\'l'n· g lucose Jllolcculc that e nt ers lsocitrate NA DH
th e mitochondria Lo as liule e xcess oxyge n as possible.
produe1io11 cl11ri 11 g 1·1Hl111 :111 < 1· , 1< 1i,it i1· , . I !J ,.., 11l.11 <·, tl1<· gh·coh·tic p; 1t li \\'; l\'. t\\'() lllokculcs or l)\'J'l(\',\le arc H o Fumarase dehydrogenase
Exc ess oxyge n exposur e in m itochond ri a c r eates reac- 2 CO2
con sid<.:rahlc cl l'1 11;11HI , ,, ,, 1l 11 · <.11 <li,,,.1-... 1rl.11 .11 1111 ('-.pi - 1"1 ,nnl'cl . Th <· n·f"orl'. l':tc h glucose m o lecule 1h;1t begins
tive oxyg e n spe c ies (ROS), whic h are toxic Lo the ce ll Fumarate
till· <·1H ·rg,·-prod1teing process in tlil' prt'Sl'nn· o f" ox,·gen a -Ketoglutarate
at high concentratio n s.'•·7 r;1t<w~· s~·'>l<· 11 1'> 1" clt-li,·1·1 11 x \ g 1·1 1 11, 11 1<' .1, ti,, · 11111,, I, ·,.
W ithin a mu scle ce ll , mitoc h ondria tend Lo b e ()x id,1 ti\'(· l' Ill·rg\· pr< Hl1111 i11 11, .11 1 , ,,1111 · t,,1111, .11 li,,ln . r l's1 tlts i11 t,,·11 crnnpktl' Krebs c,-c lcs. FADH 2 ~ Succinate a -Ketoglutarate
dr,1tt·s (s tarti11g \\'itl1 g l\( "h,i, 1 111 f.11-. . .-\ s cll'pictcd in 'J. Y,/J (,111d sho\\'11 in more detail in FAD / dehydrogenase dehydrogenase
locali zed along the p eriphe r y of th e fiber, with hig h er
densities n ear capillarie s . This arrange me nt fun c tio11s Iigu n · '.!.. q). t hl' co11,·t-rsi 011 of s11cci 11\'I ( :o.-\ to s 11cc i n atc
Succinate
to c re ate grad ie nts in the oxygen conce ntration from Ox idation o f C a r b ohy d ra t e i11 tlw Kn·bs <Tck re sults i11 thl' gl'11L·;-;11io11 of"g11a11osi11l'
th e capillary to th e mitoch o ndri a Lo fac ilita te th e fl ow t rip l1 os1>li;11c. or ( :Tl'. a h i•d l-l'll l'l""Y c ur111)otllld si111 iL1r
As s ho wn in fi g1 11T '.!. .K. ,, x icL1li\1· j>l<Hl11, ti,,11 , ,I .\I"\' ;-, ,'.""\ .
Succinyl CoA
to .-\Tl'. ( :11;11l()si 11t· tripliosph,lll' thl·n transfers a P, to
of o xygen into tJ1 e mitochondria. H aving mitochondria f'r<Hn c 1rbol 1\'C l r,1 t<·, i11,·" I\'( ·, 1l1 1<·<· I'' "' 1·.....,1·,:
.-\DI' to form .-\Tl'. T h ese l\\·o .-\TPs ( per molec ule of"
• ChT<1lysis ( fi g 11 n·
Cytosol
Glucose
'.!..Kr1 )

• Tlit· Krt'l>s nTll' ( li g·11r1· '.!..K/i )

g h1cosl') ;in· f<>rnH·d h>· s u hs tratc -len·I p lrnsp lwnfa ti o n .
So at tit <· encl o f the Krebs c,-clc. (\\' O acldi tion;d m oles
of" .- \TI' l1:1,·t· b ee n formed di;·l·cth·• an d the ori 1" ,ri n ;tl car-
U°p
GTP

At ~
• Thl't'll'ctrrn1 t1·;111~111ll·t c li:1i11 ( li g1111 · '.!..K ,)
hoh\'Clr:1t<· l1:1.s ht'l'll b rokt·11 elm,·;, into cirbon dioxide
2J$ir 2 NAO+ ,111cl li\'Clrogt· 11.

4* (2 net)

2 Pyruvate
2 NADH + H+
:\s i11 the other p ,1t h \,·ays innih-cd in cncrg,· metab-
olism. Kre b s cycl l' l'n1.,·111cs arc r cg11la1ccl ])\' nl'gati\'l·
ked hack ;11 s<·n-ral steps in the n ·cle . The ra te-limiting
t·11zy1 11 t· i11 the Krebs C\'ck is isoc itrate dc h n lrogenasc.
,,·liic h . likl' l'FK, is in l.1 ihi1cd b , · :\TP and ;1Ct i,·'.11ed b,·
*
F IGUR E 2.9 The seri es o f reacti ons th at t ake p lace duri ng
the Krebs cycle, showing t h e com p ounds fo rmed and enzym es
invo lved.
G
.\DI' ;111d 1' a s is the elect r on tt.'anspon chai n . Be cause
0 2 NAO+ 1

n111sclc co111ractio11 relies on th e a\'ailabilit,· of calciu m ade nine d inucleotidc ( :\.-\D ) and lla,·i n adenin e dinu-
Mitochondria Mitochondria in the ce ll. L'xet·ss l'alciulll a lso s timu lates ~he rate-lim-
2 CO2
2 NA DH + H+
____c@
© iti n g t·111x111t· isocitratl' deh\'Clrogenasc.
cleotide ( FAD ) . c on\'ertin g e a c h to its r t'd un:'d fo rm
(Nr\DH and F:\DH~. respe cti\'eh ) . Dur i11g e ach kre bs
E lectron T ran s port C h a in Duri1w ,rh -col\'sis. n ·cle . three mole cules n{· \:.-\DH and one m olecule of
I t"'I t"t .

11\:drog cn io11 s ,lrl· n· lt" ascd \\' h e n glucosL' is 111 L·t ;1h-
.
F..\DI-1., are produc ed. The se e arn th e h ,dro,,.e n atoms
2 Acetyl CoA Electron
ol11:ed to p\'n1,·ic .rcid . .-\dditional h \'Clrogen ion s arc (ekcu:ons ) to the e ll' n ron t r.1ns port c li,1i11. :7grlllljJ u l·
transport
chain F I GURE 2.8 In t h e p rese n c e of rclcascd in thc co11,Trsio n o f" p,-ru,·ate to acl' td C:oA mitochondrial p rotein complexes loc 1Le d in th e inr1l' r
mitochondrial membrane ( fi g ure 'J.. I () ) .

W-----t►~
o xyg e n, a fte r g lu c o se (o r g ly co gen) .t rHI a t St'\'tTal s teps in th e Kr ebs c,-cle. If" thesl' h \'C-Jro-
h as b een redu ced t o p yruv a t e , (a) the gl'n ions rc111;1ined in the s\'sLem. th l' in side of th l' T hese protei11 c o mpkxe s con u i11 a ser il':-- llfl'n /\'tnl's
6 NADH + p yruvate is first c a t a lyzed t o ace tyl Cl' ll \\'<>ttld htT0 111t· too acidic. \\'hat ha ppens w this a n d irn n-co 11ta ining p rote ins knu,\·11 as l.Ttoch1·mne s .
co e n z y m e A (a ce t yl Co A) , whi c h ll\·drog('11 ? These p r o teins st-rn· as t·knron m ;1g nl'ts ~h .11 tr.111sfc r
c an en t e r (b) th e Kre b s c y cle , wh e re e kctrons. \\·here till' ti r:--t cnmpkx . lb\'ill 11H>1Hrn11c k -
2FAD ( Tli c Kn· hs c\'t'k is c oupled to a series of r e a ctions
o x id a ti v e p h osph o ry l a t i o n occurs. 01i d c ( F!\ I:\ ) . is a s1ro11ger mag 11e1 fo r l'lcct r u11s th,111
knrnrn as I lie electron tnmsport chain ( ligurc 'J..~ 1) . The
______..© Hydro g e n ions re leased durin g t h e
Kre b s cy c le then comb in e w it h coe n . li\'Clrog<·n ions rl'il';1sed durin g th e processes ul' g h ·cuh ·- \:AD H. the scc o11d ni111pk x is a , t nll1u·cr m,wnct th ,lll
sis. t Ill· l'o11,·t-rsio11 uf p,-ru,·il· ,Kid to acetd Cu.-\. and the till· rirst. and S tl on dll\\'11 th e c h ,1i11 . . \s ~ igh-l'l~-rg, ckt'-
zy m es th a t ca rry th e hyd rogen io n s
e G t o (c ) th e e lec t ron t ra n spo rt L h a in . Kn·lis l' \'l' k c1 >111lii 1H· \\'i tli t\,·u U> <· ri;:,·rn c ~: 11in>ti11amiclc trollS .r re passnl fr u 111 n>rnpkx tu (·1irn p l<·, .d,111g thi:--
64 Physiology of Sport and E xerci se Fuel for Exercise: Bioenergetics and Muscle Metabolism 65

