Regulation of human skeletal muscle perfusion and its heterogeneity during exercise in moderate hypoxia

Heinonen, Ilkka; Kemppainen, Jukka; Kaskinoro, Kimmo; Peltonen, Jari; Borra, Ronald; Lindroos, Markus M.; Oikonen, Vesa; Nuutila, Pirjo; Knuuti, Juhani; Boushel, Robert; Kalliokoski, Kari K.

doi:10.1152/ajpregu.00056.2010

Cited by 54 publications

(44 citation statements)

References 46 publications

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“…Baseline FBF, absolute peak FBF, and peak DFBF in ml 100 ml -1 min -1 ; baseline FVC, absolute peak FVC, and peak DFVC in ml 100 ml -1 min -1 100 mmHg -1 ; total DFBF in ml 100 ml -1 ; total DFVC in ml 100 ml -1 100 mmHg -1 * P \ 0.05 versus saline trial # P \ 0.05 versus APH alone 2000; Tabaie et al 1977), whereas in human studies APH has been linked with small reductions in flow at varying intensities of exercise (Casey and Joyner 2011;Martin et al 2006b), but failed to show any change in blood flow during hypoxic exercise Heinonen et al 2010;Marshall 2007). Thus, our findings are in line with observations during hypoxia in humans showing that ADO blockade does not blunt exercise hyperemia ).…”

Section: Discussionmentioning

confidence: 98%

Ischemic exercise hyperemia in the human forearm: reproducibility and roles of adenosine and nitric oxide

et al. 2011

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The roles of local metabolites in reactive and exercise hyperemia remain incompletely understood. A maximum metabolic stimulus caused by ischemic exercise (IE) could potentially fully activate all vasodilator pathways and limit potential redundancy amongst vasoactive substances. We tested the hypotheses that IE elicits a reproducible hyperemic response in the forearm and that adenosine (ADO) and nitric oxide (NO) contribute to this response. In separate protocols, forearm blood flow (FBF) was measured with venous occlusion plethysmography following IE trials consisting of 5 min of ischemia and rhythmic forearm handgrip exercise (performed during last 2 min of ischemia). In protocol 1 (n = 8), FBF was measured after three trials of IE. In protocol 2 (n = 9), subjects performed IE during control (saline), aminophylline (APH; adenosine receptor antagonist), and combined APH/N (G)-monomethyl-L-arginine (L-NMMA; NOS inhibition) infusions. In protocol 1, coefficients of variation for total (area under the curve) ΔFBF and ΔFVC (forearm vascular conductance) following IE were 10.4 ± 1.0% and 14.9 ± 1.0%, respectively. In protocol 2, peak ΔFBF was similar for saline and APH trials. Peak ΔFBF for the APH+L: -NMMA trial was greater than that of the APH trial (P = 0.03), and peak ΔFVC was marginally non-significant (P = 0.053). Total ΔFBF (54.8 ± 3.9, 55.2 ± 5.4, and 60.4 ± 4.8 ml 100 ml(-1); P = 0.43) and ΔFVC (51.4 ± 3.5, 52.1 ± 5.5, and 56.5 ± 5.0 ml 100 ml(-1) 100 mmHg(-1); P = 0.52) were similar for saline, APH, and APH+L: -NMMA, respectively. Our data suggest that (1) the hyperemic response to IE is reproducible and (2) inhibition of ADO alone or combined ADO and NO does not blunt the hyperemic response following IE.

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Section: Discussionmentioning

confidence: 98%

Ischemic exercise hyperemia in the human forearm: reproducibility and roles of adenosine and nitric oxide

et al. 2011

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“…sympathetic neural activity). The former mechanism tends to increase blood flow and capillary recruitment, particularly to metabolically active tissues (Heinonen et al, 2010). By contrast, the latter mechanism can promote a redistribution of blood flow away from peripheral tissues during hypoxia in favor of hypoxiasensitive tissues, such as the heart and brain (Hochachka, 1985).…”

