נק' מוניטין:
58,705
Effect of high-fat and high-carbohydrate diets on pulmonary O2 uptake kinetics during the transition to moderate-intensity exercise
J. A. Raper , L. K. Love , D. H. Paterson , S. J. Peters , G. J. F. Heigenhauser , J. M. Kowalchuk
Journal of Applied PhysiologyPublished 1 December 2014Vol. 117no. 11, 1371-1379DOI: 10.1152/japplphysiol.00456.2014
ABSTRACT
Mitochondrial pyruvate dehydrogenase (PDH) regulates the delivery of carbohydrate-derived substrate to the mitochondrial tricarboxylic acid cycle and electron transport chain. PDH activity at rest and its activation during exercise is attenuated following high-fat (HFAT) compared with high-carbohydrate (HCHO) diets. Given the reliance on carbohydrate-derived substrate early in transitions to exercise, this study examined the effects of HFAT and HCHO on phase II pulmonary O2 uptake (V̇O2p) kinetics during transitions into the moderate-intensity (MOD) exercise domain. Eight active adult men underwent dietary manipulations consisting of 6 days of HFAT (73% fat, 22% protein, 5% carbohydrate) followed immediately by 6 days of HCHO (10% fat, 10% protein, 80% carbohydrate); each dietary phase was preceded by a glycogen depletion protocol. Participants performed three MOD transitions from a 20 W cycling baseline to work rate equivalent to 80% of estimated lactate threshold on days 5 and 6 of each diet. Steady-state V̇O2p was greater (P < 0.05), and respiratory exchange ratio and carbohydrate oxidation rates were lower (P < 0.05) during HFAT. The phase II V̇O2p time constant (τV̇O2p) [HFAT 40 ± 16, HCHO 32 ± 19 s (mean ± SD)] and V̇O2p gain (HFAT 10.3 ± 0.8, HCHO 9.4 ± 0.7 ml·min−1·W−1) were greater (P < 0.05) in HFAT. The overall adjustment (effective time constant) of muscle deoxygenation (Δ[HHb]) was not different between diets (HFAT 24 ± 4 s, HCHO 23 ± 4 s), which coupled with a slower τV̇O2p, indicates a slowed microvascular blood flow response. These results suggest that the slower V̇O2p kinetics associated with HFAT are consistent with inhibition and slower activation of PDH, a lower rate of pyruvate production, and/or attenuated microvascular blood flow and O2 delivery.
J. A. Raper , L. K. Love , D. H. Paterson , S. J. Peters , G. J. F. Heigenhauser , J. M. Kowalchuk
Journal of Applied PhysiologyPublished 1 December 2014Vol. 117no. 11, 1371-1379DOI: 10.1152/japplphysiol.00456.2014
ABSTRACT
Mitochondrial pyruvate dehydrogenase (PDH) regulates the delivery of carbohydrate-derived substrate to the mitochondrial tricarboxylic acid cycle and electron transport chain. PDH activity at rest and its activation during exercise is attenuated following high-fat (HFAT) compared with high-carbohydrate (HCHO) diets. Given the reliance on carbohydrate-derived substrate early in transitions to exercise, this study examined the effects of HFAT and HCHO on phase II pulmonary O2 uptake (V̇O2p) kinetics during transitions into the moderate-intensity (MOD) exercise domain. Eight active adult men underwent dietary manipulations consisting of 6 days of HFAT (73% fat, 22% protein, 5% carbohydrate) followed immediately by 6 days of HCHO (10% fat, 10% protein, 80% carbohydrate); each dietary phase was preceded by a glycogen depletion protocol. Participants performed three MOD transitions from a 20 W cycling baseline to work rate equivalent to 80% of estimated lactate threshold on days 5 and 6 of each diet. Steady-state V̇O2p was greater (P < 0.05), and respiratory exchange ratio and carbohydrate oxidation rates were lower (P < 0.05) during HFAT. The phase II V̇O2p time constant (τV̇O2p) [HFAT 40 ± 16, HCHO 32 ± 19 s (mean ± SD)] and V̇O2p gain (HFAT 10.3 ± 0.8, HCHO 9.4 ± 0.7 ml·min−1·W−1) were greater (P < 0.05) in HFAT. The overall adjustment (effective time constant) of muscle deoxygenation (Δ[HHb]) was not different between diets (HFAT 24 ± 4 s, HCHO 23 ± 4 s), which coupled with a slower τV̇O2p, indicates a slowed microvascular blood flow response. These results suggest that the slower V̇O2p kinetics associated with HFAT are consistent with inhibition and slower activation of PDH, a lower rate of pyruvate production, and/or attenuated microvascular blood flow and O2 delivery.
