INSTITUTO

UNIVERSIÁRIO
DA MAIA ISMAI

Fisiologia do Esforço
e Traumatologia no
Treino Desportivo

Pedro Figueiredo
ISMAI, 2019
 Metabolic Response and Fatigue
in Soccer
Jens Bangsbo, Fedon Marcello Iaia, and Peter Krustrup

The physical demands in soccer have been studied intensively, and the aim of
the present review is to provide an overview of metabolic changes during a game
and their relation to the development of fatigue. Heart-rate and body-temperature
measurements suggest that for elite soccer players the average oxygen uptake
596 M. Mohr et al.
during a match is around 70% of maximum oxygen uptake (VO2max). A top-class
vated concentrationsplayer of has 150 to 250 brief
catecholamine intense actions
(Bangsbo, during
game. a game, muscle
Recently, indicating thatobtained
tissue the rates before and
1994; Galbo, 1983). of creatine-phosphate
The results of studies (CP) utilization
using and
afterglycolysis
a soccer aregamefrequently high during
was analysed for muscle fibre
dietary manipulationa game, which
indicate thatis supported by findings of
lowered muscle reduced
type muscle
specific CP levels
glycogen and several-
depletion, using the PAS-
glycogen contributesfoldtoincreases in blood and
the development muscle lactate
of fatigue concentrations.
staining technique Likewise,
(Krustrup muscle pH
et al., 2003a). It was
during long-term isintermittent
lowered and exercise
muscle inosine
(Balsom,monophosphate
shown that (IMP)
after elevated
the gameduring a soccer
about half of the type I and
Gaintanos, Søderlund,
game.&Fatigue
Ekblom, 1999;toBangsbo,
appears type during
occur temporarily IIA fibres were almost
a game, but it isornot
completely
likely to depleted of
Nørregaard, & Thorsøe, 1992c). In a number of muscle glycogen. Thus,
be caused by elevated muscle lactate, lowered muscle pH, or change in muscle- fatigue at the end of soccer
studies, muscle glycogen has been determined games may be caused by glycogen depletion of
energy status. It is unclear what causes the transient reduced ability of players to
before, during and after a game. In a study by Saltin individual muscle fibres. Hypoglycaemia has also
(1973), the muscle perform maximally.
glycogen storesMuscle glycogen is reduced
were almost by 40% toto90%
been suggested during
cause a game
fatigue and long-term
during
is probably the most important
depleted at half time when the pre-match levels were substrate for energy production, and fatigue toward
exercise (Fitts, 1994), but the blood glucose con-
low (*200 mmolthe ! kgend
71 of a game might be related to depletion of glycogen in some muscle fibers.
dry weight). When the centration does not reach critical values during a
players started theBlood
game glucose and catecholamines
with normal muscle glyco- are elevated
soccer and
game insulin lowered
(Bangsbo, during
1994; a game.
Ekblom, 1986; Krustr-
gen concentrationsThe (*400bloodmmol ! kg71 dry weight),
free-fatty-acid levels increaseupprogressively
et al., 2003a). during
Othera factors
game, probably
such as dehydration
reflecting
the values were still rather an increasing
high fat oxidation
at half time, but compensating
and hyperthermia for the
havelowering
also been of suggested
muscle as agents
below 50 mmol ! kg 71
dry weight
glycogen. Thus, at thesoccer
elite end ofplayers
the have responsible
high aerobicfor the development
requirements of fatigue in the later
throughout
game. Others obtained
a gamemuscle biopsies anaerobic
and extensive before anddemands stages of aperiods
during soccerofgamea match(Reilly, 1997).
leading to During a
after a game and found the glycogen concentrations soccer game played in a normal thermal environ-
major metabolic changes, which might contribute to the observed development
to be *200 mmol ! kg71 dry weight after the game ment, many players lose more than 3 litres of fluid
of fatigue
(Jacobs, Westlin, Karlson, during and&toward
Rasmusson, the end of (Bangsbo,
Houghton, a game. 1994; Reilly, 1997), which may have a
1982; Smaros, 1980), indicating that muscle glyco- negative effect on performance towards the end of
gen stores are notKey Words:
always muscleduring
depleted lactate,a glycogen,
soccer CP,
theammonia, glucose,
match (Saltin, FFA,Itheart
1964). rate demonstrated
has been
that a loss in body mass of only 1 – 2% contributes to
A considerable number of scientific an studies haveinfocused
elevation core temperature
et
Performance
on the overall
al.,
physi-
as well as cardio-
ological demands of soccer by performing physiological measurements before and the
vascular strain (Hoffman 1994). In soccer,
average core temperature ranges from 39.0 to 39.58C
after a game or at halftime.1-6 Some studies have also examined changes in both
performance and physiological response1978). throughout
In thesethe game,individual
studies, with specialDistância
(Ekblom, 1986; Mohr et al., 2004a; Smodlaka,
valuesfocus
were above
on the most demanding activities and periods. 408C, which may be high enough towith
6,7
This brief review deals thecentral
present knowledge about the metabolicfatigue response during a soccer game, &
induce
with
due to a deterioration in cerebral functiona
intensidade
(Nybo & Nielsen; 2001). However, Mohr et al.
(2004a) found no differences in core temperature
between the end of the first and the second halves. In
The authors are with the Institute of Exercise and Sport Sciences,
a hot University
and humid of Copenhagen,
environment, a Copenhagen
decrease in body
Muscle Research Center, Universitetsparken 132 Copenhagen
fluid of 4 – 52100,
litresDenmark.
(Mustafa & Mahmoud, 1979) can
occur and hyperthermia may become a key factor in
the development of fatigue in the final stage of the
111 597
Fatigue in soccer
game.

Impaired performance in the initial phase of the

second half
It has been shown that top-class male soccer players
perform less high-intensity running in the first
5 min of the second half compared with the first
half (see Figure 5). In the following two 5-min
periods, no differences were found between the two
halves (Mohr et al., 2003a). This pattern is also
seen in the women’s game (unpublished observa-
tions) and in match officials (Krustrup & Bangsbo,
2001; Krustrup, Mohr, & Bangsbo, 2002). Such
findings lead to the proposal that the normal
routines of resting during the entire 15-min half- Figure 5. High-intensity running by elite soccer players during the
Figure 3. Distance covered by sprinting during 15-min periods initial phase of the first (&) and second (&) halves of competitive
time interval in soccer is not an optimal preparation
throughout competitive soccer games at the highest international games (n = 42). * Significant difference between the two Mohr et al., 2009
halves
level (A,forn =the
18) second half, which
and distribution has intervals
of 15-min been suggested
with the to Figure
(data4.from
High-intensity running and sprinting during the final
Mohr et al., 2003a).
most (&)relate to a (&)
and least decline in running
intense muscle for
temperature
elite players(Bangsbo,
during 15 min of a game by players participating in the entire game (&)
1995).
competitive matches (B, n = 93). * Significant difference from the and substitutes only participating in the second half (&). *
Several
first four 15-min studies
periods of thehave
game found a from
(modified closeMohr
relationship
et al., Significant difference between substitutes and players participating
2003a). between muscle temperature and high-intensity in the entire game (data from Mohr et al., 2003a).
 Fisiologia
Lactato
PH
Glicogénio

