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Energy Supply for Muscle Contraction  constant (! p. 75 B). The several minutes that
                                       pass before this steady state is achieved are
       Adenosine triphosphate (ATP) is a direct  bridged by anaerobic energy production, in-
       source of chemical energy for muscle contrac-  creased O 2 extraction from the blood and
       tion (! A, pp. 40 and 64). However, a muscle  depletion of short-term O 2 reserves in the
       cell contains only a limited amount of ATP–  muscle (myoglobin). The interim between the
       only enough to take a sprinter some 10 to 20 m  two phases is often perceived as the “low
       or so. Hence, spent ATP is continuously re-  point” of physical performance.
                                        The O 2 affinity of myoglobin is higher than
       generated to keep the intracellular ATP con-  that of hemoglobin, but lower than that of res-
    Nerve and Muscle, Physical Work  1. Dephosphorylation of creatine phosphate  oxygen to the mitochondria during brief arte-
       centration constant, even when large quanti-
                                       piratory chain enzymes. Thus, myoglobin is
       ties of it are needed. The three routes of ATP re-
                                       normally saturated with O 2 and can pass on its
       generation are (! B ):
                                       rial oxygen supply deficits.
       2. Anaerobic glycolysis
                                        The endurance limit, which is some 370 W
       3. Aerobic oxidation of glucose and fatty acids.
                                       (! 0.5 HP) in top athletes, is mainly dependent
       Routes 2 and 3 are relatively slow, so creatine
                                       on the speed at which O 2 is supplied and on
       phosphate (CrP) must provide the chemical
                                       how fast aerobic oxidation takes place. When
       energy needed for rapid ATP regeneration. ADP
       derived from metabolized ATP is immediately
                                       the endurance limit is exceeded, steady state
       transformed to ATP and creatine (Cr) by mito-
                                       ously (! p. 75 B). The muscles can temporarily
       CrP reserve of the muscle is sufficient for
                                       compensate for the energy deficit (see above),
    2  chondrial creatine kinase (! B1 and p. 40). The  cannot occur, the heart rate then rises continu-
       short-term
                high-performance
                                            +
                                       but the H -consuming lactate metabolism can-
                             bursts
                                   of
       10–20 s (e.g., for a 100-m sprint).  not keep pace with the persistently high level
         Anaerobic glycolysis occurs later than CrP  of anaerobic ATP regeneration. An excess of
       dephosphorylation (after a maximum of ca.  lactate and H ions, i.e. lactacidosis, therefore
                                               +
       30 s). In anaerobic glycolysis, muscle glycogen  develops. If an individual exceeds his or her
       is converted via glucose-6-phosphate to lactic  endurance limit by around 60%, which is about
                   +
       acid (! lactate + H ), yielding 3 ATP molecules  equivalent to maximum O 2 consumption
       for each glucose residue (! B2). During light  (! p. 74), the plasma lactate concentration
       exercise, lactate is broken down in the heart  will increase sharply, reaching the so-called
                 !
                    +
       and liver whereby H ions are used up. Aerobic  anaerobic threshold at 4 mmol/L. No significant
       oxidation of glucose and fatty acids takes place  increase in performance can be expected after
       approx. 1 min after this less productive an-  that point. The systemic drop in pH results in
       aerobic form of ATP regeneration. If aerobic ox-  increasing inhibition of the chemical reactions
       idation does not produce a sufficient supply of  needed for muscle contraction. This ultimately
       ATP during strenuous exercise, anaerobic gly-  leads to an ATP deficit, rapid muscle fatigue
       colysis must also be continued.  and, finally, a stoppage of muscle work.
                                        CrP metabolism and anaerobic glycolysis
       In this case, however, glucose must be imported  enable the body to achieve three times the per-
       from the liver where it is formed by glycogenolysis
       and gluconeogenesis (see also p. 282f.). Imported  formance possible with aerobic ATP regenera-
       glucose yields only two ATP for each molecule of glu-  tion, albeit for only about 40 s. However, these
       cose, because one ATP is required for 6-phosphoryla-  processes result in an O 2 deficit that must be
       tion of glucose.                compensated for in the post-exercise recovery
                                       phase (O 2 debt). The body “pays off” this debt
       Aerobic regeneration of ATP from glucose
       (2 + 34 ATP per glucose residue) or fatty acids is  by regenerating its energy reserves and break-
       required for sustained exercise (! B3). The car-  ing down the excess lactate in the liver and
       diac output (= heart rate"stroke volume) and  heart. The O 2 debt after strenuous exercise is
       total ventilation must therefore be increased  much larger (up to 20 L) than the O 2 deficit for
   72  to meet the increased metabolic requirements  several reasons.
       of the muscle; the heart rate then becomes
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
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