oo till'li 11 :d :1cct'pto r of' l'kct ro 11s a nd H ·. it is referre d to ph osp h u t-Ytuion within th e Kre b s cycle i1w ol\'ing the
0 Glucose ;1s o x ich1i, ·1· pl1 osp li ord atio11. m o lecule GTP adds a n o the r rwo ATP molecules.
o l o F, 1r 1·,·1-r\· p:1 ir of' l' k c tnrns transported to th e clec- Accoun ting f'o r lh e e n e rgy cosl of s huttling e lectrons
ADP+®
,
)
l
Glycolysis t rCJ11 1r:11 1s port c ha in b,· \:.·\DI I. thrl'C molecules or across lh e miwc h o nclrial m e m brane is a relati\'e ly new

~ e,L. ® ADP
Oute r
.-\Tl' :1 rt· f'c>rtlll'd . whi le the elect ro n s passed through
tl1<· l'kct rrn1 tr;111 sport c hain b\· F.-\DH~ \·ic ld o nly lwo
111 Cl lt·ct rlt·s C>f' .-\Tl'. I lmH·n-r. because the \:.-\DH and
F.-\1 )1 1~ :1n· 011tsidt· till' 111t.·111 bran e of' th e rn itoch o 11-
con cepl in e xercise physio logy. a nd m any textbooks still
refe r lO n e l e n e rgy pro du c t ion s o f 36 lo 39 ATPs per
m o lecule o f' g lucose.
m1 toc t1onclr1;it
d ri;1. til l' I 1· rn11s t ht.· sh ut tkd th roug h the m e mbran e . Oxidation of Fat
- 13-oxidation \\'hich rt'Cpt in·s t· 11t-rgY to h e used. Su. in rcali t,·. the n e t
As n o lecl earli e r. fa l a lso co ntrib11les impo rta ntly to the
yit· lcls an· 0 11h· '.2.:1 .-\Tl's per \:.-\DH a nd l.:"l .-\ TPs per
.._,, n eed s. M11scle and Ii,·er b
m usclc 's e n e rgy o-iycoo-en
. b stores
F.-\DI I~. can pre.wide 0 11Iy - '.2.:"i00 kcal o f e n e rgy, b ul th e fat swred
Inte r memtJr ane
Cytoplasm sp;,ce Energy Yield From O x idation of Carbohy- in side m uscle fibe rs and in fa t cells can s u p ply a l least
drate Tltl' crnnpktt· oxid ation or g luco!'> e can ge n- 70.000 to 7:':>.000 kcal. e \'en in a lean adu ll. .--\ Jthough
l'r:1t l' '.{'.! 111oll'ct rl 1·s ol'.-\TP. " ·hill' '.)'.) .-\TPs arc pro duced ma1w ch e mi cal compo unds (su c h as lrig lyce rides, ph os-
f'ro111 () l\l.' 111olcc1 1k or lllllSClc g h-cogen . The silcs or p h o li pids, and c h o leste r o l) are c lassifi e d as fats. o n h·
.-\Tl' prod11 ct io 11 ;1n· s11111111;1ri1.cd in figure '.2. 1'.2. The tri1.!.'h·ccridcs are m a1·o r e n e roy
.___. I - b.
sources. Tri bo-lvcerides
.

lll't pr()(lttcliCJ11 or.-\Tl' from substrate -Ic,-cl ph nsp h n r- a rc swred in fat cells a n d between a nd within s ke letal
mitoc hondrial
transport membrnnc \'la1io11 i11 lli l' gh-coh·1ic pat h \\'a~· leading in to th e Krebs muscle fibers. To b e used fo r e n e rgy. a trig lyceride must
chain c \'cll' rt·s1tl1s i11 ;1 11 c 1 g:ti n of' t\\'o .-\TPs (or three from be broke n clmn1 lo ils basic un its: o n e m o lecu le of

0 FIGURE 2 10 Locations of the processes of glycolysis (c t

. ·. . . b an e)
port chain (inner m 1tochondna l rnern r ·
Y op Iasm), the
K rebs c y c le (m ,toc h o ndria). drH I th,· r,/cc tro n trans- g h'Cl>gl' rt ) . :\ total or 10 :---.: .-\DH molecu les leading inlo
lit e c kctrotl tr;111sport c hain- t\\'O in g l\'coh·s is. two
g lycerol and three FFA m o lec ules. Th is process is called
lipolysis and is contro lled by e n zym es known as Ii pases.
in till· co11\'l-rsio 11 o r pHu,·ic ac id to acc td C:oA. a n d Free fatty a cids a re th e p rimary e n ergv source for fat
c h a in , som e o f the e n e rgy r e leased b y tl? ose r caCLio n s . \TI' is /'o nt H·cl. T l1i -.. li 1i; tl -..1< ·11 1('(111 i11·, .111 1·1 11,·1111: six i11 tlt t· Krl' hs cyclc-\'il'ld s '.2:1 net .-\TP molec u les. m clabolism. On ce lib e rated f'ro rn g lycerol. FFAs can
d i)( 1 r
is used to pump H - fro m the mitoc h 0 nd n a l matrix into - ~A rl' s,·111lt;1:-,(' _:\ 11l w1 ·1Hl c>lll1<· 1 l1.111 .
1. 1I l l ' 11 · Rc111 t·11 il w r 1ha1 \\' h ilc :rn .-\ T Ps arc act uall~- p roctuccct, e nte r th e blood a n d be tra n sported thro ug h o u t th e
k n o"·n , 1., · .
the o ute r mitoch o n d ria l compartme n t. A<; these h ydro- . ,-s \\·i1l1 (JX\'(J'('IJ 1<> !()1·111 \\':tl('J, 1l111, plt '\ ('llllll g the l' IH-rg,· cos t of' 1r;11 1sporting .-\TP ac ross m embran es b ock e n lcring muscle fi bers by e ither sim p le d iffusion
CO J11 I) Jl h - · · ,-, '
gen io ns move back ac ross the m e mbran e d own th e ir - - - .. 11i o 11 of' t it(' ('(·II. Tl1i -.. i, ill11 , 11 .11, ·d i11 li ~ 111·t· u ses fin· or 1ltos(· ATPs. The l\\'O FAD molec ules in th e o r transponc r-m ed ia le d (facilitated ) diffusion. Their
11
ac1c11c, ·
ra te of e ntry in to th e m u scle fi bers d e p e nds on th e
Kre bs n ·ck th ;1t a rc im·ol\'cd in clcclro n transport resu lt
con centration g r adie nt, e n e rgy is transfe rre d to ADP, 2 _11. Bt•ca 11sc th is c1,·<-r; tll pr<>< '<'"" 1c.· li <'-.. lll l <>X\)-!.l' lt ;1s
i11 tlirl'l' addit io11 al ne t ATPs. And fi nalh·. s11bst ra tc-lc\'el con centratio n grad ie nt. In creasin g th e con centration
Mitochondria
Glucose

