Presentation on theme: "Diversification of Sports Nutrition Products"— Presentation transcript:
1Diversification of Sports Nutrition Products Integrating scientific knowledge and research intothe development of useful sports nutrition products for the athlete -Dr. Trent Stellingwerff, BSc, PhD- BSc, Nutrition, Cornell University, USAPhD, Exercise Physiology, Univ of Guelph,CanadaPost-Doctorate Fellowship, Univ. of Maastricht,Netherlands
6Sports 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, USAPhD, Exercise Physiology, Univ of Guelph,CanadaPost-Doctorate Fellowship, Univ. of Maastricht,Netherlands
7Diversification 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 protocolIV. Future Research Ideas/Directions- development of sportand/or gender specific nutrition recommendations/products.V. Conclusions- Take home message…
8Diversification of Sport Nutrition ProductsI. Historical perspective on sports performance products- from none to millions.
91972 Olympic Marathon Silver medalist - Frank Shorter’s “sports drink” Wow…this glucose andcaffeine is reallymaintaining my blood sugarand increasing my CNSstimulation and adiposetissue lipolysis.Cox G.R.et al. Effect of different protocolsof caffeine intake on metabolism andendurance performance. JAP. 93:, 2002.1972 Olympic Marathon Silver medalist- Frank Shorter’s “sports drink”
11‘sports nutrition products’ Consumers current options when it comes to sports nutrition:“Google” searched‘sports nutrition products’and got 54 million hits!
12claim ergogenic effects? Is there a lack of brand loyalty due to so much clutter and ubiquity of sports nutrition products that ALLclaim 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.
13Diversification of Sport Nutrition Products II. Research efficacy- what needs to be considered?
14Research 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?
15Research Design Concerns Amount- too little or too much may show no effectSubject- may only be effective in ‘untrained’ vs. trained or vice versa“value” is determined by the subjectTask- may only work in power events and not endurance or vice versaUse- acute (short term) may show effect but chronic may be compromisingSensitivity 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.)
16Assessing 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 raceGold :35.78Bronze- 3:36.72 (-0.44%)8th place- 3:38.19 (-1.12%)Sydney Men’s m raceGold :18.20Silver :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%!)
17Ergogenic 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?
18Research 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.
19Research Design Concerns So many issues and specific intricacies with eachand every product, and there are thousandsof products.HOW DOES THE GENERAL CONSUMER WADETHROUGH SO MANY POTENTIALISSUES/PRODUCTS?HOW MUCH TIME DOES THE CONSUMER HAVE FOR STUDIES TO COMPLETED?+?
20Diversification of Sport Nutrition ProductsIII. Time and effort-Fat-adaptation training and dietary protocol- 8+ years of ideas and testing…
21Decreased 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
22Initial 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!
23So what is this FAT-adaptation (FAT-adapt) nutritional & exercise intervention?
24General schematic of FAT-adaptation protocol Day Day Day Day Day Day Day 7Diet FAT or CHO FAT or CHO FAT or CHO FAT or CHO FAT or CHO CHO RestorationTestingTrialTraining Interval h long h Interval h long resttraining ride hill ride training rideTwo experiment trials: Hi FAT (FAT-adapt) vs. Hi CHO (HCHO)Two diets while training for 5-daysHCHO: 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)
25Unlike 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 andit abolishes the effect of elevated FFA normally present after a high-fat diet.Persistence of an ~ 2-fold increased whole-body fat oxidation despiteCHO 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 includedglucose 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 areequivocal, but would be expected to involve either an up and/or downregulation of key regulatory enzymes in the pathways of skeletal musclefat and CHO metabolism.
26fatty acyl-CoA fatty acyl-CoA TCA cycle LactateFFA-ALBGlucosebloodPMcytosolGlucoseGlycogenHKPHOSHSLIPASETGFFA-FABPG-6-PG-1-PPFKATPADPNADfattyacyl-CoAATPCrPCrNADHNADNADHATPADPPyruvateLactateCPT-ILDHOMCATPDHIMCPT-1IATPADPmatrixNADNADHb-oxidationH+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-CoAfattyacyl-CoANADNADNADHTCAcycleETCCO2NADHH+H+H20O2
27Regulation of PDH ? + + P - + + NAD NADH Pyruvate Dehydrogenase b (at rest)+PyruvateDehydrogenase b(inactive)ATPADP+PPDK1PDK2PDK3PDK4PDP1PDP2pyruvate-PDH kinasePDH phosphataseacetyl-CoACoASH+(rest only)Ca2++Epi?PyruvateDehydrogenase a(active)PiPipyruvate,CoASH, NADacetyl-CoA, H+,NADH, CO2
28PurposeTo 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.Hypothesis1. 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.
