The effects of carbohydrate feeding on metabolic responses to sub-maximal steady state exercise

Introduction

Energy is required for muscle contraction during exercise and the main molecule that

enables muscle contraction is ATP (Baker et al., 2010). ATP is a high energy

molecule that is produced by various energy systems. The four main energy systems

are the phosphagen system, glycolytic system, oxidative phosphorylation system

and adenylate kinase system. These energy systems interact simultaneously during

exercise and these energy systems are affected by exercise intensity and duration.

During sub-maximal exercise, mainly glycolysis and oxidative phosphorylation are

the main energy systems that provide ATP however the flux of these energy systems

is dependent on the availability of fuels and the activity of key enzymes. During

exercise there are various fuel sources. The main fuels are lipids, carbohydrates

(CHO) and amino acids.

Fuel utilisation is particularly effected by intensity and duration. Based on previous

research (Romijn et al., 1993), lipid oxidation is maximised during low-moderate

intensity exercise and CHO sources are mainly utilised during high intensity

exercise. Duration effects fuel utilisation by increases in fat oxidation and decreases

in CHO oxidation as exercise time increases (Watt et al, 2002). These differences in

fuel utilisation are due to the switching on-off of key regulatory sites for CHO and

lipid metabolism. In this study we are aiming to investigate fuel utilisation during sub-

maximal exercise.

During sub-maximal exercise, fuel utilisation is regulated by key enzymes which are

allosterically regulated. Glycogenolysis is a key regulatory site for CHO metabolism

which is catalysed by enzymes glycogen phosphorylase and phosphoglucomutase.

These enzymes are particularly activated by Ca2+ ions, ADP, AMP and Pi and

adrenaline however inhibited by high ATP and glucose-6-phosphate (G-6-P)

concentrations (Dyck et al., 1996). Glycogenolysis rate is greatest during high

intensity exercise due to greater concentrations in AMP and P i (Dyck et al., 1996).

Glycolysis is also a key regulatory site which is the process of breaking down

glucose. This mechanism has three rate limiting enzymes: hexokinase,

phosphofructokinase (PFK) and pyruvate dehydrogenase (PDH). PDH activity

particularly increases with increasing power output due to large increases in

pyruvate, Ca2+, ADP, AMP and Pi concentrations (Howlett et al., 1998). Increases in

G-6-P have been found to inhibit hexokinase activity during high intensity due to a

greater glycogenolysis rate (Wilson, 2003) whereas glucose availability will increase

hexokinase activity. PFK is allosterically inhibited with high ATP, H+ and citrate

concentrations (Uyeda & Racker, 1965) however high concentrations of ADP, AMP

and Pi will activate PFK.

A regulatory site for lipid oxidation is lipolysis which is catalysed by hormone

sensitive lipase (HSL) in the adipose tissue, liver and skeletal muscle. Peak HSL

activity is during low-moderate intensity exercise due to elevation in adrenaline and

low insulin concentrations (Watt et al., 2003). However HSL activity is inhibited

during high intensity exercise due to increases in AMP concentrations and the

activity of AMPK, which inhibits HSL activity (Watt et al., 2005). Lastly another

regulatory site is the transfer of long chain fatty acids (LCFA) across the

mitochondrial membrane. Malonyl-CoA is an inhibitor of carnitine palmitoyl

transferase I (CPT-I) and is usually activated when acetyl-CoA concentrations is high

(Jeukundrup, 2002) and in the presence of insulin, however intensity does not

significantly affect malonyl CoA concentrations (Odland et al., 1998). There is also

evidence to suggest that carnitine availability is key and during high intensity

exercise, carnitine concentrations is reduced due to high a rate of acetyl-carnitine

production (Roepstorff et al., 2004).

Based on availability of glucose and free fatty acids (FFA), previous research has

looked at the effects of feeding on metabolic responses during exercise. In

competition, athletes are advised to have a pre-exercise meal before performance to

replenish muscle glycogen and liver glycogen stores (Jeukendrup & Gleeson, 2010).

A pre-exercise meal maximises muscle glycogen content and there is a proportional

relationship between muscle glycogen content and cycling performance (Bergstrom,

1967). Research has also looked at the effects of a lipid diet on performance.

