Diversification of Sports Nutrition Products

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.

1972 Olympic Marathon Silver medalist - Frank Shorter’s “sports drink”
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: , 2002. 1972 Olympic Marathon Silver medalist - Frank Shorter’s “sports drink”

} Est. 1965 Est. 1986

‘sports nutrition products’
Consumers current options when it comes to sports nutrition: “Google” searched ‘sports nutrition products’ and got 54 million hits!

claim ergogenic effects?
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.

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- may only be effective in ‘untrained’ vs. trained or vice versa “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
Assessing sport performance- how thin can you slice? - clinical relevance vs. practical/applied relevance - Atlanta Men’s 1500m race Gold :35.78 Bronze- 3:36.72 (-0.44%) 8th place- 3:38.19 (-1.12%) Sydney Men’s m race Gold :18.20 Silver :18.29 (-0.005%!) Bronze :19.57 (-0.08%) 4th 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 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.

So many issues and specific intricacies with each and every product, and there are thousands of products. HOW DOES THE GENERAL CONSUMER WADE THROUGH SO MANY POTENTIAL ISSUES/PRODUCTS? HOW MUCH TIME DOES THE CONSUMER HAVE FOR STUDIES TO COMPLETED? + ?

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 Stellingwerff1, Lawrence L. Spriet1, Matthew J. Watt3, Nick E. Kimber2, Mark Hargreaves2, John A. Hawley3, Louise M. Burke4

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

fatty acyl-CoA fatty acyl-CoA TCA cycle
Lactate FFA-ALB Glucose blood PM cytosol Glucose Glycogen HK PHOS HSLIPASE TG FFA-FABP G-6-P G-1-P PFK ATP ADP NAD fatty acyl-CoA ATP Cr PCr NADH NAD NADH ATP ADP Pyruvate Lactate CPT-I LDH OM CAT PDH IM CPT-1I ATP ADP matrix NAD NADH b-oxidation H+ CHO can act as a fuel for both anaerobic glycolysis (substrate phosphorylation) and aerobic CHO metabolism (oxidative phosphorylation), while fat is exclusively oxidized aerobically within mitochondria. CHO contribution to aerobic energy production is dependent upon rate-limiting enzyme pyruvate dehydrogenase activation (PDHa) PDH is an important regulatory enzyme as it catalyses the oxidative decarboxylation of pyruvate to acetyl-CoA within the mitochondria. It serves as the first irreversible step and a gateway for CHO to enter the tricarboxylic cycle (TCA) within the mitochondria to ultimately be metabolized via oxidative phosphorylation. 1 millimole (mmol) of glucose or glucosyl unit (6 carbons) results in two pyruvate units (3 carbons each), that when consumed via oxidative phosphorylation result in ~39 mmol of ATP produced. Conversely, the most significant cytosolic fate of pyruvate is its conversion to lactate, with the reduction of NADH to NAD+ by the LDH reaction. During intense exercise situations, when substrate phosphorylation dominates, 1 mmol glucosyl unit (6 carbons) are metabolized to two lactate units (3 carbons) and there is a production of either 2 or 3 mmol of ATP if the glucosyl units originate from exogenous glucose of endogenous glycogen respectively. acetyl-CoA fatty acyl-CoA NAD NAD NADH TCA cycle E T C CO2 NADH H+ H+ H20 O2

Regulation of PDH ? + + P - + + NAD NADH Pyruvate Dehydrogenase b
(at rest) + Pyruvate Dehydrogenase b (inactive) ATP ADP + P PDK1 PDK2 PDK3 PDK4 PDP1 PDP2 pyruvate - PDH kinase PDH phosphatase acetyl-CoA CoASH + (rest only) Ca2+ + Epi ? Pyruvate Dehydrogenase a (active) Pi Pi pyruvate, CoASH, NAD acetyl-CoA, H+, NADH, CO2

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% VO2peak. 2. Decreased pyruvate levels and reduced levels of AMPf, ADPf and Pif would explain the found enzymatic changes. 3. The increase in whole body fat oxidation can partially be explained by increased HSL activation.

20 min steady state cycling at ~70% VO2peak (63% of PPO)
Experimental Protocol 1 min 150% PPO 20 min steady state cycling at ~70% VO2peak (63% of PPO) Biopsy Blood sampling Pulmonary gas collection 2 trials: 1) CON vs. FAT-ADAPT

Blood, glycogen and respiratory measures
No differences in plasma lactate, glucose, insulin, FFA, epinephrine or norepinephrine FAT-adapt reduced the RER during 70% VO2peak cycling (FAT-adapt: 0.85  0.02 vs. HCHO: 0.91  0.01) Which resulted in a: 45% increase in whole-body fat oxidation and a 30% decrease in CHO oxidation

Decreased calculated glycogenolysis
G6P + (pyruvate + lactate accumulation)/2 + lactate efflux (20-30% of lactate accumulation)/2 + PDH flux (use 1 min value/2)

Muscle pyruvate contents

Decreased PDHa after FAT-adapt

HSLa augmented after FAT-adapt
Trial p=0.116 P=0.091

High Energy Phosphates
No change in any of the high energy phosphates (PCr, ATP, ADPf, AMPf or Pif) after FAT-adapt as compared to HCHO during 70% VO2peak ride. After the 1-min 150% PPO sprint after FAT-adapt as compared to HCHO: ADPf AMPf

 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 - PDH kinase PDH phosphatase p=0.09 acetyl-CoA CoASH + (rest only) NO CHANGE Pi Ca2+ + EPI Pyruvate Dehydrogenase a Pi (active) pyruvate, CoASH, NAD acetyl-CoA, H+, NADH, CO2

