The role of vascular function on exercise capacity in health and disease

Abstract

Three sentinel parameters of aerobic performance are the maximal oxygen uptake (V̇O2normalmax), critical power (CP) and speed of the V̇normalO2 kinetics following exercise onset. Of these, the latter is, perhaps, the cardinal test of integrated function along the O2 transport pathway from lungs to skeletal muscle mitochondria. Fast V̇normalO2 kinetics demands that the cardiovascular system distributes exercise‐induced blood flow elevations among and within those vascular beds subserving the contracting muscle(s). Ideally, this process must occur at least as rapidly as mitochondrial metabolism elevates V̇normalO2. Chronic disease and ageing create an O2 delivery (i.e. blood flow × arterial [O2], Q̇normalO2) dependency that slows V̇normalO2 kinetics, decreasing CP and V̇O2normalmax, increasing the O2 deficit and sowing the seeds of exercise intolerance. Exercise training, in contrast, does the opposite. Within the context of these three parameters (see Graphical Abstract), this brief review examines the training‐induced plasticity of key elements in the O2 transport pathway. It asks how structural and functional vascular adaptations accelerate and redistribute muscle Q̇normalO2 and thus defend microvascular O2 partial pressures and capillary blood–myocyte O2 diffusion across a ∼100‐fold range of muscle V̇normalO2 values. Recent discoveries, especially in the muscle microcirculation and Q̇normalO2‐to‐V̇normalO2 heterogeneity, are integrated with the O2 transport pathway to appreciate how local and systemic vascular control helps defend V̇normalO2 kinetics and determine CP and V̇O2normalmax in health and how vascular dysfunction in disease predicates exercise intolerance. Finally, the latest evidence that nitrate supplementation improves vascular and therefore aerobic function in health and disease is presented.

Blood flow restriction training: You can occlude your veins, but not your oxygen transport

“…Enlargement of femoral diameter may present one of the underlying factors that contributed to a higher post-training Journal Club J Physiol 598.18 blood flow rate to the BFR-leg compared to the CON-leg at submaximal intensity (Christiansen et al 2020). In line with previously reported haemodynamic principles (Poole et al 2020), it was calculated that even a small increase (4%) in vessels radius may have contributed to higher blood flow rate to exercising muscle (20%) (Christiansen et al 2020). This functional adaptation may have contributed to an increase in blood flow and subsequently improved convective O 2 transport to the BFR-leg during the submaximal intensity exertion (Christiansen et al 2020).…”

August Krogh's theory of muscle microvascular control and oxygen delivery: a paradigm shift based on new data

“…Any putative model for capillary function must incorporate a sufficiently fast kinetics response to match the physiological behaviours demonstrated across the lungs (review: Poole & Jones, 2012) and also the contracting muscles (Behnke et al 2001(Behnke et al , 2002reviews: Poole, 2019;Poole et al 2020a). A, increase of capillary red blood cell (RBC) flux (filled circles) and microvascular P O 2 (P mvO 2 , triangles) in rat spinotrapezius (a mixed fibre type muscle with an oxidative capacity similar to the human vastus lateralis) conflated to estimate oxygen uptake (V O 2 ) (open circles) in response to 1 Hz electrically induced contractions (initiated at time = 0 s) normalized to 100% response amplitude.…”

“…Intriguingly, fast-twitch muscles regulate theirQ O 2 -to-V O 2 ratio such that microvascular and interstitial P O 2 values are lower than in their slow twitch counterparts ( Fig. 6B; Dawson et al 1987;Behnke et al 2003;McDonough et al 2005;Hudlická, 2011;Poole et al 2020a). Krogh (1919a,b,c) (1) Capillary architecture "In a muscle stretched to its normal length during rest, the capillaries are more or less straight, but in contracted muscle they become very sinuous; they anastomose to a certain extent forming long meshes about the fibres."…”

Indices of leg resistance artery function are independently related to cycling V̇O 2 max

“…Since VȮ 2 max strongly influences exercise performance and is also a strong predictor of cardiovascular risk (Poole et al, 2020), there is great interest in identifying what limits or reduces an individual's VȮ 2 max (Wagner, 2008) so that appropriate steps may be taken to improve it. With resistance artery function being related to both maximum exercise blood flow (Hanson et al, 2020) and VȮ 2 max (Table 2), noninvasive assessments, like passive-leg movement (PLM)-induced hyperemia, may conceivably be used to easily determine the likelihood that impairments in muscle resistance artery function and leg blood flow impair a person's VȮ 2 max.…”

“…One's maximum rate of oxygen consumption (VȮ 2 max) strongly influences exercise performance and is also a strong predictor of cardiovascular risk (Poole, Behnke, & Musch, 2020). While many systems may limit VȮ 2 max (Wagner, 2008), the cardiovascular system often serves as a significant bottleneck, with untrained individuals often exhibiting a much lower cardiac output and muscle blood flow than endurance-trained individuals (Gifford et al, 2016;Levine, 2008).…”