2* :rp - -... ►t- Substrate-level phosphorylation

4 ATP (-2 ATP used) - - - - - - - - - - - - - - - ' - - - = - _ _ ; ' - - - - - - - - -

Outer Oxidative phosphorylation

2 NADH + W - - - - - Electron transport system
mitochondrial
(2.5 ATP per NADH + W)
compartment
ATP
2 Pyruvate '-------..:....----=------...:..._________

~
synthase
NADH + H' _ _ _ _ _ _ _ _ _ ____;(_
2._5_A_:r_P..:..
p_e_r N_A_D_H
_ +_H_+..:..
) _ _ _ _ ____.,.
2
2 Acetyl CoA

Inner {
mitochondrial ~ ---1- 6 NADH + W (2.5
_ __ _ _ _ _ _.....:... ATP
__ __:per
__ NADH
_ _+_W
__:)_ __ __ _ __
membrane
(1.5 ATP per FADH2 )
2 FADH2 ------------'-----'-----=----------
Substrate-level
NADH + W NAO+
FAD phosphorylation from GTP

Matrix
Accounting for transport o f ATP across Total energy yield
FIGURE 2.11 The final step in the aerobic production of adenosine tri - the m itochondrial membrane , o x1dat1on o f
phosphate (ATP) is the transfer of e nergy from th e h ig h -e nergy electrons
o f reduced nicotinamide adenine dinucleotide (NADH) and reduced flavin
each NADH results in 2 .5 ATPs wh ile
o xidation o f each FADH 2 results in a ne t 0 FIGURE 2.12 Th e net energy production from th e oxidation of on e molecu le of gluco se is 32 molecules of adenosine
triphosph ate (ATP) . O xidation of g lycogen as the original substrate would yie ld one add1t1o nal ATP.
1.5 ATPs.
adenine dinucleotide (FADH 2) with in th e mitochondria, follow ing a series of
steps known as the e lectro n transport c hain .

.....
66 Physiology of Sport and E xercise Fuel for E xercise: Bioenergetics and Muscle Metabolism 67