Section: Tissue O 2 Transportmentioning

confidence: 99%

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

354

343

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SummaryHigh-altitude environments provide ideal testing grounds for investigations of mechanism and process in physiological adaptation. In vertebrates, much of our understanding of the acclimatization response to high-altitude hypoxia derives from studies of animal species that are native to lowland environments. Such studies can indicate whether phenotypic plasticity will generally facilitate or impede adaptation to high altitude. Here, we review general mechanisms of physiological acclimatization and genetic adaptation to high-altitude hypoxia in birds and mammals. We evaluate whether the acclimatization response to environmental hypoxia can be regarded generally as a mechanism of adaptive phenotypic plasticity, or whether it might sometimes represent a misdirected response that acts as a hindrance to genetic adaptation. In cases in which the acclimatization response to hypoxia is maladaptive, selection will favor an attenuation of the induced phenotypic change. This can result in a form of cryptic adaptive evolution in which phenotypic similarity between high-and low-altitude populations is attributable to directional selection on genetically based trait variation that offsets environmentally induced changes. The blunted erythropoietic and pulmonary vasoconstriction responses to hypoxia in Tibetan humans and numerous high-altitude birds and mammals provide possible examples of this phenomenon. When lowland animals colonize high-altitude environments, adaptive phenotypic plasticity can mitigate the costs of selection, thereby enhancing prospects for population establishment and persistence. By contrast, maladaptive plasticity has the opposite effect. Thus, insights into the acclimatization response of lowland animals to high-altitude hypoxia can provide a basis for predicting how altitudinal range limits might shift in response to climate change.

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“…Scanning began simultaneously with the bolus infusion of the tracer and scanning consisted of the following frames; 6 ϫ 5 s, 12 ϫ 10 s and 7 ϫ 30 s. Arterial blood radioactivity was also sampled continuously with a detector during imaging for blood flow quantification. The data analysis was performed using standard models (14) and methods (11)(12)(13)32). Blood flow was analyzed from calf musculature, with specific regions of interest including the soleus and gastrocnemius muscles, but avoided all apparent blood vessels and bone structures ( Fig.…”

Section: Subjectsmentioning

confidence: 99%

“…The PET-radiowater technique measures only blood flow in tissues where there is an exchange of water molecules, i.e., where exchange of nutrients and oxygen occurs. This technique has the capacity to quantify perfusion through different tissues (such as skin and skeletal muscle), while providing three-dimensional insight into capillary level blood flow in tissues at rest, as well as in contracting skeletal muscle (13,32). The objective of the present study was thus to test the hypothesis that both local and indirect whole body heating increase skeletal muscle blood flow as evaluated by PETradiowater measures.…”

mentioning

confidence: 99%

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

Heinonen

Kemppainen

Knuuti

et al. 2011

Journal of Applied Physiology

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149

140

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Heinonen I, Brothers RM, Kemppainen J, Knuuti J, Kalliokoski KK, Crandall CG. Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow. J Appl Physiol 111: 818-824, 2011. First published June 16, 2011 doi:10.1152 doi:10. /japplphysiol.00269.2011cades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positronemission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 Ϯ 1.0°C to 37.4 Ϯ 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 Ϯ 0.5 to 2.3 Ϯ 1.2 ml·100 g Ϫ1 ·min Ϫ1 (P Ͻ 0.05), whereas skin blood flow under the heating source increased from 0.7 Ϯ 0.3 to 5.5 Ϯ 1.5 ml·100 g Ϫ1 ·min Ϫ1 (P Ͻ 0.01). While whole body heat stress increased intestinal temperature by ϳ1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 Ϯ 0.5 ml·100 g Ϫ1 ·min Ϫ1 ; heat stress: 1.7 Ϯ 0.3 ml·100 g Ϫ1 ·min Ϫ1 ; P ϭ 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 Ϯ 1.5 ml·100 g Ϫ1 ·min Ϫ1 ) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress. positron-emission tomography; skin blood flow; bone blood flow; heat stress WHEN HUMANS ARE EXPOSED to acute heat stress several cardiovascular adjustments occur primarily directed toward increasing skin blood flow, which are necessary to adequately dissipate an internal heat load. These responses are accomplished through a combination of local and neurally mediated cutaneous vasodilation, coupled with elevated cardiac output and redistribution of blood flow and volume away from central vascular beds, such as the splanchnic and renal circulations, to the cutaneous circulation (4, 9, 21, 29 -31). In addition, skin and muscle sympathetic nerve activities (SNA) increase during heat stress (3,5,6,17,23,34), with increases in skin SNA being responsible for sweating and cutaneous vasodilation, while increases in muscle SNA have a less clear end result.Earlier studies p...

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Regulation of human skeletal muscle perfusion and its heterogeneity during exercise in moderate hypoxia

Cited by 54 publications

References 46 publications

Ischemic exercise hyperemia in the human forearm: reproducibility and roles of adenosine and nitric oxide

Ischemic exercise hyperemia in the human forearm: reproducibility and roles of adenosine and nitric oxide

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

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