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During evolution, mitochondrial DNA haplogroups of arctic populations may have been selected for lower coupling of mitochondrial respiration to ATP production in favor of higher heat production. We show that mitochondrial coupling in skeletal muscle of traditional and westernized Inuit habituating northern Greenland is identical to Danes of western Europe haplogroups. Biochemical coupling efficiency was preserved across variations in diet, muscle fiber type, and uncoupling protein-3 content. Mitochondrial phenotype displayed plasticity in relation to lifestyle and environment. Untrained Inuit and Danes had identical capacities to oxidize fat substrate in arm muscle, which increased in Danes during the 42 days of acclimation to exercise, approaching the higher level of the Inuit hunters. A common pattern emerges of mitochondrial acclimatization and evolutionary adaptation in humans at high latitude and high altitude where economy of locomotion may be optimized by preservation of biochemical coupling efficiency at modest mitochondrial density, when submaximum performance is uncoupled from VO2max and maximum capacities of oxidative phosphorylation.

AIM: It is an ongoing discussion the extent to which oxygen delivery and oxygen extraction contribute to an increased muscle oxygen uptake during dynamic exercise. It has been proposed that local muscle factors including the capillary bed and mitochondrial oxidative capacity play a large role in prolonged low-intensity training of a small muscle group when the cardiac output capacity is not directly limiting. The purpose of this study was to investigate the relative roles of circulatory and muscle metabolic mechanisms by which prolonged low-intensity exercise training alters regional muscle VO2 .METHODS: In nine healthy volunteers (seven males, two females), haemodynamic and metabolic responses to incremental arm cycling were measured by the Fick method and biopsy of the deltoid and triceps muscles before and after 42 days of skiing for 6 h day(-1) at 60% max heart rate.RESULTS: Peak pulmonary VO2 during arm crank was unchanged after training (2.38 ± 0.19 vs. 2.18 ± 0.2 L min(-1) pre-training) yet arm VO2 (1.04 ± 0.08 vs. 0.83 ± 0.1 L min(1) , P < 0.05) and power output (137 ± 9 vs. 114 ± 10 Watts) were increased along with a higher arm blood flow (7.9 ± 0.5 vs. 6.8 ± 0.6 L min(-1) , P < 0.05) and expanded muscle capillary volume (76 ± 7 vs. 62 ± 4 mL, P < 0.05). Muscle O2 diffusion capacity (16.2 ± 1 vs. 12.5 ± 0.9 mL min(-1) mHg(-1) , P < 0.05) and O2 extraction (68 ± 1 vs. 62 ± 1%, P < 0.05) were enhanced at a similar mean capillary transit time (569 ± 43 vs. 564 ± 31 ms) and P50 (35.8 ± 0.7 vs. 35 ± 0.8), whereas mitochondrial O2 flux capacity was unchanged (147 ± 6 mL kg min(-1) vs. 146 ± 8 mL kg min(-1) ).CONCLUSION: The mechanisms underlying the increase in peak arm VO2 with prolonged low-intensity training in previously untrained subjects are an increased convective O2 delivery specifically to the muscles of the arm combined with a larger capillary-muscle surface area that enhance diffusional O2 conductance, with no apparent role of mitochondrial respiratory capacity.

Studies regarding mitochondrial modifications in human skeletal muscle following acclimatization to high altitude are conflicting, and these inconsistencies may be due to the prevalence of representing mitochondrial function through static and isolated measurements of specific mitochondrial characteristics. The aim of this study, therefore, was to investigate mitochondrial function in response to high-altitude acclimatization through measurements of respiratory control in the vastus lateralis muscle. Skeletal muscle biopsies were obtained from 10 lowland natives prior to and again after a total of 9-11 days of exposure to 4559 m. High-resolution respirometry was performed on the muscle samples to compare respiratory chain function and respiratory capacities. Respirometric analysis revealed that mitochondrial function was largely unaffected, because high-altitude exposure did not affect the capacity for fat oxidation or individualized respiration capacity through either complex I or complex II. Respiratory chain function remained unaltered, because neither coupling nor respiratory control changed in response to hypoxic exposure. High-altitude acclimatization did, however, show a tendency (P = 0.059) to limit mass-specific maximal oxidative phosphorylation capacity. These data suggest that 9-11 days of exposure to high altitude do not markedly modify integrated measures of mitochondrial functional capacity in skeletal muscle despite significant decrements in the concentrations of enzymes involved in the tricarboxylic acid cycle and oxidative phosphorylation.

