Christopher Martens Headshot CHRISTOPHER MARTENS, PhD

Postdoctoral Fellow
Integrative Physiology of Aging Laboratory
University of Colorado Boulder

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Personal Statement

The number of older adults in the United States is expected to double by the year 2050, resulting in a new epidemic of age-related disability and associated healthcare costs. Treatments designed to slow the progression of aging itself, are likely to be more effective at reducing the age-associated decline in physiological function than targeting individual age-related diseases. My postdoctoral research in the Integrative Physiology of Aging Laboratory is related to the identification of novel lifestyle and dietary (nutraceutical) interventions to delay or reverse the age-associated decline in physiological function, increase "healthspan", and promote healthy aging.

Education

2009-2014
Ph.D. Applied Physiology
University of Delaware, Newark, DE
Dissertation: L-arginine transport and endothelial dysfunction in chronic kidney disease: The role of exercise
Advisor: David G. Edwards
2005-2009
B.S. Exercise Science
University of Delaware, Newark, DE
Concentration: Exercise Physiology
Minor: Biological Sciences

Experience

2014-
Postdoctoral Fellow, Department of Integrative Physiology
University of Colorado, Boulder, CO
2009-2014
Research Assistant, Department of Kinesiology & Applied Physiology
University of Delaware, Newark, DE
2009-2011
Teaching Assistant, Department of Kinesiology & Applied Physiology
University of Delaware, Newark, DE
2008-2009
Research Contractor, US Army Research Institute of Environmental Medicine, Thermal and Mountain Medicine Division
Natick, MA

Professional Development

2011
O'Brien Center Rodent Kidney Physiology/Injury Workshop
VA San Diego Healthcare System
University of California, San Diego, CA
2009
Rat & Mouse Microsurgical Workshop
Department of Orthopedic Surgery
Wake Forrest Medical School, Winston-Salem, NC

Professional Memberships

2009-
American College of Sports Medicine
2010-
American Physiological Society
2010-
American Heart Association
2011-2013
American Society of Nephrology

Honors & Awards

2013
Caroline tum Suden/Frances Hellbrandt Professional Opportunity Award
The American Physiological Society
2013
Dissertation Fellowship, University of Delaware
2012
University Graduate Fellowship, University of Delaware
2012
Professional Development Award
Office of Graduate and Professional Education, University of Delaware
2010-
Doctoral Student Investigator Award
American College of Sports Medicine- Mid Atlantic Chapter

Extramural Funding

  • Industry Contract
  • ChromaDex, Inc.
  • "NIAGEN Supplementation for Improving Physical and Metabolic Function in Midlife and Older Adult Humans"
  • Period: 2015-2016
  • Role: PI
  • Direct Costs: $65,000
  • UL1 TR001082 (P&F Grant)
  • Colorado Clinical & Translational Sciences Institute
  • "Nicotinamide Riboside Supplementation for Improving Physiological Function in Middle-Aged and Older Adults"
  • Period: 2015-2016
  • Role: PI
  • Direct Costs: $30,000
  • Postdoctoral Fellowship
  • Glenn/AFAR Program for Translational Research on Aging
  • "Nicotinamide Riboside Supplementation for Improving Physiological Function in Older Adults"
  • Period: 2015-2016
  • Role: PI
  • Direct Costs: $49,980
  • T32 AG00027912
  • NIH National Institute on Aging (NIA)
  • "Integrative Physiology of Aging Institutional Training Grant"
  • Period: 2014-2015
  • Role: Fellow (PI: Schwartz, R)
  • Direct Costs: $42,000
  • Foundation Grant
  • American College of Sports Medicine (ACSM)
  • "Exericse and Vascular Function in Chronic Kidney Disease"
  • Period: 2012-2013
  • Role: PI
  • Direct Costs: $5,000

Recent Publications

Kuczmarski, JM, Martens, CR, Kim, J, Lennon-Edwards, S, Edwards, DG. Cardiac function is preserved following 4 Weeks of voluntary wheel running in a rodent model of chronic kidney disease. J. Appl. Physiol. 2014. 117(5):482-91.