2920 min steady state cycling at ~70% VO2peak (63% of PPO) Experimental Protocol1 min 150% PPO20 min steady state cycling at ~70% VO2peak (63% of PPO)BiopsyBloodsamplingPulmonary gascollection2 trials: 1) CON vs. FAT-ADAPT
30Blood, glycogen and respiratory measures No differences in plasma lactate, glucose, insulin,FFA, epinephrine or norepinephrineFAT-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 a30% decrease in CHO oxidation
34HSLa augmented after FAT-adapt Trial p=0.116P=0.091
35High 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:ADPfAMPf
36 in PDHa after a high-fat diet despite CHO restoration ↑ NADH/NAD (at rest andexercise onset) increase inredox state with high fat diet?+Hi-Fat Diet = inc. inPDK protein/activityATPADP+PyruvateDehydrogenase b(inactive)Pyruvate-PDH kinasePDH phosphatasep=0.09acetyl-CoACoASH+(rest only)NO CHANGEPiCa2++EPIPyruvateDehydrogenase aPi(active)pyruvate,CoASH, NADacetyl-CoA, H+,NADH, CO2
37Over-riding hypothesis GlycogenGlycogenolysisG-6-PG-1-P+FFA-FABPcytosolPyruvateLactateCPT-IOMCATPDH+IMCPT-1ITCA cyclematrixb-oxidationOxidative 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-CoAfattyacyl-CoAIMTG ?Oxidative ATP Provision+NADH O ADP + PiNC
38“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.”
39IV. 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.
40Future Research Ideas & Directions Tapping into fat- the holy grail?
41Body Energy Stores of a 155 pound (~70kg) person
42What 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?
44Role of acetylcarnitine- buffer for Acetyl CoA? OM IMTCACycleAcetyl CoA, H+,NADH, CO2Pyruvate, CoASHNAD+PDHcarnitineCATAcetylcarnitine,CoASH, NAD+cytosol
45Increasing exercise intensity Inc. glycolytic flux (Odland, AJP-Endo,1998)(Roepstorff, AJP-Endo,2005)
46Correlation between acetylcarnitine and fat oxidation BUT, correlation does not always mean causation!What is the actual concentration of free carnitine between the outer and innermitochondrial 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)
47Endurance performance effects with carnitine supplementation? - No clear consensus -1) “IF” there is an positive metabolic / performance effect, long-term supplementation seems to beneeded 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.
48Future Research Ideas & Directions Post exercise optimization ofprotein balance and energy stores- a secret formula?
49What drink causes the highest insulin secretion? Drink 1: CHO only (1.2g/kg/hr)Drink 2: CHO + PH (0.2g/kg/hr) PH= protein hydrolysateDrink 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)
50AA w/ CHO supplementation on glycogen replenishment *113%170%CHO (0.8g/kg/hr)CHO + PRO(PH+leucine+phenyl)0.8g + 0.4gCHO + CHO1.2 g/kg/hrThe addition of protein hydrolysates and AA to CHO containingsolutions can further stimulate glycogen synthesisHOWEVER,Glycogen synthesis can also be accelerated by just increasingCHO intake to high levels when supplements are providedevery 30 min.(van Loon et al, Am J Clin Nutr, 2000)
51So what is it about leucine ?--- molecular signalling ? Combined ingestion of protein and free leucine with carbohydrateincreases 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 ?
55Future Research Ideas & Directions III. Other ideas- in brief.
56General 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. elderlyII. 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 pursuitsIII. Development of different products for different times of the season…- ie. base training versus tapering before big events
57Diversification of Sport Nutrition ProductsVI. Conclusions-Take home message…
58Is there currently too much selection and choice, in terms of sports nutrition products, for theconsumer?OR are there too many products without theproper scientific testing supportingtheir claims?How does a company gain the trust and supportof the consumer through the development ofadditional sports nutrition products?
