The aim was to investigate the effects of low-load resistant training combined with vascular occlusion or normobaric hypoxic exposure, on neuromuscular function. In a randomised controlled trial, well-trained athletes took part in a 5-week training of knee flexor/extensor muscles in which low-load resistant exercise (20% of one repetition maximum, 1-RM) was combined with either (1) an occlusion pressure of approximately 230 mmHg (KT, n = 10), (2) hypoxic air to generate an arterial blood oxygen saturation of ~80% (HT, n = 10), or (3) with no additional stimulus (CT, n = 10). Before and after training, participants completed the following tests: 3-s maximal voluntary contraction (MVC₃), 30-s MVC, and an endurance test (maximal number of repetitions at 20% 1-RM, Reps₂₀). Electromyographic activity (root mean square, RMS) was measured during tests and the cross-sectional area (CSA) of the quadriceps and hamstrings was measured pre- and post-training. Relative to CT, KT, and HT showed likely increases in MVC₃ (11.0 ± 11.9 and 15.0 ± 13.1%, mean ± 90% confidence interval), MVC₃₀ (10.2 ± 9.0 and 18.3 ± 17.4%), and Reps₂₀ (28.9 ± 23.7 and 23.3 ± 24.0%). Compared to the CT group, CSA increased in the KT (7.6 ± 5.8) and HT groups (5.3 ± 3.0). KT had a large effect on RMS during MVC₃, compared to CT (effect size 0.8) and HT (effect size 0.8). We suspect hypoxic conditions created within the muscles during vascular occlusion and hypoxic training may play a key role in these performance enhancements.

No abstract

Optimizing traditional training methods to elicit greater adaptations is paramount for athletes. Ischemic preconditioning (IPC) can improve maximal exercise capacity and up-regulate signaling pathways involved in physiological training adaptations. However, data on the chronic use of IPC are scarce and its impact on high-intensity training is still unknown. We investigated the benefits of adding IPC to sprint-interval training (SIT) on performance and physiological adaptations of endurance athletes. In a randomized controlled trial, athletes included eight SIT sessions in their training routine for 4 weeks, preceded by IPC (3 × 5 min ischemia/5 min reperfusion cycles at 220 mmHg, n = 11) or a placebo (20 mmHg, n = 9). Athletes were tested pre-, mid-, and post-training on a 30 s Wingate test, 5-km time trial (TT), and maximal incremental step test. Arterial O 2 saturation, heart rate, rate of perceived exertion, and quadriceps muscle oxygenation changes in total hemoglobin (Δ[THb]), deoxyhemoglobin (Δ[HHb]), and tissue saturation index (ΔTSI) were measured during exercise. Blood samples were taken pre- and post-training to determine blood markers of hypoxic response, lipid-lipoprotein profile, and immune function. Differences within and between groups were analyzed using Cohen's effect size (ES). Compared to PLA, IPC improved time to complete the TT (Mid vs. Post: −1.6%, Cohen's ES ± 90% confidence limits −0.24, −0.40;−0.07) and increased power output (Mid vs. Post: 4.0%, ES 0.20, 0.06;0.35), Δ[THb] (Mid vs. Post: 73.6%, ES 0.70, −0.15;1.54, Pre vs. Post: 68.5%, ES 0.69, −0.05;1.43), Δ[HHb] (Pre vs. Post: 12.7%, ES 0.24, −0.11;0.59) and heart rate (Pre vs. Post: 1.4%, ES 0.21, −0.13;0.55, Mid vs. Post: 1.6%, ES 0.25, −0.09;0.60). IPC also attenuated the fatigue index in the Wingate test (Mid vs. Post: −8.4%, ES −0.37, −0.79;0.05). VO 2 peak and maximal aerobic power remained unchanged in both groups. Changes in blood markers of the hypoxic response, vasodilation, and angiogenesis remained within the normal clinical range in both groups. We concluded that IPC combined with SIT induces greater adaptations in cycling endurance performance that may be related to muscle perfusion and metabolic changes. The absence of elevated markers of immune function suggests that chronic IPC is devoid of deleterious effects in athletes, and is thus a safe and potent ergogenic tool.

This study aimed to determine the impact of short-term normobaric hypoxia on physiology and performance in highly trained athletes. Twelve (7 male and 5 female) athletes were randomly assigned into two groups and spent 8 h per night for two consecutive nights a week over 3 weeks under either short-term normobaric hypoxia (simulating 3636 m altitude, inspired O 2 = 13%) or in normobaric normoxia in a single-blind study. Following a 3 week washout period, athletes were then exposed to the other condition. Athletes were tested for maximal oxygen consumption and time to exhaustion on an electromagnetically braked cycle ergometer before and after each treatment in addition to being tested for anaerobic performance (Wingate test) on a modified Monark cycle ergometer. Blood samples were taken throughout the experiment and vastus lateralis muscle biopsies were taken before and after each treatment. Increases in red blood cell count, haematocrit, haemoglobin, platelet number and erythropoietin concentration were observed following short-term normobaric hypoxia. Except for a modest decrease in phosphofructokinase activity following short-term normobaric hypoxia, no changes were observed in muscle enzyme activities, buffer capacity, capillary density or morphology. No performance measures were changed following short-term normobaric hypoxia or normobaric normoxia. Although short-term normobaric hypoxia exposure increased levels of a number of haematological parameters, this was not associated with improved aerobic or anaerobic performance in highly trained athletes.