Diversification of Sports Nutrition Products

-

Integrating scientific knowledge and research into the development of useful sports nutrition products for the athlete -

Dr. Trent Stellingwerff, BSc, PhD

- BSc, Nutrition, Cornell University, USA - PhD, Exercise Physiology, Univ of Guelph, Canada - Post-Doctorate Fellowship, Univ. of Maastricht, Netherlands

2005 World Track and Field Champs in Helsinki

2006 Commonwealth Games Melbourne, Australia

Sports Nutrition Where we’ve come from; Where we’re at; Where can we go?

- from the perspective of an athlete, coach, physiologist and scientist -

Dr. Trent Stellingwerff, BSc, PhD

- BSc, Nutrition, Cornell University, USA - PhD, Exercise Physiology, Univ of Guelph, Canada - Post-Doctorate Fellowship, Univ. of Maastricht, Netherlands

Diversification of Sport Nutrition Products

I. Historical perspective on sports performance products-

from none to millions.

II. Research efficacy-

what needs to be considered?

III. Time and effort-

Fat-adaptation training and dietary protocol

IV. Future Research Ideas/Directions-

development of sport and/or gender specific nutrition recommendations/products.

V. Conclusions-

Take home message…

Diversification of Sport Nutrition Products

I. Historical perspective on sports

performance products- from none to

millions.

Wow…this glucose and caffeine is really maintaining my blood sugar and increasing my CNS stimulation and adipose tissue lipolysis.

Cox G.R.et al. Effect of different protocols of caffeine intake on metabolism and endurance performance. JAP. 93: 990-999, 2002.

1972 Olympic Marathon Silver medalist Frank Shorter’s “sports drink ”

Est. 1965 Est. 1986

Consumers current options when it comes to sports nutrition:

“Google” searched ‘sports nutrition products’ and got 54 million hits!

Is there a lack of brand loyalty due to so much clutter and ubiquity of sports nutrition products that

ALL

claim ergogenic effects?

The major increase and proliferation of available ergogenic products has far outstripped the scientific communities ability to test for actual ergogenic effects or “claims” of such products.

Diversification of Sport Nutrition Products II. Research efficacy- what needs to be

considered?

Research and Science Principles

- What do scientists

and

the consumer need to think about or examine when weighing the potential efficacy of a sports nutrition product or when evaluating a certain “claim” or study or when developing new products?

Research Design Concerns

 Amount- too little or too much may show no effect  Subject versa may only be effective in ‘untrained’ vs. trained or vice – “value” is determined by the subject  Task- may only work in power events and not endurance or vice versa  Use- acute (short term) may show effect but chronic may be compromising  Sensitivity of method to assess performance in laboratory setting (time trial vs. amount of work completed vs. time to exhaustion vs. wattage area under the curve vs. peak wattage etc.)

Assessing sport performance- how thin can you slice?

- clinical relevance vs. practical/applied relevance Atlanta Men’s 1500m race Gold 3:35.78

Bronze- 3:36.72 (-0.44%) 8 th place- 3:38.19 (-1.12%) Sydney Men’s 10 000m race Gold Silver 27:18.20

27:18.29 (-0.005%!) Bronze 4 th 27:19.57 (-0.08%) place- 27:20.44 (-0.14%) 2005 NYC Marathon: Tergat wins over Ramaala (winning margin: 0.004%!)

Ergogenic Aid Potential??

What a researcher needs to know… • Is it degraded in the stomach?

– the stomach is VERY acidic!

• Can it be absorbed in the ‘intact’ in the blood?

• Liver Processes (first crack at everything)- metabolized or broken down?

• Kidney- how much is lost into the urine?

• How large is the original concentration in the blood and how long is it elevated? (if there is elevation, then there may be ‘potential’ ergogenic effect) • FINALLY, does it interact with the target site OR is it taken up by the target organ? How much of it is taken up?

Research Design Concerns

• Research needs to be completed by an unbiased outside source, in well establish and controlled laboratory setting using well established methods and then published in a peer-reviewed scientific journal to be truly valid.

Research Design Concerns

So many issues and specific intricacies with each and every product, and there are thousands of products.

THROUGH SO MANY POTENTIAL ISSUES/PRODUCTS?

HOW MUCH TIME DOES THE CONSUMER HAVE FOR STUDIES TO COMPLETED? + ?

