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Oxidative phosphorylation provides most of the ATP that higher animals and plants use to support life and is responsible for setting and maintaining metabolic homeostasis. The pathway incorporates three consecutive near equilibrium steps for moving reducing equivalents between the intramitochondrial [NAD+]/[NADH] pool to molecular oxygen, with irreversible reduction of oxygen to bound peroxide at cytochrome c oxidase determining the net flux. Net flux (oxygen consumption rate) is determined by demand for ATP, with feedback by the energy state ([ATP]/[ADP][Pi]) regulating the pathway. This feedback affects the reversible steps equally and independently, resulting in the rate being coupled to ([ATP]/[ADP][Pi])3. With increasing energy state, oxygen consumption decreases rapidly until a threshold is reached, above which there is little further decrease. In most cells, [ATP] and [Pi] are much higher than [ADP] and change in [ADP] is primarily responsible for the change in energy state. As a result, the rate of ATP synthesis, plotted against [ADP], remains low until [ADP] reaches about 30 μm and then increases rapidly with further increase in [ADP]. The dependencies on energy state and [ADP] near the threshold can be fitted by the Hill equation with a Hill coefficients of about −2.6 and 4.2, respectively. The homeostatic set point for metabolism is determined by the threshold, which can be modulated by the pO2 and intramitochondrial [NAD+]/[NADH]. The ability of oxidative phosphorylation to precisely set and maintain metabolic homeostasis is consistent with it being permissive of, and essential to, development of higher plants and animals.
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It has been proposed that athletes with high initial values of hemoglobin mass (Hbmass) will have a lower Hbmass increase in response to 'live high-train low' (LHTL) altitude training. To verify this assumption, the relationship between initial absolute and relative Hbmass values and their respective Hbmass increase following LHTL in male endurance and team-sport athletes was investigated. Overall, 58 male athletes (35 well-trained endurance athletes and 23 elite male field hockey players) undertook an LHTL training camp with similar hypoxic doses (200–230 h). Hbmass was measured in duplicate pre- and post-LHTL with the carbon monoxide rebreathing method. While there was no relationship (r = 0.02, P = 0.91) between initial absolute Hbmass (g) and percentage increase in absolute Hbmass, a moderate relationship (r = −0.31, P = 0.02) between initial relative Hbmass (g·kg−1) and percentage increase in relative Hbmass was detected. Mean absolute and relative Hbmass increased to a similar extent (P ≥ 0.81) in endurance (from 916 ± 88 to 951 ± 96 g, +3.8%, P < 0.001 and from 13.1 ± 1.2 to 13.6 ± 1.1 g·kg−1, +4.1%, P < 0.001) and team-sport (from 920 ± 120 to 957 ± 127 g, +4.0%, P < 0.001 and from 11.9 ± 0.9 to 12.3 ± 0.9 g·kg−1, +4.0%, P < 0.001) athletes following LHTL. The direct comparison study using individual data of male endurance and team-sport athletes and strict methodological control (duplicate Hbmass-measures, matched-hypoxic dose) indicated that even athletes with higher initial Hbmass can reasonably expect Hbmass gain post-LHTL.
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