59Final 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 companysupports sound unbiased research of their products.III. Knowledge/education coupled with brand identity results in empowerment and trust for the consumer or athlete…
62Diversification of Sport Nutrition ProductsIII. Time and effort-Fat-adaptation training and dietary protocol- 8+ years of ideas and testing…
63Decreased 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
64Chronic 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 highfat diet (Peters et al., 1998 & 2001)BUT current study had a 24 hour CHO restorationperiod…Increase in IMTG leading to an increase in HSL? (20%differences between trials?)
65Major 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”
67Body Energy Stores of a 155 pound (~70kg) person
68Fuel Utilization at Different Exercise Intensities 25% VO2max % VO2max %VO2max(Brisk Walking Pace) (~Marathon Pace) (~5 to 10km race pace)FatsMuscle GlycogenBlood Glucose (sugar)- 30 min of exercise after an overnight fast:Romijn, J.A. et al.- American Journal of Physiology, E380, 1993.
69HSL and IMTG use- substrate content and gender? +-IMTG-+Aerobic oxidation via TCA Cycle in mitochondriaLCFA-CoAPutative control of skeletal muscle HSL(Spriet and Watt, REVIEW, Proc of Nutr Soc., 2004)
70Integration between exercise, AMPK, M-CoA, pH and free carnitine on subsequent LCFA-CoA oxidation.pH-(Kiens, Physiol Rev, 2006)
71NADH pH & CPT-I Free carnitine Malonyl-CoA AMPK FAT/CD36 “magical” fuel sensing switch toalter mito. fat oxidation?NADHpH & CPT-IFree carnitineMalonyl-CoAAMPKFAT/CD36Small parts of the complexmetabolic fuel sensing andadapting machinery?
72Blood shunting during exercise - from Martin and Coe: Training Distance Runners
73Future Research Ideas & Directions Effects of caffeine – mechanism: from increased lipolysis to CNS stimulation
74? ? ? ? ? ? ? ? Caffeine supplementation and increased adipose tissue lipolysis?NOTE: Need high doseto get FFA differences,BUT get ergogeniceffect with low doses ?(Graham & Spriet, JAP, 1995)caffeineEPI, NEadenosineEPI, NE(6-8 mg /kg BW)+++-12A1nicotinicacid?-GsGi+insulinAC?-?+nicotinicphosphodiesteraseATPcAMPAMP?+AMP kinase+LEPTINinactivePKAactivePKA+??+TGdropletLEPTINinsulin?-HSLHSL-P?phosphatase+TGFFA &glycerolleptinFFA &glycerolto workingmuscleSensitivity:2 > 1PKA, protein kinase A
75in human skeletal muscle during exercise. Caffeine ingestion does not alter skeletal carbohydrate or fat metabolismin 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 CHOoxidation.
76Low dose-caffeine supplementation results in increased CNS stimulation and decreased RPE
77Future Research Ideas & Directions IV. Gender differences in fuel metabolism
78Fuel 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)MenWomen
79Gender 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)
80Gender 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 levelPrior 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)
81Future Research Ideas & Directions III. Other ideas- in brief.
82Diversification of Sport Nutrition Products 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 ROSor cortisol inflammatory responses post-training- time course, short-term vs. long-term supplementation, amounts- or is the cortisol response a necessary for training adaptation?
83Diversification of Sport Nutrition Products IV. Gender differences- differences in CHO and fat metabolism?- differing protocols/products needed for CHO loading? (evidencesuggests 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 ???
84Effects of carnitine supplementation on metabolism and performance.
85Effects of carnitine supplementation on metabolism and performance.
86Future Research Ideas & Directions Tapping into fat- the holy grail?
87What about replenishing IMTG’s post-exercise? (similar to glycogen replenishment?)
88IMTG 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)
89(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)
90Even IMTG utilization during resistance exercise Significant 27% decrease in Type IIMTG after resistance exercise.(Koopman et al. EJAP, 2006 – 45 min of resistance exercise)
91trained than in sedentary subjects. Postexercise fat intake repletes intramyocellular lipids but no faster intrained than in sedentary subjects.(Decombaz et al., AJP-Reg, 2001; 2 hrs at 50% VO2max with 55 and 15% fat diets for recoverymeasured via 1H-MRS)55% fat in recovery diet 15% fat in recovery diet
92triglyceride content in trained males. Influence of prolonged endurance cycling and recovery diet on intramusculartriglyceride content in trained males.(van Loon et al., AJP-Endo 2003; 3 hrs at 55% Wmax with 39 and 24% fat diets for recoverymeasured via 1H-MRS)39% fat in normal fat 24% low fat diet
93Could 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)
94BUT, 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)