Diversification of Sport Nutrition Products

III. Time and effort-

Fat-adaptation training and dietary protocol 8

+

years of ideas and testing…

Decreased PDH activation during exercise following short-term high-fat dietary adaptation with carbohydrate restoration.

Trent Stellingwerff 1 , Lawrence L. Spriet 1 , Matthew J. Watt 3 , Nick E. Kimber 2 , Mark Hargreaves 2 , John A. Hawley 3 , Louise M. Burke 4

Initial idea….about 10 years ago…

• Only a finite amount of stored glycogen, therefore a shift towards increased fat oxidation at a given exercise intensity should spare glycogen for later in a sporting event, and “in theory” increase endurance sport performance.

• What if you could shift metabolism towards the oxidation of more fat, yet still have ample stored carbohydrate available?

...best of both worlds!

So what is this FAT-adaptation (FAT adapt) nutritional & exercise intervention?

General schematic of FAT-adaptation protocol Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Diet FAT or CHO FAT or CHO FAT or CHO FAT or CHO FAT or CHO CHO Restoration Training Interval 3-4 h long 2-3 h Interval 3-4 h long rest training ride hill ride training ride Day 7 Testing Trial • Two experiment trials: Hi FAT (FAT-adapt) vs. Hi CHO (HCHO) – Two diets while training for 5-days • HCHO: 10.3 g · kg -1 • FAT-adapt: 4.6 g · kg · day -1 -1 · day CHO or ~70% of total energy (total intake of ~18MJ daily (4300 kcals) -1 FAT or ~67% of total energy (total intake of ~18MJ daily (4300 kcals)

Unlike previous high fat studies, unique FAT-adapt protocol, with a day of CHO restoration, has shown: Fully restored glycogen stores so ample CHO available during exercise and it abolishes the effect of elevated FFA normally present after a high-fat diet.

- Persistence of an ~ 2-fold increased whole-body fat oxidation despite CHO restoration (Burke et al., J. Appl. Physiol., 2000; Burke et al., Med. Sci. Sports Ex., 2002; Carey et al., J. Appl.

Physiol., 2001; Staudacher et.al, 2001).

These shifts in fuel utilization still present during a 4-hour ride that included glucose supplementation of ~100 g/ hour (Carey et al., J. Appl. Physiol., 2001) Strong trend towards sparing glycogen with biopsy measurments (P=0.06) and statistical glycogen sparing via indirect tracer methods (Burke et al., J. Appl. Physiol., 2000; Carey et al., J. Appl. Physiol., 2001) Potential mechanisms responsible for these shifts in fuel utilization are equivocal, but would be expected to involve either an up and/or down regulation of key regulatory enzymes in the pathways of skeletal muscle fat and CHO metabolism.

FFA-ALB Glucose blood cytosol Glucose HK Glycogen PHOS TG OM IM HSLIPASE FFA-FABP fatty acyl-CoA CPT-I CAT CPT-1I NADH NAD G-6-P PFK ATP NADH G-1-P NAD Pyruvate Lactate LDH matrix

b

-oxidation NAD fatty acyl-CoA NAD NADH NADH acetyl-CoA CO PDH 2 TCA cycle Lactate ATP Cr ATP ATP ADP NAD NADH H + E T C ADP PCr ADP H H + + PM H 2 0 O 2

Regulation of PDH

pyruvate NAD NADH (at rest) + ATP ADP + Pyruvate Dehydrogenase b (inactive) P PDH kinase + acetyl-CoA CoASH (rest only) P i

PDK1 PDK2 PDK3 PDK4 PDP1 PDP2

PDH phosphatase Pyruvate Dehydrogenase a (active) P i + Ca 2+ acetyl-CoA, H + , NADH, CO 2 pyruvate, CoASH, NAD + ?

Epi

Purpose

• To investigate the effects of a 5-day high-fat diet with 1 day of CHO restoration (FAT-adapt) as compared to a 6-day isoenergetic high CHO diet (HCHO) on the regulation of key enzymes (PDHa and HSL) involved in skeletal muscle CHO and FAT metabolism.

Hypothesis

• 1. FAT-adapt would result in decreased muscle glycogenolysis at the onset of exercise, and decreased PDHa throughout exercise at 70% VO 2peak .

• 2. Decreased pyruvate levels and reduced levels of AMP f , ADP f would explain the found enzymatic changes.

and Pi f • 3. The increase in whole body fat oxidation can partially be explained by increased HSL activation.

