Sensitivity of V̇O2max, critical power and V̇O2 on-kinetics to O2 concentration/delivery and other factors in skeletal muscle

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Abstract

<p class="first" id="d1152082e51">Relative sensitivities of the maximal oxygen uptake (V̇O2max), critical power (CP) and transition time of the primary phase II of the V̇O2 on-kinetics (t0.63) to selected factors in skeletal muscle are simulated using a computer model of the skeletal muscle bioenergetic system. In normoxia, V̇O2max is significantly positively sensitive to peak Pi (Pipeak, Pi at which exercise is terminated because of fatigue), OXPHOS (oxidative phosphorylation) activity (kOX) and ESA (each-step-activation) intensity (AOXmax), and negatively sensitive to the accessible phosphate (and total creatine) pool (Pacc). CP is additionally moderately positively sensitive to critical Pi (Picrit, Pi at which the additional ATP usage appears) and negatively sensitive to the additional ATP usage activity (kadd). t0.63 is significantly positively sensitive to Pacc and negatively to kOX and AOXmax. The positive sensitivity of V̇O2max and CP, and negative sensitivity of t0.63 to O2 concentration/delivery is low at normoxic and hyperoxic O2 levels, but increases significantly at severely hypoxic O2 levels. </p>

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Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species. Many different activities lead to fatigue, and an important challenge is to identify the various mechanisms that contribute under different circumstances. Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.

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Jason R. Richardson, Elizabeth A. Noyszewski, K Kendrick … (1995)

The assumption that cellular oxygen pressure (PO2) is close to zero in maximally exercising muscle is essential for the hypothesis that O2 transport between blood and mitochondria has a finite conductance that determines maximum O2 consumption. The unique combination of isolated human quadriceps exercise, direct measures of arterial, femoral venous PO2, and 1H nuclear magnetic resonance spectroscopy to detect myoglobin desaturation enabled this assumption to be tested in six trained men while breathing room air (normoxic, N) and 12% O2 (hypoxic, H). Within 20 s of exercise onset partial myoglobin desaturation was evident even at 50% of maximum O2 consumption, was significantly greater in H than N, and was then constant at an average of 51 +/- 3% (N) and 60 +/- 3% (H) throughout the incremental exercise protocol to maximum work rate. Assuming a myoglobin PO2 where 50% of myoglobin binding sites are bound with O2 of 3.2 mmHg, myoglobin-associated PO2 averaged 3.1 +/- .3 (N) and 2.1 +/- .2 mmHg (H). At maximal exercise, measurements of arterial PO2 (115 +/- 4 [N] and 46 +/- 1 mmHg [H]) and femoral venous PO2 (22 +/- 1.6 [N] and 17 +/- 1.3 mmHg [H]) resulted in calculated mean capillary PO2 values of 38 +/- 2 (N) and 30 +/- 2 mmHg(H). Thus, for the first time, large differences in PO2 between blood and intracellular tissue have been demonstrated in intact normal human muscle and are found over a wide range of exercise intensities. These data are consistent with an O2 diffusion limitation across the 1-5-microns path-length from red cell to the sarcolemma that plays a role in determining maximal muscle O2 uptake in normal humans.