of FFAs in th e b lood increases the ra te o f the ir transport l\\'CJ :\Tl'-,f,,1 ,II ti, .1t i,,1 1 li111, 1111l1 k, · i.:h , ,, h,1,, 111, .. ltitl' , <:, >11-, idt'r t ht' t'Xa111plc or pal m i tic a c id. a rat her Lactic Acid as a Source
in to muscle fibe rs. llll .\Tl'-, cli11· ( th . ;tli1111d;1111 I h-c1r ho11 FF.-\. The co mbine d reac tio n s of'
()x ida 1i<>11. the Kr t' hs n"Clc. and th e elec t ro n tra nsp o rt of Energy During Exercise
~-Oxidation Recall that fats are s to re d in t h e Krebs Cycl e and th e El ectron Tr a n s port
c li a i11 pr()(\itn · I()(; 111oknd cs or .-\TP fro m o n e m o lc- Lac tic acid is in a state or con stan t turno\·e r within
b ody in two places, ·within muscle fi bers a nd in adipose Chain .\f tl'1 13-<>,icl.,1 i,,11 . 1.,1 111, ·1.i1, .. 11,111 1.. 11, >\,,
ndt· ()f'p;d1 nitic ;1cid (st·,· 1ahk 2.2 ) . compare d \1·ith o nh· ct:lls. bei n g produced by g lvcolysis a n d r emo\·ed fro m
tissu e cells call ed a clipocytes. The sto rage form or f;i t-; Ih l· ,a 11 H· p; 1t Ii ;1" 1, :-.. icl . 1ti ,,· 1 .11 I ,. ,I " , I 1. 1t, · 111e · t. ii,. ,Ii, 111 .
:{~ Ill< ,It-nil,·:-- ( ,r :\TJ> rn >Ill cr]u
n cosc or 3:~ fro m ncrh·u
. wt:11°
n · th e c t:11 , primarily throug h oxida lio n . Thus . d espi te its
is trig lyce ride , whic h is broke n clown into FFAs and :\ Cl'l\] C:o.\ 11,1111\'cl I>\ 11-<> \.l <l. 111 , ,11 , ·111, ·1, ill<' l, 11 ·h,
reputa tio n as a ca use o r faligu e . lac tic acid can be. a n d
g lyce rol for e n e rgy m e tabo lism. Be fore FFAs can b c cyc le. Till' K1 eii-, c, cl, · g 1·11\' 1.11, ·, l1\ll111c:, ·11. ,, lt1.!1 i,
Oxidation of Protein is. u st:cl as an a c tual fuel sou rce during exercise. This
u sed for e n e rgy p rod u c tion , th ey must b t: co1wc rtc d t r;i n-; po rt c cl t c> 1l 11 · c· I<- c t 1, " 1 11.111, I , , , 1 t , I 1. 11 1, . ii, 11 1i.: , , 1t h
. \ s ll()tt·d t· ;1rlil'r. c;1 rho li ydra1 cs and f.1u~· a cids art: th e occurs thro 11gh sc\'t:ra l m echani sm s .
to ace tyl CoA in th e mitoc h ondria, a process callcd th c h ~-cl r()g <·11 g, · 111 ·1. 1t c·cl d 111111 g I)-•,, 1< l.111, 111 t, , 11 1"le- 1I.! , 1
pn·l't-rn ·d f't1d stthst r;1tt'S. Bu t p ro tt·ins. or r,1thc r 1he First. we 110\\' k n o \\· that !act.alt: produ ced by glycolysis
[3-oxidation. Acety l CoA is th e commo n in te rme d ia te ox idatin· p l1<,..,pl1<,n l. 1ti<>11. .\ , 11 1 i.: 111< , ..._, . 11wt.d1<d1,111.
;11 11 i11<> ;1c ids 11! ;11 crn11 p ost· p r<>tl'ins . a rc also used !'or in the cyto p lasm of a muscle fibe r can be taken up b\'
through whic h a ll s ubstrates e nte r th e Kre bs cycle: for th e 1)\-pr()dJ H h <>f FF.\ ., :,. , icl.11 i, ,11 .11 , · \ 11 '. 11 < l . . 111d
t·11t·q..,':· tt11 clt-r sc>llH' circu111stan ccs. Some am ino acids the mi tochond r ia within that sam e fibe r a nd direct!\'
oxidative m etabolism. ca rbo 11 cl i< ,x id c· ( ( :< >: ) . I I,,,, ,.,,· 1. 1I 1e · , , 11111 , I, · 1, · , , , 11 ii 111,-
c;111 1H' ,·rn1,·c·r1t'd i11 to g lt1cost·. a process called g luco- oxi dized. Th is occu rs m osth·• in cells \1·ith a h iO'h
0
densir~.
·
f3-0xidation is a se ri es of ste p s in wh ic h two-carbo n t io n of an FF:\ 11 1,,kc 1il , · 11·, 111i1 ,·, 111<,1, · , ,,, -..: , ·11 l11 ·, .111-..t•
11!"< 1gt'11csis (sl't' fi g t1n· '.Z. l ) . :\lll'n 1at i,-ch·. some can o r mi toch ond ria like l~'F>e I ( hig h o xidati\'e) muscle
acyl uni ts are c hoppe d o ff o r th e carbo n c hain o f' the , lll FF:\ Jll ()ic( 1ilt· ( (IJJ l:1i 11-- ( <111 ,1< 1, ·1. il >h l l l l l l ( " ( .1il ll1Jl
ht' co11n'l'tt·cl i111 0 ,·a r io us i11t l'r111l'dia tcs ·o f' oxidati\'c libt: rs. cardiac muscle , a nd li\'cr cel ls.
FFA. T h e acyl un its b ecom e ace tyl CoA, whic h thc n n1olcn dt·, tl1 ;111 ;1 g lt1 , ,,.,,. 111.,J.-, 1d 1·. St:co ncl . lactate p ro d uced in a muscle fibe r can be
T It l' ; l< 1\-;t II i; tg <· , >I I 1;1\ i I I g I I l< 11 <· <. 1I I >c , 11 111, , I<•< 1l It-, i 11 11H·L 1ho lis 111 (s 11 c li ,ts p,Tt1,·atc or acctd Co.-\) to e nt e r
e nters the Krebs cycle fo r the fo rmati o n of ATP. The transpo rtt:d awa\' from its site o f' prod uc tio n and u sed
FF..\s t l1a1 1 i11 g l11 <<)',t ' i, 111 ;11 111< n , .. 11 , ·t, I ( , , \ i, I, 11111t·cl IIH· o x id:ttin· pnHTSS.
number of ste p s d e p e nds o n th e numbe r o r carbons clsewht:re by a p r ocess ca lled th e lactate sh u ttle. firsl
fr()m tlw n1t· t;tl J() li, 111 c, I :1 gi \1·1 1 .11111111111 "'I.it .,., 111llre l'r()tt'i1 1"s 1·1 1c rg,· ,·icld is n ot as casih· clctl' r mint:d
in the FFA, u su a lly b e tween 14 and 24 carbons. For I , ' •
clcscribed by D r. Ge01·gt: Brooks. Lactate is produced
acc1~·l C:o:\ ,·111,·r-, i ll(' l,1, ·I,-, <, ,I<- .111d 11 11111· .. I, ·, 11 <>11 :-; as t Ital or c:1rhoh~·dra1t· o r !'a t beca use protein a lso
exampl e, if an FFA orig inall y h as a 16-ca rbon c hain , prima rily by type 11 muscle fibers but can be t ran sported
arc se nt(() ill<' !' it·< tr<>11 11 :11 1-,1>••• 1 1 l1. 1i 11 . I Iii, i, "Ii" c <>11L 1i11s 11i1rog t·1 1. \\'h l'n ;1111i110 acids arc ca tabolizccl.
f3-oxidatio n yie ld s e ig ht m o lecules of' ace tyl CoA. LO acUacc n t typ e I fibers b\' cl i ffus ion or active tra n sport.
!'at 111ctal>()li..,111 c: 111 g,·1H· 1:itc· 11111< 11 111.,1<· ,·1 1e ·1g, 111.1 11 so111t· of' t lH· rt'k ,tsl'd nitroge n is used to f'nrm n c \,·
On e n tering the muscle fibe r, FFAs must be e n zymat- In that rt:gard , m ost or the lacta te produced in a muscle
g li1c o sc 111l't :tl ,()li .., 111. l ' 1ili kt· g l111 .,.._.. c,J g h, c,g 1·11. I.it s ;1111i110 a c ids. h 111 lhl' rl'm:1i11i11,t,r n it ro<rcn c:111n o 1 be
t")
ically activated with energy from ATP, pre paring them n e ver leaves that muscle. It ca n also be tra ns p o rted
arc l1ct<"r()g t·1H'<>11s. ;111cl t ill' ;11 11.,11111 ,,1 . \ 11' 1>1 1><ll1t 1·d oxicli ;:l'cl h~· tht' body. l ns1ead ii is co n n-rtc d in to urea
for catabo lism (breakdown ) within th e mitochondria . thro ugh the circ u la tion to sites wh e re it can be di rect ly
d epe nds 011 1111' s pt T ific 1;11 <>:-;i cli 1,·c l. :111cl t h e11 l'XC l'l' lccl. p ri111 .1ri h· in the urine. This com·c r-
Like g lycolysis, [3-oxida tion re quires a n input e n e q..,';' of oxidi zed. The lac ta le sh u u le a llows f'o r gh·co lysis in
s i()ll n ·q11ir<'s 1hc use or :\ r°P. so some c ncrg,· is spen t
one ce ll lo sup p ly fue l f'or use b:, ano t her cell. Specia l
i1 1 1his proct'ss.
tra 11spo rtc 1·s called monoca.-!Jox,·late tra n spon ( MC:T)
\\'hl'll prot<·i11 is broke n down th rough combust ion
p rotei ns fa cilitate the m m·eme nt of la c tate b en,·een
i11 till' l:tlio r;1ton. tilt' <· n ng,· ,·icld is :'i.6:'i kcal/g. H cl\\·-
RESEA RCH PERSPECTIVE 2.1 l'HT. llt' C:II ISl' or Ilic t'lll'J'O"\'
cells and tissues a n d li kely \,·ith in cells. Duri ng exercise.
~- t:Xj)e ndcd in COl1\'Crt in ~o· approximateh· 80% to 90% of lac ta te is transferred
White, Brown, and (Perhaps) Beige Fat in Humans 11it rog t·11 to ttrt',I \\'lil'n p rotein is m e tabo lized in thl'
across th e sarcolem ma e it h e r b,· p assi\'e d iffus ion orb\'
bo d y. lhl' l'lll'l'g,· \'il'l d is onh· abo ut -I. I kcal/g.
~rown adipose tissue (BAT), often ca lled brown fat, is found in almost every species of mamma l, especia lly facilita ted transport through tvlC:Ts. Th ese transpo rters
To acn 1ra1 t'h· assess the rate of p rotein metabo lism,
in those that hibernate. Unlike white adipose t issue, which is specialized for lip id sto rage a nd brea kdown can b e e x.pressed in d ifferi n g numbe rs . de p endin g on
th e ;11110111 1t or 11 it rogcn being e limi nated fro m the b o d\·
(lipolysis) to meet long-duration metabol ic demands, the function of brown a dipose is to transfer e n e rgy the p rope rties of'the cells and tissu es h elpi ng to mo, e
111 11s1 lw dctc r111 inl'd. T his re quires urine collec tion ro·r
from food directly into heat. Brown adipose cel ls contain many sma ll lipid drop lets and many mitochondria , lactate in the cells that are the most m etabolicalh· actin · .
I '.Z I<> ~--1 h pc r iods. ;1 timl'-consuming process. Ikca use
which give the tissue its brown appearance. BAT cells also have more blood vessels t h an wh it e adipose Using lactate as a n1t-·ta bo lic fuel accou n ts fo r a p proxi-
th e hcal1h y hoch · u se s little protein du ri ng rest and
