Effects of a moderate intake of beer on markers of hydration after exercise in the heat: a crossover study

Background: Exercise in the heat causes important water and electrolytes losses through perspiration. Optimal rehydration is crucial to facilitate the recuperation process after exercise. The aim of our study was to examine whether a moderate beer intake as part of the rehydration has any negative effect protocol after a short but dehydrating bout of exercise in the heat.Methods: Sixteen active male (VO2max, 56 ± 4 mL/kg/min), were included in a crossover study and performed a dehydrating exercise (≤1 h running, 60 %VO2max) twice and 3 weeks apart, in a hot laboratory setting (35 ± 1 °C, humidity 60 ± 2 %). During the two hours following the exercise bouts participants consumed either mineral water ad-libitum (W) or up to 660 ml regular beer followed by water ad-libitum (BW). Body composition, hematological and serum parameters, fluid balance and urine excretion were assessed before, after exercise and after rehydration.Results: Body mass (BM) decreased (both ~ 2.4 %) after exercise in both trials. After rehydration, BM and fat free mass significantly increased although BM did not return to baseline levels (BM, 72.6 ± 6.7 to 73.6 ± 6.9; fat free mass, 56.9 ± 4.7 to 57.5 ± 4.5, no differences BW vs W). Beer intake did not adversely affect any measured parameter. Fluid balance and urine excretion values did not differ between the rehydration strategies.Conclusions: After exercise and subsequent water losses, a moderate beer (regular) intake has no deleterious effects on markers of hydration in active individuals.This study was partially supported by the “Centro de Información Cerveza y Salud” (n° C-2534-00)

Respiratory and muscle oxygenation responses to two constant-load exercise intensities

Objective: We investigated the respiratory and vastus lateralis oxygenation responses to exhaustive, constant-load cycling at two exercise intensities. Methods: Eight moderately-trained male randomly cycled to exhaustion at 75% and 85% of maximal work-load (CL75 and CL85, respectively) measured during a maximal incremental test. From continuous recordings of respiratory variables and near-infrared spectroscopy signals of the vastus lateralis muscle, VO2 slow component (SC) and deoxyhemoglobin (HHb) SC were calculated. Results: At exhaustion, VO2 (+19 ± 25%), VO2 SC (+59 ± 24%) and minute ventilation (+14 ± 14%) were significantly higher during CL85 vs. CL75, whereas oxyhemoglobin (-67 ± 22%) and total hemoglobin (-36 ± 3%) responses were lower (all p<0.05). Additionally, VO2 SC during CL75 and CL85 were strongly correlated (r=0.88, p<0.001). The HHb SC did not differ between CL75 and CL85 (3.10 ± 0.75 vs. 3.44 ± 1.1 A.U, respectively; p=0.60). HHb SC and VO2 SC during CL85 (r=0.94, p<0.001), but not during CL75 (r=-0.08, p=0.90), were correlated. Finally, HHb SC during CL75 and CL85 were unrelated (r=-0.20, p=0.70). Conclusion: Our results highlight that only the contribution of locomotor muscles to the VO2 SC magnitude is affected by the exercise intensity and not that of ventilation

Effect of prior exercise on pulmonary O2 uptake and estimated muscle capillary blood flow kinetics during moderate-intensity field running in men

