Ingesting a combined carbohydrate and essential amino acid supplement compared to a non-nutritive placebo blunts mitochondrial biogenesis-related gene expression after aerobic exercise

Abstract

Background: Whether load carriage (LC), an endurance exercise mode composed of the aerobic component of traditional endurance exercise [e.g., cycle ergometry (CE)] and contractile forces characteristic of resistive-type exercise, modulates acute mitochondrial adaptive responses to endurance exercise and supplemental nutrition [carbohydrate + essential amino acids (CHO +EAA)] is not known. Objective: The aim of this study was to examine the effects of LC and CE, with or without CHO+EAA supplementation, on acute markers of mitochondrial biogenesis. Methods: Twenty-five adults performed 90 min of metabolically matched LC (treadmill walking, wearing a vest equal to 30% of body mass) or CE exercise during which CHO+EAA (46 g carbohydrate and 10 g essential amino acids) or non-nutritive control (CON) drinks were consumed. Muscle biopsy samples were collected at rest (pre-exercise), post-exercise, and after 3 h of recovery to assess citrate synthase activity and the expression of mRNA (reverse transcriptase-quantitative polymerase chain reaction) and protein (Western blot). Results: Citrate synthase and phosphorylated p38 mitogen-activated protein kinase (p38 MAPK)Thr180/Tyr182 were elevated postexercise compared with pre-exercise (time main effect, P < 0.05). Peroxisome proliferator-activated γ-receptor coactivator 1α (PGC-1α) expression was highest after recovery for CE compared with LC (exercise-by-time effect, P < 0.05). Sirtuin 1 (SIRT1) expression postexercise was higher for CONthan for CHO+EAA treatments (drink-by-time, P,0.05). Tumor suppressor p53 (p53), mitochondrial transcription factor A (TFAM), and cytochrome c oxidase subunit IV (COXIV) expression was greater for CON than for CHO+EAA treatments (drink main effect, P < 0.05). PGC-1α and p53 expressions were positively associated (P < 0.05) with TFAM (r = 0.629 and 0.736, respectively) and COXIV (r = 0.465 and 0.461, respectively) expressions. Conclusions: Acute mitochondrial adaptive responses to endurance exercise appear to be largely driven by exogenous nutrition availability. Although CE upregulated PGC-1α expression to a greater extent than LC, downstream signaling was the same between modes, suggesting that LC, in large part, elicits the same acute mitochondrial response as traditional, non-weight-bearing endurance exercise. This trial was registered at clinicaltrials.gov as NCT01714479.