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Abstract: The purpose of this investigation was to determine the effect of 4 wk of voluntary wheel running on cardiac performance in the 5/6 ablation-infarction (AI) rat model of chronic kidney disease (CKD). We hypothesized that voluntary wheel running would be effective in preserving cardiac function in AI. Male Sprague-Dawley rats were divided into three study groups: 1) sham, sedentary nondiseased control; 2) AI-SED, sedentary AI; and 3) AI-WR, wheel-running AI. Animals were maintained over a total period of 8 wk following AI and sham surgery. The 8-wk period included 4 wk of disease development followed by a 4-wk voluntary wheel-running intervention/sedentary control period. Cardiac performance was assessed using an isolated working heart preparation. Left ventricular (LV) tissue was used for biochemical tissue analysis. In addition, soleus muscle citrate synthase activity was measured. AI-WR rats performed a low volume of exercise, running an average of 13 ± 2 km, which resulted in citrate synthase activity not different from that in sham animals. Isolated AI-SED hearts demonstrated impaired cardiac performance at baseline and in response to preload/afterload manipulations. Conversely, cardiac function was preserved in AI-WR vs. sham hearts. LV nitrite + nitrate and expression of LV nitric oxide (NO) synthase isoforms 2 and 3 in AI-WR were not different from those of sham rats. In addition, LV H2O2 in AI-WR was similar to that of sham and associated with increased expression of LV superoxide-dismutase-2 and glutathione peroxidase-1/2. The findings of the current study suggest that a low-volume exercise intervention is sufficient to maintain cardiac performance in rats with CKD, potentially through a mechanism related to improved redox homeostasis and increased NO.

Martens, CR, Kuczmarski, JM, Kim, J, Guers, JJ, Harris, MB, Lennon-Edwards, S, Edwards, DG. Voluntary wheel running augments aortic L-arginine transport and endothelial function in rats with chronic kidney disease. Am. J. Physiol Renal Physiol. 2014. 307(4):F418-26.

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Abstract: Reduced nitric oxide (NO) synthesis contributes to risk for cardiovascular disease in chronic kidney disease (CKD). Vascular uptake of the NO precursor L-arginine (ARG) is attenuated in rodents with CKD, resulting in reduced substrate availability for NO synthesis and impaired vascular function. We tested the effect of 4 wk of voluntary wheel running (RUN) and/or ARG supplementation on endothelium-dependent relaxation (EDR) in rats with CKD. Twelve-week-old male Sprague-Dawley rats underwent 5/6 ablation infarction surgery to induce CKD, or SHAM surgery as a control. Beginning 4 wk following surgery, CKD animals either remained sedentary (SED) or received one of the following interventions: supplemental ARG, RUN, or combined RUN+ARG. Animals were euthanized 8 wk after surgery, and EDR was assessed. EDR was significantly impaired in SED vs. SHAM animals after 8 wk, in response to ACh (10-9-10-5 M) as indicated by a reduced area under the curve (AUC; 44.56 ± 9.01 vs 100 ± 4.58, P < 0.05) and reduced maximal response (Emax; 59.9 ± 9.67 vs. 94.31 ± 1.27%, P < 0.05). AUC was not improved by ARG treatment but was significantly improved above SED animals in both RUN and RUN+ARG-treated animals. Maximal relaxation was elevated above SED in RUN+ARG animals only. L-[3H]arginine uptake was impaired in both SED and ARG animals and was improved in RUN and RUN+ARG animals. The results suggest that voluntary wheel running is an effective therapy to improve vascular function in CKD and may be more beneficial when combined with L-arginine.

Kuczmarski, JM, Martens, CR, Lennon-Edwards, S, Edwards, DG. Cardiac Function and Tolerance to Ischemia-Reperfusion Injury in Chronic Kidney Disease. Neph. Dial. Transplant. 2014. 29(8):1514-24.

