Carbohydrate ingestion reduces skeletal muscle acetylcarnitine availability but has no effect on substrate phosphorylation at the onset of exercise in man

Abstract

This study investigated the effect of reduced acetylcarnitine availability on oxidative metabolism during the transition from rest to steady-state exercise. Eight male subjects completed two randomised exercise trials at 68 % of the peak rate of O(2) uptake (V((O(2)),peak)). On one occasion subjects ingested 1 g (kg body mass)(-1) glucose 75 min prior to exercise (CHO), whereas the other trial acted as a control (CON). Muscle samples were obtained pre- and 75 min post-ingestion, and following 1 and 10 min of exercise. Plasma glucose and insulin were elevated (P < 0.05), and plasma free fatty acids (FFA) were lower at the onset of exercise in CHO. Acetylcarnitine (CON, 4.8 +/- 1.8; CHO, 1.5 +/- 0.9 mmol (kg dry mass (d.m.))(-1), P < 0.05) and acetyl CoA (CON, 13.2 +/- 2.3; CHO, 6.3 +/- 0.6 micromol (kg d.m.)(-1), P < 0.05) were lower at rest, whereas pyruvate dehydrogenase activation (PDHa) was greater in CHO compared with CON (CON, 0.78 +/- 0.07; CHO, 1.44 +/- 0.19 mmol min(-1) (kg wet mass (w.m.))(-1)). Respiratory exchange ratio (RER) was significantly elevated during exercise in CHO. The acetyl groups increased at similar rates at the onset of exercise (1 min) and there was no difference in substrate phosphorylation as determined from lactate accumulation and phosphocreatine degradation between trials. Subsequently, oxidative metabolism during the transition from rest to steady-state exercise was not affected by prior carbohydrate ingestion. Although exercise resulted in the rapid activation of PDH in both trials, PDHa was greater at 1 min in CHO (CON, 2.36 +/- 0.22; CHO, 2.91 +/- 0.18 mmol min(-1) (kg w.m.)(-1)). No differences in muscle metabolite levels and PDHa were observed after 10 min of moderate exercise between trials. In summary, at rest, carbohydrate ingestion induced multiple metabolic changes which included decreased acetylcarnitine availability and small increases in PDHa. The prior changes in PDHa and acetylcarnitine availability had no effect on substrate phosphorylation and oxidative metabolism at the onset of exercise. These data suggest that acetylcarnitine availability is unlikely to be the site of metabolic inertia during the transition from rest to steady-state moderate intensity exercise.

Figure 1

Blood glucose (A) and plasma insulin (B) at rest and during 10 min of exercise at 68 % V̇_O2,peak with (CHO) or without (CON) prior carbohydrate ingestion. Values are means ± s.e.m., n = 8. * Significantly different from -75 min for CHO; † significantly different from corresponding time point for CON (P < 0.05).

Figure 2

Muscle acetylcarnitine (A) and acetyl CoA (B) at rest and during 10 min of exercise at 68 % V̇_O2,peak with (CHO) or without (CON) prior carbohydrate ingestion. Values are means ± s.e.m., n = 8. * Significantly different from -75 min for CHO; † significantly different from corresponding time point for CON (P < 0.05).

Figure 3

PDH activation at rest and during 10 min of exercise at 68 % V̇_O2,peak with (CHO) or without (CON) prior carbohydrate ingestion. Values are means ± s.e.m., n = 8. * Significantly different from -75 min for CHO; † significantly different from corresponding time point for CON (P < 0.05).