Exercise twice-a-day potentiates markers of mitochondrial biogenesis in men.

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-É£ coactivator 1-alpha (PGC-1α), peroxisome proliferator-activated receptor-alpha (PPARα), and peroxisome proliferator-activated receptor beta/delta (PPARß/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.

Caffeine Increases Work Done above Critical Power, but Not Anaerobic Work.

PURPOSE: The assumption that the curvature constant (W') of the power-duration relationship represents anaerobic work capacity is a controversial, unresolved question. We investigated if caffeine ingestion could increase total work done above critical power (CP), and if this would be accompanied by greater anaerobic energy expenditure and by an enhanced maintenance of maximal oxidative metabolic rate. METHODS: Nine men (26.6 ± 5.3 yr, V˙O2max 40.6 ± 5.8 mL·kg·min) cycled until exhaustion at different exercise intensities on different days to determine the CP and W'. On separated days, participants cycled until exhaustion in the severe-intensity domain (136% ± 7% of CP) after ingesting either caffeine (5 mg·kg body mass) or a placebo. RESULTS: Time to exhaustion was 34% longer with caffeine compared with placebo, and this was accompanied by a greater work done above CP (23.7 ± 5.7 vs 17.5 ± 3.6 kJ; 130% ± 30% vs 95% ± 14% of W', P < 0.01). Caffeine increased the aerobic energy expenditure (296.4 ± 91.0 vs 210.2 ± 71.9 kJ, P < 0.01), but not anaerobic lactic, anaerobic alactic, and total anaerobic (lactic + alactic) energy expenditure. The end values of heart rate and ventilation were higher with caffeine, but the V˙O2 end was similar between conditions and was not different from V˙O2max. Caffeine did not change time to reach V˙O2max but increased time maintained at V˙O2max (199.3 ± 105.9 vs 111.9 ± 87.1 s, P < 0.05). CONCLUSIONS: Caffeine increased total work done above CP, but this was not associated with greater anaerobic work. Rather, this was associated with a higher tolerance to maintain exercise at maximal oxidative metabolic rate.

Effect of caffeine ingestion on anaerobic capacity quantified by different methods.

We investigated whether caffeine ingestion before submaximal exercise bouts would affect supramaximal oxygen demand and maximal accumulated oxygen deficit (MAOD), and if caffeine-induced improvement on the anaerobic capacity (AC) could be detected by different methods. Nine men took part in several submaximal and supramaximal exercise bouts one hour after ingesting caffeine (5 mg·kg-1) or placebo. The AC was estimated by MAOD, alternative MAOD, critical power, and gross efficiency methods. Caffeine had no effect on exercise endurance during the supramaximal bout (caffeine: 131.3 ± 21.9 and placebo: 130.8 ± 20.8 s, P = 0.80). Caffeine ingestion before submaximal trials did not affect supramaximal oxygen demand and MAOD compared to placebo (7.88 ± 1.56 L and 65.80 ± 16.06 kJ vs. 7.89 ± 1.30 L and 62.85 ± 13.67 kJ, P = 0.99). Additionally, MAOD was similar between caffeine and placebo when supramaximal oxygen demand was estimated without caffeine effects during submaximal bouts (67.02 ± 16.36 and 62.85 ± 13.67 kJ, P = 0.41) or when estimated by alternative MAOD (56.61 ± 8.49 and 56.87 ± 9.76 kJ, P = 0.91). The AC estimated by gross efficiency was also similar between caffeine and placebo (21.80 ± 3.09 and 20.94 ± 2.67 kJ, P = 0.15), but was lower in caffeine when estimated by critical power method (16.2 ± 2.6 vs. 19.3 ± 3.5 kJ, P = 0.03). In conclusion, caffeine ingestion before submaximal bouts did not affect supramaximal oxygen demand and consequently MAOD. Otherwise, caffeine seems to have no clear positive effect on AC.

Correction: Effect of caffeine ingestion on anaerobic capacity quantified by different methods.

[This corrects the article DOI: 10.1371/journal.pone.0179457.].