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Abstract: BACKGROUND: Cardiac dysfunction is an independent risk factor of ischemic heart disease and mortality in chronic kidney disease (CKD) patients, yet the relationship between impaired cardiac function and tolerance to ischemia-reperfusion (IR) injury in experimental CKD remains unclear. METHODS:Cardiac function was assessed in 5/6 ablation-infarction (AI) and sham male Sprague-Dawley rats at 20 weeks of age, 8 weeks post-surgery using an isolated working heart system. This included measures taken during manipulation of preload and afterload to produce left ventricular (LV) function curves as well as during reperfusion following a 15-min ischemic bout. In addition, LV tissue was used for biochemical tissue analysis. RESULTS: Cardiac function was impaired in AI animals during preload and afterload manipulations. Cardiac functional impairments persisted post-ischemia in the AI animals, and 36% of AI animals did not recover sufficiently to achieve aortic overflow following ischemia (versus 0% of sham animals). However, for those animals able to withstand the ischemic perturbation, no difference was observed in percent recovery of post-ischemic cardiac function between groups. Urinary NOx (nitrite + nitrate) excretion was lower in AI animals and accompanied by reduced LV endothelial nitric oxide synthase and NOx. LV antioxidants superoxide dismutase-1 and -2 were reduced in AI animals, whereas glutathione peroxidase-1/2 as well as NADPH-oxidase-4 and H2O2 were increased in these animals. CONCLUSIONS: Impaired cardiac function appears to predispose AI rats to poor outcomes following short-duration ischemic insult. These findings could be, in part, mediated by increased oxidative stress via nitric oxide-dependent and -independent mechanisms.

Martens, CR, Kuczmarski, JM, Lennon-Edwards, S, Edwards, DG. Impaired L-arginine uptake but not arginase contributes to endothelial dysfunction in rats with chronic kidney disease. J. Cardiovasc Pharmacol. 2014. 61(1):40-8.

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Abstract: Reduced nitric oxide bioavailability contributes to increased cardiovascular disease risk in patients with chronic kidney disease (CKD). Arginase has been implicated as a potential therapeutic target to treat vascular dysfunction by improving substrate availability for endothelial nitric oxide synthase. The purpose of this study was to determine if arginase contributes to endothelial dysfunction in the 5/6 ablation infarction (AI) rat model of CKD. Endothelium-dependent relaxation of aortic rings to acetylcholine was significantly impaired in AI animals versus sham after 8 weeks and was not improved by arginase inhibition (S-(2-Boronoethyl)-L-cysteine hydrochloride) alone or in combination with L-arginine. Additionally, scavenging of superoxide (Tempol, Tempol + L-arginine, Tempol + L-arginine + S-(2-Boronoethyl)-L-cysteine hydrochloride) was not effective, suggesting that a mechanism independent of oxidative stress contributes to endothelium-dependent relaxation in moderate to severe CKD. Aortic uptake of radiolabeled L-arginine was attenuated in AI animals and was associated with a reduced expression of the L-arginine transporter CAT-1. These data suggest that arginase does not contribute to endothelial dysfunction in CKD; however, impaired L-arginine transport may play an important role in diminishing substrate availability for nitric oxide production leading to endothelial dysfunction.

Martens, CR, Edwards, DG. Peripheral Vascular Function in Chronic Kidney Disease. Cardiology Research & Practice. 2011 2011, 2011:267257.

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Abstract: There is an increased prevalence of cardiovascular disease- (CVD-) related mortality in patients with chronic kidney disease (CKD). Endothelial dysfunction is a primary event in the development of atherosclerosis and hypertension and likely contributes to the elevated cardiovascular risk in CKD. Endothelial dysfunction has been shown to occur in the peripheral vasculature of patients with both severe and moderate CKD. Mechanisms include oxidative stress, L-arginine deficiency, and elevated plasma levels of ADMA. Interventions designed to restore vascular function in patients with CKD have shown mixed results. Evidence from cell culture studies suggest that the accumulation of uremic toxins inhibits L-arginine transport and reduces nitric oxide production. The results of these studies suggest that endothelial dysfunction may become less reversible with advancing kidney disease. The purpose of this paper is to present the current literature pertaining to potential mechanisms of peripheral vascular dysfunction in chronic kidney disease and to identify possible targets for treatment.