LOW CHO / HIGH FAT (LCHF) FOR ATHLETES WHAT DOES THE EVIDENCE SAY? - PowerPoint PPT Presentation

LOW CHO / HIGH FAT (LCHF) FOR ATHLETES – WHAT DOES THE EVIDENCE SAY? Trent Stellingwerff, PhD Canadian Sport Institute Pacific Saturday Jan. 13 th , 2018 10:35 – 11:15am (40min) Canadian Nutrition Society; Toronto Ontario

Conflict of Interest / Funding Disclosures – Grants/Research Support: Own The Podium i4G funding, MITACS Funding, Canadian Foundation for Innovation (CFI) Equipment Grant My real over-riding conflict of interest: – Speakers Bureau/Honoraria: Post Cereals – PowerBar (2015- Making Olympic athletes go faster in 2016); Pepsi-Co – Gatorade (2015-2016); B2ten (2015-current) Olympic events within the rules of – Consulting Fees: Post Cereals – sport PowerBar (2015-2016); B2ten (2015-current) – Other: Employee of Canadian Sport Institute Pacific, Victoria, B.C.

Presentation overview 1) Physiology of High Intensity Endurance 2) LCHF: Fat Adaptation vs. Ketogensis 3) Fat Adaptation & Ketogensis and Performance 4) What do Champion Endurance Athletes Eat? 5) Summary

PHYSIOLOGY OF HIGH INTENSITY ENDURANCE PERFORMANCE

Athlete energetic demands - Lots of misconceptions? • Some/many believe that fat oxidation plays an important role in elite athlete performance and training in events up to 3 to 4hrs. • Some/many believe that the substrate for the “aerobic” system is primarily fat at training and competition intensities in elite athletes. • Some/many believe there is no difference in the whole-body efficiency / cost in metabolizing CHO vs. FAT for ATP production • Some/many believe that PCr is the only substrate for maximal power/speed production under durations of 10 sec and for resistance (weight-room) training

FFA-ALB Glucose blood PM Transport cytosol Glucose Glycogen (Rxn 2) LIPASE HK (Rxn 3) PHOS TG FFA-FABP G-6-P G-1-P PFK (Rxn 4) ATP ADP (Rxn 1) NAD fatty ATP Cr PCr acyl-CoA NADH NAD NADH ATP ADP Pyruvate Lactate LDH CPT-I (Rxn 6) OM CAT IM PDH CPT-1I (Rxn 5) ATP ADP (Rxn 7) NAD NADH matrix b -oxidation H + acetyl-CoA fatty NAD acyl-CoA NAD NADH TCA E (Rxn 8) cycle T CO 2 NADH C H + H + H 2 0 O 2

Energy production during exercise Glycogen AEROBIC (CHO CHO Energy stores) Production Pyruvate PDHa = 36 ATP! TCA ANAEROBIC Lactic acid Cycle Energy Production La - + H + = 3 ATP! Blood Lactate MCT Mitochondria Aerobic PowerHouse

Body Energy Stores of a ~70kg person (~65,000 Kcals = 21 marathons!) 300000 275000 250000 Muscle glycogen Liver glycogen 200000 Stored Energy (kJ) Adipose tissue (fat) Muscle Triglycerides (fat) 150000 100000 (~1600 (~500 (~1,300 50000 kcals) kcals) kcals) Energy required 7000 5500 2000 for 65kg to run 0 a marathon: 1 ~3000 to Rapoport, B. I. (2010). Metabolic factors limiting performance in marathon runners. PLoS Comput Biol, Type of Energy 6(10), e1000960. 3500 kcals

Fuel Utilization at different exercise intensities Romijn et al Am J Physiol 265: E380, 1993 Energy expenditure HR (% HRmax) (kcal/kg/min) Exercise intensity (%VO 2 max) Fernandez-Garcia et Recovery / Soft-Pedaling ~30% of ~30-40% of al MSSE 32(5): ~10-20% of Tour Cycling Tour Cycling 1002-1006, 2000 Tour Cycling Fuel utilization during marathon ~85% CHO metab. RQ ~0.93 to 0.97 running in elite athletes? ~15% Fat metab. Bosch et al Eur. J. Appl. Physiol. 61: 68-72, 1990. O’Brien et al MSSE 25: 1009 -1017, 1993.

CHO Energy production during exercise is more efficient! 5.5% more kcals of energy produced per liter of oxygen consumed when utilizing 100% CHO vs. 100% fat (= lower VO2 per given power = 5.5% more efficient!) OR ~ 1% more energy liberated per L of O2 consumed for a 0.05 increase in RQ Prof. Andy Jones estimates a 0.05 increase in RQ (more CHO dependent) could be worth a 60-90 sec faster marathon performance!