However based on the glucose-fatty acid cycle (Randle et al., 1963), increases in

free fatty acid availability will reduce glycolytic flux. This reduction in CHO utilisation

has found a decline in performance during steady state exercise (Starling et al.,

1997). Therefore as there was no significant effect of increased fat availability on

performance, the aim is to investigate the effect of CHO feeding before and during

exercise on metabolism rather than increasing lipid availability. As nutritional

strategies are important for maximal performance, this study aims to investigate the

effect of feeding immediately before and during exercise on metabolism. My

hypothesis is CHO ingestion will increase CHO utilisation compared to fasted group

based on a greater CHO availability. Also exercising in a fasted state, will utilise

more lipids compared to fed state.

Methods

Participants: Twenty-three healthy students (19 Males, 4 Females) volunteered to

participate in the study with the subject characteristics are on table 1. Participants

were randomly selected into two groups; a group that were fed CHO before and

during exercise (13 participants), and a group which fasted overnight and was only

permitted to drink water during exercise (10 participants). All participants had no

breakfast on the morning of testing and was only allowed to drink water. They was all

informed of the protocol before experimental trials and with verbal consent they was

able to participate in the study.

Design: The experimental design was a two-way design with repeated measures.

Two groups were used which was a fed group and a fasted group. Both groups

exercised for 30 minutes at an intensity of 130 W and maintaining a speed of 70 rpm.

Fed group were given 500ml of Lucozade sport before exercise and was given 150

ml of Lucozade Original during exercise (at 15 minutes) however fasted group only

consumed water. We measured glucose (Glucose HemoCue Hb 201+ system,

HemoCue, Sweden), lactate (Lactate Pro, Arkray, Japan), glycerol, and NEFA

(Randox Laboratories, Antrim, UK) concentrations before and during exercise. We

collected expired gas during exercise by using Douglas Bags (for 1 minute) and the

gas was analysed by using the servomex and the dry gas meter to measure %VO 2

and %VCO2, and amount of gas expired respectively. Heart rate was measured

using a heart rate monitor (Polar

S610i, Kempele, Finland) and lastly

the participants RPE was verbally

described by the participant.

Protocol: Participants arrived at the

laboratory and their height and

weight was measured. They rested

Table 1. Mean ± SD of Age, Height, Weight and BMI for the fasted group and fed group

Fasted Fed

Age, yr 21 ± 1.2 22.2 ± 1.2

Height, m 1.77 ± 1 1.80 ± 6.1

Weight, kg 72.9 ± 15.1 78.4 ± 12.6

BMI 23.15 ± 2.73 24.07 ± 3.08

for 5 minutes on a chair in an upright position, and we measured their resting blood

sample using the capillary finger prick technique (Safety Lancet, Sarstedt, Germany)

to measure blood metabolites. All blood samples was collected in a microcuvette

tube, which was labelled and stored in an ice bucket for future analysis. Then the

participants consumed their 500ml drink of either Lucozade Sport (fed group) or

water (fasted group). Then blood samples were collected before exercise and we

also recorded their heart rate and RPE. Then the participants cycled on a cycle

ergometer for 30 minutes at an intensity of 130 W, and maintaining a speed of 70

rpm. Participants consumed their drink at 15 minutes of exercise. Heart rate and

RPE was collected at 10, 20 and 30 min of exercise. Blood metabolites were

collected at 15 and 30 min of exercise. Gas was collected using the Douglas bags at

10 and 25 min of exercise. Gas was analysed by the servomex and dry gas meter to

measure the VO2 and VCO2 concentrations, and the temperature and volume of gas

in the Douglas bags. CHO and Lipid oxidation was calculated by using the formula:

CHO oxidation (g/min) = (4.21 x VCO2)–(2.962 x VO2)

Lipid Oxidation (g/min) = (1.695 x VO2)–(1.701 x VCO2)

(Jeukendrup & Wallis, 2005)

Statistical Analysis: Mean and standard deviation of the blood metabolites, RPE,

heart rate, and oxidation rates was calculated in Microsoft Excel (2013). Statistical

analysis was performed by using a two-way mixed ANOVA for all measured

variables apart from oxidation rates of CHO and lipids, which was performed by

independent t-test. Statistical analysis was performed on SPSS 23.

