Effect of high-fat and high-carbohydrate diets on pulmonary O2 uptake kinetics during the transition to moderate-intensity exercise

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 (V̇o2 p) 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 V̇o2 p was greater (P < 0.05), and respiratory exchange ratio and carbohydrate oxidation rates were lower (P < 0.05) during HFAT. The phase II V̇o2 p time constant (τV̇o2 p) [HFAT 40 ± 16, HCHO 32 ± 19 s (mean ± SD)] and V̇o2 p 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 τV̇o2 p, indicates a slowed microvascular blood flow response. These results suggest that the slower V̇o2 p 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.

Keywords: O2 uptake kinetics; high-carbohydrate diet; high-fat diet; muscle deoxygenation; near-infrared spectroscopy; substrate oxidation.

Fig. 1.

Calculated respiratory exchange ratio (RER) (A), and fat and carbohydrate oxidation rates (B and C, respectively) for steady-state baseline (20 W) cycling, and moderate-intensity exercise following the high fat (HFAT, open bars) and high carbohydrate (HCHO, solid bars) diets. Values are means ± SD. *Significant difference (P < 0.05) between the high-fat and high-carbohydrate diets; +significant difference (P < 0.05) from baseline within a given dietary condition.

Fig. 2.

Group mean pulmonary O₂ uptake (V̇o_2p) response at baseline and throughout the transition to moderate-intensity exercise during the HFAT (open symbols) and HCHO (closed symbol) diets.

Fig. 3.

The time constant for the phase II V̇o_2p response (τV̇o_2p) during the HFAT and HCHO diets; individual responses (open symbols); group mean (± SD) response (closed symbol). Values are means ± SD; τV̇o_2p was significantly greater (P < 0.015) in HFAT vs. HCHO.

Fig. 4.

Group mean muscle deoxygenation (Δ[HHb]) response at baseline and throughout the transition to moderate-intensity exercise during the HFAT (open symbols) and HCHO (closed symbols) diets.