A well-implemented 3- or 4-wk training camp may impair performance immediately but clearly improves performance even in elite swimmers after a period of SL recovery. Hi-HiLo for 4 wk improves performance in swimming above and beyond altitude and SL controls through complex mechanisms involving altitude living and SL training effects.
When ascending to a higher altitude, changes in air density and oxygen levels affect the way in which explosive actions are executed. This study was designed to compare the effects of acute exposure to real or simulated moderate hypoxia on the dynamics of the force-velocity relationship observed in bench press exercise. Twenty-eight combat sports athletes were assigned to two groups and assessed on two separate occasions: G1 (n = 17) in conditions of normoxia (N1) and hypobaric hypoxia (HH) and G2 (n = 11) in conditions of normoxia (N2) and normobaric hypoxia (NH). Individual and complete force-velocity relationships in bench press were determined on each assessment day. For each exercise repetition, we obtained the mean and peak velocity and power shown by the athletes. Maximum power (Pmax) was recorded as the highest Pmean obtained across the complete force-velocity curve. Our findings indicate a significantly higher absolute load linked to Pmax (∼3%) and maximal strength (1RM) (∼6%) in G1 attributable to the climb to altitude (P<0.05). We also observed a stimulating effect of natural hypoxia on Pmean and Ppeak in the middle-high part of the curve (≥60 kg; P<0.01) and a 7.8% mean increase in barbell displacement velocity (P<0.001). No changes in any of the variables examined were observed in G2. According to these data, we can state that acute exposure to natural moderate altitude as opposed to simulated normobaric hypoxia leads to gains in 1RM, movement velocity and power during the execution of a force-velocity curve in bench press.
Our aim was to investigate the presence of mechanical hypersensitivity and active trigger points (TrPs) in the neck-shoulder muscles in elite swimmers with/without unilateral shoulder pain. Seventeen elite swimmers with shoulder pain; 18 swimmers without shoulder pain; and 15 elite athletes matched controls were recruited. Pressure pain thresholds (PPT) were assessed over the levator scapulae, sternocleidomastoid, upper trapezius, infraspinatus, scalene, subscapularis and tibialis anterior muscles. TrPs in the levator scapulae, upper trapezius, infraspinatus, scalene, sternocleidomastoid and subscapularis muscles were also explored. Swimmers with shoulder pain showed significant lower PPT in all muscles compared with controls (P<0.01). No differences in PPT were found between swimmers with and without shoulder pain, underlining widespread mechanical hypersensitivity. The mean number of TrPs for elite swimmer with and without shoulder pain was, respectively, 4.7 ± 1 (2.1 ± 1.5 active; 2.6 ± 1.4 latent) and 4.7 ± 1.3 (1.3 ± 1.3 active; 3.4 ± 1.5 latent), whereas healthy athletes only showed latent TrPs (2.4 ± 1.2). Elite swimmers with shoulder pain showed higher number of active TrPs than swimmers without pain, whereas it was the opposite for the number of latent muscle TrP (P<0.05). The reported mechanical hypersensitivity suggests that active TrPs play a role in the development of shoulder pain in elite swimmers.
Using a controlled parallel group longitudinal trial design, we investigated the effects of different training interventions on the prooxidant/antioxidant status of elite athletes: living and training at moderate altitude for 3 (Hi-Hi3) and 4 weeks (Hi-Hi), and for 4 weeks too, living high and training high and low (Hi-HiLo) and living and training at sea level (Lo-Lo). From 61 swimmers, 54 completed the study. Nitrites, carbonyls, and lipid peroxidation (LPO) levels were assessed in plasma. Enzymatic antioxidants glutathione peroxidase (GPx) and glutathione reductase (GRd), and non-enzymatic antioxidants total glutathione (GST), reduced glutathione (GSH) and oxidized glutathione (GSSG) were analysed in the erythrocyte fraction. At the end of the intervention, nitrites levels were similar in all altitude groups but higher than in the Lo-Lo controls (P = .02). Hi-HiLo had greater GPx activity than Hi-Hi and Hi-Hi3 during most of the intervention (P ≤ .001). GRd activity was higher in Lo-Lo than in Hi-Hi at the end of the training camp (P ≤ .001). All groups showed increased levels of LPO, except Lo-Lo, and carbonyls at the end of the study (P ≤ .001). Training at altitude for 3 or 4 weeks drives oxidative stress leading to cellular damage mainly by worsening the antioxidant capacities. The GSSG/GSH ratio appears to be related to perceived exertion and fatigue. The stronger antioxidant defence showed by the Hi-HiLo group suggests an inverse relationship between redox alterations and performance. Further studies are required to investigate the role of oxidative stress in acclimatization, performance, and health.
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