, and glycogen (C) before and after a soccer game as well as after intense periods in the first and second
FIGURE 1—Muscle lactate (A), pH (B), and glycogen (C) before and after a soccer game as well as after intense periods in the first and second
halves. Individual values are presented.

second halves (157 T 15 vs 155 T 13 bpm), whereas peak heart between the two halves (j14.4 to 27.8 mmolIkgj1 d.w.),
rate reached in the first half was higher (P G 0.05) than in the with a CV value of 74%. Muscle pH was 6.96 T j1 0.03 after
Krustrup et al., 2006
3 bpm), whereas peak heart between the two halves (j14.4 to 27.8 mmolIkg d.w.),
second half (186 T 9 vs 181 T 10 bpm). an intense period in the first half, which was lower (P G
0.05) than after an intense period in the second half (7.07 T
gher (P G 0.05) than in the with a CV value of 74%. Muscle pH was 6.96 T 0.03 after
Muscle Metabolites and pH during 0.02) and at rest (7.24 T 0.02) (Fig. 1B). The corresponding
bpm). Match Play an intense period in the first half, which was lower (P G
0.05) than after an intense period in the second half (7.07 T
Muscle metabolite concentrations, water content, and pH
before, during, and after a soccer game are presented in
0.02) and at rest (7.24 T 0.02) (Fig. 1B). The corresponding
Fisiologia
during Table 1.
Muscle adenosine nucleotides and CP. Muscle
ATP was 22.6 T 1.0 (T SEM) mmolIkgj1 d.w. after an in-

ns, water content, and pH

tense period in the second half, which was lower (P G 0.05)
than at rest (26.4 T 2.3 mmolIkgj1 d.w.). Muscle IMP was Glicogénio
0.6 T 0.2 mmolIkgj1 d.w. after an intense period in the
second half, which was higher (P G 0.05) than at rest.
r game are presented in Muscle CP was 67 T 3 mmolIkgj1 d.w. after an intense
period in the second half, which was lower (P G 0.05) than
at rest (88 T 2 mmolIkgj1 d.w.) and during the first half
tides and CP. Muscle (76 T 3 mmolIkgj1 d.w.).

molIkgj1 d.w. after an in-

Muscle lactate and pH. Muscle lactate after intense
periods in the first and second halves was 15.9 T 1.9 and
16.9 T 2.3 mmolIkgj1 d.w., respectively, which was about
hich was lower (P G 0.05) FIGURE 2—Relative glycogen content in ST, FTa, and FTx fibers as
fourfold higher (P G 0.05) than at rest (Fig. 1A). Large
well as all fibers before and immediately after a soccer match. Values
1
d.w.). Muscle IMP was intraindividual variations were found in muscle lactate
are means (N = 10).

an intense period in the

1168 Official Journal of the American College of Sports Medicine http://www.acsm-msse.org

(P G 0.05) than at rest.

Copyright @ 2006 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
j1
d.w. after an intense
was lower (P G 0.05) than
and during the first half

uscle lactate after intense

alves was 15.9 T 1.9 and
ctively, which was about
FIGURE 2—Relative glycogen content in ST, FTa, and FTx fibers as
at rest (Fig. 1A). Large well as all fibers before and immediately after a soccer match. Values
found in muscle lactate are means (N = 10).

an College of Sports Medicine http://www.acsm-msse.org Krustrup et al., 2006

rican College of Sports Medicine. Unauthorized reproduction of this article is prohibited.

 100
75
% Contribution
50
25
0

10 120 240 500

Time (s)

Aerobic Anaerobic
predicted aerobic predicted anaerobic

Cycle
Cycle Run
Run Swim
Swim
100
100
75
75

50%
50
50
25
0

10
10 120
120 240
240 500
500 10
10 120
120 240
240 500
500 10
10 120
120 240
240 500
500
Time
Time (s)
(s)
Aerobic
Aerobic Anaerobic
Anaerobic
predicted
predicted aerobic
aerobic predicted
predicted anaerobic
anaerobic
Graphs
Graphs by
by type
type of
of exercise
exercise
 Intensidade vs. Duração
Capacidade vs. Potência

110 Vescovi, Falenchuk, and Wells

20.0
18.0
_ - 16.0
•| 14.0

E 12.0
Z 10.0
"Z 8.0
X 6.0
S
"• 4.0
I Men O Wotnen
2.0
Troup, 1990
0.0 4 - - - ' - --
Freestyle Backstroke Breaststroke Butterfly IM

Figure 1 — Comparison of mean postrace [BLa[ between men (n = 66 races) and women
(n = 83 races) swimmers for each swim stroke. *Women's IM [BLa] higher compared with
women's freestyle, breaststroke, and butterfly {P < .034). **'Women's freestyle [BLa] lower
compared with women's backstroke and butterfly (P < .(X) 1 ) and also men's freestyle {P = .049).

O Freestyle •*
20.0
• »ackstrokc * * •
18.0
A IJrcaststrokc ***
16.0 O ButtciHy t

1 14.0 • IM
lUI)

i
12.0
2 10.0
flfi
g 8.0
6.0

1 4.0
2.0
0.0
50 100 200 400 800 1500
Race distance (m)

Figure 2 — Comparison of mean postrace [BLa] for each distances and stroke—men {n =
66 races) and women (« = 83 races) combined. *Breaststroke [BLa] lower compared with
the butterfly and backstroke in the 50 {P= .021) and 100 (P= .018) m races, respectively.
**Freestyle [BLa] lower after 50. 800 and 1500 m races compared with 100. 200 and 400
m races (P< .010). ***Backstroke and breaststroke [BLa] lower after 50 m races compared
[Vescovi et al., 2011]
with 100 and 200 m races (P < .001). tButterfly [BLa] lower after 50 m races compared
with 200 m races (P = .002).
 [Gastin, 2001]

Fontes de energia e metabolismo

Fosfatos de alta energia

ADENOSINA TRIFOSTATO (ATP)

SÍNTESE

ADP + Pi → ATP

QUEBRA

ATP ATPase ADP + Pi + Energia

Fuels for Exercise

Hidratos de Carbono

GLICOSE

Açúcar sanguíneo

GLICOGÉNIO

• Amazenado no fígado e músculo

• Sintetizado pela enzima glicogénio sintetase
• Glicogenólise = Quebra do glicogénio em glicose
 Fuels for Exercise
Lípidos

ÁCIDOS GORDOS
• Principal tipo de gordura usado pelo músculo
• Triglicerídeos
• Forma de armazenamento de gordura no músculo e
tecido adiposo
• Quebrado em glicerol e ácidos gordos

