Relationship between vertical jumping ability and endurance capacity with internal training loads in professional volleyball players during preseason.

BACKGROUND: This study aimed to quantify internal training load and changes in vertical jumping ability and endurance capacity of professional volleyball players during the preseason, and to explore relationships between players' physical qualities at the beginning of the preseason with internal training load accumulated during the first two weeks of training. METHODS: Sixteen male professional volleyball players from a team participating in the Brazilian National Super League took part in the study. Before and after a 10-week preseason, their vertical jumping ability and endurance capacity were assessed by squat jump, countermovement jump without and with arm swing, and YoYo endurance test, level 1. The internal training load was quantified by the session rating of perceived exertion method. Results were analyzed using analysis of variance, magnitude-based inference and Pearson's correlation. RESULTS: The internal training load varied between 1388±111 arbitrary units (a.u.) and 3852±149 a.u., and performance in all the tests was positively changed (small to moderate effect sizes) at end of preseason training. Significant (P<0.05) very large and large correlations were observed between squat jump (r=-0.81) and YoYo endurance test (r=-0.64) performances and internal training load accumulated during the first two training weeks, respectively. CONCLUSIONS: The internal training load and training strategies undertaken by the investigated team were effective to improve players' vertical jumping ability and endurance capacity. Coaches need to improve these physical qualities of volleyball players in order to improve their tolerance to training.

Ischemic preconditioning boosts post-exercise but not resting cardiac vagal control in endurance runners.

PURPOSE: High cardiac vagal control in endurance athletes has been generally associated with adequate recovery from training and readiness to cope high-intensity training. A method that improves cardiac vagal control in endurance athletes could therefore be advantageous. Accordingly, we sought to test whether ischemic preconditioning (IPC) could enhance cardiac vagal control in endurance runners. METHODS: Fifteen subjects underwent IPC, sham ultrasound (SHAM) or control (CT), in random order. Subjects were informed both IPC and SHAM would be beneficial vs. CT (i.e., similar placebo induction), and IPC would be harmless despite ischemia sensations (i.e., nocebo avoidance). Resting cardiac vagal control was assessed via respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) indexes. Post-exercise cardiac vagal control was assessed via heart rate recovery [HR time constant decay (T30) and absolute HR decay (HRR30s)] during 30-s breaks of a discontinuous incremental test. Capillary blood samples were collected for lactate threshold identification. RESULTS: RSA and HRV were similar among interventions at pre- and post-intervention assessments. Lactate threshold occurred at 85 ± 4% of maximal effort. T30 was similar among interventions, but IPC increased HRR30s at 70% and 75% of maximal effort vs. SHAM and CT (70%: IPC = 31 ± 2 vs. SHAM = 26 ± 3 vs. CT = 26 ± 2 bpm, mean ± SEM, P < 0.01; 75%: IPC = 29 ± 2 vs. SHAM = 25 ± 2 vs. CT = 24 ± 2 bpm, P < 0.01). CONCLUSION: IPC did not change resting cardiac vagal control, but boosted fast post-exercise cardiac vagal reactivation at exercise intensities below lactate threshold in endurance runners.

Effect of Ischemic Preconditioning on the Recovery of Cardiac Autonomic Control From Repeated Sprint Exercise.