~50% of a 6 sec sprint is CHO dependent! Parolin et al.- AJP, 1999 (anaerobic) (aerobic energy – mainly via CHO pyruvate disposal) Sprint #1 Sprint #3 3 bouts of 30 second sprints with 4’ rests with measurements at rest, 6, 15 and 30 seconds (all measurements based on biopsy data, not whole-body respiratory data, which violates methodological principles as non-steady state)

Fuel utilization during training in elite athletes ( NOT fasted!) “Why, for example, should athletes involved in prolonged submaximal exercise — probably the most common form of exercise performed by most elite and recreational athletes in training and competition — need always to eat high carbohydrate diets … . Surely our abundant body fat stores could provide most if not all the energy necessary to fuel activities of a submaximal intensity?” Noakes T, Volek JS, Phinney SD. Low-carbohydrate diets for athletes: what evidence? Br J Sports Med. 2014;48(14):1077-8. Athletics Canada Testing Data Base // Male avg VO2max = 71.0 +/- 2.9 ml/kg/min Avg tested easy run pace = 3:39 to 4:50 min/km pace (~60 to 85% of VO2max) Boorsma RK, Whitfield J, Spriet LL. Beetroot juice supplementation does not improve performance of elite 1500-m runners. Med Sci Sports Exerc. 2014;46(12):2326-34.

LCHF: FAT-ADAPTATION (3 TO 5 DAYS) VS. KETOGENSIS (>3 WEEKS)

Training with periodic low CHO-availability is NOT chronically training on a low CHO (or high fat) diet. LCHF: Amount of CHO and timing of diet are not scientifically validated and inconsistent. But, fat-adaptation can occur in as little as 3 to 5 days and ketogensis in ~3 weeks, w/ some athletes saying a few years are needed for optimal adaptation. In most instances, LCHF approach requires <50g CHO / day

Keto-adaptation

Ketogenic Adaptation can more than double fat oxidation! FASTER Study- Dr. Jeff Volek (FASTER=Fat-Adapted-Substrate oxidation in-Trained-Elite-Runners) 1.5 g/min 1 g/min Volek, J.S., et al., Metabolic characteristics of keto-adapted ultra-endurance runners. Metabolism, 2016. 65(3): p. 100-10. 1.5g FAT/min = 90 g FAT/hr = Volek JS, Noakes T, Phinney SD. Rethinking fat as a fuel 810 calories of fuel per hour for endurance exercise. Eur J Sport Sci. 2015;15(1):13- 20. at 60% VO2peak

Decreased PDHa after FAT-adapt (or a 5 day low CHO diet) 5 † PDHa (mmol ·kg w.w. -1 · min -1 ) 4 FAT-adapt HCHO 3 * * ‡ 2 * * 1 0 0 10 20 Time (min) Post 1 min Sprint @ 150% PPO Stellingwerff T, Spriet LL, Watt MJ, et al. Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration. Am J Physiol Endocrinol Metab 2006;290:E380-8.

FAT ADAPTATION OR KETOGENSIS & PERFORMANCE

Glycogen and performance during high-intensity exercise 9 * Time to exhaustion (min) 8 6 males undertook at 105% Vo2max 7 3 dietary conditions for 6 2.5 days preceding # 5 TTE tests 4 Normal Diet (3.9g CHO/kg/day) High CHO (6.1g CHO/kg/day) 3 Low CHO (0.3g CHO/kg/day) 2 1 0 Normal Diet High CHO Low CHO Maughan RJ, and Poole DC. The effects of a glycogen-loading regimen on the capacity to perform anaerobic exercise. Eur J Appl Physiol Occup Physiol 46: 211-219, 1981.

Ketogenic Data – Phinney 1983 five well-trained cyclists were fed a eucaloric balanced diet (EBD) for one - 84’ week providing 35-50 kcal/kg/d, 1.75 g protein/kg/d and 66% CHO, then followed by four weeks 146’ 130’ of a eucaloric ketogenic diet (EKD, less than 20g of With Subject JP Without Subject JP CHO). p-value here = 0.9488 // p-value here = 0.4943 // Change in ES = -0.03 (trivial at best) Change in ES = -0.33 (small to moderate) Cycling endurance test was ride to exhaustion (ENDUR) Odds ratios of clinical or mechanistic Odds ratios of clinical or mechanistic at 62%-64% of Vo2max relevance: relevance: (~2.5hrs) 32% possibly positive, 15% possibly positive, 32% possibly trivial 24% possibly trivial 36% possibly negative. 61% possibly negative. Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism. 1983;32(8):769-76..

Performance Improvement or Decrement? Havemann et al. Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance J Appl Physiol. 100: 194 – 202, 2006.

“… 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 caused a reduction in the activity of pyruvate dehydrogenase; this change would act to impair rates of glycogenolysis...[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. ”