FOSFOLÍPIDOS
Não são usados como fonte
energética

Fuels for Exercise

Proteína

• Composta de aminoácidos
• Alguma pode ser convertida em glicose no fígado
– Gluconeogénese
• Outros podem ser convertidos em intermediários metabólicos
– Contribuem como fonte energética no músculo
• Na generalidade, a proteína não é uma fonte primária de
energia durante o exercício
 • descending'motor'activation'and'α7motoneuron'excitation'
• neuromuscular'transmission'
• sarcolemma'and't7tubule'excitation'
• excitation7contraction'coupling'–'SR'Ca2+'release'
contractile'activation'–'actin7myosin'cross7bridge'cycling'
Fontes de energia e metabolismo
•
• ATP'utilization'at'various'steps'
'
ATP7dependent'process'in'skeletal'muscle:'
cross7bridge'cycling'(myosin'ATPase)'
Sistemas energéticos no músculo esquelético:
sarcolemmal'excitability'(Na+/K+'ATPase)'
calcium'pumping'into'sarcoplasmic'reticulum'(SERCA'–'Ca2+'ATPase)'
'
Skeletal'muscle'ATP'generation'during'exercise:'
Substrate'level'phosphorylation'
• Fosfagénios • ATP/CP'
• “anaerobic”'glycolysis'
• Glicólise anaeróbia (glicose
Oxidative'phosphorylation' lactato)
• CHO'and'lipid/fat'(small'contribution'from'protein)'
'
• Metabolismo oxidativo de CHO e gordura (pequena contribuição da proteína)
'

'
'
'
'
'
Fontes de ATP para a Contração Muscular
'
$ $

Muscle'Study'Guide' ' The'University'of'Melbourne'7'2013'

Contribuição dos sistemas energéticos

Interaction Between Aerobic/Anaerobic ATP Production

Contribuição Aeróbia/Anaeróbia na Produção de ATP
 Interaction Between Aerobic/Anaerobic ATP Production
Contribuição Aeróbia/Anaeróbia na Produção de ATP

Fosforilação ao nível do substrato

(Catalisada pela
creatina quinase)

(Catalisada pelo
adenilato quinase)

(glicólise)
 Bioenergetics
Ácido láctico ou lactato?

Bioenergetics
Glicólise
 Bioenergetics
Glicólise

Bioenergetics
Conversão de Ácido Pirúvico em Ácido Lático
 Produção aeróbia de ATP

Requer O2, ADP e Pi, e dadores de eletrões

Fosforilação oxidativa (NADH, FADH2) produzidos pelo metabolismo
dos CHO e gordura

Glicose + 6O2 + 36ADP 6CO2 + 6H2O + 36ATP

Ácidos gordos + 23O2 + 130ADP 16CO2 + 16H2O + 130ATP

Quociente Respiratório (QR = VCO2/VO2)

QR para lípidos

C16H32O2 + 23 O2 → 16 CO2 + 16 H2O

VCO2 16 CO2
R= = = 0.70
VO2 23 O2

QR para CHO

C6H12O6 + 6 O2 → 6 CO2 + 6 H2O

VCO2 6 CO2
R= = = 1.00
VO2 6 O2
Wilmore and Costill, 1999
 substancialmente. Como consequência, a quantidade de O 2 necessária para o
catabolismo desses compostos vai depender, naturalmente, do tipo de substrato oxidado.
A calorimetria indirecta mede a quantidade de CO 2 libertado (VCO 2 ) e de O2
Quociente Respiratório (QR = VCO2/VO2)
consumido (VO 2). O quociente entre estes dois valores (VCO2/VO2) designa-se por
quociente respiratório (QR) (quadro 5).

QR = VCO2/VO2
HC
C6 H12 O6 + 6O 2 ! 6CO2 + 6H2O + 38ATP
Substrato Kcal/lO2 QR Kcal/g QR = 6 CO2 / 6 O 2 = 1,0
Lípidos Bioenergética
Glúcidos 5.05 1.00 4.2 C16 H32 O2 + 23O2 ! 16CO2 + 16H2O + 129ATP
QR = 16 CO2 / 23 O 2 = 0,7
Lípidos 4.69 370.71 9.5
durante o exercício , uma vez que têm uma finalidade Proteínas
essencialmente estrutural
Proteínas 4.46 0.80 QR = 63 CO2 / 77 O 2 = 0,8
(formam tecidos de suporte), razão4.2
pela qual o seu contributo energético é praticamente
desprezível.
Quadro 5. Representação do QR em função dos vários substratos catabolizados (Brooks et al. 2000).
Durante a oxidação dos HC verifica-se que o O2 consumido é idêntico ao CO2 produzido, por isso o
QR
QR=1. Já os lípidos e as proteínas implicam um Energia
consumo superior% kcal % kcal
de O2, razão pela qual o seu QR<1.
Dito de outra forma, do ponto de vista energético (kcal/lO 2)
a oxidação (HC)HC é claramente
dos (lípidos) vantajosa, porque
0.71(kcal) por cada
assegura uma maior produção energética 4.69 litro de O 2 0consumido. 100
0.75 4.74 15.6 84.4
Deste modo, uma vez determinado
0.80 38 o QR através
4.80 da medição
33.4 dos66.6
gases respiratórios, o
valor encontrado pode ser comparado
0.85 a uma tabela (quadro
4.86 50.7 6) de 49.3
forma a determinar o
0.90 4.92
tipo de mistura alimentar que está a ser oxidada. Por 67.5 32.5
exemplo, se o QR=1, então isso
0.95 4.99 84.0 16.0
significa que as células estão a1.00
utilizar apenas
5.05
glucose
100.0
e glicogénio
0
como substrato
energético e que por cada litro de oxigénio consumido são gerados 5.05kcal de energia.
Quadro 6. Relação entre o QR e os equivalentes calóricos correspondentes, sendo ainda referido o
Em termoscontributo energéticocom
comparativos, (%kcal) dado pelos
o mesmo HCde
litro e lípidos
O só(Wilmore
poderiam e Costill 1999).
ser gerados
2 4.69kcal a
partir da
Nooxidação lipídica.salientar
entanto, convém As proteínas,
que só éde uma forma
possível geral,
efectuar uma não são catabolizadas
avaliação correcta do gasto
energético da actividade física por calorimetria indirecta se se verificarem os seguintes

Calorimetria indireta
35
pressupostos:
Os espiroergómetros, (1) designados
vulgarmente se o esforço for são
por oxímetros, sub-máximo e constante;
equipamentos delicados (2)(custam
e dispendiosos se todo ATPa
entre 15.000 for
30.000 euros) que incorporam, entre outras coisas, um sensor de O 2 , um sensor de CO2 e um fluxómetro, este último destinado a
medir o volume de ar mobilizado durante a ventilação.
produzido através da respiração celular; (3) se a intensidade de exercício for inferior ao
36
O cálculo do dispêndio energético por calorimetria indirecta, assenta no pressuposto de que toda a energia produzida pelo
organismo limiar
durante asanaeróbio; (4) sedepende
actividades aeróbias o QR<1; (5) sedooOVO
da utilização 2 conseguir
2. Quando uma mistura estabilizar
de HC, lípidosao fim de é3min.
e proteínas oxidada,
libertam-se cerca de 4,82kcal/lO 2 . No entanto, este valor sofre ligeiras oscilações consoante a mistura utilizada. De forma a
simplificar os cálculos relativos ao dispêndio energético, utiliza-se frequentemente o valor fixo de 5 kcal como correspondendo ao
Toda a energia produzida pelo organismo acaba por
consumo de 1litro de O2. Assim se, por exemplo, os músculos estiverem a utilizar exclusivamente glucose e o organismo apresentar
37
um consumo Do de Oponto
2 (VOde vista
2 ) de energético,
3l/min, então aoprodução
contributo do catabolismo
energética será de das proteínas(3lO
15kcal/min e aminoácidos só tem algum significado durante o
2 /min x 5kcal).

