Exercise twice‐a‐day potentiates markers of mitochondrial biogenesis in men

Abstract

Endurance exercise begun with reduced muscle glycogen stores seems to potentiate skeletal muscle protein abundance and gene expression. However, it is unknown whether this greater signaling responses is due to performing two exercise sessions in close proximity—as a first exercise session is necessary to reduce the muscle glycogen stores. In the present study, we manipulated the recovery duration between a first muscle glycogen‐depleting exercise and a second exercise session, such that the second exercise session started with reduced muscle glycogen in both approaches but was performed either 2 or 15 hours after the first exercise session (so‐called “twice‐a‐day” and “once‐daily” approaches, respectively). We found that exercise twice‐a‐day increased the nuclear abundance of transcription factor EB (TFEB) and nuclear factor of activated T cells (NFAT) and potentiated the transcription of peroxisome proliferator‐activated receptor‐ɣ coactivator 1‐alpha (PGC‐1α), peroxisome proliferator‐activated receptor‐alpha (PPARα), and peroxisome proliferator‐activated receptor beta/delta (PPARβ/δ) genes, in comparison with the once‐daily exercise. These results suggest that part of the elevated molecular signaling reported with previous “train‐low” approaches might be attributed to performing two exercise sessions in close proximity. The twice‐a‐day approach might be an effective strategy to induce adaptations related to mitochondrial biogenesis and fat oxidation.

Achieving energy balance with a high‐fat meal does not enhance skeletal muscle adaptation and impairs glycaemic response in a sleep‐low training model

“…Recent findings from our group show no difference in markers of skeletal muscle adaptation between LCHO low energy and LCHO high fat (energy balance) during two consecutive aerobic training sessions (Hammond et al., 2019). However, the lack of differences observed in this study can be due to the overriding effect of the short time frame (2.5 h) between the two consecutive training sessions of the ‘twice‐a‐day’ model used (Andrade‐Souza et al., 2019). To eliminate this confounding factor, the ‘sleep‐low, train‐low’ model has emerged as a particularly potent strategy to prolong the period of CHO and energy restriction between two sessions (Bartlett et al., 2013; Lane et al., 2015).…”

Genome wide association study of response to interval and continuous exercise training: the Predict-HIIT study

“…A study also found PGC-1α expression can be increased through the dephosphorylation and nuclear translocation of TFEB [ 60 ]. With these points in mind, a recent study found completing two high-intensity exercise sessions within a short time frame (2 h) increased the nuclear abundance of TFEB and the transcription of PCG-1α in 8 healthy young men [ 61 ]. Furthermore, overexpression of PGC-1α has been associated with improved V̇O 2 peak at baseline and following endurance training in several studies [ 62 , 63 ].…”

Impact of pre‐exercise feeding status on metabolic adaptations to endurance‐type exercise training

“…Skeletal muscle AMPK activation also stimulates enduring adaptations to exercise including increases in the GLUT4 protein levels and mitochondrial biogenesis via transcription factors including PGC1α (Wojtaszewski et al 2000;Ojuka et al 2002). Enhanced AMPK activation in response to exercise commenced with reduced muscle glycogen concentrations (35-45% of basal) may explain increased mitochondrial adaptations compared to the same exercise started with higher muscle glycogen concentrations (Morton et al 2009;Hulston et al 2010;Bartlett et al 2013;Andrade-Souza et al, 2020). This may be important as obesity and peripheral insulin resistance have been associated with a lower mitochondrial oxidative capacity (Kelley et al 1999;Simoneau et al 1999).…”