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Physiological basis of temperature-dependent biogeography: trade-offs in muscle design and performance in polar ectotherms

H. O. Pörtner

Alfred-Wegener-Institut für Polar- und Meeresforschung, Ökophysiologie, Postfach 12 01 61, D-27515 Bremerhaven, Germany

View larger version (23K): [in a new window]   Fig. 1. Simplified model of thermal tolerance and eurythermal temperature adaptation in animals (modified after Pörtner, 2001a) considering (A) contributions to metabolic heat production () by oxygen consumption (O2) and anaerobic metabolism (anae). The model is based predominantly on data for water-breathers. Mechanisms shifting the respective tolerance thresholds include a change in overall mitochondrial functional capacity (B), which causes a shift in both lower (I) and upper (II) pejus temperature (Tp, the onset of a decrease in aerobic scope) and critical temperature (Tc, the onset of anaerobic metabolism). Reductions in oxygen demand and anaerobic heat production are expected to result from a decrease in mitochondrial densities and capacities during warming (indicated by arrows in A).

View larger version (19K): [in a new window]   Fig. 2. Patterns of changes in rates of oxygen consumption (O2, mg h-1 kg-1, red lines) with increasing exercise levels in Atlantic cod (Gadus morhua) and Greenland cod (Gadus ogac) from various latitudes based on data for North Sea cod (Schurmann and Steffensen, 1997) and for the Greenland populations of both species (Bushnell et al., 1994). Solid lines depict the actual performance range up to the critical swimming velocity (Ucrit). Dashed lines depict extrapolated costs at higher swimming speeds (not reached) for a comparison between acclimation temperatures. For comparison, results at 0°C for Antarctic stenotherms (Notothenia neglecta and Pagothenia borchgrevinki) are included (Johnston et al., 1991; Forster et al., 1987). (A) In accordance with a compensatory increase in mitochondrial densities and overall aerobic metabolic capacities (see text), the intersection of extrapolated lines suggests that cold-acclimation at 10 or 5°C compared with 15°C causes a larger metabolic increment for the same exercise level in cod (as well as a rise in temperature-specific standard metabolic rate, SMR; not shown, see text). Metabolic cold adaptation observed in northern cod populations (at 4°C) also elevates SMR. However, the metabolic increment with rising swimming speed reflects enhanced energy efficiency and a somewhat higher Ucrit. (B) A model of the transitions between acute warming and long-term warm acclimation (from 5 to 15°C) based on data for cod by Claireaux et al. (1995) and Schurmann and Steffensen (1997). The reduction in baseline oxygen demand associated with a warm-induced decrease in mitochondrial densities should contribute to the increase in Ucrit observed during long-term warm acclimation. For further explanation, see the text.

View larger version (26K): [in a new window]   Fig. 3. Temperature-compensated aerobic scopes depending on standard metabolic rates (SMRs) in warm-adapted fish or other ectotherms compared with cold-compensated SMRs in eurytherms (Northern hemisphere) and reduced SMRs in Antarctic (and possibly Arctic) polar stenotherms. As a consequence of metabolic adjustments to cold, active metabolic rates at maximum aerobic activity (given as the metabolic rate at the critical swimming speed, Ucrit) may be cold-compensated in eurytherms, whereas lower rates may result for those Antarctic stenotherms with low SMRs (see, however, Fig. 2A and the text for a balanced view of these patterns). The low SMR in polar stenotherms despite high mitochondrial densities suggests that capacities are downregulated to levels expected from the Q10 relationship, possibly because of high Arrhenius activation energies (see text). For each of the four groups (warm-adapted versus temperate eurythermal versus cold eurythermal versus polar), straight vertical arrows depict the relationship between standard and maximum aerobic metabolic rate. The warm-water situation is interpreted to be the original situation (on evolutionary time scales) and, accordingly, to represent `the hub of metabolic cold adaptation' according to Pörtner et al. (2000).

View larger version (26K): [in a new window]   Fig. 4. High performance characteristics are required for moderate activity levels in Antarctic fish muscle. The trend from carbohydrate to lipid metabolism and the associated accumulation of intracellular lipid, favoured by high mitochondrial densities and, most likely, excess citrate levels at low standard metabolic rates (SMRs), contribute to energy savings in the cold by reducing energy-dependent membrane transport and neutral buoyancy. Low SMRs correlate with extreme stenothermy in the cold (see text).

View larger version (15K): [in a new window]   Fig. 5. The phosphorus spectra of Antarctic and temperate eelpout (Pachycara brachycephalum) reflect the higher concentration of phospholipids in the Antarctic species. GPC, glycerophosphatidylcholine; GPE, glycerophosphatidylethanolamine; PC, phosphatidylcholine; PCr, phosphocreatine; PE, phosphatidylethanolamine; Pi, inorganic phosphate; X, unassigned phosphodiester (adapted from Bock et al., 2001).

View larger version (27K): [in a new window]   Fig. 6. Simple qualitative model of tissue design limits for aerobic metabolism and performance levels as a function of body temperature. In a trade-off between the cellular space required by mitochondria, sarcoplasmic reticulum (SR) and myofilaments, the increased mitochondrial energy production at warm temperatures allows muscular power output at high body temperatures to be maximized. Design limits for aerobic metabolism are reached at lower performance levels in Antarctic fish. The model takes account of the higher mitochondrial densities seen in Antarctic fish than in mammal and bird muscles (see text).