The effect of prior exercise on pulmonary O2 uptake (V̇o2 p) and estimated muscle capillary blood flow (Q̇m) kinetics during moderate-intensity, field-based running was examined in 14 young adult men, presenting with either moderately fast (16 s \u3c τV̇o2 p \u3c 30 s; MFK) or very fast V̇o2 p kinetics (τV̇o2 p \u3c 16 s; VFK) (i.e., primary time constant, τV̇o2 p). On four occasions, participants completed a square-wave protocol involving two bouts of running at 90–95% of estimated lactate threshold (Mod1 and Mod2), separated by 2 min of repeated supramaximal sprinting. V̇o2 p was measured breath by breath, heart rate (HR) beat to beat, and vastus lateralis oxygenation {deoxy-hemoglobin/myoglobin concentration (deoxy-[Hb+Mb])} using near-infrared spectroscopy. Mean response time of Q̇m (Q̇m MRT) was estimated by rearranging the Fick equation, using V̇o2 p and deoxy-[Hb+Mb] as proxies of muscle O2 uptake (V̇o2) and arteriovenous difference, respectively. HR, blood lactate concentration, total hemoglobin, and Q̇m were elevated before Mod2 compared with Mod1 (all P \u3c 0.05). τV̇o2 p was shorter in VFK compared with MFK during Mod1 (13.1 ± 1.8 vs. 21.0 ± 2.5 s, P \u3c 0.01), but not in Mod2 (12.9 ± 1.5 vs. 13.7 ± 3.8 s, P = 1.0). Q̇m MRT was shorter in VFK compared with MFK in Mod1 (8.8 ± 1.9 vs. 17.0 ± 3.4 s, P \u3c 0.01), but not in Mod2 (10.1 ± 1.8 vs. 10.5 ± 3.5 s, P = 1.0). During Mod2, HR kinetics were slowed, whereas mean deoxy-[Hb+Mb] response time was unchanged. The difference in τV̇o2 p between Mod1 and Mod2 was related to Q̇m MRT measured at Mod1 (r = 0.71, P \u3c 0.01). Present results suggest that local O2 delivery (i.e., Q̇m) may be a factor contributing to the V̇o2 kinetic during the onset of moderate-intensity, field-based running exercise, at least in subjects exhibiting moderately fast V̇o2 kinetics

Parasympathetic reactivation after repeated sprint exercise

The purpose of this study was to examine the effects of muscular power engagement, anaerobic participation, aerobic power level, and energy expenditure on postexercise parasympathetic reactivation. We compared the response of heart rate (HR) after repeated sprinting with that of exercise sessions of comparable net energy expenditure and anaerobic energy contribution. Fifteen moderately trained athletes performed 1) 18 maximal all-out 15-m sprints interspersed with 17 s of passive recovery (RS), 2) a moderate isocaloric continuous exercise session (MC) at a level of mean oxygen uptake similar to that of the RS trial, and 3) a high-intensity intermittent exercise session (HI) conducted at a level of anaerobic energy expenditure similar to that of the RS trial. Subjects were immediately seated after the exercise trials, and beat-to-beat HR was recorded for 10 min. Parasympathetic reactivation was evaluated through 1) immediate postexercise HR recovery, 2) the time course of the root mean square for the successive R-R interval difference between successive 30-s segments (RMSSD30s) and 3) HR variability vagal-related indexes calculated for the last 5-min stationary period of recovery. RMSSD30s increased during the 10-min period after the MC trial, whereas RMSSD30s remained depressed after both the RS and HI trials. Parasympathetic reactivation indexes were similar for the RS and HI trials but lower than for the MC trial (P \u3c 0.001). When data of the three exercise trials were considered together, only anaerobic contribution was related to HR trial-derived indexes. Parasympathetic reactivation is highly impaired after RS exercise and appears to be mainly related to anaerobic process participation

Excess VO2 during ramp exercise is positively correlated to intercostal muscles deoxyhemoglobin levels above the gas exchange threshold in young trained cyclists.

We assessed respiratory muscles oxygenation responses during a ramp exercise to exhaustion and further explored their relationship with the non-linear increase of VO2 (VO2 excess) observed above the gas-exchange threshold. Ten male cyclists completed a ramp exercise to exhaustion on an electromagnetically braked cycle-ergometer with a rate of increment of 30Wmin(-1) with continuous monitoring of expired gases (breath-by-breath) and oxygenation status of intercostal muscles. Maximal inspiratory and expiratory pressure measurements were taken at rest and at exhaustion. The VO2 excess represents the difference between VO2max observed and VO2max expected using linear equation between the VO2 and the intensity before gas-exchange threshold. The deoxyhemoglobin remained unchanged until 60% of maximal aerobic power (MAP) and thereafter increased significantly by 37±18% and 40±22% at 80% and 100% of MAP, respectively. Additionally, the amplitude of deoxyhemoglobin increase between 60 and 100% of MAP positively correlated with the VO2 excess (r=0.69, p&lt;0.05). Compared to exercise start, the oxygen tissue saturation index decreased from 80% of MAP (-4.8±3.2%, p&lt;0.05) onwards. At exhaustion, maximal inspiratory and expiratory pressures declined by 7.8±16% and 12.6±10% (both p&lt;0.05), respectively. In summary, our results suggest a significant contribution of respiratory muscles to the VO2 excess phenomenon