Experimental Protocol

1 min sprint @ 150% PPO 20 min steady state cycling at ~70% VO 2peak (63% of PPO) Biopsy Blood sampling Pulmonary gas collection 2 trials: 1) CON vs. FAT-ADAPT

Blood, glycogen and respiratory measures

1000 No differences in plasma lactate, glucose, insulin,

* *

FAT 600 CHO FAT-adapt reduced the RER during 70% VO 2peak (FAT-adapt: 0.85  0.02 vs. HCHO: 0.91  cycling 0.01) 400 200 Which resulted in a: 45% increase in whole-body fat oxidation and a REST FINISH Time (min)

Decreased calculated glycogenolysis 70 30 20 10 60 50 40 FAT-adapt HCHO

†

*

* †

0 0 to 1 min Time (min) 20 to 21 min G6P + (pyruvate + lactate accumulation)/2 + lactate efflux (20-30% of lactate accumulation)/2 + PDH flux (use 1 min value/2)

Muscle pyruvate contents

0.6

0.4

0.2

0.0

1.6

1.4

1.2

1.0

0.8

0 FAT-adapt HCHO

p = 0.09

10 Time (min) 20 Post 1 min Sprint @ 150% PPO

1 2 3 4 5

Decreased PDHa after FAT-adapt

†

FAT-adapt HCHO

* * * * ‡

0 0 10 Time (min) 20 Post 1 min Sprint @ 150% PPO

HSLa augmented after FAT-adapt

8 6 4

* *

2

P=0.091

0 0

* Trial p=0.116

*

FAT-adapt HCHO 10 Time (min) 20 Post 1 min Sprint @ 150% PPO

High Energy Phosphates

• No change in any of the high energy phosphates (PCr, ATP, ADP f , AMP f or Pi f ) after FAT-adapt as compared to HCHO during 70% VO 2peak ride.

• After the 1-min 150% PPO sprint after FAT-adapt as compared to HCHO:

- ADP

f

- AMP

f

 in PDHa after a high-fat diet despite CHO restoration

↑ NADH/NAD (at rest and exercise onset) increase in redox state with high fat diet?

+ Hi-Fat Diet = inc. in PDK protein/activity ATP ADP Pyruvate Dehydrogenase b

(inactive)

+ Pyruvate

p=0.09

NO CHANGE PDH kinase + acetyl-CoA CoASH (rest only) P i acetyl-CoA, H + , NADH, CO 2 Pyruvate Dehydrogenase a

(active)

PDH phosphatase P i + Ca 2+ pyruvate, CoASH, NAD EPI

Over-riding hypothesis

G-6-P Glycogen Glycogenolysis G-1-P + FFA-FABP cytosol OM IM IMTG ?

Pyruvate Lactate CPT-I CAT CPT-1I fatty acyl-CoA

b

-oxidation PDH + acetyl-CoA +

TCA cycle

Oxidative ATP Provision NADH O 2 matrix ADP + Pi

“There is now evidence that what was initially viewed as “glycogen sparing” after FAT-adapt may be, in fact, a down regulation of CHO metabolism or “glycogen impairment”. [Stellingwerff et al.] recently reported that FAT-adapt protocols are associated with a reduction in the activity of pyruvate dehydrogenase; this change would act to impair rates of glycogenolysis at a time when muscle CHO requirements are high…. [it may] compromise the ability of well-trained cyclists to perform a high-intensity sprint when they need it most- at the end of a race.”

IV. Future Research Ideas and Directions-

development of sport, age, training status and/or gender specific nutrition recommendations and products.

I. Tapping into fat- the holy grail?

II. Exercise optimization of protein balance and energy stores- a secret formula?

III. Other ideas- in brief.

Future Research Ideas & Directions I. Tapping into fat- the holy grail?

Body Energy Stores of a 155 pound (~70kg) person

300000 250000 200000 Muscle glycogen Liver glycogen Adipose tissue (fat) Muscle Triglycerides (fat) 150000 275000 100000 50000 0 7000 2000 1

Type of Energy

5500

What regulates mitochondrial lipid oxidation?

• Contemporary mechanism (s) that have been suggested to help explain the shifts in fuel utilization found during increasing exercise intensity or durations: - Mitochondrial NADH regulating fuel utilization?

- Muscle decrease in pH down-regulating CPT-1?

