Endurance Is Improved in Female Rats After Living High-Training High Despite Alterations in Skeletal Muscle

Abstract

Altitude camps are used during the preparation of endurance athletes to improve performance based on the stimulation of erythropoiesis by living at high altitude. In addition to such whole-body adaptations, studies have suggested that high-altitude training increases mitochondrial mass, but this has been challenged by later studies. Here, we hypothesized that living and training at high altitude (LHTH) improves mitochondrial efficiency and/or substrate utilization. Female rats were exposed and trained in hypoxia (simulated 3,200 m) for 5 weeks (LHTH) and compared to sedentary rats living in hypoxia (LH) or normoxia (LL) or those that trained in normoxia (LLTL). Maximal aerobic velocity (MAV) improved with training, independently of hypoxia, whereas the time to exhaustion, performed at 65% of MAV, increased both with training (P = 0.009) and hypoxia (P = 0.015), with an additive effect of the two conditions. The distance run was 7.98 ± 0.57 km in LHTH vs. 6.94 ± 0.51 in LLTL (+15%, ns). The hematocrit increased >20% with hypoxia (P < 0.001). The increases in mitochondrial mass and maximal oxidative capacity with endurance training were blunted by combination with hypoxia (−30% for citrate synthase, P < 0.01, and −23% for Vmax glut−succ, P < 0.001 between LHTH and LLTL). A similar reduction between the LHTH and LLTL groups was found for maximal respiration with pyruvate (−29%, P < 0.001), for acceptor-control ratio (−36%, hypoxia effect, P < 0.001), and for creatine kinase efficiency (−48%, P < 0.01). 3-hydroxyl acyl coenzyme A dehydrogenase was not altered by hypoxia, whereas maximal respiration with Palmitoyl-CoA specifically decreased. Overall, our results show that mitochondrial adaptations are not involved in the improvement of submaximal aerobic performance after LHTH, suggesting that the benefits of altitude camps in females relies essentially on other factors, such as the transitory elevation of hematocrit, and should be planned a few weeks before competition and not several months.

Training at moderate altitude improves submaximal but not maximal performance-related parameters in elite rowers

“…This is consistent with Jacobs et al (Jacobs et al, 2012), who found that 28 days at a high altitude (3454-m) enhances efficiency in human skeletal muscle mitochondria. However, contrary to the above, Malgoyre et al (Malgoyre et al, 2021) did not observe significant changes in mitochondrial enzymes linked to efficiency applying a LHTH model; although this valuable study was carried out in female rats, we do not rule out the possibility that it occurs in humans. In addition, the lower supply of oxygen at altitude in conjunction with endurance training induces the activation of mechanisms associated with mitochondrial biogenesis and angiogenesis, mediating skeletal muscle adaptations, promoting the optimization of glucose transport, and an increase in glycolytic enzymes activity (Zoll et al, 2006).…”

Male and Female Mitochondria Respond Differently after Exercising in Acute Hypoxia

“…It is important to note that the results mentioned earlier were obtained only from male subjects. In contrast, a study conducted on trained female rats in chronically hypoxic conditions found that respiration through complex I and with lipid substrates was reduced after hypoxia, despite the expected improvement from training [25].…”

Hacd2 deficiency in mice leads to an early and lethal mitochondrial disease

“…Protein concentration was assessed using the bicinchoninic acid assay (Pierce BCA Protein Assay Kit −23225). Total activity of cytochrome oxidase (COX) and citrate synthase (CS) was assayed at 30 °C, pH 7.5, using standard spectrophotometric assays [ 45 ].…”