Results

Blood glucose concentrations: There was a significant main effect for group

(F1,21=7.386, P=0.01) on blood glucose levels where blood glucose levels was

greater at pre-exercise and at 15 minutes of exercise for the fed group compared to

fasted group (Fig. 1). However glucose levels were similar between both groups at

30 minutes of exercise. There was a significant effect for the time (F2.2, 45.2=17.578,

P<0.001) where the fed groups blood glucose levels increased when CHO was

ingested and then gradually decreased during exercise. However for the fasted

group, glucose levels were unchanged (5.1 mmol/L). There was a significant

interaction (F2.2,45=15.467, P<0.001) where both groups had similar blood glucose

levels at pre-feeding and at the end of exercise, however blood glucose levels was

higher at post feeding (8.3 mmol/L) and at 15 minutes (5.9 mmol/L) during exercise

for the fed group. Fed groups blood glucose levels returned to normal at 30 minutes

of exercise (5.3 mmol/L)

Blood Lactate concentrations: There was not a significant main effect for fed state

during exercise (F1, 21=1.86, P=0.19). However fasted group had a larger blood

lactate concentration at 15 minutes of exercise by a difference of 1.3 mmol/L (Fig. 2). There was a significant main effect for time (F1.6, 33.3=100.498, P<0.001) on blood

lactate levels where lactate levels increase during exercise for both groups to a

concentration of 4.9-6.2 mmol/L and lactate concentrations decreased towards the

end of exercise. However there was no significant interaction (F1.6, 33.3= 1.71,

P=0.174) of time and group.

Blood NEFA concentrations: There is a significant main effect of group (F1,21=11.61,

P=0.003) on the concentration of NEFA (Fig. 3) during exercise where there were

increases in NEFA concentration for the fasted group with the greatest NEFA

concentration was at 30 minutes of exercise (0.67 mmol/L). However there was a

gradual decrease in NEFA concentrations in the fed group by a difference of 0.07

mmol/L. There was also a significant main effect of time ( F1.7, 36.5= 4.689, P=0.02)

where there were increases in NEFA concentrations during exercise for the fasted

group however there was a decrease in NEFA for the fed group. Lastly there was a

significant interaction between group and time (F1.74, 36.5= 17.23, P=0.001).

Blood Glycerol concentrations: There was not a significant main effect for group (F1,

21=4.102, P>0.05). However there was a significant main effect of time (F1.76,

37=28.55, P=0.001) on glycerol concentrations (Fig. 4) where the fasted group

gradually increased glycerol concentrations throughout exercise with glycerol levels

was at its highest at 30 minutes during exercise (218 mmol/L). However for fed

group there was a slight decrease when ingesting CHO and then there were small

increases in glycerol concentration during exercise by a difference of 10 mmol/L at

30 minutes of exercise. Lastly there was a significant interaction (F1.76, 37.02=16.91,

P=0.001) between group and time of measurement.

Heart Rate: There was not a significant main effect of group (F1,21= 2.507, P>0.05) on

heart rate (Fig. 5). However there was a significant main effect of time (F1.6,

35.24=227.73, P=0.001) where both fasted and fed group increased heart rate as time

increases until 10 minutes where the heart rate plateaus. Lastly there was not a

significant interaction between group and time (F1.68, 35.24=2.04, P>0.05) however

fasted group had a higher heart rate at time points of 10 minutes, 15 minutes and 30

minutes of exercise by a difference of approximately 15 bpm. The maximal heart rate

for fasted group and fed group was 155 bpm and 139 bpm respectively.

RPE: There was no significant main effect of group (F1,21=0.191, P>0.05) on RPE

(Fig. 6), where RPE was similar throughout exercise. There was a significant main

effect of time (F1.95, 41.04=100.89, P=0.001) on RPE, where RPE increased with time to

about 11-12 RPE at 10 minutes and then plateaus. Lastly there is no significant

interaction (F1.95, 41.04=0.31, P>0.05) between group and time.

