Skeletal muscle vasodilatation during maximal exercise in health and disease

Abstract

Maximal exercise vasodilatation results from the balance between vasoconstricting and vasodilating signals combined with the vascular reactivity to these signals. During maximal exercise with a small muscle mass the skeletal muscle vascular bed is fully vasodilated. During maximal whole body exercise, however, vasodilatation is restrained by the sympathetic system. This is necessary to avoid hypotension since the maximal vascular conductance of the musculature exceeds the maximal pumping capacity of the heart. Endurance training and high-intensity intermittent knee extension training increase the capacity for maximal exercise vasodilatation by 20-30%, mainly due to an enhanced vasodilatory capacity, as maximal exercise perfusion pressure changes little with training. The increase in maximal exercise vascular conductance is to a large extent explained by skeletal muscle hypertrophy and vascular remodelling. The vasodilatory capacity during maximal exercise is reduced or blunted with ageing, as well as in chronic heart failure patients and chronically hypoxic humans; reduced vasodilatory responsiveness and increased sympathetic activity (and probably, altered sympatholysis) are potential mechanisms accounting for this effect. Pharmacological counteraction of the sympathetic restraint may result in lower perfusion pressure and reduced oxygen extraction by the exercising muscles. However, at the same time fast inhibition of the chemoreflex in maximally exercising humans may result in increased vasodilatation, further confirming a restraining role of the sympathetic nervous system on exercise-induced vasodilatation. This is likely to be critical for the maintenance of blood pressure in exercising patients with a limited heart pump capacity.

Repeated Double-Poling Sprint Training in Hypoxia by Competitive Cross-country Skiers

“…Then, high-intensity intermittent training (e.g., knee extension) was reported to increase the capacity for maximal exercise vasodilation by 20%-30% (9). The latter may in turn partly explain the twofold higher amplitude of blood perfusion variations observed after RSN (Fig.…”

No Improved Performance With Repeated-Sprint Training in Hypoxia Versus Normoxia: A Double-Blind and Crossover Study

“…In this respect, it is mainly accepted that exercise in hypoxia results in a nitric oxide (NO)-dependent increase in muscle blood flow, matching oxygen delivery to demand if allowed by peak circulation levels 17,18 . As peak muscle perfusion is likely not reached with RS 19 , it follows that RS in hypoxia must be associated with elevated muscle blood flow and plausibly increased endothelial shear stress, which along with NO and hypoxia may stimulate angiogenesis in skeletal muscle [20][21][22] . In fact, enhanced capillary-to-fiber ratio has been "Repeated Sprint Training in Hypoxia Versus Normoxia Does Not Improve Performance: A Double-Blind and Cross-Over Study" by Montero D, Lundby C International Journal of Sports Physiology and Performance © 2016 Human Kinetics, Inc. observed after 3 weeks of moderate intensity hypoxic vs. normoxic training 23 .…”

Exaggerated haemodynamic and neural responses to involuntary contractions induced by whole‐body vibration in normotensive obese versus lean women

“…The delayed restoration of SVR to baseline during recovery from vibration in our obese group and the significant correlation of this response with body fat percentage are, however, suggestive of early alterations in vasomotor ability following physiological stress (Calbet & Lundby, 2012). Our data agree with the view that alterations in resting vasodilatation or resting NO levels do not necessarily modify mechanical exercise-induced hyperaemia; however, in the immediate postexercise period, alterations in vasodilatory state, possibly by changes in NO synthase, can delay or speed the return of blood flow to baseline (Joyner & Wilkins, 2007).…”

“…Vibration increased SV and cardiac indices to a greater extent in obese than lean women, which is in accordance with data reported in obese adults during voluntary aerobic exercise (Vella et al 2009). The greater increase in cardiac output index in our obese group could be the result of a reduced capacity for oxygen extraction, linked to alterations in glucose uptake and mitochondrial density reported in obesity (Kumagai et al 2002;Calbet & Lundby, 2012). An impaired distribution of blood flow between inactive and active tissues, along with alterations in skeletal muscle microvessels, can also require larger increases in cardiac output in order to meet the oxygen needs of the active skeletal muscle, as shown in obese Zucker rats (Frisbee et al 2011).…”