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Maximal external work (i.e. power output) is largely dependent on the duration of exercise. Osimertinib concentration Power output is estimated to peak between 100 and 140 W (kg body weight)?1 in athletes (di Prampero et al. 2005). Forceful contractions can, however, only be maintained for a fraction of a second owing to the high demand on energy flux (Wilkie, 1980; Beneke & Boning, 2008). Consequently, with continued duration of a workout the maximally sustainable power declines considerably to reach ?4�C5 W (kg body weight)?1 (300�C400 W for 75 kg of body weight) in trained subjects working for up to 10 min (Fig. 1). In contrast, the relation between energy input (i.e. metabolic cost) and external muscle work is kept in a narrower range within 0.14�C0.27 along the power continuum (Bangsbo, 1996; Beneke & Boning, 2008). The different optima in power output during high-intensity exercise essentially reflect modified energy transfer from creatine phosphate to actin�Cmyosin ATPase (Greenhaff & Timmons, 1998). Existing creatine phosphate pools are depleted with contractions lasting more than a few seconds (Sahlin et al. 1998) and need to be replenished to allow sarcomeres to shorten. This recharging is coupled to increased ATP production from the combustion of carbohydrates and fatty acids with exercise (Fig. 2; Saks et al. 1996; Jeukendrup, 2003). The increased energy demand after onset of contractions is met by production of ATP through the conversion of glucose into pyruvate (Greenhaff & Timmons, 1998; Wasserman Alectinib in vitro & Halseth, 1998). This glycolytic ATP production is very powerful but can only be maintained for a short duration. The deficit is compensated by a drop in exercise output along with increases in blood flow and substrate import GPX4 and the elevation of mitochondrial metabolism in contracting muscle fibres (Greenhaff & Timmons, 1998; Clifford & Hellsten, 2004). The resulting oxidation of pyruvate produces a considerably larger number of ATP molecules than the conversion of pyruvate into lactate (i.e. 36 versus 2 ATP) and alleviates muscle fibres from the consequences of metabolite accumulation (Sahlin et al. 1998). Concurrently, the slower mitochondrial oxidation of fatty acids via ��-oxidation and the Krebs cycle delivers a considerable amount of ATP per fatty acid molecule (i.e. 131 ATP per palmitate). Henceforth, oxidation of pyruvate and fatty acids is the choice for endurance-type activities when economic energy production becomes a priority to fuel mechanical output for a prolonged period (Romijn et al. 1993; Beneke & Boning, 2008). With prolonged duration of muscle work, an increasing role is assigned to supply of substrates from intramuscular, hepatic and adipose stores (Jeukendrup, 2003; Beneke & Boning, 2008) and the containment of wasteful metabolic products (Wade et al. 2000; Weibel, 2002).