CHO oxidation: There is a significant difference in CHO oxidation (Fig. 7) (t17.87=2.68,

P=0.016) between fasted group (1.87±0.76 g/min) and fed group (2.68±0.66 g/min)

where the fed group had a higher CHO oxidation rate compared to fasted group. The

95% confidence interval for the mean of differences was between 0.19-1.42 g/min.

Lipid Oxidation: The fasted group (0.7±0.25 g/min) had a significantly (t11.85=5.19,

P=0.001) greater lipid oxidation (Fig. 8) rate during exercise compared to fed group

(0.27±0.03 g/min) by a difference of 0.43 g/min. The 95% confidence interval for the

mean of differences was between 0.27-0.59 g/min.

Discussion

The aim of this study was to investigate the effect of CHO feeding before exercise on

fuel utilisation during submaximal exercise. The main findings in this present study

was that lipid oxidation rate (Fig. 8) was significantly higher in the fasted group

compared to fed group by a difference of 0.43 g/min during exercise. This was

supported by gradual increases in blood NEFA and glycerol concentrations for the

fasted group (Fig. 3 & 4 respectively) however remained constant for the fed

group. Fed group (2.68 g/min) had a significantly higher CHO oxidation rate (Fig. 7) compared to fasted group (1.88 g/min). These results were similar to Bergmen and

Brooks (1999) study, where they also found that the fed group utilised more CHO

sources and less lipid sources during moderate intensity (40% VO2max) exercise

whereas the fasted group utilised more lipids and less CHO.

Regulation of lipolysis: During moderate intensity exercise, more lipid oxidation is

usually observed due to a higher HSL activity which is caused by increases in

adrenaline and lower AMPK activity (Watt et al., 2003; Watt et al., 2005). In our

study, fasted group displayed increases in NEFA and glycerol concentrations (Fig. 3 & 4 respectively) as a result of increases in HSL activity and lipolysis. The fed

group maintained glycerol levels and NEFA concentrations decreased. Horowitz et

al. (1997) had similar blood glycerol and plasma FFA concentrations compared to

this study, and discussed that ingesting CHO caused the inhibition of HSL activity as

a result of the insulinemic response (Febbraio et al, 2000a). Horowitz et al. (1997)

reported that increases in insulin supresses lipolysis by >60%, which explains why

there is a lower glycerol and NEFA concentrations in the fed state.

Regulation of GLUT-4, Glycogenolysis, Glycolysis and PDH: On figure 1, there was

an increase in blood plasma glucose from pre-feeding to pre-exercise for the fed

group which was also found by Horowitz et al. (1997). This is due to ingestion of high

GI CHO and absorption of glucose into the bloodstream. Then during exercise (15

min), there was a large decrease in glucose concentrations in the fed group. This is

due to a high insulin concentration (Richter & Hargreaves, 2013), which activates the

translocation of GLUT-4 to the muscle plasma membrane for the uptake of glucose

into the muscle. Muscle glycogen phosphorylase activity has been reported to be

augmented in the fed state compared to fasted, due to greater concentrations of

AMP and Pi (Dyck et al., 1996). Increases in glucose uptake would also increase the

glycolytic flux (hexokinase and PFK) and produce sufficient quantities in pyruvate to

allosterically activate PDH and convert pyruvate into acetyl CoA.

The fasted group had a lower CHO oxidation rate (Fig. 7) compared to the fed group

due to lower plasma glucose concentrations therefore depend on the muscle

glycogen stores and FFA from the adipose tissue and muscle. In the fasted group

there was less glycogen utilisation as there was increases in FFA availability (due to

lipolysis), causing the decrease in AMP and P i concentrations (Horowitz et al, 1997).

This will cause the decrease in glycogen phosphorylase activity and glucose-6-

phosphate availability. Also based on the glucose-FA cycle, increases in FFA

availability reduces the glycolytic flux and PDH activity (Jeukendrup, 2002).

Increases in blood glucose concentrations was not observed for the fasted group

(Fig. 1), and Horowitz et al. (1997) also found no significant changes in blood

glucose concentrations during exercise.