A large number of enzyme systems are examined for the diagnosis of mitochondrial myopathies including the pyruvate dehydrogenase complex, tricarboxylic-acid-cycle enzymes and respiratory-chain complexes. These investigations can be carried out in frozen tissue. For the study of oxidative phosphorylation in intact mitochondria, fresh muscle tissue is required, and isolation of mitochondria from large amounts of tissue (at least 500-1000 mg) is necessary. For ethical reasons this imposes a serious limitation, especially in paediatric patients. Radiochemical measurment of oxidation rates of various substrates in 600g supernatant from 100-300 mg amounts of muscle tissue has partly overcome this problem (Bookelman et al 1978)

The ciliated gill of bivalve molluscs is situated at an interface between animal and environment. Cilia propel water past the gills to deliver oxygen and nutrition to the animal. Ciliary activity is driven by dynein ATPases and requires a continual supply of ATP at a rate sufficient to match the rate of ATP hydrolysis. Control of the balance between ATP supply and demand in the ciliated gill, and how this balance may be altered by environmental stresses, is unknown. In this pilot study, metabolic flux of excised gills from the marine mussel Mytilus edulis was examined in response to oxygen availability and to serotonin-stimulated ciliary activity. Heat flux and oxygen flux were measured simultaneously with calorespirometry. In parallel experiments, the redox state of mitochondrial cytochromes was determined with in vivo spectrophotometry. Above 4 kPapO2, heat flux was supported by aerobic metabolism. Anoxic heat flux was less than 5% of aerobic heat flux. Heat and oxygen fluxes nearly doubled in gills in the presence of 10 μM serotonin; however, half-maximal pO2 for heat and oxygen fluxes and for reduction of mitochondrial cytochromes remained unchanged from control levels. In gills having inactive cilia in half-strength seawater, half-maximal pO2 for heat and oxygen fluxes and for cytochrome reduction nearly doubled compared with values in full-strength seawater. These data indicate that limitation to oxygen delivery imposed by boundary layers may be reduced when ciliary beat frequency is elevated, leading to enhanced oxygen flux to intracellular mitochondria which matches the increased energy demand by the cilia. © 1993 Wiley-Liss, Inc.

This survey on calorimetry and thermodynamics of anoxibiosis applies classical and irreversible thermodynamics to interpret experimental, direct calorimetric results in order to elucidate the sequential activation of various biochemical pathways. First, the concept of direct and indirect calorimetry is expanded to incorporate the thermochemistry of aerobic and anoxic metabolism in living cells and organisms. Calorimetric studies done under normoxia as well as under physiological and environmental anoxia are presented and assessed in terms of ATP turnover rate. Present evidence suggests that unknown sources of energy in freshwater and marine invertebrates under long-term anoxia may be important. During physiological hypoxia, thermodynamically grossly inefficient pathways sustain high metabolic rates for brief periods. On the contrary, under long-term environmental anoxia, low steady-state heat dissipation is linked to the more efficient succinate, propionate, and acetate pathways. In the second part of this paper these relationships are discussed in the context of linear, irreversible thermodynamics. The calorimetric and biochemical trends during aerobic-anoxic transitions are consistent with thermodynamic optimum functions of catabolic pathways. The theory predicts a decrease of rate with an increase of thermodynamic efficiency; therefore maximum rate and maximum efficiency are mutually exclusive. Cellular changes of pH and adenylate phosphorylation potential are recognized as regulatory mechanisms in the energetic switching to propionate production. While enzyme kinetics provides one key for understanding metabolic regulation, our insight remains incomplete without a complementary thermodynamic analysis of kinetic control in energetically coupled pathways.

Unusually high pH values up to 9.6 measured during low tide in a calcareous sandy beach were correlated with high in situ temperatures..Daily fluctuations of up to 1.5 pI1 units are limited to the topmost layer of sediment. Light, by controlling photosynthesis, is the causal factor in determining high pH at the surface; subsurface sediments do not respond to experimental light changes. Indications of such fluctuations are lacking in the literature. These fluctuations could influence community respiration.