depender da utilização do O2
exercício prolongado, quando o organismo se encontra fortemente depleccionado de glicogénio. Mesmo assim, o seu catabolismo
não assegura mais de 5-10% do dispêndio energético total, sendo o ciclo alanina-glucose o responsável pela produção de cerca de
metade dessa energia.
38
O valor do QR em repouso situa-se, habitualmente, entre 0.78 e 0.80.
28
•4,82kcal/lO2 quando uma mistura de CH, Lípidos e
Proteínas são consumidos

•Ocorrem variações consoante a mistura

Geralmente utiliza-se o valor de: 5 kcal/lO2

 Cálculo do gasto energético por
calorimetria indireta
Problema 1

Numa corrida submáxima com 30min de duração são consumidos,

em termos médios, 4lO2/min e produzidos 3,5lCO2/min

1. Calcule a energia dispendida nessa actividade

2. Calcule a % de energia produzida à custa dos HC e dos Lípidos

3. Calcule as gramas de HC utilizados

4. Calcule as gramas de Lípidos utilizados

Cálculo do gasto energético por

calorimetria indireta

Resposta 1

1. QR ? QR = 3,5 /4 = 0,88
Ver tabela equiv. Energético para 1 L O2= 4,89 kcal
Totalidade de O2 consumido = 30 x 4 = 120 L
120 x 4,89 = 586,8 kcal

2. Ver tabela % de CH e % de Lípidos: CH 60,8% = 357 kcal

Líp 39,2% = 230 kcal

3 e 4. Gramas CH = 357 / 4,2 = 85g

Líp = 230 / 9,5 = 24 g
 Cálculo do gasto energético por
calorimetria indireta
Problema 2

Atleta A gasta em média 45 ml/kg/min; v=12km/h; 60kg de

peso
Atleta B gasta em média 40 ml/kg/min; v=12km/h; 75kg de
peso

1. Num mesmo treino de 30 min, em percurso plano e a

velocidade estável, qual dispendeu mais energia?

2. Quantas Kcal gasta por minuto?

3. Quantas Kcal gasta por cada km percorrido?

Cálculo do gasto energético por

calorimetria indireta

Resposta 1.

Atleta A
VO2 total: [(60 x 45) x 30] : 1000 =81 L; 81 x 5 = 405Kcal
Atleta B
VO2 total: [(75 x 40) x 30] : 1000 =90 L; 90 x 5 = 450 Kcal

Respostas 2 e 3.
Atleta A
405 / 30 = 13,5 kcal /min; 405 / 6 = 68 Kcal /km
Atleta B
450 /30 = 15 Kcal /min; 450 / 6 = 75 Kcal /km
 Bioenergetics
Fosforilação oxidativa

Bioenergetics
Ciclo de Krebs
 Bioenergetics
Relação entre o Metabolismo de Proteínas, Hidratos de
carbono e Lípidos

Bioenergetics
Cadeia transportadora de eletrões
 Bioenergetics
Beta Oxidação

Control of Bioenergetics
Controlo da Bioenergética

Pathway Rate-Limiting Stimulators Inhibitors

Enzyme

ATP-PC system Creatine kinase ADP ATP

Glycolysis Phosphofructokinase AMP, ADP, Pi, ↑pH ATP, CP, citrate, ↓pH

++
Krebs cycle Isocitrate ADP, Ca , NAD ATP, NADH
dehydrogenase

Electron transport Cytochrome Oxidase ADP, Pi ATP

chain
Potência dos sistemas energéticos

Sahlin et al, 1998

Capacidade dos sistemas energéticos

Sahlin et al, 1998

 Energy Requirements at Rest
Necessidades energéticas em repouso

• Quase 100% do ATP é produzido pelo sistema aeróbio

• Lactato sanguíneo baixo (<1.0 mmol/L)
• O2 de repouso:
– 0.25 L/min
– 3.5 ml/kg/min

Rest-to-Exercise Transitions
Transição Repouso-Exercício

• Produção de ATP aumenta imediatamente

• O consumo de O2 aumenta rapidamente
– Chega a um steady state em 1-4 min
– Após o steady state ser atingido, o ATP necessário é conseguido
pela via aeróbia
• Produção inicial de ATP através das vias anaeróbias
• ATP-PC
– Glicólise
• Défice de O2
Sistemas energéticos no início do exercício

control (thin line

delivery to metab
ation of muscle c
cause, through “c
HR by parasympa
well as resetting
muscle contractio
an increase in m
increase in flow
such that total bl
of flow directed to
muscle pump act
flow to the requ
Figure 1. Schematic illustrating the potential sources of ATP, expressed (10,14).
in V̇O2 energy equivalents, at the onset of moderate intensity exercise
(steady-state V̇O2 # 1750 mL/min or 50% V̇O2peak for individual with “Feedback Con
V̇O2peak # 3500 mL/min). The major source of energy in the first seconds The achievem
of exercise is PCr hydrolysis. The net contribution from anaerobic glycolysis Hughson et al, 2001
state O2 deliver
to ATP supply will be expected to vary as a function of the rate of increase
in oxidative phosphorylation during this transition in metabolic demand. control mechan
The biphasic na
Sistemas energéticos em exercício de alta intensidade(10,14) is consi
We believe that this debate can be reduced to one primary control of musc
question. distinct pathway
propriate match
Can O2 Supply During the Entire Adaptation Phase feedback can co
Precisely Anticipate or Exceed O2 Demand? activation (e.g.,
Because there is an approximately linear relationship in tion (e.g., adeno
the steady state between metabolic rate (V̇O2) and each of oxidative metab
heart rate (HR), cardiac output, and muscle blood flow of ATP (e.g., P
(7,12), the O2 utilization hypothesis requires that O2 demand accumulation ac
must somehow be “anticipated” so that O2 supply can be O2 supply and d
precisely matched to or exceed the demand by feed forward itself would cau
control. With the exception of very light exercise, there does unless the bar
not appear to be an overshoot in the O2 delivery response, through further
further highlighting the need for exquisite precision of this system (SNS) ac
mechanism. stroke volume a
vascular beds of n
“Feed Forward” Control of O2 Delivery
skeletal muscle)
Figure 2 indicates potential mechanisms for feed forward delivery of O2 to
tonically active,
vated by the accu
of low blood flo
Paroling et al, 1999
An additional
adequate in addit
hemoglobin (Hb
Evolução do défice acumulado de O2
Série anaeróbia de 7x (20s a 170% pVO2max I=10 s)