- Muscle cystolic malonyl-CoA (M-CoA) inhibition of CPT-1?

AMPK’s role as a fuel-sensing molecule for regulation?

- Interaction of CPT-1 with fatty acid translocase (FAT/CD36) ?

- Availability of free-carnitine for CPT-1 reaction?

cytoplasm Acetyl-CoA

+

Feeding = Citrate & Insulin

PPAR’s LCFA (?) Contract (?)

ACC (active)

+ FAT/CD36 ?

MCD

LCFA-CoA

pH M-CoA

FFA-albumin IMTGs carnitine ACT CPT- II

ACC

P +

AMPK

CoASH LCFA-lcarnitine

Exercise Fasting LCFA (Watt, epud, 2006) OM IM

LCFA-lcarnitine carnitine ?

CoASH LCFA-CoA

b

-oxidation

mitochondria

Acetyl-CoA units TCA cycle

Role of acetylcarnitine- buffer for Acetyl CoA?

OM IM Pyruvate, CoASH NAD + PDH TCA Cycle Acetyl CoA, H + , NADH, CO 2 carnitine CAT cytosol Acetylcarnitine, CoASH, NAD+

Increasing exercise intensity Inc. glycolytic flux (Odland, AJP-Endo,1998) (Roepstorff, AJP-Endo,2005)

Correlation between acetylcarnitine and fat oxidation BUT, correlation does not always mean causation! (Kiens, Physiol Rev, 2006) What is the actual concentration of free carnitine between the outer and inner mitochondrial membrane? Is it actually limiting?(compartment methodological issues) As K m of CPT-1 for carnitine is very low (0.5mM at pH 7.4) (carnitine (1 to 4mM)

Endurance performance effects with carnitine supplementation?

- No clear consensus 1) “IF” there is an positive metabolic / performance effect, long-term supplementation seems to be needed to get very small increases in muscle carnitine contents.

2) Improvements in performance may be too small to clinically detect.

3) Seems to be no negative side-effects.

Future Research Ideas & Directions II. Post exercise optimization of protein balance and energy stores a secret formula?

What drink causes the highest insulin secretion?

Drink 1: CHO only (1.2g/kg/hr) Drink 2: CHO + PH (0.2g/kg/hr) PH= protein hydrolysate Drink 3: CHO + PH (0.4g/kg/hr) Drink 4: CHO + PH (0.1g/kg/hr) + leucine (0.05g/kg/hr) + phenylalanine (0.05 g/kg/hr) Drink 5: CHO + PH (0.2 g/kg/hr) + leucine (0.1 g/kg/hr) (van Loon et al, J Nutr, 2000)

AA w/ CHO supplementation on glycogen replenishment

*

170% CHO (0.8g/kg/hr) -The addition of protein hydrolysates and AA to CHO containing 113% solutions can further stimulate glycogen synthesis (PH+leucine+phenyl) 0.8g + 0.4g

HOWEVER, CHO + CHO 1.2 g/kg/hr Glycogen synthesis can also be accelerated by just increasing CHO intake to high levels when supplements are provided every 30 min.

(van Loon et al, Am J Clin Nutr, 2000)

Combined ingestion of protein and free leucine with carbohydrate increases post-exercise muscle protein synthesis in vivo in male subjects.

(Koopman et al., AJP Endo, 2005 / 45’ resistance exercise, 3 drinks, 6 hours recovery) So what is it about leucine ?--- molecular signalling ?

Leucine ?

Increase in S6K1 phosphorylation in human skeletal muscle following resistance exercise occurs mainly in type II muscle fibers.

(Koopman et al., AJP Endo, 2006 / 45’ resistance exercise, 4 biopsies )

Leucine ?

Future Research Ideas & Directions III. Other ideas- in brief.

General Summary: Diversification of Sport Nutrition Products

I.

Possibility for development of different products for different sub section of the population…

- professional athletes vs. recreational - male vs. female differences - young vs. elderly

II. Possibility for different products for different athletic situations…

- speed and power athletes vs. endurance athletes - nutrition pre, during and post event - aerobic vs. anaerobic - weight dependant vs. weight independent pursuits

III. Development of different products for different times of the season…

- ie. base training versus tapering before big events

Diversification of Sport Nutrition Products

VI. Conclusions-

Take home message…

Is there currently too much selection and choice, in terms of sports nutrition products, for the consumer?

