Muscular exercise, lactic acid, and the supply and utilisation of oxygen.—Parts ӏ-ӏӏӏ

Abstract

In a recent paper under the general title of this series A. V. Hill and Lupton (1) gave a preliminary account of experiments made on man, in an attempt to press to its logical conclusion the physico-chemical view of muscular contraction arrived at by the investigation of the isolated muscle. The present series of papers contains a more adequate account of these experiments, which are still in progress. ( a ) The “ Initial ” Process . In the isolated muscle the complete cycle of contraction and relaxation, as distinguished from recovery, appears to be accompanied by no chemical change of any importance, other than the conversion of glycogen into lactic acid, and the subsequent neutralisation of the latter (2) (4). These “ initial ” phases of muscular activity are entirely non-oxidative in character (3), and the following “ balance sheet ” (Table I) shows that, if any other chemical changes do actually occur, they are negligible from the energy standpoint.

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

“…They also are consistent with the effects of inspired hypoxia (1,11,19,25,29,38) and hyperoxia (1,11,19,38) on decreasing and increasing performance, respectively. Because we also found that the magnitude of locomotor muscle fatigue was attenuated by preventing EIAH and exacerbated by increasing arterial hypoxemia, does this mean that locomotor muscle fatigue caused the changes in performance?…”

“…This finding was interpreted to reflect an increase in motor unit recruitment to compensate for the fatigue (47). In contrast, it has been argued that systemic hypoxemia may reflexively inhibit central motor output to locomotor muscles to ensure that a catastrophic failure of homeostasis does not occur during exercise (3,19). This proposal is supported by the finding that cycle exercise during chronic severe hypoxia is terminated without evidence of peripheral muscle fatigue, again as inferred by the absence of hypoxic effects on limb muscle EMG activity (26).…”

Oxygen uptake kinetics as a determinant of sports performance

“…The second important property of the V O 2 Ápower output relationship is that there is an upper limit to the increase in V O 2 (V O 2max ). The concept of V O 2max was originally established using discontinuous constant-load exercise testing (Å strand & Saltin, 1961a;Hill & Lupton, 1923), but it is well known that the peak V O 2 observed in the more common ramp test is identical to V O 2max measured using constant power output exercise ( Figure 1C; see also Day, Rossiter, Coats, Skasick, & Whipp, 2003).…”

“…Since the work of Krogh and Lindhard (1920) and Hill and Lupton (1923), it has been widely appreciated that sustaining exercise beyond a few seconds depends upon the appropriate supply and utilization of oxygen. However, the widespread use of incremental exercise tests on the one hand, and Douglas bag or mixing chamber analyses in which pulmonary gas exchange data are averaged over periods of 30 Á 60 s on the other, has led to the common misconceptions that: (1) following a ''lag'' in V O 2 at the onset of constant-load exercise (the ''oxygen deficit''), a steady state is always achieved within about 3 min; and (2) V O 2 increases linearly as power output increases to V O 2max .…”

Intertemporal Decision Making: A Mental Load Perspective

“…[26], [27], [3], [4]) a new hyperbolicexponential discounting model has been derived. This hyperbolic-exponential discounting model makes use of the concept critical power which indicates the level of power that can be provided without increasing fatigue (e.g., [8], [11], [12], [15], [19], [26], [27]). Moreover, the assumption was made that the considered power spent is kept constant over time.…”