Long chain fatty acid transport: Investigating the mechanisms of fatty acid uptake

and oxidation in the mitochondria was difficult as a result of not collecting muscle

biopsies and arteriovenous sampling. However we have found greater lipid oxidation

in the fasted group compared to fed group (Fig. 8) therefore there should be a

greater uptake of LCFA into the mitochondria in the fasted group to undergo β-

oxidation. For fed group as lipolysis rate has decreased there will be less FFA

availability, decreasing FAT/CD36 activity and LCFA uptake into mitochondria.

Carnitine availability is key for lipid oxidation as it is essential for LCFA transport into

the mitochondria (Jeukendrup, 2002). In fed groups, there was greater acetyl-CoA

and acetyl-carnitine concentrations, therefore decreasing carnitine availability which

explains the lower lipid oxidation rates for fed groups (Roepstorff et al., 2004).

However for fasted groups, there was a reduction in glycolytic flux and PDH activity

(Stephens et al., 2007) which increases carnitine availability therefore increasing the

capacity to transport of LCFA into mitochondria to undergo β-oxidation.

Effect of Glycaemic Index, timing and quantity on Fuel Utilisation: Glycaemic index

(GI) is the rate of digestion and absorption of CHO sugars (Brouns et al., 2005). In

this study, Lucozade ‘sport’ and ‘original’ was used which is classed as a high GI

carbohydrate (Jenkins et al., 1981). Based on Horowitz et al. (1997), different GI

effects the rate of insulin release, where high GI has a greater insulin concentration

compared to low GI therefore greater inhibition of lipolysis. Both this study and theirs

found a significantly lower blood FFA concentrations and greater CHO oxidation

during exercise when ingested high GI CHO. However if we had used low GI CHO in

our study, we would observe greater blood FFA concentrations and greater lipid

oxidation (Febbraio et al., 2000) due to less inhibition of lipolysis. Jeukendrup and

Jentjens (2000) also found that ingesting high GI glucose and low GI fructose

together will increase overall CHO oxidation compared to just high GI CHO.

Timing of CHO intake is important as it effects muscle glycogen content and

availability of blood glucose for exercise. Febbraio et al. (2000b) looked at timings of

feeding on metabolism and found that CHO oxidation rates and blood glucose levels

remained constant, when CHO was ingested before (30 minutes before exercise)

and during exercise (15 minute intervals). However when ingested just before

exercise, they found a steady decrease in blood glucose concentration and increase

in lipid oxidation. Therefore ingestion during exercise maintains blood glucose

concentrations. In this study, participants ingested CHO before and at 15 minutes of

exercise. A greater blood glucose concentrations was observed at pre-exercise

however when consumed CHO at 15 minutes of exercise, blood glucose levels was

less than pre-exercise. This is probably due to a high glucose uptake in the

exercising muscles (Coggan & Swanson, 1992). If CHO was ingested only before

exercise, lower blood glucose concentrations would be observed during exercise.

Quantity of CHO ingestion is another factor that can manipulate fuel utilisation.

Increasing concentrations of carbohydrates have been found to increase the

dependence of CHO oxidation (Wallis et al., 2007) and increased glycogen

phosphorylase activity. This is probably due to a greater insulin spike and greater

availability of endogenous CHO. However excessive ingestion of CHO can supress

endogenous glucose production during exercise (Jeukendrup et al., 1999) therefore

promote liver and muscle glycogen sparing. However CHO quantity has been found

to not effect performance (Jetjens et al., 2003). It is recommended that CHO supply

rate of 40-75 g/hour during exercise is sufficient for a maintained CHO oxidation rate

(Coggan & Swanson, 1992). However lower concentrations of ingested CHO will

cause a decrease in CHO oxidation and increased lipid oxidation (Wallis et al.,

2007).

Implications: Based on this study and previous literature, increasing endogenous

CHO availability will increase utilisation of CHO. In a performance aspect, research

has found that sufficient CHO ingestion during exercise increases muscle glycogen

sparing (Tsintzas et al., 1995) which may improve performance (Bergstrom et al.,

1967) during prolonged exercise however needs to be investigated further. Training

in a fasted state has been found to increase oxidative capacity by inducing oxidative

enzyme adaptation (Morton et al., 2009) and mitochondrial biogenesis (Bartlett et al.,

2013). Therefore training in a fasted state and performing in a fed state may improve

endurance performance at a low-moderate intensity. Based on GI, a higher GI will

provide quicker rate of CHO availability for fuel utilisation for a short period of time

therefore high GI is best consumed during exercise (Walton & Rhodes, 1997).