cells to supply the tissue w ith oxygen and nutrients and distribute the h eat produced in the cells t o the m a te ly 70 % to 75 % of lactate remo\'al during exercise.
<'X<'1T isc ( u su alh· 1101 morl' than 10 % of total cne roy ~-
rest of t ~e body. :he inner membrane of the m itochondria of BAT cells has a specia li zed p rote in ca ll ed .
Fi n a lly. som e o r l h e lactic acid p r o duct'd in the
exp e nded ). <-·st i m ates o r total c 11 en2,· e XJ)endi t u re bn-en-
~ncoupling protein that uncouples the e lectron transport c hain from th e c reation of ATP (phosph oryla- {J.
muscle is transporte d b\' t h e blood to the li\'er. \d1t're
crally ignorl' pro te in metabo lism.
tion). While white fat generates ATP for e nergy, brown fat's primary ro le is to produce h eat and in crease it is reconve n ed to J)\Tll\'ic
. acid and b a c k to bo·\u cose
metabolism, especially at rest. (gluconeoge n esis) anc\ trans p orted hack to t h e \\'t) rk-
Brown adipose is abundant in newborn babies and young ch ildren. However, for a long time, it was ing muscle. T h is is cal le e\ th e Cori C\'cle. \•\'itho u t th is
beli e ve d that brown ad ipose sto res we re absent in adult humans. In 2009, a study pub lished in the N ew TABLE 2 .2 ATP Produced From On e recyc li n g o f lactate into g lu cose fo r . use as an energT
3
En~land Jo urnal of Medic ine showed that adult humans have functionally active brown adipose t issue. Molecule of Palmitic Acid sou rce. p ro longecl e xercise \\'Oulc\ he sc, -ereh· lirni tc,d .
Us ing positron-emission tomog raphy and computed tomography (PET-CT) scans, resea rche rs found that Direct On a mo re in tegrati\'t:' k\'cl. !acu te pruc\ucl·~I in ,·xt-r-
th~ most common location for this brown adipose tissue in adults was near the clav icl es, that brown (substrate-level By oxidative cising skeletal muscle is ta ke n up ,rn c\ tlxid i;:ed in 1hc
~dipose was m o re frequently found in women tha n in men, and that individua ls with a h ig h er body mass Stage of process oxidation) phosphorylation b rain . T hus, lactate n ot onl\' is in tegralh· inniln·d ;1s , l
tndex_have _less br?wn fat. Because BAT promotes e nergy dissipation rathe r than energy storage (the ro le Fatty acid 0 -2 m etabolic l'u el b ut also resp ond s to c hanges in nu1 r it·n1
of ~~tte adipose tissue), it_s discovery in humans sparked great inte rest in the possibility of increasing the activation sensing as di ffe ren t n it·ta hol ic 1·u c ls art· used d u ring-
act1v1ty of BAT ~o target diseases like obesity and type 2 diabetes. ~-oxidation 0 28 cxcJT tst· .
~ev_eral studies have recently reported that chronic endura n ce exercise m ay promote the e xpress ion (occurs 7 t imes)
of similar the rmogenic (heat-producing) genes in white adipose tissue, resu lting in t h e brown ing of white
fa t . In '?ne an imal study, training-induced c hanges in fat type resu lted in increases in resting e n e rgy
Krebs cycle 8 72 Summary of Substrate
(occurs 8 times)
expenditure of up to 17% in trained rats. 2 It is still unclear whether exe rc ise training increases BAT mass Metabolism
o r prom?tes the browning of white a dipose tiss u e in human s , but stud ies are now underway to use the Subtotal 8 98
.-\s sl1tn,·11 in lig-11n· '.2. 1:~. liil' .1hili1, t(> prild 11n· 1n11s1·k
metabolic p otentia l of BAT to in crease whole-body e n ergy expend iture. Th e ult imate goa l of these studies Total 106 ('()ll ll'.tl'litll l f'u r ('Xl'l'l'i:--,· i:-- , I 111.ll ll'I' 111 ('llt'J'g, ,1 q1 ph
is to treat obesity and oth e r m e tabolic diseases.
 Fue l for Exercise: Bioenerget ics and Musc le Metabolism 69
R ESEA RCH PERSPECTIV E 2.2
Lifelong Training Can Lead to More Efficient Fuel Utiliza tion ;111d 1·111·rgY clv111;111d. Buth Lh c contractio n o f skelc.: tal
Inte raction o f the Ene rg y
1111 1-;clt- lilwrs ;11Hl th L·ir rL'bx;1tio11 r equ ire en c r1-,1;·. That
While aging is associated with a decrease in exercise capacity and spo rt p e rfo rmance, it is clear that the
skeletal muscle of o lder adu lts can be trained to meet the demand s of exe rcise . Re m ain ing physically active
t·1H-r1-,n. crn 1H·s fro111 foodstuff-; in th e diet ;i ncl stored Syst ems
1·11vrgY i 11 1he i>llrh-. T h e .-\TP-PC:r s~·s1crn operat es ,,·it h i n
throughout a person's life protects against some of the age-relat ed decremen t s in muscle-fiber size, fiber Th e three energy systems do not work inde pendentlY of
1IIL· n ·1c 1sn l of ti ll· ce ll. as docs g l~-col~·sis. and n ei th er
type, mitochondria l number, and oxidative capacity when comp are d to old e r sed e ntary people. These o n e another, and no acti,·i ty is 100 % suppo n e d bY any
n·q1 1in·s ox~·gl' 11 for .-\Tl' produc ti o n. Ox iclatin: phos-
age-related changes and adaptations are discussed si n g le eneq..,ry syst em. \ 1\'hen a p er son e x e r cises a t the
pltrn·~·l;i1 irn1 t;1 k1·s place " ·ith i 11 th e mitoc h o ndria. \!ote
in greater detail in chapter 18. hig h est in tensit~· possible , from the shortest sprints (l ess
'2 4,000 - 1li ;11 1111ckr ;1l'r< ,hi e co nditions. b o th rn;~jor substratcs-
A recent study performed at the University than 10 s) t o endurance evenL<, (greater than 30 min ) .
E
of Pittsburgh sought to determine whether the Cl
E
-- Younger carhol 1n l r;1t1·s ;111d E1 ts-;u T rccl 11cccl to th e com mon
i 1111-r111t"cli;1 11· ;HTtd C :o.-\ 1lta1 enters the Krebs n. ·ck.
eac h or th e energy systems is co ntributing t o the total
skeletal muscles of older masters ath letes had the - 3000 - - Older . e11<.- rs1;· n eed s or the body. Generally. o n e e n er g-· system
c '
same substrate storage and capacity for oxidation .Q dominates ene r gy prod u c ti on. except w h e n there is a
of those fuels as those of younger athletes who ro In Review tran si tion f"rom the p1·cdominance o f one energy syste m
trained similarly (i.e., used the same mode of ~X 2 ' 000 - to an oth el'. As an example. in a I O s. I 00 m sp r i nt. the
0
0 Th e oxidative system involv es the breakdown of
exercise and frequency of training). 4 That study a, r\TP-PC r sYstem is th e predom inant energy system. but
found that lifelong masters athl etes have greater E substrat e s in the presence o f oxygen. This system
both the anaerobic g l ycol \'li c and the oxidati,·e s,·st em s
-g_ 1,000 - -.-,,........---- - - - yi e lds more energy than the ATP-PCr or the g lyco-
triglyceride stores in their muscle fibers and a .s:::. p rm·idc a small p orti o n of t h e en e r gy nee d ed. A t th e
0 lytic syste m .
g reater proportio n of oxidative fibers compared ...co
.0
0 Oxidation of carbohydrate involves g lycolysis, the
o th er extr em e , in a 30 min . 10.000 m ( 10.936 )·d ) nm .
to the you ng athletes. These d ifferences resu lted u 0 _ . .... the oxidatiYe system is predominant. but both th e ATP-
20% 60% 9 0°0 Kre bs cycle, and the electron transport chain. The
in better metabolic efficiency-a lower reliance on PCr and anaerobic gl)·col~•tic sYst em s contribute some
Relative exercise intensity end result is H 7 0, CO 7 , and 32 or 33 ATP molecules
carbohydrate oxidation- during exercise at high energv as well.
p e r c arbohydrate molecule.
intensities in the o lder ath letes (see figure). Lifelong Figure 2. 14 shows th e r eciprocal r e latio n among t he
A simplified illustration o f carbohydrate ox ida ti o n a t dif- 0 Fat oxid ation begins with ~-oxidation of FFAs and
endurance exercise protects against some of the ferent r elative exercise inte n sities in young e r a nd o ld e r en er gy systems w i th r espe ct to pmn.T and capacitY. The
th e n follows the same path as carbohydrate oxida-
age-associated decreases in oxidative potential and adu lt athletes. Life long m ast e r s e ndurance a thl e t e s r e ly ATP-PCr en er gy system can prO\·ide en er gy at a fast r a te
tion : ace tyl CoA moving int o the Krebs cycl e and
provides older ath letes w ith an increased capacity less on carbohydrate oxidation at high e r exer c ise inte n- but has a ve1·y low cap a ci ty for energy production. Thus
the electron transport chain. The energy yield for
for fat oxidation to produce ATP during exercise. sities compare d to similarly trained young e r athl e t e s.
fat oxidation is much h igher than for carbohydrate
oxidation, and it varies with the FFA being oxi-
dize d . Howeve r, the maximum rate of high-energy
'en

