Changes in metabolism but not myocellular signaling by training with CHO-restriction in endurance athletes

Abstract

Carbohydrate (CHO) restricted training has been shown to increase the acute training response, whereas less is known about the acute effects after repeated CHO restricted training. On two occasions, the acute responses to CHO restriction were examined in endurance athletes. Study 1 examined cellular signaling and metabolic responses after seven training‐days including CHO manipulation (n = 16). The protocol consisted of 1 h high‐intensity cycling, followed by 7 h recovery, and 2 h of moderate‐intensity exercise (120SS). Athletes were randomly assigned to low (LCHO: 80 g) or high (HCHO: 415 g) CHO during recovery and the 120SS. Study 2 examined unaccustomed exposure to the same training protocol (n = 12). In Study 1, muscle biopsies were obtained at rest and 1 h after 120SS, and blood samples drawn during the 120SS. In Study 2, substrate oxidation and plasma glucagon were determined. In Study 1, plasma insulin and proinsulin C‐peptide were higher during the 120SS in HCHO compared to LCHO (insulin: 0 min: +37%; 60 min: +135%; 120 min: +357%, P = 0.05; proinsulin C‐peptide: 0 min: +32%; 60 min: +52%; 120 min: +79%, P = 0.02), whereas plasma cholesterol was higher in LCHO (+15–17%, P = 0.03). Myocellular signaling did not differ between groups. p‐AMPK and p‐ACC were increased after 120SS (+35%, P = 0.03; +59%, P = 0.0004, respectively), with no alterations in p‐p38, p‐53, or p‐CREB. In Study 2, glucagon and fat oxidation were higher in LCHO compared to HCHO during the 120SS (+26–40%, P = 0.03; +44‐76%, P = 0.01 respectively). In conclusion, the clear respiratory and hematological effects of CHO restricted training were not translated into superior myocellular signaling after accustomization to CHO restriction.

Acute and sustained effects of a periodized carbohydrate intake using the sleep‐low model in endurance‐trained males

“…It was recently reported, though, that in highly trained endurance athletes, acute exercise with low CHO availability did not induce superior myocellular signaling (eg, through AMPK) when investigated in the accustomed state. 29 A limitation of the present study is that we did not directly measure muscle glycogen levels to verify whether the sleep-low model lowered endogenous CHO availability as intended. However, in a crossover design, muscle glycogen levels were lower with the sleep-low model when compared to high CHO availability.…”

“…Moving forward, however, adaptations related to mitochondrial biogenesis (through AMPK and PGC‐1α signaling) following exercise commenced with low CHO availability remain the dominant hypothesis within the field of diet‐exercise strategies to optimize the intramuscular response to exercise. It was recently reported, though, that in highly trained endurance athletes, acute exercise with low CHO availability did not induce superior myocellular signaling (eg, through AMPK) when investigated in the accustomed state …”

“…Notwithstanding, we suggest that the sleep‐low model applied in the present study — which is comparable to other prolonged studies — remains a useful approach to study the sustained effects of commencing exercise repeatedly with high reliance on fat as fuel during exercise. Although performing the acute study during the last 3 weeks of the intervention does not let us account for potential training effects during the intervention, fat oxidation rates were higher during exercise with low CHO availability in the seventh training block of a prolonged CHO periodization study . This suggests that repetitive manipulation of fat oxidation in endurance‐trained cohorts over an intervention is possible.…”

“…Although performing the acute study during the last 3 weeks of the intervention does not let us account for potential training effects during the intervention, fat oxidation rates were higher during exercise with low CHO availability in the seventh training block of a prolonged CHO periodization study. 29 This suggests that repetitive manipulation of fat oxidation in endurance-trained cohorts over an intervention is possible.…”

“…Based on these findings, we decided to add a crosssectional investigation of the influence of aerobic training state on protein expression of the proteins in Figure 5. Therefore, we compared all thirteen pre-values from the present study with a reference group, including seven recreationally active men (VO 2 -max = 49.8 ± 4.6 mL·kg −1 ·min −1 , range 41.1-55.1 mL·kg −1 ·min −1 ) from a previous study performed in our laboratory with similar age, sex, and BMI (median (range) age of 27 (24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) year; BMI of 24 (23-29) kg·m −2 ). 23 V O 2 -max was significantly different between groups (unpaired t test, P < .001).…”