Post-Game High Protein Intake May Improve Recovery of Football-Specific Performance during a Congested Game Fixture: Results from the PRO-FOOTBALL Study.

The effects of protein supplementation on performance recovery and inflammatory responses during a simulated one-week in-season microcycle with two games (G1, G2) performed three days apart were examined. Twenty football players participated in two trials, receiving either milk protein concentrate (1.15 and 0.26 g/kg on game and training days, respectively) (PRO) or an energy-matched placebo (1.37 and 0.31 g/kg of carbohydrate on game and training days, respectively) (PLA) according to a randomized, repeated-measures, crossover, double-blind design. Each trial included two games and four daily practices. Speed, jump height, isokinetic peak torque, and muscle soreness of knee flexors (KF) and extensors (KE) were measured before G1 and daily thereafter for six days. Blood was drawn before G1 and daily thereafter. Football-specific locomotor activity and heart rate were monitored using GPS technology during games and practices. The two games resulted in reduced speed (by 3-17%), strength of knee flexors (by 12-23%), and jumping performance (by 3-10%) throughout recovery, in both trials. Average heart rate and total distance covered during games remained unchanged in PRO but not in PLA. Moreover, PRO resulted in a change of smaller magnitude in high-intensity running at the end of G2 (75-90 min vs. 0-15 min) compared to PLA (P = 0.012). KE concentric strength demonstrated a more prolonged decline in PLA (days 1 and 2 after G1, P = 0.014-0.018; days 1, 2 and 3 after G2, P = 0.016-0.037) compared to PRO (days 1 after G1, P = 0.013; days 1 and 2 after G2, P = 0.014-0.033) following both games. KF eccentric strength decreased throughout recovery after G1 (PLA: P=0.001-0.047-PRO: P =0.004-0.22) in both trials, whereas after G2 it declined throughout recovery in PLA (P = 0.000-0.013) but only during the first two days (P = 0.000-0.014) in PRO. No treatment effect was observed for delayed onset of muscle soreness, leukocyte counts, and creatine kinase activity. PRO resulted in a faster recovery of protein and lipid peroxidation markers after both games. Reduced glutathione demonstrated a more short-lived reduction after G2 in PRO compared to PLA. In summary, these results provide evidence that protein feeding may more efficiently restore football-specific performance and strength and provide antioxidant protection during a congested game fixture.

Improved Exercise Tolerance with Caffeine Is Associated with Modulation of both Peripheral and Central Neural Processes in Human Participants.

BACKGROUND: Caffeine has been shown to enhance exercise performance and capacity. The mechanisms remain unclear but are suggested to relate to adenosine receptor antagonism, resulting in increased central motor drive, reduced perception of effort, and altered peripheral processes such as enhanced calcium handling and extracellular potassium regulation. Our aims were to investigate how caffeine (i) affects knee extensor PCr kinetics and pH during repeated sets of single-leg knee extensor exercise to task failure and (ii) modulates the interplay between central and peripheral neural processes. We hypothesized that the caffeine-induced extension of exercise capacity during repeated sets of exercise would occur despite greater disturbance of the muscle milieu due to enhanced peripheral and corticospinal excitatory output, central motor drive, and muscle contractility. METHODS: Nine healthy active young men performed five sets of intense single-leg knee extensor exercise to task failure on four separate occasions: for two visits (6 mg·kg-1 caffeine vs placebo), quadriceps 31P-magnetic resonance spectroscopy scans were performed to quantify phosphocreatine kinetics and pH, and for the remaining two visits (6 mg·kg-1 caffeine vs placebo), femoral nerve electrical and transcranial magnetic stimulation of the quadriceps cortical motor area were applied pre- and post exercise. RESULTS: The total exercise time was 17.9 ± 6.0% longer in the caffeine (1,225 ± 86 s) than in the placebo trial (1,049 ± 73 s, p = 0.016), and muscle phosphocreatine concentration and pH (p < 0.05) were significantly lower in the latter sets of exercise after caffeine ingestion. Voluntary activation (VA) (peripheral, p = 0.007; but not supraspinal, p = 0.074), motor-evoked potential (MEP) amplitude (p = 0.007), and contractility (contraction time, p = 0.009; and relaxation rate, p = 0.003) were significantly higher after caffeine consumption, but at task failure MEP amplitude and VA were not different from placebo. Caffeine prevented the reduction in M-wave amplitude that occurred at task failure (p = 0.039). CONCLUSION: Caffeine supplementation improved high-intensity exercise tolerance despite greater-end exercise knee extensor phosphocreatine depletion and H+ accumulation. Caffeine-induced increases in central motor drive and corticospinal excitability were attenuated at task failure. This may have been induced by the afferent feedback of the greater disturbance of the muscle milieu, resulting in a stronger inhibitory input to the spinal and supraspinal motor neurons. However, causality needs to be established through further experiments.