Energy s u pply Energy dema n d

p hosph ate format ion from lipid oxidation is too
low to match t h e rate o f uti lization of high-energy
'E
en
en
ro
8

>- 6
phosphate during high er-intensity exercise, and the -0
at the intestine
j Contraction I energy yield of fat per o xygen molecule used is much Cl

l
Glycogen ~ 4
less than that for carbohydrate. a..
Rest
Exe ,clse ADP
+
) 0 A lthough fat provides more kilocalories of energy per !;;: 2
Myosin gram than carbohydrate, fat oxidation requires more 0
Glycolysis ® ATPase oxygen t h an carbohydrate oxidation. The energy
E 0
E PCr Glycolysis C HO Fat
(anaerobic) yield from fat is 5.6 ATP molecules per oxygen mole- oxidation oxidation
~

Lactic ,.
acid
•t
Pyruvate .,,,
AT P '.<
+
Ca -AT Pase
\
I Relaxation j
cule used, compared with carbohydrate's yield of 6.3
ATP per oxygen molecule . Oxygen delive ry is limited
by th e oxygen transport system, so carbohydrate
is the preferred fuel during high-intensity exercise .
O Maximal rate of ATP generation

100 -
Not limited
Fatty ~ Acetyl CoA Creatine
acids 0 Th e m axi mum rate of ATP production from lipid 80
t
+
Triglycerides Oxidative
phosphorylation
and citric acid
cycle
(aerobic)
I( J~
Creatine -® (PCr)
o x idation is too low to m a tch the rat e o f utilization
of ATP during high-intensity e xercise . This explains
th e reductio n in an at h le te's ra ce pace when car-
b o hydrate stores are d e pleted and fat , by default,
b e comes th e p redominant fue l source .
a.. 60
~
0
E 40

20
,!-
ADP 0 Measurement of protein oxidat io n is more complex
0
Muscle fiber b ecau se am ino acids contain nitrogen, which cannot PCr Glycolys1s CHO Fat
b e oxidize d . Pro t e in contributes re latively little to oxidation oxidation
e ne rgy p roduction, generally less t han 10%, so its 4:) Maximal available energy
m e tabolism is often considered ne gligible .
F IGUR E 2.13 The metabolism of carbohydrate, fat, and (to a lesse r extent) p ro te in sh ares som e c omm o n p a thw a y s within 0 D espite its rep utation as a potential fa cto r in causing FI GURE 2 .14 The vario us ene rgy syst em s have a recip-
t h e muscl e fibe r. The adenosine triphosphate (ATP) molecule s g ene rat ed by o xid ative and n onoxi da tiv e m e t a b o li sm are rocal re lati o n with resp ect t o (a) t h e maxima l rate at w h ich
fa tigue, lact ic acid can be , and is, used as an imp ort-
use d by t hose steps in muscl e contracti o n and relaxati o n th at d e m and energ y. energ y can b e p rod uced and (b ) th e cap acity to p ro duce
an t fu e l source durin g e xercise .
that energy.

68
70 Physiology of Sport a n d Exerci se Fuel for E xercise: B ioe nerget ics and Muscle Metabo lism 71

it suppo r ts exe rcise that is intense but o r VCJ'}' s h o n

duratio n . By contras t , fat oxida tio n ta kes lo n ger to
gear up a nd pro duces e n e rgy a t a slowe r rate; h mvc,-c r.
100 -
~ 90
tj - 100
- '.)0
0
:I:
u
( >Xi<b ti \'l· c;1p;1c it,· u ll illl,ttl'I~· dq1l'11cls 011 its ox id a ti,·e
1·111,·111<· co11n· 11 1r;11ions. lil)t'r type C<>lllposit ion . a11 d
<ix,·gl· 11 ;l\·;1 i h hi Ii t ,·.
o r oxidati\'C: enzymes . T,·1x· II fibers are beue r suited
for g lyco h-tic e nergy production. Thus, in ge n eral.
the more tv p e I fibers in one 's muscles, the greate1·
the a m o un t of energy it can pro duce is un li mite d . The
c h a r ac t e ristics o f t h e muscle fibe r's e n e rgy systems a rc
lis te d in table 2.3.
E
0
-=
"C
Ql
>
~~-- -l-
60 - -
- 80
- ;-o
- GO
E
~
"O
C
Enzyme Activity
th e o:xiclati\'C' capacit, · o r th ose muscles. Elite dista n ce
r unners. ror exam p le:, p ossess more type I fi b e rs. m o re
mitoc hond r ia. and h ig h e r muscle o:xidati,·e enzyme
·;:: >
Ql
so - - - 50 ~ Tl1l' c 1p;1ci1,· (Jr 1n11sclt- lilwrs 10 oxidi1c carhohnlr,11c
"C C aCLi\'it ics than do un trai ned indi,·iduals.
>- 40 - - - ,l O
"O ;11 1d L11 i.., cl inin d1 I<> d,·11-rmint·. :\u1n,-rous st udies han_•
~ >- End u ra n ce trai n ing enhanc es t h e oxiclati\'c capac-
The Crossover Concept Ql
C: 30 - 30
~
c.,
s liow11 ;1 clo~, · n·h1io11 l)t't\\'l'l'll a m 11sck"s ahilit,· to
ity or all libcrs. cspl'cia lly t:-pc II fibers. T raining that
w C:
w 1wrr( ll'lll pn il rn 1g,·d :ll'rohic t'Xl'l'Cisc a n d th t' act i,·i ,~-or
T h e crossover concept was first described by Brooks a nd ~ 20 - - ?O placcs ckm,111cls 011 o:xiclatiH· phosphoryla tio n stim u-
0 0
i 1s <>Xid;11 i\'l · 1·1 11,·1111 ·s. lkc11 1Sl' 111;111,· cl i rkrcn t c 11 z,·m cs
Mercier1 to d escribe th e r e la ti ve bala n ce b<.:tween ca r-
o-
- 10 lates the musc le lilwrs to dc,·elop more m itoc h o ndria.
;1n · n·q1 1i r,·cl lor ox id ;11i011. !ht· t' ll /~'lllt' ;1ct i,·it,· o r the
bohydrate (CHO ) a nd fat m e tabolism during sustain e d 0 0 large r m itoc h o 11 dria. and more o:xicbt i,·c enzymes per
Res t 20 '10 60 80 t OO 1n11.... c k lil wrs pro,·ic k s a n ·ason ahk i11d ic11io11 or 1lwir
exercise. A t r est a nd during e xe rcise at low to modera te mi1 ochonclr io11 . B,· increasin g the libcrs' en1.~·m es for
% Maximal oxygen uptake <ixicLtt in· p( >t1·1 1t i;tl.
inte n sities (below 60 % of m axim al oxyge n uptake) . f3-oxidation. this tra inin g a lso e nables th e muscle to
\k;1s1 11·i11g ;ill til l' l'll/.\'llll'S in 11111scks is impossible,
lipids serve as th e m a in s ubstrate fo r gen e rating r\TP. FIGURE 2 .15 The rel ation b0tv1c:c ·11 th<· l(• l.1t 1v1· < ontr,bu- rely more on En ror a e n1bic r\TP prod u ction. Thus.
S(> ;1 rt·\,· rl' p n·s,·11 1,11in· 1·11 1~·1111·s lt ;1n· hcl.'11 st'kctcd 10
During hi g h-intensity exerc ise (above 75 % of max imal tions of fat and ca rboh ydrat0 (C HO) util11.1t,c>r 1 t o overall \\"ith endur,IIHT train in g. L'\'l' ll people with large p er-
rl'lk ct llil' ;ll' ro hi c c;1p;1ci 1y o r !li t· fiht-rs. T ht· l'll /.\'lllt'S
oxygen up take), in creases in muscle g lyco ge n o lys is ene rgy exp endi ture as a funct,011 o f \'X(•I c ,.,._. ,n t,•n~, y The centages or typc 11 liblTs c 111 increase their muscles ·
11 H is l l rnp 11·111 I~· 1111·as11n·cl ;ire s11ccinate ckhnlroge n asc
a nd t h e r ecruitm e nt o f m o re type II muscle: fib e rs point at which t he two lines ,ntc:rsc:ct illuc;tr.itv'-. tlH' c.. l<1ss1c al'rnbi c capacitil's. But it is gentTal ly agTe cd that an
;111cl ci1 ra 1<· ,,·111 lt;1st·. 1ni1oc ho11drial l'll/\'lllL'S inn>h-ccl in
promote a shift to C HO as the pre d om in a nt substrate crossover concep t. . . L'nd u ran ce-trainecl type II fib<..T will not d c , ·clop the
t Iii' Kn·hs nT k (s,·,· lig1 1rt· ~-~l ) . Figure ~- 1li illustr;1tt·s
for gen e rating ATP. The crossover p o in t is the intensity samc h igh l'nduran cc capacit\' as ,1 simi la rh· tra ined
IIii' c I( >S<· corrcLt t io11 h l' I\\'t't'n s ucci na t,· rk hnlrogc11;1se type I libl'r.
wh e r e fat a nd carb o h ydra te utilization inte rsect (fi g ure s upply ;111d '-.l()rl"'-. ) ;111cl pi i, 11 ,· x , ·1, 1,, . I il.1 , ,,·,, ,11d.u-,.- ;1cti\'i1~- i11 tlil' , ·;1st 11s L11 t·r;tlis muscle ;111d 1hat muscle's
2. 15) as the ener gy from fat decreases a nd th e e n cq.,,-y ro h-s in dl"l<"l"llli 11i 11 g tlw li;1L 111 , ,. 11( ,1 il i, 11 .11, ·, 111ili /:l- , >x icL11in· ca p;1ci1~-- F11d1 1r;111n· ;11h lt-tt's' muscles hm-c
fro m carbo h ydrate in creases. Beyond t his c rossm·er
tio11 d11ri11g s 1il >111;1x i111 ;tl <"X<" I < i,1 ·. oxicL11in· 1·111,·1n1· ac 1i,·i1it·s t\,·o to ru11r tim es g reater
point, further in c reases in power are m et with further
tlt ;111 llt ost· 1>1· 11111 r;1 i11 l'd 1111·11 a11cl \\'Ollll' ll .
in crements in CHO utilization a nd d ecremc n Ls in fat
oxidation . The Oxidative Capacity Fiber Type Composition
Th e cr ossover point is affected by both th e exercise
inte n sity a nd e ndura n ce training s tatus. E nduran ce of Muscle and Endurance Training
tr a ini ng res u lts i n bi och e mical ada pta tio ns within th e \\'e haH· scT 11 1li;11 tl w pr<>n·..,-...·, <>I 11 :-.. icl.11i" · 111,·t:1 h u -
.-\ 1111 1sck's lil )('r t,-pt· co1nposit ion primarih detern1ines
m uscle fibe rs tha t p romote a nd suppo rt oxidatio n o r lism lt a\'C· llt C" l1igl1l"S I 1·1l<'rg, , ·i,·lck 11 " ·"1tlcl lH" idl';tl if'
its <>Xi<Litin· c;1paci1~·- .-\ s nott'd in chapt er 1. t,-pc I (slcl\\·-
FFAs, including an increase in th e numbe r o f mito- 1hcsc prolTssc·s;tl w;1~·s l1111 <"1i ,i111·cl ;11 IH';1k , ;q >; 1<" i1 , . 1\111 .
t \,·i Ic It ) Ii l)l'rs h ,1n· ,1gn·,ll lT capaci t,· ror aerobic an iYi 1y
chondria, increased oxida tive e n zymes, a nd c h a n ges as wi th a ll pli ysio log ic; tl .,,·s 1c·11 1'-. . 111 1·, "IH'r;11,· \\·i1 lt i n
11!,111 1,-pc II ( L1sl-l\,·i1 ch ) fihns because tYpc I fibers
in f3-oxidatio n and the e lectro n t ra n sp o rt ch a in - all certa in co11s1r;1i11ts. T II<' oxicL1 1i n· <;1p;1, it, " ' 111 11sc lc..· h ,1, ·1· 111111T mitoc li o 11dria and hi,,.hcr conn·111ra tio n s
;--,
impo r tan t d e te ,-m ina n ts o f fat m etabo lism. The result of (QO) is ;1 IJlc;1s 111T ol i1s 111 ;1x i11i;tl ,·;1p;1ci1,· I<> 11se
tr a ining is to a ll ow the body to sp a re muscle g lycogen , oxygen. Tlti s 111l'as11n·111 <·111 j-; 11 1;1clc· i11 Ill<' l;tlH> r; 1to1·~--
since carbo h ydrate s tores within th e body are limited. wh ere ;1 s111 ,dl ;1111 0 1111t o f 11111scl <" 1iss1 ll' <";11 1 IH' 1,·st,·d 18 -
These training-ind uced a d aptatio ns shift the crossover to cletc rrni11 c i1 s c;1p;1c i1~- t<1 c<> 11 -;11 111 ,· <>X\'g"l'll ,,· li<'n C)