Tabata et al, 1997

Armazenamento de glicogénio e glucose

 Substratos energéticos para o exercício - intensidade

SUBSTRATE UTILIZATION DURING EXERCISE E387

3oo f/$j Muscle Glycogen Table 2. Plasma concentrations of catecholamines
• l Muscle Triglycerides at rest, during exercise, and after 60 min of recovery
q Plasma FFA
q Plasma Glucose
v- Exercise Exercise, min Recovery
Intensity, Rest (60 min)
% iTo max 30 120

Epinephrine
25 38rt6 59+3* 52+8* 36+4
65 58217 199+18*t 239+28*t 62ztl7
85 36+7 625+86*$ 4428
Norepinephrine
25 231rt43 388+54* 372+41* 223+27
65 291+31 1,694+237*t 1,851&286*t 424+130
85 266219 5;085+914*$ 293+52
25 65 85 Values are means rt SE in mg/l. * P < 0.05 vs. rest. t P < 0.05 vs.
% of V02 max
exercise at 25% of ~osmax. $ P-C 0.01 vs. exercise at 25 and 65% of
vo2 max.
Fig. 8. Maximal contribution to energy expenditure derived from glu-
cose and FFA taken up from blood and minimal contribution of muscle
triglyceride and glycogen stores after 30 min of exercise, expressed as FFA turnover with increasing exercise intensity was off-
function of exercise intensity. Total amount of calories (Cal) available set by progressive increases in blood Romijnglucose turnover.
et al, 1993
from plasma does not change in relation to exercise intensity. Therefore the contribution of plasma substrates to ca-
loric expenditure remained essentially constant over this
wide range of exercise intensities. The changes in lipid
metabolism occurred concurrently with changes in car-
Substratos energéticos para o exercício - duração bohydrate metabolism, consistent with what would have
been predicted from previous work, namely that glucose
:: tissue uptake and especially muscle glycogen utilization
w 60 Plasma FFA
increased roughly exponentially in relation to exercise
%
$ 40 intensity.
5
Evaluation of Methods
‘ii 20
The use of stable isotope tracers for quantification of
s glucose and palmitate turnover is well established (35).
0
-15 30 45 60 75 90 105 120 Whole body oxidation rates of fat and carbohydrate were
calculated by indirect. calorimetry. This method relies on
B loo the assumption that VO, and VCO~ accurately reflect tis-
t sue 0s consumption and COB production (14). There is
little controversy with respect to VO,, of which there are
no large stores in the body. However, at exercise intensi-
ties that cause hyperventilation, VCO~ may overestimate
tissue CO2 production (13). This can potentially result in
the overestimation of the rate of carbohydrate oxidation
and, concomitantly, an underestimation of fat oxidation
(13). Therefore, before the present study, we conducted a
preliminary study that developed a new breath 13C-toJ2C
ratio method for the calculation of carbohydrate and fat
oxidation during exercise at low to high intensities that is
15 30 45 60 75 90 105 120
completely independent of the measurement of VCO~
Time (mln) (26). This new method proved that carbohydrate and fat
Fig. 9. Relative contribution of blood-borne and intramuscular sub- oxidation calculated by indirect calorimetry during exer-
strates to energy production during 120 min of exercise at 25% Voz maX cise is valid, including during exercise at 85% VO, max in
(B) and 65% (A) VO, mBx.Tg, triglycerides.
trained subjects, as performed in the present study.
The rates of fat and carbohydrate oxidation in excess of
Angus et al, 2002
lipolysis was high during low-intensity exercise and did the measured blood glucose and plasma FFA uptake are
not increase further with more intense exercise. However, assumed to equal the oxidation of intramuscular triglyc-
little lipolysis of muscle triglycerides occurred during low- eride and glycogen, respectively. There is no reason to
intensity exercise (i.e., 25% Vo, ,,,) compared with ex- believe that there are major fates other than oxidation for
glucose and FFA taken up by the tissues during exercise
Fatores que influenciam o metabolismo

• Intensidade e duração do exercício

• Dieta
• Treino
• Temperatura ambiente
• Idade e género

Estes efeitos são mediados pela

disponibilidade do substrato, nível
hormonal e características
bioquímicas do músculo esquelético

Metabolismo dos CHO durante o exercício

Spriet, 2002
Uso do glicogénio muscular durante o exercício

Gollnick et al, 1974

Regulação da glicogenólise muscular durante o exercício

Ca2+, Pi
Adrenalina
Músculo [glicogénio]
Glicose sanguínea ??, FFA
Temperatura
 Vias metabólicas preferenciais de acordo com o tipo de fibra

Schiaffino and Reggiani, 2011

Treino e glicogénio muscular durante o exercício

RYLASE REGULATION FOLLOWING ENDURANCE TRAINING

calculated free ADP, Aerobic contribution

ercise before and 225
1 E2Muscle lactate contribution
z 200- Blood lactate contribution
-u
7.5 min 15 min 2ii+ u) 175-
-A
;E .- 150-
26.61+ 1.50 25.79” 1.99 friiF5 125-
28.16 + 0.89 27.75 + 1.86
mv1
08 loo-
‘zi=3
grr, 75-
31.4 + 4.3* 29.3 + 4.3* 50-
45.1+ 4.1 41.5 + 4.7

PRE POST
337 *39-f- 364 t 42t
O-15 min
276 2 23 306 2 28
Fig. 6. Estimated anaerobic and aerobic contributions from muscle
glycogenolysis during 15 min of exercise at 80% of VOzlnax before (Pre)
4.68 + 1.39* 5.32 + 1.29* and after (Post) training. For assumptions and calculations see
2.71+ 0.48 3.42 ‘-+ 0.66 METHODS.

Chelsea et al, 1996

74.5 k 6.9* 78.7 k 8.P days of moderate intensity endurance training. Train-
52.0 k 6.0 55.4 + 7.6 ing resulted in a pronounced reduction of muscle
(n = 5) (n = 5) glycogen use during 15 min of exercise at 80% of VOzmax.
The plasma Epi response during exercise was blunted
 niques have been used to characterize exercise-induc
Leg glucose uptake ( atts creases in microvascular blood volume, an index of m
2 130 W
capillary recruitment, in rats and humans (56, 133,
Glicose durante o exercício 307). Although the extraction of glucose across a wo
1
tts 65 Wa muscle in vivo under most conditions is relatively low
8%), ERIKan increase in tissueAND
A. RICHTER glucose uptakeHARGREA
MARK has the pot
to decrease interstitial glucose concentrations; howeve
increase in glucose delivery and rapid transfer of gl
0
4 30 ence only increase
0 10 20 40 from ttsthe capillaries to the interstitium through the end
pores ensures that interstitialInglucose
addition to the
0W a
Time (min) 20lial levels are

Leg glucose uptake (mmol · min-1)

