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PurposeTo investigate whether caffeine ingestion counteracts the morning reduction in neuromuscular performance associated with the circadian rhythm pattern.MethodsTwelve highly resistance-trained men underwent a battery of neuromuscular tests under three different conditions; i) morning (10:00 a.m.) with caffeine ingestion (i.e., 3 mg kg−1; AMCAFF trial); ii) morning (10:00 a.m.) with placebo ingestion (AMPLAC trial); and iii) afternoon (18:00 p.m.) with placebo ingestion (PMPLAC trial). A randomized, double-blind, crossover, placebo controlled experimental design was used, with all subjects serving as their own controls. The neuromuscular test battery consisted in the measurement of bar displacement velocity during free-weight full-squat (SQ) and bench press (BP) exercises against loads that elicit maximum strength (75% 1RM load) and muscle power adaptations (1 m s−1 load). Isometric maximum voluntary contraction (MVCLEG) and isometric electrically evoked strength of the right knee (EVOKLEG) were measured to identify caffeine's action mechanisms. Steroid hormone levels (serum testosterone, cortisol and growth hormone) were evaluated at the beginning of each trial (PRE). In addition, plasma norepinephrine (NE) and epinephrine were measured PRE and at the end of each trial following a standardized intense (85% 1RM) 6 repetitions bout of SQ (POST).ResultsIn the PMPLAC trial, dynamic muscle strength and power output were significantly enhanced compared with AMPLAC treatment (3.0%–7.5%; p≤0.05). During AMCAFF trial, muscle strength and power output increased above AMPLAC levels (4.6%–5.7%; p≤0.05) except for BP velocity with 1 m s−1 load (p = 0.06). During AMCAFF, EVOKLEG and NE (a surrogate of maximal muscle sympathetic nerve activation) were increased above AMPLAC trial (14.6% and 96.8% respectively; p≤0.05).ConclusionsThese results indicate that caffeine ingestion reverses the morning neuromuscular declines in highly resistance-trained men, raising performance to the levels of the afternoon trial. Our electrical stimulation data, along with the NE values, suggest that caffeine increases neuromuscular performance having a direct effect in the muscle.

To determine the effect of circadian rhythm on neuromuscular responses and kinematics related to physical tennis performance, after a standardised warm-up, 13 highly competitive male tennis players were tested twice for serve velocity/accuracy (SVA), countermovement vertical jump (CMJ), isometric handgrip strength (IS), agility T-test (AGIL) and a 10-m sprint (10-m RUN). In a randomised, counter-balance order, tennis players underwent the test battery twice, either in the morning (i.e., AM; 9:00 h) and in the afternoon (i.e., PM; 16:30 h). Paired t-tests were used to analyse differences due to time-of-day in performance variables. Comparison of morning versus afternoon testing revealed that SVA (168.5 ± 6.5 vs. 175.2 ± 6.1 km · h; P = 0.003; effect size [ES] = 1.07), CMJ (32.2 ± 0.9 vs. 33.7 ± 1.1 cm; P = 0.018; ES = 1.46), AGIL (10.14 ± 0.1 vs. 9.91 ± 0.2 s; P = 0.007; ES = 1.23) and 10-m RUN time (1.74 ± 0.1 vs. 1.69 ± 0.1 s; P = 0.021; ES = 0.67) were significantly blunted during the morning testing. However, IS was not affected by time-of-day (P = 0.891). Thus, tennis performance may be reduced when competing in the morning in comparison to early evening. Therefore, coaches and tennis players should focus on schedule the SVA, power, speed and agility training sessions in the afternoon.

Beetroot juice (BJ) contains high levels of inorganic nitrate (NO3−) and its intake has good evidence in increasing blood nitrate/nitrite concentrations. The ingestion of BJ has been associated with improvements in physical performance of endurance sports, however the literature in intermittent sports is scarce. The aim of this study was to investigate whether BJ could improve physical performance in tennis players. Thirteen well-trained tennis players (25.4 ± 5.1 years) participated in the study during their preparatory period for the tennis season. Subjects were randomly divided into two groups and performed a neuromuscular test battery after either BJ or placebo (PLA) consumption. Both trials were executed on two separate days, in randomized order, with one week of wash out period. The test battery consisted of serve velocity test (SVT), countermovement jump (CMJ), isometric handgrip strength (IHS), 5-0-5 agility test (5-0-5), and 10 m sprint (10-m). No significant differences were found in SVT (1.19%; p = 0.536), CMJ (0.96%; p = 0.327), IHS (4.06%; p = 0.069), 5-0-5 dominant and nondominant side (1.11–2.02%; p = 0.071–0.191) and 10-m (1.05%; p = 0.277) when comparing BJ and PLA ingestion. Thus, our data suggest that low doses of BJ (70 mL) consumption do not enhance tennis physical performance.

Iron deficiency is a frequent and multifactorial disorder in the career of athletes, particularly in females. Exercise-induced disturbances in iron homeostasis produce deleterious effects on performance and adaptation to training; thus, the identification of strategies that restore or maintain iron homeostasis in athletes is required. Hepcidin is a liver-derived hormone that degrades the ferroportin transport channel, thus reducing the ability of macrophages to recycle damaged iron, and decreasing iron availability. Although it has been suggested that the circulating fraction of hepcidin increases during early post-exercise recovery (~3 h), it remains unknown how an acute exercise bout may modify the circulating expression of hepcidin. Therefore, the current review aims to determine the post-exercise expression of serum hepcidin in response to a single session of exercise. The review was carried out in the Dialnet, Elsevier, Medline, Pubmed, Scielo and SPORTDiscus databases, using hepcidin (and “exercise” or “sport” or “physical activity”) as a strategy of search. A total of 19 articles were included in the review after the application of the inclusion/exclusion criteria. This search found that a single session of endurance exercise (intervallic or continuous) at moderate or vigorous intensity (60–90% VO2peak) stimulates an increase in the circulating levels of hepcidin between 0 h and 6 h after the end of the exercise bout, peaking at ~3 h post-exercise. The magnitude of the response of hepcidin to exercise seems to be dependent on the pre-exercise status of iron (ferritin) and inflammation (IL-6). Moreover, oxygen disturbances and the activation of a hypoxia-induced factor during or after exercise may stimulate a reduction of hepcidin expression. Meanwhile, cranberry flavonoids supplementation promotes an anti-oxidant effect that may facilitate the post-exercise expression of hepcidin. Further studies are required to explore the effect of resistance exercise on hepcidin expression.