Repeated sprint exercise (RSE) acutely impairs post-exercise heart rate (HR) recovery (HRR) and time-domain heart rate variability (i. e., RMSSD), likely in part, due to lactic acidosis-induced reduction of cardiac vagal reactivation. In contrast, ischemic preconditioning (IPC) mediates cardiac vagal activation and augments energy metabolism efficiency during prolonged ischemia followed by reperfusion. Therefore, we investigated whether IPC could improve recovery of cardiac autonomic control from RSE partially via improved energy metabolism responses to RSE. Fifteen men team-sport practitioners (mean ± SD: 25 ± 5 years) were randomly exposed to IPC in the legs (3 × 5 min at 220 mmHg) or control (CT; 3 × 5 min at 20 mmHg) 48 h, 24 h, and 35 min before performing 3 sets of 6 shuttle running sprints (15 + 15 m with 180° change of direction and 20 s of active recovery). Sets 1 and 2 were followed by 180 s and set 3 by 360 s of inactive recovery. Short-term HRR was analyzed after all sets via linear regression of HR decay within the first 30 s of recovery (T30) and delta from peak HR to 60 s of recovery (HRR60s). Long-term HRR was analyzed throughout recovery from set 3 via first-order exponential regression of HR decay. Moreover, RMSSD was calculated using 30-s data segments throughout recovery from set 3. Energy metabolism responses were inferred via peak pulmonary oxygen uptake ( V ˙ O 2 peak), peak carbon dioxide output ( V ˙ O 2 peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of V ˙ O 2 decay within 360 s of recovery and blood lactate concentration ([Lac-]). IPC did not change T30, but increased HRR60s after all sets (condition main effect: P = 0.03; partial eta square (η2 p ) = 0.27, i.e., large effect size). IPC did not change long-term HRR and RMSSD throughout recovery, nor did IPC change any energy metabolism parameter. In conclusion, IPC accelerated to some extent the short-term recovery, but did not change the long-term recovery of cardiac autonomic control from RSE, and such accelerator effect was not accompanied by any IPC effect on surrogates of energy metabolism responses to RSE.

Effect of Ischemic Preconditioning on Endurance Performance Does Not Surpass Placebo.

PURPOSE: Recent studies have reported ischemic preconditioning (IPC) can acutely improve endurance exercise performance in athletes. However, placebo and nocebo effects have not been sufficiently controlled, and the effect on aerobic metabolism parameters that determine endurance performance (e.g., oxygen cost of running, lactate threshold, and maximal oxygen uptake [V˙O2max]) has been equivocal. Thus, we circumvented limitations from previous studies to test the effect of IPC on aerobic metabolism parameters and endurance performance in well-trained runners. METHODS: Eighteen runners (14 men/4 women) were submitted to three interventions, in random order: IPC; sham intervention (SHAM); and resting control (CT). Subjects were told both IPC and SHAM would improve performance compared to CT (i.e., similar placebo induction), and IPC would be harmless despite circulatory occlusion sensations (i.e., nocebo avoidance). Next, pulmonary ventilation and gas exchange, blood lactate concentration, and perceived effort were measured during a discontinuous incremental test on a treadmill. Then, a supramaximal test was used to verify the V˙O2max and assess endurance performance (i.e., time to exhaustion). RESULTS: Ventilation, oxygen uptake, carbon dioxide output, lactate concentration, and perceived effort were similar among IPC, SHAM, and CT throughout the discontinuous incremental test (P > 0.05). Oxygen cost of running, lactate threshold, and V˙O2max were also similar among interventions (P > 0.05). Time to exhaustion was longer after IPC (mean ± SEM, 165.34 ± 12.34 s) and SHAM (164.38 ± 11.71 s) than CT (143.98 ± 12.09 s; P = 0.02 and 0.03, respectively), but similar between IPC and SHAM (P = 1.00). CONCLUSIONS: IPC did not change aerobic metabolism parameters, whereas improved endurance performance. The IPC improvement, however, did not surpass the effect of a placebo intervention.

Ischemic Preconditioning and Repeated Sprint Swimming: A Placebo and Nocebo Study.

PURPOSE: Ischemic preconditioning (IPC) has been shown to improve performance of exercises lasting 10-90 s (anaerobic) and more than 90 s (aerobic). However, its effect on repeated sprint performance has been controversial, placebo effect has not been adequately controlled, and nocebo effect has not been avoided. Thus, the IPC effect on repeated sprint performance was investigated using a swimming task and controlling placebo/nocebo effects. METHODS: Short-distance university swimmers were randomized to two groups. One group (n = 15, 24 ± 1 yr [mean ± SEM]) was exposed to IPC (ischemia cycles lasted 5 min) and control (CT) (no ischemia); another (n = 15, 24 ± 1 yr) to a placebo intervention (SHAM) (ischemia cycles lasted 1 min) and CT. Seven subjects crossed over groups. Subjects were informed IPC and SHAM would improve performance compared with CT and would be harmless despite circulatory occlusion sensations. The swimming task consisted of six 50-m all-out efforts repeated every 3 min. RESULTS: IPC, in contrast with SHAM, reduced worst sprint time (IPC, 35.21 ± 0.73 vs CT, 36.53 ± 0.72 s; P = 0.04) and total sprints time (IPC, 203.7 ± 4.60 vs CT, 206.03 ± 4.57 s; P = 0.02), moreover augmented swimming velocity (IPC, 1.45 ± 0.03 vs CT, 1.44 ± 0.03 m·s; P = 0.049). Six of seven subjects who crossed over groups reduced total sprints time with IPC versus SHAM (delta = -3.95 ± 1.49 s, P = 0.09). Both IPC and SHAM did not change blood lactate concentration (P = 0.20) and perceived effort (P = 0.22). CONCLUSION: IPC enhanced repeated sprint swimming performance in university swimmers, whereas a placebo intervention did not.