Over-riding hypothesis
Glycogen Glycogenolysis G-6-P G-1-P + FFA-FABP cytosol Pyruvate Lactate CPT-I OM CAT PDH + IM CPT-1I TCA cycle matrix b-oxidation Oxidative phosphorylation, via mitochondrial respiration, is responsible for aerobic ATP production, and this process is accomplished by the ETC. The ETC is a four enzyme complex that oxidized mitochondrial reducing equivalents (NADH and FADH2) by transferring electrons to reduce both H2O and O2 (117). In turn, this ETC enzyme complex converts its substrates of ADP and Pi to the product of ATP. The rate of oxidative phosphorylation is regulated by the ratios of [NAD+] to [NADH], [ATP] to [ADP][Pi] and the availability of O2 (David Wilson) When one of these two ratios or O2 availability is altered, a compensatory change occurs in the other ratio to maintain the same driving force for oxidative phosphorylation. The process of mitochondrial respiration is stimulated by increased ADP and Pi caused by muscle contractions at exercise onset. The phosphorylation state is also intimately associated with the regulation of substrate phosphorylation ATP production. acetyl-CoA fatty acyl-CoA IMTG ? Oxidative ATP Provision + NADH O ADP + Pi NC

“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. 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
Tapping into fat- the holy grail?

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

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?

? ? OM IM Acetyl-CoA ACC (active) MCD ACC P + + + AMPK M-CoA - pH
cytoplasm Acetyl-CoA ACC (active) MCD ACC P + Feeding = Citrate & Insulin + PPAR’s LCFA (?) Contract (?) FAT/CD36 ? + AMPK Exercise Fasting LCFA (Watt, epud, 2006) M-CoA - pH LCFA-CoA FFA-albumin IMTGs CoASH LCFA-lcarnitine carnitine CPT-1 CPT - I OM ACT IM ? CPT- II carnitine LCFA-lcarnitine CoASH LCFA-CoA b-oxidation Acetyl-CoA units TCA cycle mitochondria

Role of acetylcarnitine- buffer for Acetyl CoA?
OM IM TCA Cycle Acetyl CoA, H+, NADH, CO2 Pyruvate, CoASH NAD+ PDH carnitine CAT Acetylcarnitine, CoASH, NAD+ cytosol

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! What is the actual concentration of free carnitine between the outer and inner mitochondrial membrane? Is it actually limiting?(compartment methodological issues) As Km of CPT-1 for carnitine is very low (0.5mM at pH 7.4) (carnitine (1 to 4mM) (Kiens, Physiol Rev, 2006)

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.

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
* 113% 170% CHO (0.8g/kg/hr) CHO + PRO (PH+leucine+phenyl) 0.8g + 0.4g CHO + CHO 1.2 g/kg/hr The addition of protein hydrolysates and AA to CHO containing solutions can further stimulate glycogen synthesis HOWEVER, 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)

So what is it about leucine ?--- molecular signalling ?
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 ?

III. Other ideas- in brief.

General Summary: Diversification of Sport Nutrition Products
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

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…

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 Stellingwerff1, Lawrence L. Spriet1, Matthew J. Watt3, Nick E. Kimber2, Mark Hargreaves2, John A. Hawley3, Louise M. Burke4

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

Fuel Utilization at Different Exercise Intensities
25% VO2max % VO2max %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 - + Aerobic oxidation via TCA Cycle in mitochondria LCFA-CoA Putative control of skeletal muscle HSL (Spriet and Watt, REVIEW, Proc of Nutr Soc., 2004)

Integration between exercise, AMPK, M-CoA, pH
and free carnitine on subsequent LCFA-CoA oxidation. pH - (Kiens, Physiol Rev, 2006)

NADH pH & CPT-I Free carnitine Malonyl-CoA AMPK FAT/CD36
“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

Effects of caffeine – mechanism: from increased lipolysis to CNS stimulation

? ? ? ? ? ? ? ? Caffeine supplementation and
increased adipose tissue lipolysis? NOTE: Need high dose to get FFA differences, BUT get ergogenic effect with low doses ? (Graham & Spriet, JAP, 1995) caffeine EPI, NE adenosine EPI, NE (6-8 mg /kg BW) + + + - 1 2 A1 nicotinic acid ? - Gs Gi + insulin AC ? - ? + nicotinic phosphodiesterase ATP cAMP AMP ? + AMP kinase + LEPTIN inactive PKA active PKA + ? ? + TG droplet LEPTIN insulin ? - HSL HSL-P ? phosphatase + TG FFA & glycerol leptin FFA & glycerol to working muscle Sensitivity: 2 > 1 PKA, protein kinase A

in human skeletal muscle during exercise.
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 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

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, min of 57% VO2peak) (Steffensen et al. AJP, 2002 – 90 min of 60% VO2peak)

Gender specific IMTG use- controversy?
Is IMTG use gender specific, OR: Substrate content specific- if you have more stored you use more and therefore more dependent upon: Training level Prior diet than gender? WHAT ABOUT HSL? IMTG quantification via 1H-magnetic resonance spectroscopy (Zehnder et al. MSSE, hours of 50% VO2peak) (While et al. J Clin Endocrinol Metab, 2003 – 1 hour of 65% VO2peak)

III. Other ideas- in brief.

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?

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.

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 57% VO2peak)

(van Loon et al. J. Physiol, 2003 – 2 hours of cycling @ 60% VO2peak)
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 60% VO2peak)

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)

trained than in sedentary subjects.
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 1H-MRS) 55% fat in recovery diet 15% fat in recovery diet

triglyceride content in trained males.
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 1H-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 57% VO2peak)

BUT, could an initially low IMTG store cause a significantly
greater glycogen use during the first min of exercise? (van Loon et al. J. Physiol, 2003 – 2 hours of 60% VO2peak)

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