point toward hig h e r exer cise inte n sities. Di e t (en e rgy c h e mi ca ll y s 1i1111 tl ,11 <·d I<> g 1·111T;11<" :\'I I'. . \ 11111 sc l1··~ ---
0
N 16

0
E 14
TABLE 2 .3 Characteristics of the Various Energy Supply Syst ems ~
~ 12
· Relative rate ATP formed per >
Oxygen Overall chemical of ATP formed molecule of Available ~
(ti
10
Energy system necessary? reaction per second substrate capacity :I:
Cl
(f)
ATP-PCr No PCr to Cr 10 1 < 15 s Q) 8
0(J)
G lycolysis No Glucose or glycogen 5 2-3 -1 m in :::,
6
~
to lactate
Oxidative Yes Glucose or glycogen 2.5 36-39* - 90 m in 0
0 2 3 4
(from carbohydrate) to CO2 and H 2 0
Oxidati ve capacity (00 2 ) (µL . g- 1 . h- 1 • 103 )
Oxidative Yes FFA o r triglycerides 1.5 > 100
(from fat) to CO 2 and H 2 0 Days FI GURE 2.16 The relation between muscle succinate dehy-
*Production of 36 to 39 ATP per m o lecule of ca rbo hydrate excludes e n e rg y cost o f transpo r1 th rough ,nernbra ,H)S Th,, 1101 1>1 odu, tH,) 11 r:;, drogenase (SDH) activity and it s oxidative capacity (00 2) ,
slightly lower (see text). measu red in a muscle biopsy sample taken from the vastus
(_r_,urr~sy of Dr Man,r- fJ1b;.,ld, Mrfvlaster Urnv']rs1ty, Harn 1lrc,n, On r r1r1fJ t ~a r i,. 1dr1
lateralis.
 ----
72 Physio logy of Spo rt and Exercise

