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The aim of this study was to investigate the effect of 3 and 6 mg of caffeine per kg of body mass (mg/kg) on whole-body substrate oxidation during an incremental cycling exercise test in healthy active women. Using a double-blind placebo-controlled counterbalanced experimental design, 14 subjects performed three identical exercise trials after the ingestion of 3 or 6 mg/kg of caffeine or placebo. The exercise trials consisted of an incremental test on a cycle ergometer with 3-min stages at workloads from 30 to 70% of maximal oxygen uptake (VO2max). Substrate oxidation rates were measured by indirect calorimetry. During exercise, there was a significant effect of substance (F = 5.221; p = 0.016) on fat oxidation rate. In comparison to the placebo, 3 mg/kg of caffeine increased fat oxidation rates at 30 to 60% of VO2max (all p < 0.050) and 6 mg/kg at 30 to 50% of VO2max (all p < 0.050). There was also a significant effect of substance (F = 5.221; p = 0.016) on carbohydrate oxidation rate (F = 9.632; p < 0.001). In comparison to placebo, both caffeine doses decreased carbohydrate oxidation rates at 40 to 60% VO2max (all p < 0.050). The maximal rate of fat oxidation with placebo was 0.24±0.03 g/min, which increased with 3 mg/kg to 0.29±0.04 g/min (p = 0.032) and to 0.29±0.03 with 6 mg/kg of caffeine (p = 0.042). Acute intake of caffeine improves the utilization of fat as a fuel during submaximal aerobic exercise in healthy active women with an effect of similar magnitude after the intake of 3 and 6 mg of caffeine per kg of body mass. Thus, the use of 3 mg/kg of caffeine would be more recommended than 6 mg/kg for women seeking increased fat utilization during submaximal exercise

Pre-exercise caffeine ingestion has been shown to increase the workload at ventilatory threshold, suggesting an ergogenic effect of this stimulant on submaximal aerobic exercise. However, the time course of tolerance to the effect of caffeine on ventilatory threshold is unknown. This study aimed to determine the evolution of tolerance to the ergogenic effect of caffeine on the ventilatory threshold. Methods: Eleven participants (age 32.3 ± 4.9 yrs, height 171 ± 8 cm, body mass 66.6 ± 13.6 kg, VO2max = 48.0 ± 3.8 mL/kg/min) took part in a longitudinal, double-blind, placebo-controlled, randomized, crossover experimental design. Each participant took part in two identical treatments: in one treatment, participants ingested a capsule containing 3 mg of caffeine per kg of body mass per day (mg/kg/day) for twenty consecutive days; in the other treatment, participants ingested a capsule filled with a placebo for the same duration and frequency. During these treatments, participants performed a maximal ramp test on a cycle ergometer three times per week and the second ventilatory threshold (VT2) was assessed by using the ventilatory equivalents for oxygen and carbon dioxide. Results: A two-way ANOVA with repeated measures (substance × time) revealed statistically significant main effects of caffeine (p < 0.01) and time (p = 0.04) on the wattage obtained at VT2, although there was no interaction (p = 0.09). In comparison to the placebo, caffeine increased the workload at VT2 on days 1, 4, 6 and 15 of ingestion (p < 0.05). The size of the ergogenic effect of caffeine over the placebo on the workload at VT2 was progressively reduced with the duration of the treatment. In addition, there were main effects of caffeine (p = 0.03) and time (p = 0.16) on VO2 obtained at VT2, with no interaction (p = 0.49). Specifically, caffeine increased oxygen uptake at VT2 on days 1 and 4 (p < 0.05), with no other caffeine–placebo differences afterwards. For heart rate obtained at VT2, there was a main effect of substance (p < 0.01), while the overall effect of time (p = 0.13) and the interaction (p = 0.22) did not reach statistical significance. Heart rate at VT2 was higher with caffeine than with the placebo on days 1 and 4 (p < 0.05). The size of the effect of caffeine on VO2 and heart at VT2 tended to decline over time. Conclusion: Pre-exercise intake of 3 mg/kg/day of caffeine for twenty days enhanced the wattage obtained at VT2 during cycling ramp tests for ~15 days of ingestion, while there was a progressive attenuation of the size of the ergogenic effect of caffeine on this performance variable. Therefore, habituation to caffeine through daily ingestion may reduce the ergogenic effect of this stimulant on aerobic exercise of submaximal intensity.

Genetic factors play a significant role in athletic performance and its related phenotypes such as power, strength and aerobic capacity. In this regard, the lack of a muscle protein due to a genetic polymorphism has been found to affect sport performance in a wide variety of ways. α-actinin-3 is a protein located within the skeletal muscle with a key role in the production of sarcomeric force. A common stop-codon polymorphism (rs1815739; R577X) in the gene that codes for α-actinin-3 (ACTN3) produces individuals with the XX genotype that lack expression of a functional α-actinin-3. In contrast, individuals with the R-allele (i.e., RX vs. RR genotypes) in this polymorphism can express α-actinin-3. Interestingly, around ~18% of the world population have the XX genotype and much has been debated about why a polymorphism that produces a lack of a muscle protein has endured natural selection. Several investigations have found that α-actinin-3 deficiency due to XX homozygosity in the ACTN3 R577X polymorphism can negatively affect sports performance through several structural, metabolic, or signaling changes. In addition, new evidence suggests that α-actinin-3 deficiency may also impact sports performance through indirect factors such a higher risk for injury or lower resistance to muscle-damaging exercise. The purpose of this discussion is to provide a clear explanation of the effect of α-actinin-3 deficiency due to the ACTN3 XX genotype on sport. Key focus has been provided about the effect of α-actinin-3 deficiency on morphologic changes in skeletal muscle, on the low frequency of XX athletes in some athletic disciplines, and on injury epidemiology.

The ergogenic effect of acute caffeine ingestion has been widely investigated; however, scientific information regarding tolerance to the performance benefits of caffeine, when ingested on a day-to-day basis, is scarce. The aim of this investigation was to determine the time course of tolerance to the ergogenic effects of a moderate dose of caffeine. Eleven healthy active participants took part in a cross-over, double-blind, placebo-controlled experiment. In one treatment, they ingested 3 mg/kg/day of caffeine for 20 consecutive days while in another they ingested a placebo for 20 days. Each substance was administered daily in an opaque unidentifiable capsule, and the experimental trials started 45 min after capsule ingestion. Two days before, and three times per week during each 20-day treatment, aerobic peak power was measured with an incremental test to volitional fatigue (25 W/min) and aerobic peak power was measured with an adapted version of the Wingate test (15 s). In comparison to the placebo, the ingestion of caffeine increased peak cycling power in the incremental exercise test by ~4.0 ±1.3% for the first 15 days (P