OR

are there too many products without the proper scientific testing supporting their claims?

How does a company gain the trust and support of the consumer through the development of

additional

sports nutrition products?

Final Thoughts…

I. Many companies make claims on their products, but you cannot “trick” consumers/athletes over the long term. Ultimately brand loyalty comes from well researched reputable products that work!

II. Further establishment of consumer contact with research center and experts:

- helps develop trust in the brands/ shows consumer that company supports sound unbiased research of their products.

III. Knowledge/education coupled with brand identity results in empowerment and trust for the consumer or athlete…

Diversification of Sport Nutrition Products

III. Time and effort-

Fat-adaptation training and dietary protocol 8

+

years of ideas and testing…

Decreased PDH activation during exercise following short-term high-fat dietary adaptation with carbohydrate restoration.

Trent Stellingwerff 1 , Lawrence L. Spriet 1 , Matthew J. Watt 3 , Nick E. Kimber 2 , Mark Hargreaves 2 , John A. Hawley 3 , Louise M. Burke 4

Chronic effects of high-fat diet while training, despite CHO restoration on PDHa and whole body fuel utilization shifts.

↓ in PDHa due to a chronic ↑ in PDK after a high fat diet (Peters et al., 1998 & 2001) BUT current study had a 24 hour CHO restoration period… Increase in IMTG leading to an increase in HSL? (20% differences between trials?)

Major conclusions by Louise Burke….

“Indeed, so concerned about the possibility of making a type II error, we embarked upon testing six more subjects with the same study design. Our interim results show [nothing]: 1 hour time trial: CON 41.92km; FAT ADAPT= 41.94km (P=0.98).” “…[even though] our FAT-adapt strategy, which has consistently been shown to spare muscle glycogen utilization during prolonged submaximal exercise, it does NOT appear to provide a clear benefit to performance”

Performance Improvement?

Body Energy Stores of a 155 pound (~70kg) person

300000 250000 200000 Muscle glycogen Liver glycogen Adipose tissue (fat) Muscle Triglycerides (fat) 150000 275000 100000 50000 0 7000 2000 1

Type of Energy

5500

Fuel Utilization at Different Exercise Intensities 25% VO2max 65% VO2max 85%VO2max

(Brisk Walking Pace) (~Marathon Pace) (~5 to 10km race pace) Fats Muscle Glycogen Blood Glucose (sugar) - 30 min of exercise after an overnight fast: Romijn, J.A. et al.- American Journal of Physiology, E380, 1993.

HSL and IMTG use- substrate content and gender?

+ +

IMTG LCFA-CoA Putative control of skeletal muscle HSL (Spriet and Watt, REVIEW, Proc of Nutr Soc., 2004) Aerobic oxidation via TCA Cycle in mitochondria

Integration between exercise, AMPK, M-CoA, pH and free carnitine on subsequent LCFA-CoA oxidation.

pH

(Kiens, Physiol Rev, 2006)

“magical” fuel sensing switch to alter mito. fat oxidation?

NADH pH & CPT-I Free carnitine Malonyl-CoA AMPK FAT/CD36 Small parts of the complex metabolic fuel sensing and adapting machinery?

Blood shunting during exercise - from Martin and Coe: Training Distance Runners

Future Research Ideas & Directions III.Effects of caffeine – mechanism: from increased lipolysis to CNS stimulation

Caffeine supplementation and increased adipose tissue lipolysis?

nicotinic acid + + EPI, NE +

nicotinic LEPTIN insulin ?

b 1

Gs

EPI, NE

AC

Gi

+

?

ATP +

inactive PKA

 2 A 1 adenosine + -

?

cAMP +

?

phosphodiesterase AMP

active PKA

+

?

?

-

HSL HSL-P

NOTE: Need high dose to get FFA differences, BUT get ergogenic effect with low doses ?

caffeine (Graham & Spriet, JAP, 1995) (6-8 mg /kg BW) AMP kinase + TG droplet

?

LEPTIN ?

+ phosphatase TG FFA & glycerol leptin PKA, protein kinase A Sensitivity:  2 > b 1 FFA & glycerol to working muscle

Caffeine ingestion does not alter skeletal carbohydrate or fat metabolism in human skeletal muscle during exercise.