However low GI foods when ingested 45 minutes before exercise has been found to

enhance endurance performance (Kirwan et al., 2001). Timing-wise, provision of

CHO before and during exercise will provide constant CHO availability, and

supplying sufficient quantities of 0.7g/kg/hr of CHO (Rodriguez et al., 2009) whilst

performing will be beneficial for performance and delay fatigue (Coyle et al., 1986).

Limitations: We did not use muscle biopsies or arteriovenous blood samples to

analyse the rate of CHO and FFA uptake, therefore use muscle biopsies or

arteriovenous blood sampling at exercising muscle to analyse CHO and lipid uptake.

We also did not look at the metabolite concentrations in the muscle to acquire a

better understanding on the effect of CHO ingestion on regulatory sites in the

muscle. This study also used both males and females in the study which can affect

the utilisation of endogenous CHO (Riddell et al., 2003) therefore one gender should

be used. This study also did not control everyday diet of participants, as they may

have different muscle glycogen content before exercise which may affect utilisation

of fuels. Lastly we also used participants with different training status, where

endurance trained subjects utilised more lipids compared to untrained subjects (Van

Loon et al., 1999), and therefore reducing the reliability of lipid oxidation results.

Future Research: Based on limitations and findings, there should be further

research into the effect of CHO ingestion at different timing points and at different

concentrations on performance. Also further investigate the effects of a combination

low GI and high GI intake during exercise on fuel utilisation. Also further investigate

the effects of training in low carbohydrate and performing with a high CHO diet on

fuel utilisation and performance in competition. Also using manipulations of timing,

quantity and GI on utilisation in groups of different gender and training status.

Conclusions: Based on the results, there was a greater lipid oxidation in the fasted

state compared to fed which confirms this study’s hypothesis. This is due to the

decrease in lipolysis rate in the fed group due to the insulin spike and a greater

carnitine availability in the fasted group for LCFA uptake into the mitochondria. The

fed group did display a significantly greater CHO oxidation which confirms the

second hypothesis. This is due to increased exogenous CHO availability and

increased flux of the glycolytic system rather than endogenous CHO sources.

Figure 3: Blood NEFA (mmol/L) levels for both fed and fasted groups at pre-feeding, post-feeding,

15 minutes of exercise and 30 minutes of exercise. There is a significant main effect of group

(F1,21=11.61, P=0.003) on the concentration of NEFA during exercise where there were increases

in NEFA concentration by a difference of 0.27 mmol/L for the fasted group however there is a

gradual decrease in NEFA concentrations in the fed group by a difference of 0.07 mmol/L (See

figure 3). There was also a significant main effect of time ( F1.7, 36.5= 4.689, P=0.02Lastly there was

a significant interaction between group and time (F1.74, 36.5= 17.23, P=0.001).

Pre-feeding Pre-exercise 15 min 30 min0

50

100

150

200

250Fasted Fed

Gyc

erol

(mm

ol/L

)

Figure 4: Glycerol concentrations (mmol/L) for both fasted and fed groups at pre-feeding, pre-

exercise a, 15 minutes of exercise and at 30 minutes of exercise. There was not a significant main

effect for group (F1, 21=4.102, P>0.05). However there was a significant main effect of time (F1.76,

37=28.55, P=0.001) on glycerol concentrations where fasted group gradually increased glycerol

concentrations throughout exercise with glycerol levels was at its highest at 30 minutes during

exercise at 218 mmol/L (see figure 4). However for fed group there was a slight decrease when

ingested CHO and then small increases in glycerol concentrations during exercise by a difference

of 10 mmol/L at 30 minutes of exercise. Lastly there was a significant interaction (F 1.76, 37.02=16.91,

P=0.001) between group and time of measurement.