URE 1. Leg glucose uptake at rest and during cycle ergometer
skeletal muscle
maintained during exercise of increasing intensity (19 du
rcise of varying intensity and duration. [Modified
3 from Wahren et capillaries which
311).] Studies in the perfused rat hindlimb glucose delivery a
have demonstrate
importance of increases in perfusion niques
for have been
the contrac
a tts
0W
13induced increases in muscle glucosecreases
uptakein microva
(118, 277,
m the sarcolemma and T-tubules. With 2 exercise, skeletal

scle hyperemia, capillary recruitment, and GLUT4

The increase in both glucose and insulin capillary recruitm
delivery, secon
nslocation to the sarcolemma and T-tubules effectively to increased perfusion, contributes307). to enhanced
Although muscl
th
cose
65 Wa tt suptake. Indeed, it has been estimated that this
muscle in vivo un acc
move delivery and transport as major1 barriers to glucose
for !30% of the total exercise-induced 8%), anincrease
increaseini
ake, with glucose phosphorylation becoming potentially
iting, especially at high exercise intensities (156, 314). glucose uptake in dogs (344). Although plasmainterst
to decrease insuli
els decline during exercise, the increase in skeletal
increase in glucos m
dies from Wasserman and colleagues,0 using isotopic glu-
0 10 blood flow 30 may increase, or at least maintain,
from insulin
the capillarie
e analogs and the principles of countertransport (104), 20 40

well as transgenic manipulation of muscle GLUT4 andTime (min) ery to contracting skeletal muscle. Muscle contraction
lial pores ensures
okinase II (HKII) expression in mice insulin activate muscle glucose transport by differen
FIGURE 1. (76,
Leg 77, 79),uptake
glucose have at rest and during cycle ergometer maintained during
lecular mechanisms (93, 97, 184, 190, 233, 312), and
vided support for this hypothesis.
exercise of varying intensity and duration. [Modified from Wahren et
al. (311).] tractions, flow, and insulin have synergistic effects on
cose uptake in perfused, contracting Studies in the (118
rat muscle perf
Glucose Delivery exercising humans (57, Richter
315). In importance
and Hargreaves, 2013
the former ofleas
at inc
interaction betweenskeletal induced increases
insulin and contractions appearsi
from the sarcolemma and T-tubules. With exercise,
letal muscle blood flow can increasehyperemia,
muscle up to 20-foldcapillary
from critically dependent
recruitment, on adenosine The
and GLUT4 increase
receptors in bo
(305).
to intense, Glicose
dynamic exercise (7). Sinceoglucose to increased perfus
durante
translocation to theuptake
exercício is
sarcolemma and T-tubules effectively
product of blood flow and the arteriovenous glucose The arterial glucose level is the other cose uptake.determ
important Indee
remove delivery and transport as major barriers to glucose
erence, this increase in blood flow is quantitatively the for !30%
of muscle glucose uptake during exercise.
uptake, with glucose phosphorylation becoming potentially of the
Because gl
ger contributor to the exercise-induced increase in mus- uptake across an exercising limb followsglucose saturation
uptake in ki
limiting, especially at high exercise intensities (156, 314).
glucose uptake since the arteriovenous glucose differ- Locais and
Studies from Wasserman de regulação
with a Km found to be around 5 mM in dog muscle
els decline during
colleagues, using isotopic glu-
cose analogs and the principles of countertransport (104), blood flow may in
ery to contracting
as Capillary
well as transgenic
Interstitium manipulation of muscle GLUT4 and
Myocyte
insulin activate m
hexokinase II (HKII) expression in mice (76,P 77, 79), have
hexokinase lecular mechanism
provided support for this hypothesis. Glycolysis
Glucose G G6P tractions, flow, an
(G) GLUT cose uptake in per
A. Glucose Delivery Glycogenesis exercising human
interaction betwee
Skeletal muscle blood flow can increase up to 20-fold from critically dependen
rest to intense, dynamic exercise (7). Since glucose uptake is
the product of blood
SUPPLY TRANSPORT flow and the arteriovenous
METABOLISM glucose The arterial glucos
• Perfusion • Surface membrane
difference, this increase
• Blood glucose
in blood flow is•• Hexokinase
GLUT abundance
activity
quantitatively
Substrate flux
the of muscle glucose
larger contributor
concentration to the exercise-induced
• Glucose gradient increase in mus- uptake across an e
cle glucose uptake • GLUTsince
activitythe arteriovenous glucose differ- with a Km found t
FIGURE 2. Potential sites of regulation of muscle glucose uptake during exercise. [From Rose and Richter
(261).]
Capillary Interstitium Myocyte
Physiol Rev • VOL 93 • JULY 2013 • www.prv.org
Richter and Hargreaves, 2013
P
hexokinase

Glucose G G6P
(G) GLUT

Gly
Regulação da expressão de GLUT4 pelo exercício

Richter and Hargreaves, 2013

Regulação da glicose muscular durante o exercício

• Aumento da entrega de glicose - aumento do fluxo

sanguíneo
• GLUT4
• Disponibilidade de substrato (glicogénio, glicose, FFA)
• Adrenalina??
 a reduction in the R,,.
-3 IO Glucose Rd (Table
cr"
trials. Mean Rd duri
0
37.3 t 4.1 pmol*min
Treino, consumo e oxidação da glicose 3.5 pmol*min-lo kg-l

T mean rate of glucose

Rd/plasma glucose con

T I/ T 1" cantly with training, f

0.57 ml*min-l*kg-l (
Z' /
*4*
confirm our previous o
i'
v* * * * *-2*HP Hormone and subst
r/
A -2-2-P
o/P-P
lin concentration aver
untrained state and
exercise (Fig. 4, top).

- 40 150
v
'WI zc
‘s,
Y
G 30 2 100
.-'c
E Un
0- 20
.-c
E 5 50
1 co
- 10 -c
>r
rr" 0
0
I 1 1 . L . 1 . I

0 30 60 90 120 600
Exercise duration (min) T-
Coogan et al, 01997
Fig. 2. Total glucose production (R,; top) and estimated rates of
gluconeogenesis (Rgng; middle) and glycogenolysis (Rgly; bottom) at z 400
rest and during prolonged exercise before (0) and after (0) endurance -
training. *Significantly lower than before training (P < 0.001). a
Treino e glicose do fígado durante o exercício u
'F; 200
a>
Q
6
0

GLY: glicogenólise 90
GNG: gliconeogénese

60

0
Before After
training training Exe
Fig. 3. Estimated contributions of gluconeogenesis (GNG) and glyco- Fig. 4. Plasma insulin (top),
genolysis (GLY) to total glucose production (in mmol.120 min. kg tom) concentrations at rest
body wt-l) during prolonged exercise before and after endurance and after (0) endurance train
training. *Significantly lower than before training (P < 0.001). training: *P < 0.05 and “rP

