SUMMARY1. The energetic cost of work performance by mouse fast-and slow-twitch muscle was assessed by measuring the rates of thermal and mechanical energy liberation of the muscles at 21 'C. Thermal energy (heat) liberation was measured using a fastresponding thermopile.2. Bundles of muscle fibres from the slow-twitch soleus and fast-twitch extensor digitorum longus (EDL) muscles were used. Work output was controlled by performing isovelocity shortenings during the plateau of an isometric tetanus. A range of shortening velocities, spanning the possible range, was used for each muscle.3. During tetanic contractions, the rate of heat production from EDL muscle was 134-2 + 11-4 mW/g. The rate of heat production by soleus muscle was only one-fifth as great (26-8 + 2-7 mW/g).4. The maximum shortening velocity (Vmax) of EDL muscles was 2*5-fold greater than that for soleus muscles and it's force-velocity relationship was less curved. Peak power output from EDL muscles was 3-fold greater than that from soleus muscle.5. During shortening, the rate of heat output from soleus muscles increased considerably above the isometric heat rate. In contrast to soleus muscle, the rate of heat production by EDL muscle increased by only a small fraction of the isometric heat rate. The magnitude of the increases in rate was proportional to shortening velocity.6. The total rate of energy liberation (heat rate + power) by EDL muscle, shortening at 0 95 Vmax was 1-62 + 0 37 times greater than the isometric heat rate. In contrast, the rate of energy liberation from soleus muscle shortening at 0 95 Vmax was 5-21 + 0-58 times greater than its isometric heat rate. The peak mechanical efficiency (power/total energy rate) of the both muscles was approximately 30%.

SUMMARY1. The average resting heat production of a muscle under zero tension is 24*8 mcal/g muscle . min at 20°C. In the majority of muscles exomined the resting heat production increases when the resting tension and muscle length are increased.2. The relation between actively developed tension and heat produced is similar to that existing in skeletal muscle. The plot of heat against developed tension can be obtained either by altering muscle length or by varying the stimulus frequency.3. The mean maximum total efficiency work/(work + heat) in the work experiments was 11-6 %. The total energy produced (work+ heat) correlates with the load rather than with the work done. 4. In isotonic contractions more heat is liberated than the heat versus tension plot predicts. This extra heat is load-dependent.

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The energy flux of rat, guinea pig, and cat papillary muscles was measured myothermically under resting, isometric, and isotonic conditions at 27 degrees C. Resting heat rate was highest in the smallest species and declined with body size. The slope of the isometric heat-stress relationship was constant across species, whereas the stress-independent heat component was least for rat muscles. The shape of the load enthalpy relationship was similar across species. Maximum mechanical efficiency, work-enthalpy, occurred with lighter loads than for skeletal muscle (approximately 0.2 Po). Rat muscle had the smallest enthalpy per beat and the highest active mechanical efficiency, but this advantage was nullified by the higher basal heat rate. The myothermic data are compared with cardiac oxygen consumption values in the literature and it is concluded, contrary to the deductions of common dimensional arguments, that cardiac energy expenditure across species is not directly proportional to heart rate. Reasons for this discrepancy are considered together with the likely contribution of cardiac metabolism (EH) to total body metabolism (EB). It seems likely that smaller species have lower EH/EB.

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The cardiac basal metabolism is the rate of energy expenditure of the quiescent myocardium. It is also called the resting metabolism or the arrested heart metabolism. It has been measured in numerous ways, and in vivo there is good evidence that it accounts for about 1/5 to 1/3 of the total energy flux. The difficulty arises, however, when the heart is stopped because the magnitude of the basal metabolism depends, as blood viscosity, on how and under what physiological condition it is measured. It is possible for the in vivo basal value to fall to less than 1/5 of its original value without cellular damage or to increase to values 5 times greater than its probable in vivo magnitude (i.e., to rise to values in excess of the energy flux of the normally beating heart) by altering the composition of the perfusion medium. We have written on this subject several times [1][2][3], but believe that developments in knowledge now make it possible for us to speculate in a more informed manner. Since several million openheart operations are performed on arrested hearts worldwide each year, it would seem imperative that we understand the cellular mechanisms that can change the magnitude of basal metabolism.A. V. Hill [4] has pointed out that in examining physiological activities, it is necessary to assume a baseline from which some quantity or rate can be measured. If the energy flux produced by the beating heart were very large compared with the energy flux of the arrested heart, baseline ambiguity would be relatively unimportant. But this is not so in regard to the heart; its basal metabolism is high. Within a species, the basal metabolism of cardiac tissue is several-fold higher than the resting metabolism of skeletal muscle and is an order of magnitude greater than the resting metabolism of amphibian skeletal muscle.Species differences are clearly evident in the magnitude of cardiac basal metabolism, and we believe that the major reason for these differences relates to the leakiness of cell membranes, such as those of the sarcolemma and sarcoplasmic reticulum and those of Japanese Journal of Physiology, 51, 399-426, 2001 Key words: whole hearts, isolated preparations, biochemical contributors, modifiers, species difference, temperature, substrate, hypoxia. Abstract:We endeavor to show that the metabolism of the nonbeating heart can vary over an extreme range: from values approximating those measured in the beating heart to values of only a small fraction of normal-perhaps mimicking the situation of nonflow arrest during cardiac bypass surgery. We discuss some of the technical issues that make it difficult to establish the magnitude of basal metabolism in vivo. We consider some of the likely contributors to its magnitude and point out that the biochemical reasons for a sizable fraction of the heart's basal ATP usage remain unresolved. We consider many of the physiological factors that can alter the basal metabolic rate, stressing the importance of substrate supply. We point out that the protective effect of hypothermia ...

SUMMARY1. Activation heat was estimated myothermically in right ventricular papillary muscles of rabbits using several different methods.2. Gradual pre-shortening of muscles to a length (Imin) where no active force development took place upon stimulation led to relatively low estimates of activation heat (1-59 + 0-26-2-06 + 057 mJ g-1 blotted wet weight, mean + S.E.M., n = 10).3. Quick releases applied during the latency period, before force development, from Imax to various muscle lengths allowed a heat-stress relation to be established.The zero-stress intercept of this relation estimated the activation heat to be 3-27 + 0 40 mJ g-'; this was close to the experimentally measured value of 3-46 + 0-39 mJ g-1 (mean + S.E.M., n = 23) found by quick release from lmax to lmin, 4. The magnitude of the activation heat measured by the quick-release technique is dependent upon the extracellular Ca2+ concentration and there is good correlation between activation heat magnitude and peak developed stress.5. In agreement with expectations based on the aequorin data of Allen & Kurihara (1982) a prolonged period of time spent at a short length is shown to depress the subsequently determined activation heat.6. Hyperosmotic solutions (2-5 x normal) only abolished active stress development at low stimulus rates (0-2 Hz) and the activation heat measured at Imax under these conditions was 2-03 + 0x12 mJ g1-(mean +S.E.M., n = 6). This value was significantly lower than the latency release estimate of activation heat in the same preparations (2-93+0-39 mJ g-1).7. The latency release method of estimating activation heat results in activation heat values that account for approximately 30 % of total active energy flux per contraction; a fraction comparable to that found in skeletal muscle. Calculations based on the data suggest that, under our experimental conditions, total Ca2" release per beat lies between 50 and 100 nmol g-1 wet weight which would produce less than half-maximal myofibrillar ATPase activity when allowance is made for the passive