Background: Training in hypoxia versus normoxia often induces larger physiological adaptations, while this does not always translate into additional performance benefits. A possible explanation is a reduced oxygen flux, negatively affecting training intensity and/or volume (decreasing training stimulus). Repeated Wingates (RW) in normoxia is an efficient training strategy for improving both physiological parameters and exercise capacity. However, it remains unclear whether the addition of hypoxia has a detrimental effect on RW performance. Purpose: To test the hypothesis that acute moderate hypoxia exposure has no detrimental effect on RW, while both metabolic and perceptual responses would be slightly higher. Methods: On separate days, 7 male university sprinters performed 3 × 30-s Wingate efforts with 4.5-min passive recovery in either hypoxia (FiO2: 0.145) or normoxia (FiO2: 0.209). Arterial oxygen saturation was assessed before the first Wingate effort, while blood lactate concentration and ratings of perceived exertion were measured after each bout. Results: Mean (P = .92) and peak (P = .63) power outputs, total work (P = .98), and the percentage decrement score (P = .25) were similar between conditions. Arterial oxygen saturation was significantly lower in hypoxia versus normoxia (92.0% [2.8%] vs 98.1% [0.4%], P < .01), whereas blood lactate concentration (P = .78) and ratings of perceived exertion (P = .51) did not differ between conditions. Conclusion: In sprinters, acute exposure to moderate hypoxia had no detrimental effect on RW performance and associated metabolic and perceptual responses.

Repeated Wingate efforts (RW) represent an effective training strategy for improving exercise capacity. Living low-training high altitude/hypoxic training methods, that upregulate muscle adaptations, are increasingly popular. However, the benefits of RW training in hypoxia compared to normoxia on performance and accompanying physiological adaptations remain largely undetermined. Our intention was to test the hypothesis that RW training in hypoxia provides additional performance benefits and more favorable physiological responses than equivalent training in normoxia. Twelve male runners (university sprinters) completed six RW training sessions (3 × 30-s Wingate "all-out" efforts with 4.5-min recovery) in either hypoxia (FiO 2 : 0.145, n = 6) or normoxia (FiO 2 : 0.209, n = 6) over 2 weeks. Before and after the intervention, participants underwent a RW performance test (3 × 30-s Wingate "all-out" efforts with 4.5-min recovery). Peak power output, mean power output, and total work for the three exercise bouts were determined. A capillary blood sample was taken for analyzing blood lactate concentration (BLa) 3 min after each of the three efforts. Peak power output (+ 11.3 ± 23.0%, p = 0.001), mean power output (+ 6.6 ± 6.8%, p = 0.001), and total work (+ 6.3 ± 5.4% p = 0.016) significantly increased from pre-to post-training, independently of condition. The time × group × interval interaction was significant (p = 0.05) for BLa. Compared to Pre-tests, BLa values during post-test were higher (+ 8.7 ± 10.3%) after about 2 in the normoxic group, although statistical significance was not reached (p = 0.08). Contrastingly, BLa values were lower (albeit not significantly) during post-compared to pre-tests after bout 2 (−9.3 ± 8.6%; p = 0.08) and bout 3 (−9.1 ± 10.7%; p = 0.09) in the hypoxic group. In conclusion, six RW training sessions over 2 weeks significantly improved RW performance, while training in hypoxia had no additional benefit over normoxia. However, accompanying BLa responses tended to be lower in the hypoxic group, while an opposite pattern was observed in the normoxic group. This indicates that different glycolytic and/or oxidative pathway adaptations were probably at play.

Repeated sprint training in hypoxia (RSH) is a potential training strategy to improve short-term high-intensity sprint ability and evoke adaptation of lactate metabolism. Therefore, the purpose of the present study was to examine the effects of RSH on Wingate sprint performance and lactate metabolism. Eight university cyclists performed 6 sessions of RSH (3 × 30sec sprint with 5-min recovery, FiO 2: 14.5%) over 6 consecutive days. Two days before (pretest) and 7-9 days after (post-test) the training intervention, subjects performed Wingate tests as performance tests. We took blood samples before and 0.5, 1, 2, 3, 4, 5, 7, 10 min after the Wingate test to evaluate physiological adaptations. Mean power outputs were unchanged after the intervention (p = 0.094, d = 0.23). Whereas, the fatigue index was significantly improved (p = 0.025, d = 0.43). According to time course change in power outputs during the Wingate test, power outputs at 26 s, 29 s and 30 s were significantly improved after the intervention (p = 0.029, 0.001 and 0.001; d = 0.54, 0.74 and 0.74, respectively). Area under the curve (AUC) of blood lactate concentration was significantly lowered after the intervention (p = 0.048, d = 0.46). Six sessions of RSH over 6 consecutive days delayed fatigue during the Wingate test. AUC of blood lactate concentration was lowered after the intervention, indicating that glycogen breakdown was reduced (glycogen sparing effect) and/or lactate oxidation was increased during and after the Wingate test when the same work was performed. The effects of glycogen sparing and increased lactate oxidation would provide a competitive advantage to athletes performing multiple sprints.

Lactate production is an important clue for understanding metabolic and signal responses to exercise but its measurement is difficult. Therefore, this study aimed (1) to develop a method of calculating lactate production volume during exercise based on blood lactate concentration and compare the effects between endurance exercise training (EX) and PGC-1α overexpression (OE), (2) to elucidate which proteins and enzymes contribute to changes in lactate production due to EX and muscle PGC-1α OE, and (3) to elucidate the relationship between lactate production volume and signaling phosphorylations involved in mitochondrial biogenesis. EX and PGC-1α OE decreased muscle lactate production volume at the absolute same-intensity exercise, but only PGC-1α OE increased lactate production volume at the relative same-intensity exercise. Multiple linear regression revealed that phosphofructokinase, monocarboxylate transporter (MCT)1, MCT4, and citrate synthase equally contribute to the lactate production volume at high-intensity exercise within physiological adaptations, such as EX, not PGC-1α OE. We found that an exercise intensity-dependent increase in the lactate production volume was associated with a decrease in glycogen concentration and an increase in P-AMPK/T-AMPK. This suggested that the calculated lactate production volume was appropriate and reflected metabolic and signal responses but further modifications are needed for the translation to humans.

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