Are heart rate deflection point and peak velocity determined in the Université of Montréal Track Test valid to approximate aerobic parameters measured in the laboratory?

BACKGROUND: The aim of this study was to compare the respiratory compensation point (RCP) and maximal aerobic velocity (vVO2max) measured in the laboratory, respectively, with the heart rate deflection point (HRDP) and the peak velocity (PV) determined in the Université of Montréal Track Test (UMTT). Beside, we investigated the relationship of these parameters with endurance performance. METHODS: Eighteen long distance runners randomly performed (in different days) two incremental exercise tests (laboratory and UMTT). RCP and vVO2max were identified in a treadmill test. The HRDP was identified using the Dmax method, while the PV was identified as the velocity of the last complete stage (PVc) and the time-corrected velocity of the last incomplete stage (PVi). Endurance performance was the reported 10-km race time from the closest race to the test visits. RESULTS: RCP heart rate (176±14 bpm) was not significantly different from HRDP (173±10 bpm). The agreement was reasonable [bias: 4 bpm (95% limit of agreement: -16 to 24 bpm)]. vVO2max (18.0±2.1 km.h-1) was not significantly different from PVi (17.6±2.1 km.h-1), but was significantly higher than PVc (17.3±2.0 km.h-1). The agreement between vVO2max and PVi was acceptable [0.4 km.h-1 (-1.6 to 2.4 km.h-1)]. Endurance performance correlations (2212±277 s) with HRDP velocity (r=-0.75) and PVi (r=-0.83) tended to be lower than with RCP velocity (r=-0.91) and vVO2max (r=-0.85). CONCLUSIONS: It is possible to estimate with reasonable accuracy the vVO2max using the UMTT. However, care must be taken to use the HRDP identified through the UMTT to prescribe training intensities.

Chemical synthesis, structure-activity relationship, and properties of shepherin I: a fungicidal peptide enriched in glycine-glycine-histidine motifs.

Although glycine-rich antimicrobial peptides (AMPs) are found in animals and plants, very little has been reported on their chemistry, structure activity-relationship, and properties. We investigated those topics for Shepherin I (Shep I), a glycine-rich AMP with the unique amino acid sequence G(1)YGGHGGHGGHGGHGGHGGHGHGGGGHG(28). Shep I and analogues were synthesized by the solid-phase method at 60 °C using conventional heating. Purification followed by chemical characterization confirmed the products' identities and high purity. Amino acid analysis provided their peptide contents. All peptides were active against the clinically important Candida species, but ineffective against bacteria and mycelia fungi. Truncation of the N- or C-terminal portion reduced Shep I antifungal activity, the latter being more pronounced. Carboxyamidation of Shep I did not affect the activity against C. albicans or C. tropicalis, but increased activity against S. cerevisiae. Carboxyamidated analogues Shep I (3-28)a and Shep I (6-28)a were equipotent to Shep I and Shep Ia against Candida species. As with most cationic AMPs, all peptides had their activity significantly reduced in high-salt concentrations, a disadvantage that is defeated if 10 µM ZnCl2 is present. At 100 µM, the peptides were practically not hemolytic. Shep Ia also killed C. albicans MDM8 and ATCC 90028 cells. Fluo-Shep Ia, an analogue labeled with 5(6)-carboxyfluorescein, was rapidly internalized by C. albicans MDM8 cells, a salt-sensitive process dependent on metabolic energy and temperature. Altogether, such results shed light on the chemistry, structural requirements for activity, and other properties of candidacidal glycine-rich peptides. Furthermore, they show that Shep Ia may have strong potential for use in topical application.