To better see the tradeoff, we derive a steady-county design (P

As we mentioned earlier, in healthy fit subjects, the central physiological tradeoffs in cardiovsincecular control require keeping errors such as CBF, SaO_dos, and ?O₂ suitably small in response to variations in W disturbance through changes in actuations such as H. _as, ?O₂) = f(H, W) from standard physiology that constrains the relationship between (P_as, ?O₂) and (H, W) independent of how H is controlled (details below). Here P_as is mean systemic arterial blood pressure, which is an important variable affecting the CBF (28, 38) and ?O₂ is the drop in oxygen content across working muscle [Notice that the model already assumes constant SaO₂, which is consistent with data measurement and literature (27).] The mesh plot in Fig. 3C is the image on the (P_as, ?O₂) plane of the Fig. 3B (H, W) mesh plot under this function f(H,W) for generic, plausible values of physiological parameters (SI Appendix). Thus, any function H = h(W) can be mapped from the (H, W) plane using model (P_as, ?O₂) = f(H, W) to the (P_as, ?O₂) plane to determine its consequences for the most important tradeoffs, which involve P_as and ?O₂. These results are shown with the black lines in Fig. 3B, which give H = h(W) curves consistent with Fig. 3A and then are mapped onto Fig. 3C.

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Hidden complexity is unavoidable in the model (P_as, ?O₂) = f(H, W), but we temporarily defer these details to focus on the general shape of the color-coded curves in Fig. 3 B and C, which have an intuitively clear explanation highlighted by the dashed red and https://datingranking.net/fr/rencontres-gamer/ purple lines. At constant workload, increased HR would greatly increase P_as while slightly decreasing ?O₂ due to greater flow rate through the muscle. For constant HR, increased workload would greatly increase ?O₂ while slightly reducing P_as due to greater oxygenation and peripheral vasodilatation. _as with increasing ?O₂, both of which are undesirable. The modest curvature of the colored meshes in Fig. 3C demonstrates a small nonlinearity in the function (P_as, ?O₂) = f(H, W). However, the solid black lines in Fig. 3 manifest a much larger nonlinearity in the control function H = h(W). We will argue that the essential sources of this nonlinearity are the tradeoff in robust homeostasis and metabolic efficiency and how it changes at different HR levels.

The hypothetical linear response at low workload in Fig. 3 can be explained in terms of purely metabolic tradeoffs. Healthy athletes can maintain the low workload almost indefinitely even in adverse (e.g., heat) conditions, a feature of human physiology thought to be an important adaptation for a successful hunter (39). Prolonged exercise necessarily requires steeply increased HR to provide sufficient tissue O₂ (low ?O₂), to maintain aerobic lipid metabolism in muscles and preserve precious carbohydrates for the brain.

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The nonlinear response in Fig. 3 (solid lines) reflects additional tradeoffs that arise at higher workload and HR, when the resulting high P_as becomes dangerous mainly due to actuator saturation of cerebral autoregulatory control. In healthy humans, CBF is autoregulated to be quite constant (28, 38) over a relatively wide range of P_as (50 < P_as < 150 mm Hg), so that no new tradeoffs at moderate exercise levels are required, because P_as is within this range. A new tradeoff does arise at P_as above 150 mm Hg when cerebral autoregulation saturates, and CBF begins to rise with the severe possible consequences of edema and/or hemorrhage. Thus, for the dashed black linear response in Fig. 3 B and C, the resulting P_as would be elevated to potentially pathologic levels, and some nonlinearity as in the solid black line is necessary. Moreover, in many subjects there may be diminishing metabolic benefit of high tissue O₂ (low ?O₂) at high workloads because muscle mitochondria saturate. Although many details of cerebral autoregulation (as well as the mitochondrial saturation) are poorly understood, the P_as at which autoregulation saturates is well-known in healthy adults, and helps to explain an important change in HRV with stressors. Ultimately, cardiac output itself saturates at sufficiently high HR due to compromised diastolic filling time with subsequent dramatic falls in stroke volume.