(Graham et al. J.Physiol, 2000 – 6mg/kg, 1 hour @ 70% VO2peak, 2 trials: CAF vs. PLA, a-v lines) But no difference net flux (uptake or release) across the working leg for FFA or glycerol, or whole body and leg fat and CHO oxidation.

Low dose-caffeine supplementation results in increased CNS stimulation and decreased RPE

Future Research Ideas & Directions IV. Gender differences in fuel metabolism

Fuel metabolism in men and women during and after long-duration exercise.

(Horton et al. JAP, 1998 – 14 females vs. 14 males; 2 hrs of cycling at 40% VO2peak; 2 hr re ) Men Women

Gender specific IMTG use- controversy?

Biochemical IMTG extraction from muscle biopsies (Roepstorff et al. AJP, 2002- 90 min of cycling @ 57% VO 2peak ) (Steffensen et al. AJP, 2002 – 90 min of cycling @ 60% VO 2peak )

Gender specific IMTG use- controversy?

IMTG quantification via 1 H-magnetic resonance spectroscopy (Zehnder et al. MSSE, 2005- 3 hours of cycling @ 50% VO 2peak ) (While et al. J Clin Endocrinol Metab, 2003 – 1 hour of cycling @ 65% VO 2peak )

Future Research Ideas & Directions III. Other ideas- in brief.

Diversification of Sport Nutrition Products

I.

Post-exercise optimization of protein balance and energy stores- a secret formula?

- how many calories and types of calories post-exercise?

- insulinatrophic amino acid supplementation (eg. Leucine) - molecular protein signalling pathways (insulin vs. protein)

II. Continued research on high MW sports drinks…

- does MW change gastric emptying rates? - and/or CHO uptake rates? - Recent evidence says NO (Rowlands et al. MSSE (37): 2005)

III. Addition of antioxidants into products to decrease ROS or cortisol inflammatory responses post-training

- time course, short-term vs. long-term supplementation, amounts - or is the cortisol response a necessary for training adaptation?

Diversification of Sport Nutrition Products

IV. Gender differences

- differences in CHO and fat metabolism?

- differing protocols/products needed for CHO loading? (evidence suggests females need >8 g CHO per kg BW) - differences in caffeine responses/supplementation?

V. Caffeine

- gender differences in CNS responses?

- dose-response at start of exercise vs. fatigued (late in race)?

- chronic supplementation = habituation effects?

VI. G.I. favorable / stable sports drinks and nutrition

- ultra endurance sport athletes and blood shunting issues.

VII . Bicarbonate, pseudoephedrine, taurine, green-tea ???

Effects of carnitine supplementation on metabolism and performance.

Effects of carnitine supplementation on metabolism and performance.

Future Research Ideas & Directions I. Tapping into fat- the holy grail?

What about replenishing IMTG’s post-exercise?

(similar to glycogen replenishment?)

IMTG use during exercise- No longer a controversy.

Time (hours) Biochemical extraction with mixed muscle (Watt et al. J. Physiol, 2002 – 4 hours of cycling @ 57% VO 2peak )

IMTG use during exercise- No longer a controversy.

Histochemical with immunofluorescence microscopy methodology- fiber type specific (van Loon et al. J. Physiol, 2003 – 2 hours of cycling @ 60% VO 2peak )

Even IMTG utilization during resistance exercise Significant 27% decrease in Type I IMTG after resistance exercise.

(Koopman et al. EJAP, 2006 – 45 min of resistance exercise)

Postexercise fat intake repletes intramyocellular lipids but no faster in trained than in sedentary subjects.

(Decombaz et al., AJP-Reg, 2001; 2 hrs at 50% VO2max with 55 and 15% fat diets for recovery measured via 1 H-MRS) 55% fat in recovery diet 15% fat in recovery diet

Influence of prolonged endurance cycling and recovery diet on intramuscular triglyceride content in trained males.

(van Loon et al., AJP-Endo 2003; 3 hrs at 55% Wmax with 39 and 24% fat diets for recovery measured via 1 H-MRS) 39% fat in normal fat 24% low fat diet

Could a lack of IMTG replenishment lead to decrements in training or performance over time?

(Watt et al. J. Physiol, 2002 – 4 hours of cycling @ 57% VO 2peak )

BUT, could an initially low IMTG store cause a significantly greater glycogen use during the first 90-120 min of exercise?

(van Loon et al. J. Physiol, 2003 – 2 hours of cycling @ 60% VO 2peak )