Exercise training in normobaric hypoxia in endurance runners. II. Improvement of mitochondrial properties in skeletal muscle

Abstract

This study investigates whether adaptations of mitochondrial function accompany the improvement of endurance performance capacity observed in well-trained athletes after an intermittent hypoxic training program. Fifteen endurance-trained athletes performed two weekly training sessions on treadmill at the velocity associated with the second ventilatory threshold (VT2) with inspired O2 fraction = 14.5% [hypoxic group (Hyp), n = 8] or with inspired O2 fraction = 21% [normoxic group (Nor), n = 7], integrated into their usual training, for 6 wk. Before and after training, oxygen uptake (VO2) and speed at VT2, maximal VO2 (VO2 max), and time to exhaustion at velocity of VO2 max (minimal speed associated with VO2 max) were measured, and muscle biopsies of vastus lateralis were harvested. Muscle oxidative capacities and sensitivity of mitochondrial respiration to ADP (Km) were evaluated on permeabilized muscle fibers. Time to exhaustion, VO2 at VT2, and VO2 max were significantly improved in Hyp (+42, +8, and +5%, respectively) but not in Nor. No increase in muscle oxidative capacity was obtained with either training protocol. However, mitochondrial regulation shifted to a more oxidative profile in Hyp only as shown by the increased Km for ADP (Nor: before 476 +/- 63, after 524 +/- 62 microM, not significant; Hyp: before 441 +/- 59, after 694 +/- 51 microM, P < 0.05). Thus including hypoxia sessions into the usual training of athletes qualitatively ameliorates mitochondrial function by increasing the respiratory control by creatine, providing a tighter integration between ATP demand and supply.

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

“…Accordingly, the apparent K m to ADP (inversely proportional to the apparent affinity of mitochondria for ADP) was high in all our athletes, regardless of the magnitude of their drop in V O 2max with moderate hypoxia, suggesting that the sensitivity to cytosolic ADP is not a key factor involved in the hypoxia tolerance in athletes with already high K m values. Nevertheless, high K m values reflect a low sensitivity of mitochondrial respiration to cytosolic ADP, as expected in endurance-trained subjects (34,47,51) with skeletal muscles featuring high oxidative capacities (8,31,48,53,55,62).…”

“…In a previous study, we showed that V max was positively correlated to V O 2max when the population ranges from sedentary (V O 2max ϭ 28.5 ml·kg Ϫ1 ·min Ϫ1 ) to moderately trained subjects (V O 2max ϭ 50 ml·kg Ϫ1 ·min Ϫ1 ) (51). However, in subsequent studies, endurance athletes with higher V O 2max (ϳ60 ml·kg Ϫ1 ·min Ϫ1 ) were shown to have similar V max values compared with their moderately trained counterparts (12,34), suggesting that the quantitative aspects of tissue oxidative capacity levels off before the highest levels of endurance training are reached. Moreover, the higher V O 2max demonstrated by endurance-trained athletes was not accompanied by any increase in enzymatic markers of quantitative aspects of mitochondrial function (34).…”

“…However, in subsequent studies, endurance athletes with higher V O 2max (ϳ60 ml·kg Ϫ1 ·min Ϫ1 ) were shown to have similar V max values compared with their moderately trained counterparts (12,34), suggesting that the quantitative aspects of tissue oxidative capacity levels off before the highest levels of endurance training are reached. Moreover, the higher V O 2max demonstrated by endurance-trained athletes was not accompanied by any increase in enzymatic markers of quantitative aspects of mitochondrial function (34). In the present study, the ACR was similar between groups, suggesting that the degree of coupling between electron transport and phosphorylation does not explain the difference in the ability to maintain the normoxic V O 2max in moderate hypoxia.…”

Usefulness of combining intermittent hypoxia and physical exercise in the treatment of obesity

“…Adaptive responses to the respiratory tract and cardiovascular system are produced and, at the same time, the mitochondrial efficiency, pH / lactate regulation [81,164], and physical performance are increased [17, 108,143].…”

Control of respiration in flight muscle from the high-altitude bar-headed goose and low-altitude birds

“…At a cellular level this can manifest as a low sensitivity to cytosolic ADP and an enhanced sensitivity to creatine for mitochondrial respiration in permeabilized muscle fibers (1,20). These characteristics are particularly evident in muscle from athletic humans (49) and are enhanced in humans after exercise training in hypoxia (31) and in rats that have been artificially selected for exercise endurance capacity (44). However, the ADP and creatine sensitivities of bird flight muscle are unknown, and it is conceivable that improved CK shuttling could benefit exercise performance at high altitude.…”