Coogan et al, 1995

 Regulação da oxidação dos CHO - PDH

Howlett et al, 1998

Treino e destreino em futebolistas

to 801 T 162 and

ity, respectively.
during repeated
ns, there was no cor-
sed as T and MRT,
0.03 and 0.001, NS),
S), and Yo-Yo IR2
NS). A correlation
changes in V̇O2 ki-
3 for T and 0.27 for
0.25) but not MRT
found between the
e in Yo-Yo IR2 per-

distribution. In HI,
FIGURE 4—Mean values T SD and individual values of the change in the
and 32.7 T 3.6 Kmol amount of PDH in trained soccer players after 2 wk of high-intensity
23.7 T 2.1 and 22.5 T training group (HI, left, n = 7) or training cessation group (TC, right,
not change (Fig. 3), n = 8). *P G 0.05, **P G 0.01, post significantly different from pre. AU,
arbitrary units. Christensen et al, 2011
ated by 17% T 14%
intervention period
28.8 T 4.8 Kmol per (P G 0.01) by 12% and 18% after the inactivation period, and
10 Beneke, Leithäuser, and Ochentel
Metabolismo do lactato durante o exercício
with the increase in power. Usually INCP tests start at a power reflecting moder-
ate exercise intensity. The exercise intensity is subsequently increased by given
increments at given times. Over a range of low power increments, the BLC remains
more or less at resting level before it increases slowly but progressively during
subsequent steps in power (Figure 1).
Blood Lactate Diagnostics 11

Figure 1 — Example of BLC during INCP; the BLC does not increase during Figureincreasing
2 — BLC during CP according to INCP (Figure 1).
power up to an intensity of 48%; at 4 mmol⋅L–1 exercise intensity is 66%, which is lower
than the MLSS intensity of 83% of maximum power at test termination.
most threshold concepts reflect just slight variations of procedures developed in
the 1970s and 1980s.29–43
Lactate thresholds are generally accepted performance indicators. The ideafirst
The of the aerobic-anaerobic threshold28 was that it may detect an exercise
intensity
BLC-based threshold concept termed the aerobic-anaerobic threshold28 detected at or close to the highest prolonged CP at which, Beneke
after anetinitial increase, a
al, 2010
constant BLC is observed. The intention to verify this idea led to the concept of the
the power at a BLC of 4.0 mmol⋅L–1 during an INCP test with relatively long
maximal lactate steady state (MLSS).10,44 The MLSS is measured during a series
lasting stages of 5 min at minimum. This threshold, also termed the 4 mmol⋅L –1
of prolonged CP tests and defines an exercise intensity that is usually sustainable
threshold, was based upon empirical observations that long lasting constant
for 30 to 60 min.45,46 It detects the highest aerobic power without metabolic energy
exercise was sustainable if the BLC stabilized after an initial increase
from indicating
continuing net lactate production. This MLSS power is highly correlated
Regulação do metabolismo de lactato durante o exercício
equilibrium between lactate appearance and elimination (Figurewith 2). Atheconstant
maximum aerobic power. The between-subject variability of the MLSS
BLC indicates that the rate of glycolytic lactate generation is similar to high
is rather its use
and the MLSS is rarely found at a BLC of 4 mmol⋅L–1. MLSS values
as fuel for the aerobic metabolism. A decrease in BLC appears ifbetweenmore pyruvate
1.9 and 7.5 mmol⋅L–1 have been reported, which corresponded to exercise
and lactate are aerobically consumed than generated via anaerobic glycolysis.
intensities between 54 and 83% of the maximum power measured during INCP
If the rate of glycolytic lactate generation exceeds the corresponding rate of
testing. Surprisingly, MLSS, and MLSS intensity are independent of maximum
aerobic lactate utilization, the resulting net lactate accumulation power.
and increase
47 There inis evidence that the MLSS differs between different sports even
the BLC indicate a demand of anaerobic metabolic energy. During prolonged
if performed by the same athlete.48,49 Consequently, depending on the individual
running exercise, a constant BLC was frequently seen above BLC but baseline but conditions, the MLSS may reflect a BLC close to that typically
also on testing
rarely above 4.0 Produção é determinada pelo balanço entre a taxa
• mmol⋅L–1.28 found at rest or at a higher BLC, which may be significantly beyond 4 mmol⋅L–1
Shortly after Mader et al28 had published their threshold idea, an excessive
(Figure 2). Under selected conditions, the average MLSS power may be close or
de formação de piruvato e a oxidação
number of other threshold concepts were put forward and this process is still
similar to ongo-
the power corresponding to a specific BLC threshold measured during a
ing. Due to this “threshold inflation,” it is nowadays almost impossible to verify
selected INCP thetesting program. However, even then the preciseness of individual
correct number • of Níveis sanguíneos determinados pela taxa de
different threshold concepts published internationally.
MLSS However,
power predictions via INCP testing remains moderate. Therefore, threshold
determinations are likely to under- or overestimate individual MLSS power.10,44,48,50
produção e remoção de lactato Obviously differently defined thresholds determine different points on the
BLC power curve. These points reflect either (a) selected BLC values, (b) defined
increases in BLC above baseline or (c) specific changes in the steepness of the BLC
• Capacidade oxidava do músculo power curve or (d) combinations of BLC measurements during INCP testing, at
INCP test termination and during recovery.30,31,51 Thresholds detecting the power
• LDH iso-enzimas
• Abastecimento de O2 no músculo em exercício
• Adrenalina
• Músculo [glicogénio]
Treino e metabolismo lático durante o exercício

Bonen et al, 1998

Destino metabólico do lactato

• Oxidação no músculo esquelético (tipo I) e cardíaco

(recuperação ativa melhora a remoção de lactato)
• Substrato para a síntese de glicogénio
• Conversão para outros metabolitos (ex. aminoácidos)
• Não aumenta o VO2 ou causa desconforto muscular
 Factors Governing Fuel Selection
Lactato como fonte energética durante o exercício

Pode ser usado como uma fonte de combustível

pelo músculo esquelético e coração
• Convertida em acetil-CoA e entra ciclo de Krebs

Podem ser convertido em glicose no fígado

• Ciclo de Cori

Transportador de Lactato
• Lactato produzido em um tecido e transportada para outro

Chapter 4 Factors Governing Fuel Selection

Ciclo de Cori: Lactato como fonte energética
Chapter 4 Recovery From Exercise: Metabolic Responses
Recuperação ativa melhora a remoção de lactato

Chapter 4 Metabolic Responses to Exercise: Influence of Duration and Intensity

Alterações no lactato sanguíneo durante exercício
incremental
 Cunniffe et al. 0–6.0 Standing, 6.0–12.0 Jogging 12.0–14.0 Cruising 14.0–18.0 Striding
[36] walking
Hartwig et al. 0–1.0 Stationary 1.0–7.0 Walking 7.0–12.0 Jogging 12.0–21.0 Striding 18.0–20.0 High-intensity [21.0 Sprint
[32] running
Chapter 4
Venter et al. [34] 0–1.0 Standing \20 %
Vmax
Walking 20–50 %
Vmax
Jogging 51–80 %
Vmax
Striding 96–100 %
Vmax
Maximum
sprint

Limiar anaeróbio e zonas de velocidade em futebol

Higham [35]
Suárez-Arrones
et al. [33]
0.1–5.9 Standing,
walking
0–7.2
6.0–11.9 Jogging
7.2–12.6
12.0–13.9 Cruising
12.6–18
14.0–17.9 Striding
18.0–21.6
18.0–19.9 High-intensity
running
[21.6
[20 Sprinting

