Repository logo

Department of Health and Exercise Science

Permanent URI for this community

https://hdl.handle.net/10217/100447
These digital collections include theses, dissertations, and faculty publications from the Department of Health and Exercise Science. Due to departmental name changes, materials from the following historical department is also included here: Physical Education.

Browse

Browsing Department of Health and Exercise Science by Author "Anna, Jacob L., author"

Now showing 1 - 1 of 1
  • Thumbnail Image
    ItemOpen Access
    Mechanisms of exercise hyperemia during elevated oxygen delivery in humans
    (Colorado State University. Libraries, 2020) Anna, Jacob L., author; Dinenno, Frank, advisor; Richards, Jennifer, advisor; Lark, Daniel, committee member; Chicco, Adam, committee member
    The coupling between skeletal muscle oxygen delivery (O2D) and metabolic demand is largely attributed to the integration of feedback, and feedforward vascular mechanisms. It has been demonstrated that blood flow responses remain intact despite pharmacological elevations in resting blood flow, suggesting the existence of a vasodilator capable of augmenting hyperemia independent of tissue oxygen demand. We hypothesized that the change in forearm blood flow (FBF) from rest to steady-state exercise is preserved independent of baseline O2D, and that reciprocal reductions in oxygen extraction coincide with elevated O2D (Protocol 1). Additionally, pharmacological blockade of Kir channels and ATPase will reduce the change in FBF. In 10 young healthy adults, we quantified forearm blood flow (FBF; Doppler ultrasound), venous oxygen saturation (SvO2), oxygen extraction (O2 extraction; deep venous blood samples), and forearm oxygen consumption (mVO2) at rest and throughout 5 minutes of mild-intensity (10% maximal voluntary contraction; MVC) rhythmic handgrip exercise under control (CON) conditions and following intra-arterial infusion of the vasodilator sodium nitroprusside (SNP) to elevate local FBF and O2D. In Protocol 1, we elevated resting FBF and O2D to levels that matched (MAT) and exceeded (EXC) steady-state FBF (FBF: MAT; 166 ± 25 ml/min, P=NS, EXC; 219 ± 27 ml/min, P<0.05) during control (CON) exercise trials (FBF: CON; 172 ± 24). Changes in blood flow remained intact (ΔFBF: CON; 135 ± 20 ml/min vs. MAT; 132 ± 19 ml/min vs. EXC; 167 ± 26 ml/min, P=NS across all conditions), despite elevations in resting FBF which were adequate to sustain steady-state contractile activity under CON conditions. Reciprocal reductions in O2 extraction were observed in the MAT (O2 extraction: CON; 63 ± 3% vs. MAT; 43 ± 5%, P<0.05) and EXC trials (O2 extraction: CON; 63 ± 3% vs. EXC; 35 ± 5%., P<0.05) compared to CON during exercise. Additionally, we measured venous K+ in a subset of participants (N=6) to evaluate changes in K+ efflux (venous [K+] x FBF/1000) as an index of K+ release during exercise, alluding to K+-mediated activation of Kir channels and the ATPase. Five participants completed Protocol 2 which included control and elevated FBF trials (Saline + Block and SNP + Block) with the addition of intra-arterial infusion of barium chloride (BaCl2) and ouabain to inhibit Kir channels and the ATPase, respectively. Blockade of these pathways reduced the change in FBF that persisted during the Protocol 1 MAT trial (ΔFBF: MAT; 148 ± 21 ml/min vs. SNP + Block; 96 ± 13 ml/min, P<0.05). From this data, we are able to determine that changes in blood flow during exercise persist despite elevations in resting O2D (via SNP) prior to the start of exercise and that trends in O2 extraction follows changes in total O2D. We believe that local skeletal muscle K+ release is capable of activating Kir channels and the ATPase in a feed-forward manner which initiates a hyperpolarizing signal, thus augmenting blood flow independent of tissue oxygen demand.