l1111 g-.. ;ind t l u· lw .11 l lw ,1h l.1 , 1< · 1 .111d 11 1"1 , . ICJH clulh.
Oxygen Needs IN CLOSING
pump i 11~ IJl () t c· "''L!c· 11.11, · d 1,1,..,<f 1.. ii i ,· 11111,dt·, .
Altho ug h t he oxidative cap acity o f a muscle is d e te r- . \ rte r iolt-, d i l.11, · ' " l. 1, il11.11 , · cl , · 11 , , · I\ 11! .11 l n 1.d blond In t his cha pter, w e focused on energy m etabolism and t he synthesis of t he st o rage form of e n ergy in t he
m in e d b y the numbe r of mitoch o ndria a nd th e a m ou nt to 11111,c le · < ,1 p i ll.1 1 i, ·,. body, ATP. W e describ ed in some detail t he t hree b asic energy systems used to gene rate AT P and t heir
o f oxidative e n zym es prese nt, oxid a tive m e tabo lism "J h c l 11 1111 .111 l1,11h , 1,,1, ·, l11 1lc- , ,, ,:_: , · 11 I li, · 1do1t•. reg ulatio n and interaction. Final ly, we highlig ht ed the imp orta nt role t hat oxygen p lays in t he susta in ed
u ltim a te ly d e p e nds o n a n a d e qua te supply o f o xrgc n . LIH· ;t l)) ()l llll "' .. , , g , · 11 1· 111 , · 1111 :..: iltc · 1,1 .... .i .,, II j>,l ' l g e n e ration of ATP for continued m uscle contraction and t he three f ib e r t y p es found in h u man ske let al
At re s t, the n eed for ATP is re la tive ly sm all, rcq1 1ir in g tli rou g li 11 11· lt 11 1g, 1, <11,, · , 1h JH 11 J•11 11 , .. ,1. t1 ,., the.• muscle. We next look at t he neural control of exercising muscle.
m inima l oxygen d e live ry. As exe rcise inte nsity inc n:,Lo;cs . a11101 1nt 11 , <·cl I I\ li w 11 .... 11< ·, I, 11 , , ,1 .J . 11 t \C · 111 , ·1.d111li -..nl .
so d o e n e rgy d e m a nds. To m eet the m , the rate o f ox i- C:0 11..,ccpn· 111 h . ,1 11 ·. 1, " 11.tl,h ·", 111 .1 1, · , ·, 111 11.11<· <> I .u.•r-
KEY TERMS
d a tive ATP pro duc tio n in creases. In a n e ffo rt to m c:c t ob ic c·1tt· f h" p1 , ,cltl( ltc, 11 < .11 1 lw 11 1.1,I, · ll\ llt t". 1,111 in ,-.-
the muscles' n eed for oxyge n , the ra te a nd ckpl1 1 o f tlic · ;111101 11 11 11 1 " ' ' g , · 11 « 11 1, 11111< · .J .11 1lt, · ltt ng , ( '-l'C..- a c etyl c o e nzym e A (acetyl CoA) cyt ochro m e lipo lysis
respira tio n inc rease, im p roving gas exch a nge in the c li a p t 1·1 : , ) . a ctivation e ne rgy e lectron t ran sport cha in m eta b olism
ad e nosine d iphosphate (ADP) enzyme mitochondria
ae robic m etabolism free fatty acid s (FFA s) n e g ative fee d b ack

RESEARCH PERSPECTIVE 2.3 anaerobic metab o lism gluconeogenesis o xidat ive p h osphorylat ion
A TP- PCr system gluco se oxid at ive system
Does the Muscle Fiber's Oxidative Capacity Determine Fitness Level? p hospho c reatine (PCr)
f3 -oxidatio n g lycogen
Max ima l oxygen uptake (VO 2max; d iscussed in d eta il in chapter 5) is a m e asure,:n e nt of ca rd i~ r~sp irat o ry
bioen ergetics glycogeno lysis phospho fru ct okina se (PFK)
fitness, so it is not surprising that well-trained endurance athlet es have a high V0 7 ,,,,, . · Th e a bil i ty to take
in and use oxygen during aerobic exercise m ay be limit ed by any n umber o f factor s alo n g th e p a th way of carbohydrat e g lycolysis p ho spho rylation
the O m o lecu le as it moves from the atmosphere to the mitochondria t o b e u se d fo r e n e rg y : pulm o nary cat abol ism kil oca lories (kca l) rat e-l imitin g e nzym e
venti l~t ion, t he oxygen-carrying capacity of t he blood, and b lood fl ow to exe rc ising m_uscle , t o name a Krebs cycle su bstrate
c reatine kinase
f ew. Max imal oxygen upt ake is also an important predicto r of health, and re du ctio n s in V0 711 ,., , a re associ-
c rossover concept lipogenesis t riglycerides
ated with a loss of m o bility and independ ence in t he e lderly and an incre a se in m orta li t y in many chronic
d iseases. Because of its crit ica l ro le, exercise physio log ist s are keen ly inte rested in t h e f ac t ors t h at limit
\/O 2max in all p eople, from chron ic heart fa ilu re p atients t ? prof essiona l ~n d _u ran ce_ at h le t es. STUDY QUESTIONS
Since the early d evelopment of m easurement techn iques to q uantify VO 2 max 1n h u m a n s, resea rchers
1 . W h at is ATP, how is it formed, and ho w d oes it p rovid e energy during met ab o lism ?
have design ed st udies to systematically examine each p o int alo ng t he oxyge n d e liv e ry p a t h way from
inspired air t o t he mitochondria w ith in muscl e fibers. 2. W h at is t he prima ry su b strat e used to provide energy at rest ? D uring h igh- intensity exercise?
Beca use it is w e ll acce pted that increasi~g o xygen 3 . W h at is t he ro le of PCr in energy p ro duction, and w hat are its limit at ions? Describe t he re lat ionsh ip
supply t o the working muscl e improves VO2max and between m uscle ATP and PCr d uring sprint exercise.
ex e rcise capa city, many scie ntists b e liev ed t hat 4. Describ e th e essenti al characteristics of t he t hree energy syst ems.
the abi lity of the mitocho ndria themselves to use
5 . Why are t he AT P-PC r and g lycolyti c energy system s consid ered anaerobic?
oxyg e n- mit o chondrial oxidative capacity-was not
a limiting factor for maximal oxygen uptake. However, / 6 . W hat role does o xygen play in the process of aerobic met abo lism?
;
a recent study exam ined how w ell the mit o cho_ndria l I 7 . D escri be the by-products of energy production from AT P-PC r, g lycolysis, and oxidat ion .
oxidat ive capacity alone was associat ed wit h VO 2max 8 . What is lactic acid, and w hy is it important ?
8
acro ss p e ople of vastly d iffere nt fitn ess_leve ls. . 9 . Di scu ss t he interaction among the th ree energy syst ems w it h respect t o t he rat e at w h ich e nergy ca n
In t hat st udy, researchers measured VO2max d uring
b e produced and t he sust ained ca p acity to produce t hat e ne rgy.
cycl ing exercise in chronic hea rt fai lure p ati ents,
healthy subjects, and e lit e cyclists. They then t ook 10 . What is m eant by t he crossover concept, and how does it chang e w ith end u rance exercise tra ining?
muscle b io p sy sa mples fro m the quadricep s of each 1 1 . H ow do type I mu scle f ib ers d iffer fro m type II fibers in t heir respective o x idat ive ca pacit ies? W hat
subj ect to m easure mitocho ndrial ox idative capac- accou nts fo r those d ifferences?
ity. To q uant ify the muscl e fibers' capacity to utilize
o xygen, they m easured the activit y of an important Mitoc hondrial ox idative cap acity STUDY GUIDE ACTIVITIES
e nzym e in the Kreb s cycle, succinate dehydrogenase. (SDH activity) In add iti o n t o t he activit ies list ed in the chapter opening o utl ine, t w o o t her activ it ies are avai lab le in t he
Interesting ly, they found that this m easure of m it o- web st udy g uid e , locat ed at
Simplified figure showing th e re lat io n b etween mito-
cho nd rial oxid ative capacity was related t o V0 2m ax cho ndrial oxidative cap acit y, m eas ure d as succinat e www. Human Kinet ics.com/ Physio logyOfSpo rtAndE xercise
across all subject s, reg ardless of fitn ess or health d ehydrogenase activity in ske let al muscle biopsy sam-
st atus (see fi g ure). Their results indicat ed t hat w hile Th e KEY TERM S act ivit y rev iew s important t e rm s, and t he end -o f-chapt e r QU IZ t e sts your unde rstand ing
p les obtained fro m t he q uad ricep s aft er cycle exerci se,
limitatio ns in oxygen supp ly certain ly limit V0 2 max' and maximal o xyg en uptake in ch ro n ic he art fa ilure of th e m ateria l covered in t he chapt er.
m aximal oxyge n upt ake d uring whole-b ody exercise pat ients (C HF) , hea lt hy ad ults, and e lite cycl ists. M ax-
is p artially d et e rmined at t he leve l of t he m uscle imal oxygen uptake is close ly re lated t o m it ochondrial
fib e r itself. oxidative ca pacity across all three subject g roups.

73