Rugby League
McLellan et al. 0–6.0 Standing/ 6.1–12 Jogging 12.1–14.0 Cruising 14.1–18.0 Striding 18.1–20.0 High-intensity [20.1 Sprint
[5, 40] walking running
Austin and Kelly 0–12 Standing, 12–14 Cruising 14–18 Striding 18–20 High- 20–24 Sprinting [24 High-
[37] walking, or intensity intensity
jogging running sprinting

GPS Technology in1034

Table 2 Zone classification of work rate patterns in team sports
Duffield et al. \14.4 Low-speed [14.5 High-speed [20 Very-high
References
[38] Zone 1 Zone 2 Zone 3 activity Zone 4 running Zone 5 Zone 6 speed
running
Speed Description Speed Description Speed Description Speed Description Speed Description Speed Sprinting
Gabbett et al. (km!h-1)a Low speed
0–3.6 [3.6
(km!h-1)a High speed (km!h-1)a (km!h-1)a (km!h-1)a (km!h-1)a
[39]
Australian
Soccer Football League (AFL)
Table 2 continued
[14.4 [20.0

Team Sports
Farrow
BarberoetAlvarez
al. [21] 0.0–0.4 Standing/stop 0.5–3.0 Walk 7.2–14.4
3.1–8.0 Moderate
Low-intensity 8.1–13.0 High
Mediumvelocity 13.1–18.0 High-intensity [18.0 Sprint
et al. [26]
References Zone 1 Zone 2 Zone 3 velocity
running or Zone 4 intensity Zone 5 running Zone 6
Brewer et al. [19] trotting [15.0 running
High- 20.0–23.0 Higher-speed [23.0 Sprint
Speed Description Speed Description Speed Description Speed Description Speed Description Speed Sprinting
Hill-Haas [29] 0–6.9 7.0–9.9 10.0–12.9 13.0–15.9 intensity run 16.0–17.9 running [19.1-1 a Sprinting
(km!h-1)a (km!h-1)a (km!h-1)a (km!h-1)a (km!h-1)a (km!h )

1033
Aughey and 15.2–18.0 Jog [18.0 [25.0
Falloonet[18]
Hill-Haas al. 0.0–0.4 Standing/stop 7.9–12.9 Jogging 13.0–17.9 Cruising Sprinting
Coutts
[30] et al. [20] 0–0.7 Standing 0.7–7.0 Walk 7.0–14.4 Jog 14.4–20.0 Run 18.0–24.9 Run 24.9–36.0 Sprint
Wisbey et
Castagna et al.
al. [24] 0–0.4
0–0.8 Standing 8.0–12.0
0.4–3.0 Walking 12.0–16.0 Jogging
3.0–8.0 16.0–18.0 Medium-
8.0–13.0 18.0–21.6
13.0–18.0 High-intensity [18.0 Sprint/
Sprinting
[25] intensity running maximum
running intensity
Aughey [17]
Casamichana 0–3.9 Stationary– 7.2–10.8 4.0–6.9 Jogging 14.4–18.0 Quick
7.0–12.9 13.0–17.9 High-intensity [18.0 Sprinting
Castellano
Rugby Union[28] walking running running
Bucheit
Hartwiget et
al.al.
[27] 0–1.0 Stationary 1.0–7.0 Walk \13
7.0–12.0 Low-intensity
Jog 13.1–16.0
12.0–21.0 High-
Stride 16.1–19.0
81.0–95.0 % Very high-
Sprinting [20.0
[21.0 Very
Sprinthigh
[31] running intensity Vmax intensity intensity
running running
Cunniffe et al. 0–6.0 Standing, 6.0–12.0 Jogging 12.0–14.0 Cruising 14.0–18.0 Striding
Harley
[36] et al. [16] Standing
walking Walking Jogging Running High-speed
running
Hartwig et al. 0–1.0 Stationary 1.0–7.0 Walking 7.0–12.0 Jogging 12.0–21.0 Striding 18.0–20.0 High-intensity [21.0 Sprint
Cricket
[32] running
Petersen et al.
Venter et al. [34] 0–1.0 Standing \20 % Standing/
Walking 7.2–12.6
20–50 % Jogging
Jogging 12.6–14.4
51–80 % Running
Striding 14.4–18.0 Striding 96–100 % Maximum
[41–43] Vmax walking Vmax Vmax Vmax sprint
Hockey
Higham [35] 0–7.2 7.2–12.6 12.6–18 18.0–21.6 [21.6
Gabbett [44]
Suárez-Arrones 0–3.6
0.1–5.9 Low intensity
Standing, 6.0–11.9 Jogging 3.6–10.8
12.0–13.9 Moderate
Cruising 10.8–18
14.0–17.9 Moderate
Striding 18–25.2
18.0–19.9 High intensity
High-intensity [20 Sprinting
et al. [33] walking intensity intensity running
Macutkiewicz
Rugby League 0–0.6 Standing Walking 6.1–11.0 Jogging 11.1–15.0 Running 15.1–19.0 Fast running
and Sunderland
McLellan et al. 0–6.0 Standing/ 6.1–12 Jogging 12.1–14.0 Cruising 14.1–18.0 Striding 18.1–20.0 High-intensity [20.1 Sprint
[46]
[5, 40] walking running
Jennings et al. 0.36–15 Lower speed [15 Hig-speed
Austin and Kelly 0–12 Standing, 12–14 Cruising 14–18 Striding 18–20 High- 20–24 Sprinting [24 High-
[45] activity running
[37] walking, or intensity intensity
Lacrosse jogging running Cummins et al,sprinting
2013
Duffield
Duffieldetetal.al. \7.0
\14.4 Low-intensity
Low-speed 7.0–14.4
[14.5 Moderate
High-speed [14.5 High-intensity [20 Very-high
[48]
[38] activity
activity intensity
running run speed
activity running

Chapter
V Gabbett 4
et al.velocity0–3.6
maximum
max
[39]
Low speed Metabolic
[3.6 HighResponses
speed to Exercise: Influence of Duration and Intensity
a
Except where otherwise stated
Soccer
Mecanismos explicativos do limiar lactatémio
Barbero Alvarez
et al. [26]
0.0–0.4 Standing/stop 0.5–3.0 Walk 3.1–8.0 Low-intensity
running or
8.1–13.0 Medium
intensity
13.1–18.0 High-intensity
running
[18.0 Sprint

trotting running
Hill-Haas [29] 0–6.9 7.0–9.9 10.0–12.9 13.0–15.9 16.0–17.9 [19.1 Sprinting

1033 C. Cummins et al.

Fatores influenciadores da re-síntese do glicogénio
muscular

Custo energético da
Locomoção
• Atividade da glicogénio sintetase
• Grau de depleção de glicogénio muscular
• Expressão de GLUT4
• Níveis de glicose sanguínea e insulina, influenciados pela
ingestão de CHO (quantidade, tipo, timing)
• Dano muscular