Pre-feeding Pre-exercise 15 min 30 min0.00

0.10

0.20

0.30

0.40

0.50

0.60

0.70

0.80

Fasted Fed

NEFA

(mm

ol/L

)

Figure 2: Blood lactate (mmol/L) levels for fed group and fasted group at pre-feeding, pre-exercise

and during exercise. There was no significant main effect (F1,21=1.86, P=0.19) for group on blood

lactate levels. There was a significant main effect for time (F1.6, 33.3=100.498, P<0.001), where both

groups increased lactate concentrations from pre exercise to 15 minutes of exercise with the

greatest lactate concentration was in the fasted group (6.2 mmol/L) compared to the fed group (5

mmol/L). However there was no significant interaction between group and time.

Figure 1: Blood glucose levels (mmol/L) for both fasted group and fed group at pre-feeding, post-

feeding and during exercise. Where there was a significant main effect for group (F1,21=7.386,

P=0.01), where blood glucose levels was higher in the fed group compared to fasted group at pre

exercise and at 15 minutes exercise with highest glucose levels of 8.2 g/min at 15 min. Fasted

group glucose levels remained constant of about 5.5 g/min.

Pre-feeding Pre-exercise 15 min 30 min4.0

4.5

5.0

5.5

6.0

6.5

7.0

7.5

8.0

8.5FastedFed

Bloo

d G

luco

se (m

mol

/L)

Pre-feeding Pre-exercise 15 min 30 min0.0

1.0

2.0

3.0

4.0

5.0

6.0

7.0

Fasted

Fed

Bloo

d La

ctat

e (m

mol

/L)

Figure 6: RPE for both fasted and fed groups at pre-feeding, pre-exercise a, 15 minutes of

exercise and at 30 minutes of exercise. There is no significant main effect of group (F1,21=0.191,

P>0.05) on RPE during exercise, where RPE was similar throughout exercise. There was a

significant main effect of time (F1.95, 41.04=100.89, P=0.001) on RPE where RPE increased with time

to about 11-12 RPE at 10 minutes and then plateaus. Lastly there is no significant interaction (F1.95,

41.04=0.31, P>0.05) between group and time.

0 10 20 3060708090

100110120130140150160

Fasted Fed

Time (Minutes)

Hear

t Rat

e (B

pm)

Figure 5: Heart rate (bpm) for both fasted and fed groups at pre-feeding, pre-exercise a, 15

minutes of exercise and at 30 minutes of exercise. There was not a significant main effect of group

(F1,21= 2.507, P>0.05) on heart rate during exercise. However there was a significant main effect of

time (F1.6, 35.24=227.73, P=0.001) where both fasted and fed group increased heart rate as time

increases until 10 minutes where the heart rate plateaus. Lastly there was not a significant

interaction between group and time (F1.68, 35.24=2.04, P>0.05) however fasted group had a higher

heart rate at time points of 10 minutes, 15 minutes and 30 minutes of exercise by a difference of

approximately 15 bpm.

0 5 10 15 20 25 305

6

7

8

9

10

11

12

13

14Fasted Fed

Time (Minutes)

RPE

References

Fasted Fed 0

0.5

1

1.5

2

2.5

3

Fed State

CH

O O

xida

tion

(g/m

in)

Figure 8: The lipid oxidation rate (g/min) during exercise for the fasted group and the fed group.

The fasted group (0.7±0.25 g/min) had a significantly (t11.85=5.19, P=0.001) greater lipid oxidation

rate during exercise compared to fed group (0.27±0.03 g/min) by a difference of 0.43 g/min. The

95% confidence interval for the mean of differences was between 0.27-0.59 g/min.

Fasted Fed 0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

Fed State

Lipi

d O

xida

tion

(g/m

in)

Figure 7: The CHO oxidation rate (g/min) during exercise for the fasted group and the fed group.

There is a significant difference in CHO oxidation (t17.87=2.68, P=0.016) between fasted group

(1.87±0.76 g/min) and fed group (2.68±0.66 g/min) where showed the fed group had a higher CHO

oxidation rate compared to fasted group. The 95% confidence interval for the mean of differences

was between 0.19-1.42 g/min.

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